PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
6312894-3	1983	For small molecules, such as cysteine, N-acetylcysteine, glutathione, and 2-mercaptoethanol, the spectrum is that of a freely rotating nitroxide while for the proteins, bovine serum albumin and myosin, the spectrum is characteristic of a strongly immobilized nitroxide spin label rigidly attached to the protein.	Acetylcysteine	39-55	albumin	Homo sapiens	176-189
2546864-3	1989	N-acetylcysteine is a powerful scavenger of hypochlorous acid (H--OCl); low concentrations are able to protect alpha 1-antiproteinase against inactivation by HOCl.	Acetylcysteine	0-16	serpin family A member 1	Homo sapiens	111-133
3029208-10	1986	Mean values of O(2)-generation induced by A23187 or by FMLP were significantly reduced for cells harvested after NAC-treatment.	Acetylcysteine	113-116	formyl peptide receptor 1	Homo sapiens	55-59
6725286-2	1984	A fully translated actin biosynthetic intermediate containing N-acetylcysteine at the NH2 terminus has been identified in homogenates of differentiated mouse BC3H1 cerebrovascular smooth muscle cells labeled with L-[35S]cysteine.	Acetylcysteine	62-78	Actin 79B	Drosophila melanogaster	19-24
6743275-10	1984	Oct-1-yn-3-one reacted non-enzymically with N-acetylcysteine at pH 7.4 and 37 degrees C with a t1/2 of about 6 s also to yield S-3-oxo-oct-l-enyl-N-acetylcysteine.	Acetylcysteine	44-60	solute carrier family 22 member 1	Homo sapiens	0-5
2556468-5	1989	N-Acetylcysteine inhibited quinone-stimulated cytochrome C reduction at high concentrations.	Acetylcysteine	0-16	cytochrome c, somatic	Homo sapiens	46-58
2852604-6	1988	In serum/plasma, the concentrations of myeloperoxidase (MPO) and elastase were reduced after NAC treatment whereas concentrations of other constituents examined were unaltered.	Acetylcysteine	93-96	myeloperoxidase	Homo sapiens	39-54
2852604-6	1988	In serum/plasma, the concentrations of myeloperoxidase (MPO) and elastase were reduced after NAC treatment whereas concentrations of other constituents examined were unaltered.	Acetylcysteine	93-96	myeloperoxidase	Homo sapiens	56-59
2833080-0	1987	Prevention of tissue damage: inhibition of myeloperoxidase mediated inactivation of alpha 1-proteinase inhibitor by N-acetyl cysteine, glutathione, and methionine.	Acetylcysteine	116-133	myeloperoxidase	Homo sapiens	43-58
2833080-1	1987	The ability of the sulphur compounds, N-acetyl cysteine, Methionine, and Glutathione to prevent inactivation of alpha 1-proteinase inhibitor by Myeloperoxidase-H2O2-Cl--system was investigated in vitro with purified components.	Acetylcysteine	38-55	myeloperoxidase	Homo sapiens	144-159
3827591-0	1986	Identification and quantitative determination of mercapturic acids formed from Z- and E-1,3-dichloropropene by the rat, using gas chromatography with three different detection techniques.	Acetylcysteine	49-66	carboxylesterase 1C	Rattus norvegicus	79-89
3827591-1	1986	Z- and E-1,3-dichloropropene, mutagenic geometric isomers and major constituents of commercial soil fumigants, were found to be metabolized to mercapturic acid derivatives by the rat.	Acetylcysteine	143-159	carboxylesterase 1C	Rattus norvegicus	0-10
33724537-10	2021	NAC treatment significantly increased the antioxidant state, testicular function beside structural germ cell and seminiferous tubules histology accompanied by upsurge of steroidogenic mRNA expressions (P450scc and 3beta-HSD) and downregulated the pro-inflammatory cytokines mRNA expression (TNF-alpha, IL-1beta).	Acetylcysteine	0-3	tumor necrosis factor	Rattus norvegicus	291-300
7387676-0	1980	Protection by N-acetylcysteine of cyclophosphamide metabolism - related in vivo depression of mixed function oxygenase activity and in vitro denaturation of cytochrome P-450.	Acetylcysteine	14-30	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	157-173
33900847-10	2021	Pre-treatment with the antioxidant N-acetyl-L-cysteine could ameliorate HUA-activated JNK and hepatic steatosis.	Acetylcysteine	35-54	mitogen-activated protein kinase 8	Homo sapiens	86-89
6821192-5	1982	Bovine serum albumin was shown to act as a carrier in place of N-acetyl-cysteine.	Acetylcysteine	63-80	albumin	Homo sapiens	7-20
33724537-10	2021	NAC treatment significantly increased the antioxidant state, testicular function beside structural germ cell and seminiferous tubules histology accompanied by upsurge of steroidogenic mRNA expressions (P450scc and 3beta-HSD) and downregulated the pro-inflammatory cytokines mRNA expression (TNF-alpha, IL-1beta).	Acetylcysteine	0-3	interleukin 1 alpha	Rattus norvegicus	302-310
33503268-12	2021	NAC supplementation to the MTA extract significantly reduced the level of IL-6 and TNF-alpha expression (P<0.05).	Acetylcysteine	0-3	interleukin 6	Homo sapiens	74-78
33404763-12	2021	Ten-minute NAC treatment downregulated the IL-6 and TNF-alpha expression, whereas the expression of Bcl-2/Bax and Mfn-2/Drp-1 ratios was upregulated at 6 h. CONCLUSIONS: Under the LPS-induced inflammatory condition, NAC stimulated APC survival and decreased inflammation.	Acetylcysteine	11-14	interleukin 6	Homo sapiens	43-47
33404763-12	2021	Ten-minute NAC treatment downregulated the IL-6 and TNF-alpha expression, whereas the expression of Bcl-2/Bax and Mfn-2/Drp-1 ratios was upregulated at 6 h. CONCLUSIONS: Under the LPS-induced inflammatory condition, NAC stimulated APC survival and decreased inflammation.	Acetylcysteine	11-14	tumor necrosis factor	Homo sapiens	52-61
33404763-12	2021	Ten-minute NAC treatment downregulated the IL-6 and TNF-alpha expression, whereas the expression of Bcl-2/Bax and Mfn-2/Drp-1 ratios was upregulated at 6 h. CONCLUSIONS: Under the LPS-induced inflammatory condition, NAC stimulated APC survival and decreased inflammation.	Acetylcysteine	216-219	BCL2 apoptosis regulator	Homo sapiens	100-105
33503268-12	2021	NAC supplementation to the MTA extract significantly reduced the level of IL-6 and TNF-alpha expression (P<0.05).	Acetylcysteine	0-3	tumor necrosis factor	Homo sapiens	83-92
34052344-10	2021	Moreover, both NAC and Drp1 ameliorated tissue damage and inflammation, and decreased expression of p-Drp1 and Drp1 in mice with periodontitis.	Acetylcysteine	15-18	dynamin 1-like	Mus musculus	102-106
33610806-13	2021	Amo and NAC significantly reduced ROS production and increased Nrf2 expression.	Acetylcysteine	8-11	NFE2 like bZIP transcription factor 2	Homo sapiens	63-67
33781788-6	2021	Pre-treatment with N-acetylcysteine (NAC, a ROS scavenger) demonstrated that reactive oxygen species (ROS) mediated T-17-induced p53-independent apoptosis.	Acetylcysteine	19-35	tumor protein p53	Homo sapiens	129-132
33781788-6	2021	Pre-treatment with N-acetylcysteine (NAC, a ROS scavenger) demonstrated that reactive oxygen species (ROS) mediated T-17-induced p53-independent apoptosis.	Acetylcysteine	37-40	tumor protein p53	Homo sapiens	129-132
34052344-10	2021	Moreover, both NAC and Drp1 ameliorated tissue damage and inflammation, and decreased expression of p-Drp1 and Drp1 in mice with periodontitis.	Acetylcysteine	15-18	dynamin 1-like	Mus musculus	102-106
33470049-3	2021	The representative ITC-ARi 13 is an AR ligand that contains an N-acetyl cysteine-masked ITC moiety and gradually releases parental unconjugated ITC 12b in aqueous solution.	Acetylcysteine	63-80	androgen receptor	Homo sapiens	23-25
33966346-0	2021	Investigating binding tendency, stability of Sulforaphane-N-acetyl cysteine in the active site of histone deacetylase 2 (HDAC2) and testing its cytotoxicity against distinct cancer lines through stringent molecular dynamics, DFT and cell based assays.	Acetylcysteine	58-75	histone deacetylase 2	Homo sapiens	98-119
33966346-0	2021	Investigating binding tendency, stability of Sulforaphane-N-acetyl cysteine in the active site of histone deacetylase 2 (HDAC2) and testing its cytotoxicity against distinct cancer lines through stringent molecular dynamics, DFT and cell based assays.	Acetylcysteine	58-75	histone deacetylase 2	Homo sapiens	121-126
33978073-5	2021	RESULTS: Data showed a reduction in malondialdehyde (MDA), myeloperoxidase (MPO), and TNF-alpha in the animals pretreated with NAC or MEL when compared to those treated with SS+iIR (p<0.05).	Acetylcysteine	127-130	tumor necrosis factor	Rattus norvegicus	86-95
33978073-7	2021	TNF-alpha levels were lower in the MEL+iIR group (91+-5 pg/mL) than in the NAC+iIR group (101+-6 pg/mL).	Acetylcysteine	75-78	tumor necrosis factor	Rattus norvegicus	0-9
33247942-13	2021	In all NAC treatment groups, levels of serum IL-6, neuronal apoptosis and brain NFkB, nNOS, Caspase 3, TNF-alpha, IL-6 and IL-1beta protein levels were significantly reduced compared to NEC group.	Acetylcysteine	7-10	tumor necrosis factor	Rattus norvegicus	103-112
33247942-13	2021	In all NAC treatment groups, levels of serum IL-6, neuronal apoptosis and brain NFkB, nNOS, Caspase 3, TNF-alpha, IL-6 and IL-1beta protein levels were significantly reduced compared to NEC group.	Acetylcysteine	7-10	interleukin 1 alpha	Rattus norvegicus	123-131
33994712-12	2021	In the NAC group, there was significant reduction in Aspartate transaminase (AST) and Alanine transaminase (ALT) levels from day 1 to day 3 (p = 0.000) compared with the non-NAC group, with no significant change in bilirubin or international normalized ratio levels.	Acetylcysteine	7-10	solute carrier family 17 member 5	Homo sapiens	53-75
33994712-12	2021	In the NAC group, there was significant reduction in Aspartate transaminase (AST) and Alanine transaminase (ALT) levels from day 1 to day 3 (p = 0.000) compared with the non-NAC group, with no significant change in bilirubin or international normalized ratio levels.	Acetylcysteine	7-10	solute carrier family 17 member 5	Homo sapiens	77-80
33760170-10	2021	Pretreatment with 5 mM N-Acetyl-L-cysteine or 10 microM pyrrolidine dithiocarbamate effectively reduced cellular damage and inhibited activation of the NF-kappaB/RAGE signaling pathway.	Acetylcysteine	23-42	advanced glycosylation end product-specific receptor	Rattus norvegicus	162-166
33858491-12	2021	NAC treatment significantly reduced oxidative stress level and expression of alpha-SMA, collagen type I in PSCs, which apparently present a quiescent-like state with a high number of lipid droplets.	Acetylcysteine	0-3	actin alpha 2, smooth muscle, aorta	Mus musculus	77-86
33411248-6	2021	Intake of N-acetylcysteine, coenzyme Q10 and melatonin is accompanied by increased Nrf2 activity.	Acetylcysteine	10-26	NFE2 like bZIP transcription factor 2	Homo sapiens	83-87
33744595-14	2021	NAC (N-acetylcysteine), a reducer reversed valtrate-induced the depletion of Stat3, p-Stat3, c-Myc, and Cyclin B1.	Acetylcysteine	0-3	signal transducer and activator of transcription 3	Homo sapiens	77-82
33744595-14	2021	NAC (N-acetylcysteine), a reducer reversed valtrate-induced the depletion of Stat3, p-Stat3, c-Myc, and Cyclin B1.	Acetylcysteine	0-3	signal transducer and activator of transcription 3	Homo sapiens	86-91
33744595-14	2021	NAC (N-acetylcysteine), a reducer reversed valtrate-induced the depletion of Stat3, p-Stat3, c-Myc, and Cyclin B1.	Acetylcysteine	5-21	signal transducer and activator of transcription 3	Homo sapiens	77-82
33946939-6	2021	The benefit of NAC was related to the modulation of signaling proteins in the AMPK-SIRT3-SOD2 axis.	Acetylcysteine	15-18	sirtuin 3	Homo sapiens	83-88
33959604-9	2021	In addition, the activation of ER stress and the JNK signaling pathway prompted by IATL and cisplatin was also reversed by NAC pretreatment.	Acetylcysteine	123-126	mitogen-activated protein kinase 8	Homo sapiens	49-52
33744595-14	2021	NAC (N-acetylcysteine), a reducer reversed valtrate-induced the depletion of Stat3, p-Stat3, c-Myc, and Cyclin B1.	Acetylcysteine	5-21	signal transducer and activator of transcription 3	Homo sapiens	86-91
33925826-7	2021	In addition, administration of antioxidants N-acetylcysteine (NAC) and GSH induced delays per se at CT14 but did not affect light-induced advances at CT18.	Acetylcysteine	44-60	sarcoma antigen 1	Homo sapiens	100-104
33925826-7	2021	In addition, administration of antioxidants N-acetylcysteine (NAC) and GSH induced delays per se at CT14 but did not affect light-induced advances at CT18.	Acetylcysteine	62-65	sarcoma antigen 1	Homo sapiens	100-104
33882750-8	2021	Treated rats with N-acetylcysteine (N-AC) and granulocyte colony stimulating factor (G-CSF) showed a decrease in serum levels of ALT, AST and LDH, while the level of ALP in the G-CSF group was still high.	Acetylcysteine	18-34	glutamic-oxaloacetic transaminase 2	Rattus norvegicus	134-137
33882750-8	2021	Treated rats with N-acetylcysteine (N-AC) and granulocyte colony stimulating factor (G-CSF) showed a decrease in serum levels of ALT, AST and LDH, while the level of ALP in the G-CSF group was still high.	Acetylcysteine	36-40	glutamic-oxaloacetic transaminase 2	Rattus norvegicus	134-137
33882750-9	2021	After administration of APAP, treatment with N-AC or G-CSF substantially reduced the level of MDA and NO while maintaining the GSH content and CAT activity.	Acetylcysteine	45-49	catalase	Rattus norvegicus	143-146
33739173-9	2021	NAC treatment significantly decreased serum ALT and AST levels and proinflammatory cytokines in the diabetic group.	Acetylcysteine	0-3	glutamic-oxaloacetic transaminase 2	Rattus norvegicus	52-55
33825597-8	2021	However, Pifithrin-alpha (p53 inhibitor) and N-Acetylcysteine (NAC) could reduce cell apoptosis, lung structural damage and oxidative stress, accelerate the expression of Bcl-2, while suppressing the expression of Bax, total caspase-3 and cleaved caspase-3.	Acetylcysteine	45-61	B cell leukemia/lymphoma 2	Mus musculus	171-176
33825597-8	2021	However, Pifithrin-alpha (p53 inhibitor) and N-Acetylcysteine (NAC) could reduce cell apoptosis, lung structural damage and oxidative stress, accelerate the expression of Bcl-2, while suppressing the expression of Bax, total caspase-3 and cleaved caspase-3.	Acetylcysteine	63-66	B cell leukemia/lymphoma 2	Mus musculus	171-176
33880372-6	2021	Compared with 200 mumol/L PFOS treatment, NAC pretreatment reversed the increase in ROS, Bax, and cleaved-caspase-3 protein caused by PFOS, lowered the apoptosis rate increased by PFOS, and increased the levels of MMP and Bcl-2/Bax ratio decreased by PFOS.	Acetylcysteine	42-45	BCL2 associated X, apoptosis regulator	Homo sapiens	89-92
33880372-6	2021	Compared with 200 mumol/L PFOS treatment, NAC pretreatment reversed the increase in ROS, Bax, and cleaved-caspase-3 protein caused by PFOS, lowered the apoptosis rate increased by PFOS, and increased the levels of MMP and Bcl-2/Bax ratio decreased by PFOS.	Acetylcysteine	42-45	BCL2 apoptosis regulator	Homo sapiens	222-227
33880372-6	2021	Compared with 200 mumol/L PFOS treatment, NAC pretreatment reversed the increase in ROS, Bax, and cleaved-caspase-3 protein caused by PFOS, lowered the apoptosis rate increased by PFOS, and increased the levels of MMP and Bcl-2/Bax ratio decreased by PFOS.	Acetylcysteine	42-45	BCL2 associated X, apoptosis regulator	Homo sapiens	228-231
32779379-8	2021	Incubation of hNECs with N-acetyl-L-cysteine (NAC) significantly attenuated BC +- pollen-induced expression of ROS, NLRP3, and IL-1beta.	Acetylcysteine	25-44	NLR family pyrin domain containing 3	Homo sapiens	116-121
32779379-8	2021	Incubation of hNECs with N-acetyl-L-cysteine (NAC) significantly attenuated BC +- pollen-induced expression of ROS, NLRP3, and IL-1beta.	Acetylcysteine	46-49	NLR family pyrin domain containing 3	Homo sapiens	116-121
33453249-7	2021	Podocytes treatment with NAC reversed Nox4, Col4a1, Acta2, and Tgfb1 increased expression but did not abrogate the reduced expression of nephrin.	Acetylcysteine	25-28	collagen type IV alpha 1 chain	Rattus norvegicus	44-50
33453249-7	2021	Podocytes treatment with NAC reversed Nox4, Col4a1, Acta2, and Tgfb1 increased expression but did not abrogate the reduced expression of nephrin.	Acetylcysteine	25-28	transforming growth factor, beta 1	Rattus norvegicus	63-68
33912174-10	2021	Notably, antioxidant N-acetylcysteine treatment influenced the microbial composition (decreased Rikenellaceae; increased Akkeransiaceae, Erysipelotrichaceae and Muribaculaceae) and attenuated the systemic autoimmunity in MRL/lpr mice.	Acetylcysteine	21-37	Fas (TNF receptor superfamily member 6)	Mus musculus	225-228
33551189-10	2021	After adding 3mM N-Acetylcysteine to HGK cultures, increased fluorescence intensity and protein amounts of Involucrin and Filaggrin indicated enhanced differentiation (p<0.05).	Acetylcysteine	17-33	mitogen-activated protein kinase kinase kinase kinase 4	Homo sapiens	37-40
33551189-10	2021	After adding 3mM N-Acetylcysteine to HGK cultures, increased fluorescence intensity and protein amounts of Involucrin and Filaggrin indicated enhanced differentiation (p<0.05).	Acetylcysteine	17-33	involucrin	Homo sapiens	107-117
33740178-6	2022	NAC treatments significantly improved TAC and IL-10, but decreased MDA and TNF-alpha values in rats that were exposed to a single and continuous dose of Cd (p < 0.05).	Acetylcysteine	0-3	tumor necrosis factor	Rattus norvegicus	75-84
33740178-9	2022	NAC treatments significantly decreased the expression of c-myc, and Ask-1 in rats exposed to single or continuous Cd.	Acetylcysteine	0-3	mitogen-activated protein kinase kinase kinase 5	Rattus norvegicus	68-73
33720480-8	2021	Additionally, NAC"s effect is not apparent on SiO2 -mediated autophagy through the PI3K/Akt/mTOR signaling pathway, but it can reduce the inflammatory response on NR8383 cells mediated by SiO2-exposed.	Acetylcysteine	14-17	AKT serine/threonine kinase 1	Rattus norvegicus	88-91
33726556-8	2022	NAC and salubrinal inhibited an increase in VEGF-A, CHOP and caspase-3 caused by ATRA in ARPE-19 cells.	Acetylcysteine	0-3	vascular endothelial growth factor A	Homo sapiens	44-50
33726556-8	2022	NAC and salubrinal inhibited an increase in VEGF-A, CHOP and caspase-3 caused by ATRA in ARPE-19 cells.	Acetylcysteine	0-3	DNA damage inducible transcript 3	Homo sapiens	52-56
33726556-8	2022	NAC and salubrinal inhibited an increase in VEGF-A, CHOP and caspase-3 caused by ATRA in ARPE-19 cells.	Acetylcysteine	0-3	caspase 3	Homo sapiens	61-70
33720480-10	2021	Taken together, our data demonstrated that SiO2 -exposed can induce pulmonary fibrosis along with autophagy both in vivo and in vitro, NAC could alleviate the inflammatory response NR8383 cells by SiO2 -exposed through non PI3K/Akt/mTOR signaling pathway, and the specific mechanism of its action needs further studying.	Acetylcysteine	135-138	AKT serine/threonine kinase 1	Rattus norvegicus	228-231
33712558-9	2021	As shown in our study, although ROS play a role in upregulating NOXA mRNA transcription, ROS scavenging in CRC cells by N-acetyl-L-cysteine (NAC) can significantly reduce CUL5 neddylation and extend the NOXA protein half-life.	Acetylcysteine	120-139	phorbol-12-myristate-13-acetate-induced protein 1	Homo sapiens	64-68
33712045-12	2021	After IR exposure, IGFBP3-induced NF-kappaB activation was inhibited by the ROS scavenger N-acetyl-L-cysteine (NAC).	Acetylcysteine	90-109	nuclear factor kappa B subunit 1	Homo sapiens	34-43
33712045-12	2021	After IR exposure, IGFBP3-induced NF-kappaB activation was inhibited by the ROS scavenger N-acetyl-L-cysteine (NAC).	Acetylcysteine	111-114	nuclear factor kappa B subunit 1	Homo sapiens	34-43
33712558-9	2021	As shown in our study, although ROS play a role in upregulating NOXA mRNA transcription, ROS scavenging in CRC cells by N-acetyl-L-cysteine (NAC) can significantly reduce CUL5 neddylation and extend the NOXA protein half-life.	Acetylcysteine	120-139	phorbol-12-myristate-13-acetate-induced protein 1	Homo sapiens	203-207
33712558-9	2021	As shown in our study, although ROS play a role in upregulating NOXA mRNA transcription, ROS scavenging in CRC cells by N-acetyl-L-cysteine (NAC) can significantly reduce CUL5 neddylation and extend the NOXA protein half-life.	Acetylcysteine	141-144	phorbol-12-myristate-13-acetate-induced protein 1	Homo sapiens	64-68
33712558-9	2021	As shown in our study, although ROS play a role in upregulating NOXA mRNA transcription, ROS scavenging in CRC cells by N-acetyl-L-cysteine (NAC) can significantly reduce CUL5 neddylation and extend the NOXA protein half-life.	Acetylcysteine	141-144	phorbol-12-myristate-13-acetate-induced protein 1	Homo sapiens	203-207
33663554-9	2021	NAC improved HTM cell viability, inhibited the activation of the NLRP3 inflammasome axis, and HTM cell contraction by scavenging ROS.	Acetylcysteine	0-3	NLR family pyrin domain containing 3	Homo sapiens	65-70
33748286-3	2021	By using antioxidants N-acetylcysteine and catalase, we found that ERK pathway was activated by a reactive oxygen species- (ROS-) dependent mechanism after exposure to urinary proteins.	Acetylcysteine	22-38	mitogen-activated protein kinase 1	Homo sapiens	67-70
33783984-0	2021	Glycine and N-acetylcysteine (GlyNAC) supplementation in older adults improves glutathione deficiency, oxidative stress, mitochondrial dysfunction, inflammation, insulin resistance, endothelial dysfunction, genotoxicity, muscle strength, and cognition: Results of a pilot clinical trial.	Acetylcysteine	12-28	insulin	Homo sapiens	162-169
33495825-6	2021	Endothelial damage was also corrected by NAC, as indicated by an increase in the expression levels of phosphorylated (p-)Akt and p-endothelial nitric oxide synthase (eNOS) in the aorta, as well as nitric oxide (NO) in the serum.	Acetylcysteine	41-44	thymoma viral proto-oncogene 1	Mus musculus	121-124
33398364-6	2021	Furthermore, N-acetyl-L-cysteine, a reactive oxygen species scavenger, inhibited NO production and HO-1 mRNA expression levels through the nuclear factor erythroid 2-related factor 2 pathway.	Acetylcysteine	13-32	heme oxygenase 1	Mus musculus	99-103
33398364-6	2021	Furthermore, N-acetyl-L-cysteine, a reactive oxygen species scavenger, inhibited NO production and HO-1 mRNA expression levels through the nuclear factor erythroid 2-related factor 2 pathway.	Acetylcysteine	13-32	nuclear factor, erythroid derived 2, like 2	Mus musculus	139-182
33398366-10	2021	However, the effects of TRIM28 overexpression were limited by the action of ROS inhibitor N-acetyl-L-cysteine.	Acetylcysteine	90-109	tripartite motif containing 28	Homo sapiens	24-30
33495825-10	2021	Furthermore, NAC may offer protection against atherosclerotic development in DM by altering aortic and systemic responses via correcting GSH-dependent MG elimination, leading to decreased oxidative stress and restoration of the p-Akt/p-eNOS pathway in the aorta.	Acetylcysteine	13-16	thymoma viral proto-oncogene 1	Mus musculus	230-233
33164240-6	2021	Downregulation of EXT-induced p-STAT3-Y705 was rescued by pretreating DU145 cells with antioxidants, such as N-acetyl-L-cysteine (NAC), indicating that reactive oxygen species (ROS) were involved in the EXT-induced inhibition of STAT3 activation.	Acetylcysteine	109-128	signal transducer and activator of transcription 3	Homo sapiens	32-37
33164240-6	2021	Downregulation of EXT-induced p-STAT3-Y705 was rescued by pretreating DU145 cells with antioxidants, such as N-acetyl-L-cysteine (NAC), indicating that reactive oxygen species (ROS) were involved in the EXT-induced inhibition of STAT3 activation.	Acetylcysteine	109-128	signal transducer and activator of transcription 3	Homo sapiens	229-234
33164240-6	2021	Downregulation of EXT-induced p-STAT3-Y705 was rescued by pretreating DU145 cells with antioxidants, such as N-acetyl-L-cysteine (NAC), indicating that reactive oxygen species (ROS) were involved in the EXT-induced inhibition of STAT3 activation.	Acetylcysteine	130-133	signal transducer and activator of transcription 3	Homo sapiens	229-234
33456508-6	2021	Furthermore, 4-OI and the antioxidant N-acetyl-L-cysteine markedly suppressed PI3K and Akt phosphorylation in LPS-treated RAW264.7 macrophage cells in vitro.	Acetylcysteine	38-57	thymoma viral proto-oncogene 1	Mus musculus	87-90
33632046-8	2021	The antioxidant N-acetyl cysteine (NAC) also showed similar effects on JNK and NF-kappaB-P65 phosphorylation and inflammatory cytokines (p < .00).	Acetylcysteine	16-33	mitogen-activated protein kinase 8	Homo sapiens	71-74
33632046-8	2021	The antioxidant N-acetyl cysteine (NAC) also showed similar effects on JNK and NF-kappaB-P65 phosphorylation and inflammatory cytokines (p < .00).	Acetylcysteine	35-38	mitogen-activated protein kinase 8	Homo sapiens	71-74
33672594-8	2021	The antioxidant N-acetylcysteine and NADPH oxidase 1 inhibitor ML171 suppressed the EtOH/POA-induced increases in ROS production, NF-kappaB activation, zymogen activation, and IL-6 expression.	Acetylcysteine	16-32	interleukin 6	Rattus norvegicus	176-180
33554313-6	2021	We found that the inhibitory effect of PP on cell proliferation and AKT protein expression induced by PP could be partially reversed by N-acetyl-L-cysteine (NAC), an ROS scavenger.	Acetylcysteine	136-155	AKT serine/threonine kinase 1	Homo sapiens	68-71
33554313-6	2021	We found that the inhibitory effect of PP on cell proliferation and AKT protein expression induced by PP could be partially reversed by N-acetyl-L-cysteine (NAC), an ROS scavenger.	Acetylcysteine	157-160	AKT serine/threonine kinase 1	Homo sapiens	68-71
33030807-9	2021	The pretreatment of N-acetyl-L-cysteine (NAC) blocked the apoptosis induced by Quina and inhibited the activities of MAPK, STAT3, and NF-kappaB signaling pathways.	Acetylcysteine	20-39	signal transducer and activator of transcription 3	Homo sapiens	123-128
33030807-9	2021	The pretreatment of N-acetyl-L-cysteine (NAC) blocked the apoptosis induced by Quina and inhibited the activities of MAPK, STAT3, and NF-kappaB signaling pathways.	Acetylcysteine	20-39	nuclear factor kappa B subunit 1	Homo sapiens	134-143
33030807-9	2021	The pretreatment of N-acetyl-L-cysteine (NAC) blocked the apoptosis induced by Quina and inhibited the activities of MAPK, STAT3, and NF-kappaB signaling pathways.	Acetylcysteine	41-44	signal transducer and activator of transcription 3	Homo sapiens	123-128
33030807-9	2021	The pretreatment of N-acetyl-L-cysteine (NAC) blocked the apoptosis induced by Quina and inhibited the activities of MAPK, STAT3, and NF-kappaB signaling pathways.	Acetylcysteine	41-44	nuclear factor kappa B subunit 1	Homo sapiens	134-143
33630121-9	2021	While induction of CIN did not affect the renal levels of catalase, glutathione peroxidase (GPx), and thiobarbituric acid reactive substances, pretreatment of animals with CoQ10/NAC showed significant increase in GPx and catalase levels versus controls.	Acetylcysteine	178-181	catalase	Rattus norvegicus	221-229
33545736-10	2021	N-Acetyl cysteine (NAC), a ROS scavenger, markedly abolished H2O2-stimulated PI3K/Akt/GSK3beta signaling, caspase-3 activation, and phosphatidylserine exposure.	Acetylcysteine	0-17	AKT serine/threonine kinase 1	Homo sapiens	82-85
33545736-10	2021	N-Acetyl cysteine (NAC), a ROS scavenger, markedly abolished H2O2-stimulated PI3K/Akt/GSK3beta signaling, caspase-3 activation, and phosphatidylserine exposure.	Acetylcysteine	0-17	caspase 3	Homo sapiens	106-115
33545736-10	2021	N-Acetyl cysteine (NAC), a ROS scavenger, markedly abolished H2O2-stimulated PI3K/Akt/GSK3beta signaling, caspase-3 activation, and phosphatidylserine exposure.	Acetylcysteine	19-22	AKT serine/threonine kinase 1	Homo sapiens	82-85
33545736-10	2021	N-Acetyl cysteine (NAC), a ROS scavenger, markedly abolished H2O2-stimulated PI3K/Akt/GSK3beta signaling, caspase-3 activation, and phosphatidylserine exposure.	Acetylcysteine	19-22	caspase 3	Homo sapiens	106-115
33633548-9	2020	Conclusion: Nicotine reinstatement, following post-deprivation of chronic oral nicotine intake, downregulates the mRNA levels of GLT-1 and xCT transporters, an effect reversed by the coadministration of N-acetylcysteine and acetylsalicylic acid, leading to a marked inhibition of nicotine intake.	Acetylcysteine	203-219	solute carrier family 1 member 2	Rattus norvegicus	129-134
32747719-7	2021	Interestingly, the degree of apoptosis and expression of ER stress-related proteins were alleviated in the presence of either N-acetyl cysteine (NAC), an ROS scavenger, or 2-aminoethyl diphenylborinate (2-APB), an IP3R-1 inhibitor, implicating ROS/calcium-dependent ER stress in LW-213-induced apoptosis.	Acetylcysteine	126-143	inositol 1,4,5-trisphosphate receptor type 1	Homo sapiens	214-220
32747719-7	2021	Interestingly, the degree of apoptosis and expression of ER stress-related proteins were alleviated in the presence of either N-acetyl cysteine (NAC), an ROS scavenger, or 2-aminoethyl diphenylborinate (2-APB), an IP3R-1 inhibitor, implicating ROS/calcium-dependent ER stress in LW-213-induced apoptosis.	Acetylcysteine	145-148	inositol 1,4,5-trisphosphate receptor type 1	Homo sapiens	214-220
33217539-10	2021	Furthermore, N-acetylcysteine (NAC) pretreatment reversed the ED-71-treatment outcomes, including increased apoptosis and autophagy and inhibition of the PI3K/Akt/mTOR pathway.	Acetylcysteine	13-29	AKT serine/threonine kinase 1	Homo sapiens	159-162
33217539-10	2021	Furthermore, N-acetylcysteine (NAC) pretreatment reversed the ED-71-treatment outcomes, including increased apoptosis and autophagy and inhibition of the PI3K/Akt/mTOR pathway.	Acetylcysteine	13-29	mechanistic target of rapamycin kinase	Homo sapiens	163-167
33217539-10	2021	Furthermore, N-acetylcysteine (NAC) pretreatment reversed the ED-71-treatment outcomes, including increased apoptosis and autophagy and inhibition of the PI3K/Akt/mTOR pathway.	Acetylcysteine	31-34	AKT serine/threonine kinase 1	Homo sapiens	159-162
33217539-10	2021	Furthermore, N-acetylcysteine (NAC) pretreatment reversed the ED-71-treatment outcomes, including increased apoptosis and autophagy and inhibition of the PI3K/Akt/mTOR pathway.	Acetylcysteine	31-34	mechanistic target of rapamycin kinase	Homo sapiens	163-167
33302164-9	2021	Low-dose NAC increased CCDN1 and decreased CASP3 and CASP8 mRNA levels (P < 0.05), whereas high-dose NAC decreased CDK4 and CCDN1 and increased CASP3 mRNA levels (P < 0.05).	Acetylcysteine	9-12	caspase 3	Homo sapiens	43-48
33302164-9	2021	Low-dose NAC increased CCDN1 and decreased CASP3 and CASP8 mRNA levels (P < 0.05), whereas high-dose NAC decreased CDK4 and CCDN1 and increased CASP3 mRNA levels (P < 0.05).	Acetylcysteine	101-104	caspase 3	Homo sapiens	144-149
33302164-11	2021	Low-dose NAC upregulated CYP19A1 mRNA expression, and high-dose NAC downregulated CYP11A1 mRNA abundance (P < 0.05).	Acetylcysteine	9-12	cytochrome P450 family 19 subfamily A member 1	Homo sapiens	25-32
33302164-11	2021	Low-dose NAC upregulated CYP19A1 mRNA expression, and high-dose NAC downregulated CYP11A1 mRNA abundance (P < 0.05).	Acetylcysteine	64-67	cytochrome P450 family 11 subfamily A member 1	Homo sapiens	82-89
33302164-12	2021	Only low-dose NAC increased NOS3 mRNA abundance and tetrahydrobiopterin reduction (BH4/BH2 ratio).	Acetylcysteine	14-17	nitric oxide synthase 3	Homo sapiens	28-32
33498402-3	2021	Recently, we showed that N-acetylcysteine (NAC) inhibits kynurenine aminotransferase II (KAT II), KYNA"s key biosynthetic enzyme, and reduces KYNA neosynthesis in rats in vivo.	Acetylcysteine	25-41	aminoadipate aminotransferase	Rattus norvegicus	57-87
33530504-0	2021	Activation of NRF2 and ATF4 Signaling by the Pro-Glutathione Molecule I-152, a Co-Drug of N-Acetyl-Cysteine and Cysteamine.	Acetylcysteine	90-107	NFE2 like bZIP transcription factor 2	Homo sapiens	14-18
33498402-3	2021	Recently, we showed that N-acetylcysteine (NAC) inhibits kynurenine aminotransferase II (KAT II), KYNA"s key biosynthetic enzyme, and reduces KYNA neosynthesis in rats in vivo.	Acetylcysteine	25-41	aminoadipate aminotransferase	Rattus norvegicus	89-95
33498402-3	2021	Recently, we showed that N-acetylcysteine (NAC) inhibits kynurenine aminotransferase II (KAT II), KYNA"s key biosynthetic enzyme, and reduces KYNA neosynthesis in rats in vivo.	Acetylcysteine	43-46	aminoadipate aminotransferase	Rattus norvegicus	57-87
33498402-3	2021	Recently, we showed that N-acetylcysteine (NAC) inhibits kynurenine aminotransferase II (KAT II), KYNA"s key biosynthetic enzyme, and reduces KYNA neosynthesis in rats in vivo.	Acetylcysteine	43-46	aminoadipate aminotransferase	Rattus norvegicus	89-95
33441976-6	2021	NAC numerically reduced diarrhea incidence (- 46.2%) and the concentrations of hydrogen peroxide and malondialdehyde, but increased claudin-1 and intestinal fatty-acid binding protein (iFABP) protein abundances and activities of catalase and glutathione peroxidase in the jejunum of beta-CG-challenged piglets.	Acetylcysteine	0-3	fatty acid binding protein 2	Homo sapiens	146-183
33441976-9	2021	Remarkably, NAC decreased Atg5 protein abundance and the LC3II/LC3I ratio (an indicator of autophagy) in the jejunum of beta-CG-challenged piglets.	Acetylcysteine	12-15	autophagy related 5	Homo sapiens	26-30
33454892-8	2021	We concluded that adding NAC to CdCl2 resulted in a decreased signaling of the NF-kappaB p65 signaling pathway.	Acetylcysteine	25-28	synaptotagmin 1	Rattus norvegicus	89-92
33183638-0	2021	Inclusion complex based on N-acetyl-L-cysteine and arginine modified hydroxypropyl-beta-cyclodextrin for oral insulin delivery.	Acetylcysteine	27-46	insulin	Homo sapiens	110-117
33183638-4	2021	In this study, a novel N-acetyl-L-cysteine and arginine modified hydroxypropyl-beta-cyclodextrin (NAC-HP-beta-CD-Arg) was successfully synthesized and characterized.	Acetylcysteine	23-42	ACD shelterin complex subunit and telomerase recruitment factor	Homo sapiens	105-112
33188856-7	2021	The genes (ApoE/TET1/TIMP2/TIMP3) suppressed by Cd were further suppressed by hydroquinone (HQ; a reactive oxygen species [ROS] producer), whereas N-acetyl-L-cysteine (NAC; a ROS scavenger) prevented the suppression of their expression by HQ.	Acetylcysteine	147-166	apolipoprotein E	Rattus norvegicus	11-15
33188856-7	2021	The genes (ApoE/TET1/TIMP2/TIMP3) suppressed by Cd were further suppressed by hydroquinone (HQ; a reactive oxygen species [ROS] producer), whereas N-acetyl-L-cysteine (NAC; a ROS scavenger) prevented the suppression of their expression by HQ.	Acetylcysteine	168-171	apolipoprotein E	Rattus norvegicus	11-15
33441976-6	2021	NAC numerically reduced diarrhea incidence (- 46.2%) and the concentrations of hydrogen peroxide and malondialdehyde, but increased claudin-1 and intestinal fatty-acid binding protein (iFABP) protein abundances and activities of catalase and glutathione peroxidase in the jejunum of beta-CG-challenged piglets.	Acetylcysteine	0-3	fatty acid binding protein 2	Homo sapiens	185-190
33441976-8	2021	Moreover, NAC increased the concentrations of citrulline and D-xylose in the plasma, as well as the expression of genes for aquaporin (AQP) 3, AQP4, peptide transporter 1 (PepT1), sodium/glucose co-transporter-1 (SGLT-1), potassium inwardly-rectifying channel, subfamily J, member 13 (KCNJ13), and solute carrier family 1 member 1 (SLC1A1) in the jejunum, demonstrating that NAC augmented intestinal metabolic activity and absorptive function.	Acetylcysteine	10-13	solute carrier family 15 member 1	Homo sapiens	149-170
33441976-8	2021	Moreover, NAC increased the concentrations of citrulline and D-xylose in the plasma, as well as the expression of genes for aquaporin (AQP) 3, AQP4, peptide transporter 1 (PepT1), sodium/glucose co-transporter-1 (SGLT-1), potassium inwardly-rectifying channel, subfamily J, member 13 (KCNJ13), and solute carrier family 1 member 1 (SLC1A1) in the jejunum, demonstrating that NAC augmented intestinal metabolic activity and absorptive function.	Acetylcysteine	10-13	solute carrier family 15 member 1	Homo sapiens	172-177
33441976-8	2021	Moreover, NAC increased the concentrations of citrulline and D-xylose in the plasma, as well as the expression of genes for aquaporin (AQP) 3, AQP4, peptide transporter 1 (PepT1), sodium/glucose co-transporter-1 (SGLT-1), potassium inwardly-rectifying channel, subfamily J, member 13 (KCNJ13), and solute carrier family 1 member 1 (SLC1A1) in the jejunum, demonstrating that NAC augmented intestinal metabolic activity and absorptive function.	Acetylcysteine	10-13	solute carrier family 5 member 1	Homo sapiens	180-211
33441976-8	2021	Moreover, NAC increased the concentrations of citrulline and D-xylose in the plasma, as well as the expression of genes for aquaporin (AQP) 3, AQP4, peptide transporter 1 (PepT1), sodium/glucose co-transporter-1 (SGLT-1), potassium inwardly-rectifying channel, subfamily J, member 13 (KCNJ13), and solute carrier family 1 member 1 (SLC1A1) in the jejunum, demonstrating that NAC augmented intestinal metabolic activity and absorptive function.	Acetylcysteine	10-13	solute carrier family 5 member 1	Homo sapiens	213-219
33441976-8	2021	Moreover, NAC increased the concentrations of citrulline and D-xylose in the plasma, as well as the expression of genes for aquaporin (AQP) 3, AQP4, peptide transporter 1 (PepT1), sodium/glucose co-transporter-1 (SGLT-1), potassium inwardly-rectifying channel, subfamily J, member 13 (KCNJ13), and solute carrier family 1 member 1 (SLC1A1) in the jejunum, demonstrating that NAC augmented intestinal metabolic activity and absorptive function.	Acetylcysteine	10-13	solute carrier family 1 member 1	Homo sapiens	298-330
33441976-8	2021	Moreover, NAC increased the concentrations of citrulline and D-xylose in the plasma, as well as the expression of genes for aquaporin (AQP) 3, AQP4, peptide transporter 1 (PepT1), sodium/glucose co-transporter-1 (SGLT-1), potassium inwardly-rectifying channel, subfamily J, member 13 (KCNJ13), and solute carrier family 1 member 1 (SLC1A1) in the jejunum, demonstrating that NAC augmented intestinal metabolic activity and absorptive function.	Acetylcysteine	10-13	solute carrier family 1 member 1	Homo sapiens	332-338
33496364-6	2021	However, an intra-peritoneal injection of the antioxidant N-acetyl-l-cysteine (NAC) and autophagy inhibitor chloroquine inhibited the inflammatory response, liver damage, and pexophagy in the liver of catalase-KO mice during prolonged fasting.	Acetylcysteine	58-77	catalase	Mus musculus	201-209
33345643-1	2021	Our previous studies have shown that intermittent exposure to a 50-Hz, 100-microT sine wave magnetic field (MF) promotes human NB69 cell proliferation, mediated by activation of the epidermal growth factor receptor (EGFR) and pathways MAPK-ERK1/2 and p38; being the effects on proliferation and p38 activation blocked by the chelator N-acetylcysteine.	Acetylcysteine	334-350	epidermal growth factor receptor	Homo sapiens	182-214
33378994-8	2021	Maternal obesity also activated cardiac Akt and mammalian target of rapamycin (mTOR) signalling in offspring, and NAC treatment restored offspring cardiac Akt-mTOR signalling to normal irrespective of sex.	Acetylcysteine	114-117	AKT serine/threonine kinase 1	Homo sapiens	155-158
33378994-8	2021	Maternal obesity also activated cardiac Akt and mammalian target of rapamycin (mTOR) signalling in offspring, and NAC treatment restored offspring cardiac Akt-mTOR signalling to normal irrespective of sex.	Acetylcysteine	114-117	mechanistic target of rapamycin kinase	Homo sapiens	159-163
33496364-6	2021	However, an intra-peritoneal injection of the antioxidant N-acetyl-l-cysteine (NAC) and autophagy inhibitor chloroquine inhibited the inflammatory response, liver damage, and pexophagy in the liver of catalase-KO mice during prolonged fasting.	Acetylcysteine	79-82	catalase	Mus musculus	201-209
33130472-15	2021	N-acetyl-L-cysteine (NAC) not only revered ROS generation triggered by LCA but also restored IFN-gamma-induced expression of PD-L1.	Acetylcysteine	0-19	interferon gamma	Homo sapiens	93-102
32864863-8	2021	Total p53 protein level increase was observed by 24 hours in HCT-116 upon NAC pre-treatment.	Acetylcysteine	74-77	tumor protein p53	Homo sapiens	6-9
33439409-15	2021	It was revealed by Western blotting analysis that NAC promoted Bcl-2 signaling and decreased p53 signaling.	Acetylcysteine	50-53	BCL2, apoptosis regulator	Rattus norvegicus	63-68
33303231-3	2021	The present investigation presents evidence regarding the role of HEMA-induced oxidative stress in the secretion of the pro-inflammatory cytokine TNFalpha from cells exposed to the antigens LTA (lipoteichoic acid) or LPS (lipopolysaccharide) of cariogenic microorganisms using BSO (L-buthionine sulfoximine) or NAC (N-acetyl cysteine) to inhibit or stabilize the amounts of the antioxidant glutathione.	Acetylcysteine	311-314	tumor necrosis factor	Mus musculus	146-154
33303231-3	2021	The present investigation presents evidence regarding the role of HEMA-induced oxidative stress in the secretion of the pro-inflammatory cytokine TNFalpha from cells exposed to the antigens LTA (lipoteichoic acid) or LPS (lipopolysaccharide) of cariogenic microorganisms using BSO (L-buthionine sulfoximine) or NAC (N-acetyl cysteine) to inhibit or stabilize the amounts of the antioxidant glutathione.	Acetylcysteine	316-333	tumor necrosis factor	Mus musculus	146-154
33303231-7	2021	RESULTS: The release of TNFalpha in both LTA- and LPS-exposed cells was decreased by HEMA, and this concentration-dependent inhibitory effect was amplified by BSO or NAC.	Acetylcysteine	166-169	tumor necrosis factor	Mus musculus	24-32
32818949-10	2021	NAC reduced the placental expression of histone deacetylase-2, suggesting that epigenetic mechanisms may be involved.	Acetylcysteine	0-3	histone deacetylase 2	Homo sapiens	40-61
33130472-15	2021	N-acetyl-L-cysteine (NAC) not only revered ROS generation triggered by LCA but also restored IFN-gamma-induced expression of PD-L1.	Acetylcysteine	21-24	interferon gamma	Homo sapiens	93-102
33371832-7	2021	Furthermore, NAC decreases TNF-alpha, IL-1beta, IL-6, IL-8, IL-10, and IL-17 serum levels in patients with sepsis, severe burns, acute liver failure, or peritoneal dialysis and may also reduce cytokine storm in COVID-19.	Acetylcysteine	13-16	tumor necrosis factor	Homo sapiens	27-36
33371832-7	2021	Furthermore, NAC decreases TNF-alpha, IL-1beta, IL-6, IL-8, IL-10, and IL-17 serum levels in patients with sepsis, severe burns, acute liver failure, or peritoneal dialysis and may also reduce cytokine storm in COVID-19.	Acetylcysteine	13-16	interleukin 6	Homo sapiens	48-52
33371832-7	2021	Furthermore, NAC decreases TNF-alpha, IL-1beta, IL-6, IL-8, IL-10, and IL-17 serum levels in patients with sepsis, severe burns, acute liver failure, or peritoneal dialysis and may also reduce cytokine storm in COVID-19.	Acetylcysteine	13-16	C-X-C motif chemokine ligand 8	Homo sapiens	54-58
32871518-7	2020	Moreover, NAC administration achieved its therapeutic effect by inhibiting ovarian apoptosis-induced by radiation through downregulating p53 and Bax levels by 33% and 16%, respectively while increasing the Bcl-2 mRNA expression by 135%.	Acetylcysteine	10-13	BCL2, apoptosis regulator	Rattus norvegicus	206-211
33426071-11	2020	The cellular expression levels of ZO-1, Occludin, and Claudin-4, which were lowered by hyperoxia, were increased by NAC.	Acetylcysteine	116-119	tight junction protein 1	Homo sapiens	34-38
33426071-11	2020	The cellular expression levels of ZO-1, Occludin, and Claudin-4, which were lowered by hyperoxia, were increased by NAC.	Acetylcysteine	116-119	claudin 4	Homo sapiens	54-63
33127645-5	2020	HPSE expression in cerebral vessels increased after stroke onset and infarct volume greatly decreased after co-administration of N-acetylcysteine (NAC)+GAG oligosaccharides as compared to NAC administration alone.	Acetylcysteine	129-145	heparanase	Homo sapiens	0-4
33127645-5	2020	HPSE expression in cerebral vessels increased after stroke onset and infarct volume greatly decreased after co-administration of N-acetylcysteine (NAC)+GAG oligosaccharides as compared to NAC administration alone.	Acetylcysteine	147-150	heparanase	Homo sapiens	0-4
33127645-5	2020	HPSE expression in cerebral vessels increased after stroke onset and infarct volume greatly decreased after co-administration of N-acetylcysteine (NAC)+GAG oligosaccharides as compared to NAC administration alone.	Acetylcysteine	188-191	heparanase	Homo sapiens	0-4
33035499-7	2020	In striatum and cortex, NAC prevented glial cells activation (GFAP and Iba-1), decreased NGF, Bcl-2 and NeuN, the increase of lipid peroxidation and PARP induced by GA in both ages.	Acetylcysteine	24-27	B cell leukemia/lymphoma 2	Mus musculus	94-99
33035499-8	2020	NAC protected against increased p75NTR induced by GA, but not in cortex of 21-day-old mice.	Acetylcysteine	0-3	nerve growth factor receptor (TNFR superfamily, member 16)	Mus musculus	32-38
33291667-6	2020	An antioxidant, N-acetyl-l-cysteine, mimicked the effects of RAGE-aptamer on AGE-exposed U937 cells.	Acetylcysteine	16-35	MOK protein kinase	Homo sapiens	61-65
33291667-6	2020	An antioxidant, N-acetyl-l-cysteine, mimicked the effects of RAGE-aptamer on AGE-exposed U937 cells.	Acetylcysteine	16-35	renin binding protein	Homo sapiens	62-65
33343802-11	2020	Moreover, DDF-induced HO-1 expression was mediated through Nrf2 phosphorylation and translocation into the nucleus which was attenuated by NAC or p38 siRNA.	Acetylcysteine	139-142	NFE2 like bZIP transcription factor 2	Homo sapiens	59-63
33343802-13	2020	Interaction between Nrf2 and the ARE-binding sites on the HO-1 promoter was revealed by chromatin immunoprecipitation assay, which was attenuated by NAC, GSH, or p38i VIII.	Acetylcysteine	149-152	NFE2 like bZIP transcription factor 2	Homo sapiens	20-24
33415010-4	2020	Pre-treatment with the anti-oxidant, N-acetylcysteine (NAC), reversed DHA-induced caspase 3 activity and prevented DHA-reduced cell proliferation.	Acetylcysteine	37-53	caspase 3	Homo sapiens	82-91
33415010-4	2020	Pre-treatment with the anti-oxidant, N-acetylcysteine (NAC), reversed DHA-induced caspase 3 activity and prevented DHA-reduced cell proliferation.	Acetylcysteine	55-58	caspase 3	Homo sapiens	82-91
32658336-0	2020	Modulation of Bleomycin-induced oxidative stress and pulmonary fibrosis by N-acetylcysteine in Ratsvia AMPK/SIRT1/ NF-Kbeta.	Acetylcysteine	75-91	protein kinase AMP-activated catalytic subunit alpha 2	Rattus norvegicus	103-107
32736244-6	2020	Moreover, the down regulating of p-Akt/Akt, p-mTOR/mTOR and subsequent up-regulation of p-AMPK/AMPK induced by NP can be rescued by pretreatment of NAC.	Acetylcysteine	148-151	AKT serine/threonine kinase 1	Rattus norvegicus	35-38
32736244-6	2020	Moreover, the down regulating of p-Akt/Akt, p-mTOR/mTOR and subsequent up-regulation of p-AMPK/AMPK induced by NP can be rescued by pretreatment of NAC.	Acetylcysteine	148-151	AKT serine/threonine kinase 1	Rattus norvegicus	39-42
32736244-6	2020	Moreover, the down regulating of p-Akt/Akt, p-mTOR/mTOR and subsequent up-regulation of p-AMPK/AMPK induced by NP can be rescued by pretreatment of NAC.	Acetylcysteine	148-151	protein kinase AMP-activated catalytic subunit alpha 2	Rattus norvegicus	90-94
32658336-0	2020	Modulation of Bleomycin-induced oxidative stress and pulmonary fibrosis by N-acetylcysteine in Ratsvia AMPK/SIRT1/ NF-Kbeta.	Acetylcysteine	75-91	sirtuin 1	Rattus norvegicus	108-113
32736244-6	2020	Moreover, the down regulating of p-Akt/Akt, p-mTOR/mTOR and subsequent up-regulation of p-AMPK/AMPK induced by NP can be rescued by pretreatment of NAC.	Acetylcysteine	148-151	protein kinase AMP-activated catalytic subunit alpha 2	Rattus norvegicus	95-99
32658336-11	2020	NAC markedly attenuated the lung histopathological changes and reduced collagen deposition.These results suggested that NAC exerted anameliorative effect against BLM-induced oxidative damage and pulmonary fibrosisvia SIRT1/ AMPK/ NF-Kbeta pathways.	Acetylcysteine	0-3	sirtuin 1	Rattus norvegicus	217-222
32658336-11	2020	NAC markedly attenuated the lung histopathological changes and reduced collagen deposition.These results suggested that NAC exerted anameliorative effect against BLM-induced oxidative damage and pulmonary fibrosisvia SIRT1/ AMPK/ NF-Kbeta pathways.	Acetylcysteine	0-3	protein kinase AMP-activated catalytic subunit alpha 2	Rattus norvegicus	224-228
32658336-11	2020	NAC markedly attenuated the lung histopathological changes and reduced collagen deposition.These results suggested that NAC exerted anameliorative effect against BLM-induced oxidative damage and pulmonary fibrosisvia SIRT1/ AMPK/ NF-Kbeta pathways.	Acetylcysteine	120-123	sirtuin 1	Rattus norvegicus	217-222
32658336-11	2020	NAC markedly attenuated the lung histopathological changes and reduced collagen deposition.These results suggested that NAC exerted anameliorative effect against BLM-induced oxidative damage and pulmonary fibrosisvia SIRT1/ AMPK/ NF-Kbeta pathways.	Acetylcysteine	120-123	protein kinase AMP-activated catalytic subunit alpha 2	Rattus norvegicus	224-228
33278022-10	2020	CONCLUSIONS: Perioperative NAC infusion following LDLT resulted in significantly lower postoperative AST and ALT levels.	Acetylcysteine	27-30	solute carrier family 17 member 5	Homo sapiens	101-104
32339540-9	2020	The use of hydrogen peroxide altered AQP3 and NOTCH1 expression, and the use of N-acetyl-L-cysteine (NAC) altered NOTCH1 expression, evidencing this is a redox-dependent process.	Acetylcysteine	80-99	notch receptor 1	Homo sapiens	114-120
32339540-9	2020	The use of hydrogen peroxide altered AQP3 and NOTCH1 expression, and the use of N-acetyl-L-cysteine (NAC) altered NOTCH1 expression, evidencing this is a redox-dependent process.	Acetylcysteine	101-104	notch receptor 1	Homo sapiens	114-120
31931659-12	2020	Collectively, our results identify ROS as central inducers of MTORC2 activation during chronic autophagy, which in turn fuels senescence activation and myofibroblast differentiation in distinct cellular subpopulations.Abbreviations: 3-MA: 3-methyladenine; ACTA2: actin, alpha 2, smooth muscle, aorta; AKT1: AKT serine/threonine kinase 1; p-AKT1: AKT1 Ser473 phosphorylation; t-AKT1: total AKT serine/threonine kinase 1; ATG4A: autophagy related 4A cysteine peptidase; ATG7: autophagy gene 7; C12FDG: 5-dodecanoylaminofluorescein Di-beta-D-Galactopyranoside; CDKN1A: cyclin dependent kinase inhibitor 1A; CDKN2A: cyclin dependent kinase inhibitor 2A; Ctl: control; DAPI: 4",6-diamidino-2-phenylindole, dilactate; ECM: extracellular matrix; GSH: L-glutathione reduced; H2O2: hydrogen peroxide; HLF: adult human lung fibroblasts; Ho: Hoechst 33342 (2"-[4-ethoxyphenyl]-5-[4-methyl-1-piperazinyl]-2.5"-bi-1H-benzimidazole); HSC: hepatic stellate cells; LY: LY294002; MAP1LC3B/LC3B: microtubule-associated protein 1 light chain 3 beta; MTORC1/2: mechanistic target of rapamycin kinase complex 1/2; N: normal growth medium; NAC: N-acetyl-L-cysteine; PBS: phosphate-buffered saline; PDGFA: platelet derived growth factor subunit A; PRKCA/PKCalpha: protein kinase C alpha; PtdIns3K: class III phosphatidylinositol 3-kinase; PTEN: phosphatase and tensin homolog; R: rapamycin; RICTOR: RPTOR independent companion of MTOR complex 2; ROS: reactive oxygen species; RPTOR: regulatory associated protein of MTOR complex 1; SA-GLB1/beta-gal: senescence-associated galactosidase beta 1; SGK1: serum/glucocorticoid regulated kinase 1; shRNA: short hairpin RNA; siCtl: control siRNA; siRNA: small interfering RNA; SQSTM1: sequestosome 1; SS: serum-free (serum starvation) medium; TP53: tumor protein p53; TUBA: tubulin alpha; V: vehicle.	Acetylcysteine	1123-1142	mechanistic target of rapamycin kinase	Homo sapiens	62-66
32467034-1	2020	AIM: To evaluate the role of nebulized N-acetyl cysteine (NAC) in liquefying the airway secretions and improving the outcome of patients of esophageal atresia with tracheoesophageal fistula (EA + TEF).	Acetylcysteine	58-61	TEF transcription factor, PAR bZIP family member	Homo sapiens	196-199
32467034-12	2020	CONCLUSION: It appears that nebulized NAC decreases the consistency of secretions in EA + TEF patients.	Acetylcysteine	38-41	TEF transcription factor, PAR bZIP family member	Homo sapiens	90-93
33281629-9	2020	The activation of the MAPK/NF-kappaB signaling was halted by NAC, EGTA, and HC030031.	Acetylcysteine	61-64	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	27-36
33201834-3	2020	Notably, CdSe/ZnS QDs treatment increased the contents of MDA and ROS, and decreased the activities of SOD, CAT and GSH-Px; however, the co-treatment of NAC and QDs relieved the oxidative damage of NRK cells.	Acetylcysteine	153-156	catalase	Rattus norvegicus	108-111
33201734-6	2021	Administration of NAC or melatonin significantly improved the lipid parameters, gonadal hormones, TNFalpha level, sperm count and abnormal morphology, oxidant/antioxidant system and the absolute testicular and epididymal mass with an enhancement of testicular architecture, AR expression and apoptosis as compared to that in the obese group.	Acetylcysteine	18-21	tumor necrosis factor	Rattus norvegicus	98-106
33139577-4	2020	As a result, Akt3-expressing cells activate the DNA damage response pathway, express high levels of p53 and its direct transcriptional target miR-34, and exhibit a proliferation defect, which is rescued by the antioxidant N-acetylcysteine.	Acetylcysteine	222-238	tumor protein p53	Homo sapiens	100-103
33191885-10	2021	Our study showed that NAC significantly increased MA in the both HFD+NAC1-12 and HFD+NAC1-6 groups, and improved HFD-induced mitochondrial and intracellular ROS expression, DNA and protein oxidative damage, and adipose tissue inflammation.	Acetylcysteine	22-25	nucleus accumbens associated 1, BEN and BTB (POZ) domain containing	Mus musculus	69-73
33191885-10	2021	Our study showed that NAC significantly increased MA in the both HFD+NAC1-12 and HFD+NAC1-6 groups, and improved HFD-induced mitochondrial and intracellular ROS expression, DNA and protein oxidative damage, and adipose tissue inflammation.	Acetylcysteine	22-25	nucleus accumbens associated 1, BEN and BTB (POZ) domain containing	Mus musculus	85-91
33198336-4	2020	Thus, we aimed to analyze effects of acute and chronic NAC treatment on the homeostasis of copper (Cu) and zinc (Zn) and on the activity of the redox-sensitive transcription factor Nrf2.	Acetylcysteine	55-58	nuclear factor, erythroid derived 2, like 2	Mus musculus	181-185
33198336-7	2020	In addition, NAC inhibited the Zn-induced Nrf2 activation and limited the concomitant upregulation of cellular GSH concentrations.	Acetylcysteine	13-16	nuclear factor, erythroid derived 2, like 2	Mus musculus	42-46
33177587-7	2020	However, pretreatment of the cells with NAC completely abrogated the NKA inhibitory activity of plumbagin and atovaquone.	Acetylcysteine	40-43	tachykinin precursor 1	Homo sapiens	69-72
33146789-10	2021	In addition, using the ROS inhibitor N-acetyl-L-cysteine (NAC), we observed abrogated mRNA expression of several ARPs and production of inflammatory cytokines/chemokines (IL-6, IL-8, MCP-1, and CCL-5) in the CSE-challenged cells suggesting an important role of ROS in regulating CSE-induced autophagy.	Acetylcysteine	37-56	interleukin 6	Homo sapiens	171-175
33146789-10	2021	In addition, using the ROS inhibitor N-acetyl-L-cysteine (NAC), we observed abrogated mRNA expression of several ARPs and production of inflammatory cytokines/chemokines (IL-6, IL-8, MCP-1, and CCL-5) in the CSE-challenged cells suggesting an important role of ROS in regulating CSE-induced autophagy.	Acetylcysteine	37-56	C-X-C motif chemokine ligand 8	Homo sapiens	177-181
33146789-10	2021	In addition, using the ROS inhibitor N-acetyl-L-cysteine (NAC), we observed abrogated mRNA expression of several ARPs and production of inflammatory cytokines/chemokines (IL-6, IL-8, MCP-1, and CCL-5) in the CSE-challenged cells suggesting an important role of ROS in regulating CSE-induced autophagy.	Acetylcysteine	58-61	interleukin 6	Homo sapiens	171-175
33146789-10	2021	In addition, using the ROS inhibitor N-acetyl-L-cysteine (NAC), we observed abrogated mRNA expression of several ARPs and production of inflammatory cytokines/chemokines (IL-6, IL-8, MCP-1, and CCL-5) in the CSE-challenged cells suggesting an important role of ROS in regulating CSE-induced autophagy.	Acetylcysteine	58-61	C-X-C motif chemokine ligand 8	Homo sapiens	177-181
33131013-7	2021	Treatment with N-acetylcysteine (NAC) blocked 27-HC-induced ROS generation and p38 signaling pathway activation, prevented beta-catenin from release from binding, and inhibited EndMT.	Acetylcysteine	15-31	mitogen-activated protein kinase 14	Homo sapiens	79-82
33131013-7	2021	Treatment with N-acetylcysteine (NAC) blocked 27-HC-induced ROS generation and p38 signaling pathway activation, prevented beta-catenin from release from binding, and inhibited EndMT.	Acetylcysteine	33-36	mitogen-activated protein kinase 14	Homo sapiens	79-82
33133334-13	2020	In cultured spleen mononuclear cells, TXNIP, MDA, SOD, ROS and inflammatory cytokines levels were altered by OVA but reversed by resveratrol or NAC.	Acetylcysteine	144-147	thioredoxin interacting protein	Mus musculus	38-43
32799012-9	2020	Oral supplementation of NAC reduced serum level of C-reactive protein (CRP) [WMD: -0.61 mg/L, 95% CI: -1.18 to -0.03, P = 0.039, I2 = 79.6%], and interleukin-6 (IL-6) [WMD: -0.43 pg/mL, 95% CI: -0.69 to -0.17, P = 0.001, I2 = 89.3%].	Acetylcysteine	24-27	C-reactive protein	Homo sapiens	51-69
32799012-9	2020	Oral supplementation of NAC reduced serum level of C-reactive protein (CRP) [WMD: -0.61 mg/L, 95% CI: -1.18 to -0.03, P = 0.039, I2 = 79.6%], and interleukin-6 (IL-6) [WMD: -0.43 pg/mL, 95% CI: -0.69 to -0.17, P = 0.001, I2 = 89.3%].	Acetylcysteine	24-27	C-reactive protein	Homo sapiens	71-74
32799012-9	2020	Oral supplementation of NAC reduced serum level of C-reactive protein (CRP) [WMD: -0.61 mg/L, 95% CI: -1.18 to -0.03, P = 0.039, I2 = 79.6%], and interleukin-6 (IL-6) [WMD: -0.43 pg/mL, 95% CI: -0.69 to -0.17, P = 0.001, I2 = 89.3%].	Acetylcysteine	24-27	interleukin 6	Homo sapiens	146-159
32799012-9	2020	Oral supplementation of NAC reduced serum level of C-reactive protein (CRP) [WMD: -0.61 mg/L, 95% CI: -1.18 to -0.03, P = 0.039, I2 = 79.6%], and interleukin-6 (IL-6) [WMD: -0.43 pg/mL, 95% CI: -0.69 to -0.17, P = 0.001, I2 = 89.3%].	Acetylcysteine	24-27	interleukin 6	Homo sapiens	161-165
32799012-11	2020	Dose-response investigation showed a non-linear association between oral NAC supplementation with CRP.	Acetylcysteine	73-76	C-reactive protein	Homo sapiens	98-101
32799012-12	2020	CONCLUSION: Oral NAC supplementation reduced serum level of CRP and IL-6, but did not affect other inflammatory biomarkers.	Acetylcysteine	17-20	C-reactive protein	Homo sapiens	60-63
32799012-12	2020	CONCLUSION: Oral NAC supplementation reduced serum level of CRP and IL-6, but did not affect other inflammatory biomarkers.	Acetylcysteine	17-20	interleukin 6	Homo sapiens	68-72
32905825-5	2020	On the other hand, the levels of p53, miR-513a-5p, and gammaH2AX were attenuated by 5 mM N-acetyl-l-cysteine (NAC) pretreatment, indicating that the reactive oxygen species (ROS)-dependent p53-miR-513a-5p was involved in DSB repair in 4-ABP-treated cells.	Acetylcysteine	89-108	tumor protein p53	Homo sapiens	33-36
32905825-5	2020	On the other hand, the levels of p53, miR-513a-5p, and gammaH2AX were attenuated by 5 mM N-acetyl-l-cysteine (NAC) pretreatment, indicating that the reactive oxygen species (ROS)-dependent p53-miR-513a-5p was involved in DSB repair in 4-ABP-treated cells.	Acetylcysteine	89-108	tumor protein p53	Homo sapiens	189-192
32905825-5	2020	On the other hand, the levels of p53, miR-513a-5p, and gammaH2AX were attenuated by 5 mM N-acetyl-l-cysteine (NAC) pretreatment, indicating that the reactive oxygen species (ROS)-dependent p53-miR-513a-5p was involved in DSB repair in 4-ABP-treated cells.	Acetylcysteine	110-113	tumor protein p53	Homo sapiens	33-36
32905825-5	2020	On the other hand, the levels of p53, miR-513a-5p, and gammaH2AX were attenuated by 5 mM N-acetyl-l-cysteine (NAC) pretreatment, indicating that the reactive oxygen species (ROS)-dependent p53-miR-513a-5p was involved in DSB repair in 4-ABP-treated cells.	Acetylcysteine	110-113	tumor protein p53	Homo sapiens	189-192
33163142-5	2020	The overproduction of reactive oxygen species (ROS) decreases NR4A3 protein abundance in VEC under OGD-R condition, which is reversed by TRIOL and N-acetylcysteine (NAC).	Acetylcysteine	147-163	nuclear receptor subfamily 4 group A member 3	Macaca fascicularis	62-67
33163142-5	2020	The overproduction of reactive oxygen species (ROS) decreases NR4A3 protein abundance in VEC under OGD-R condition, which is reversed by TRIOL and N-acetylcysteine (NAC).	Acetylcysteine	165-168	nuclear receptor subfamily 4 group A member 3	Macaca fascicularis	62-67
32838966-7	2020	Up-regulation of CRTAC1 promoted HLECs pyroptosis, while the ROS inhibitor N-acetyl-l-cysteine blocked the effects of CRTAC1 overexpression.	Acetylcysteine	75-94	cartilage acidic protein 1	Homo sapiens	118-124
33149614-10	2020	However, the ROS scavenger N-acetylcysteine (NAC) and MAPK inhibitors inhibited zeaxanthin-induced apoptosis, and under the action of zeaxanthin, MAPK regulated NF-kappaB and STAT3, and reduced their protein expression levels.	Acetylcysteine	27-43	nuclear factor kappa B subunit 1	Homo sapiens	161-170
33149614-10	2020	However, the ROS scavenger N-acetylcysteine (NAC) and MAPK inhibitors inhibited zeaxanthin-induced apoptosis, and under the action of zeaxanthin, MAPK regulated NF-kappaB and STAT3, and reduced their protein expression levels.	Acetylcysteine	27-43	signal transducer and activator of transcription 3	Homo sapiens	175-180
33149614-10	2020	However, the ROS scavenger N-acetylcysteine (NAC) and MAPK inhibitors inhibited zeaxanthin-induced apoptosis, and under the action of zeaxanthin, MAPK regulated NF-kappaB and STAT3, and reduced their protein expression levels.	Acetylcysteine	45-48	nuclear factor kappa B subunit 1	Homo sapiens	161-170
33149614-10	2020	However, the ROS scavenger N-acetylcysteine (NAC) and MAPK inhibitors inhibited zeaxanthin-induced apoptosis, and under the action of zeaxanthin, MAPK regulated NF-kappaB and STAT3, and reduced their protein expression levels.	Acetylcysteine	45-48	signal transducer and activator of transcription 3	Homo sapiens	175-180
33067169-12	2021	At the end of the intervention period (16 weeks) and 6 weeks post-intervention, the mean fecal calprotectin, serum erythrocyte sedimentation rate, and hs-CRP levels were significantly lower in the NAC group compared with the placebo group (p < 0.05).	Acetylcysteine	197-200	C-reactive protein	Homo sapiens	154-157
32868342-8	2020	In addition, compared to SS2-infected STEC, PCV2/SS2 coinfection and pretreatment of STEC with NAC prior to SS2 infection both down-regulated the expression of inflammatory cytokines IL-6, TNF-alpha and IL-1beta.	Acetylcysteine	95-98	interleukin 6	Homo sapiens	183-187
32868342-8	2020	In addition, compared to SS2-infected STEC, PCV2/SS2 coinfection and pretreatment of STEC with NAC prior to SS2 infection both down-regulated the expression of inflammatory cytokines IL-6, TNF-alpha and IL-1beta.	Acetylcysteine	95-98	tumor necrosis factor	Homo sapiens	189-198
32868342-9	2020	Further research found that activation of p38/MAPK promoted the expression of inflammatory cytokines in SS2-infected STEC; however, PCV2/SS2 coinfection or NAC pretreatment of STEC inhibited p38 phosphorylation, suggesting that coinfection of STEC with PCV2 and SS2 weakens the inflammatory response to SS2 infection through reduced ROS production.	Acetylcysteine	156-159	mitogen-activated protein kinase 14	Homo sapiens	42-50
32868342-9	2020	Further research found that activation of p38/MAPK promoted the expression of inflammatory cytokines in SS2-infected STEC; however, PCV2/SS2 coinfection or NAC pretreatment of STEC inhibited p38 phosphorylation, suggesting that coinfection of STEC with PCV2 and SS2 weakens the inflammatory response to SS2 infection through reduced ROS production.	Acetylcysteine	156-159	mitogen-activated protein kinase 14	Homo sapiens	42-45
32504923-8	2020	NAC has also been shown to inhibit the NLRP3 inflammasome pathway (IL1beta and IL18) in vitro, and decrease plasma TNF-alpha in human clinical trials.	Acetylcysteine	0-3	NLR family pyrin domain containing 3	Homo sapiens	39-44
32726657-11	2020	NAC significantly decreased malondialdehyde (MDA) (SMD = -1.44 mumol/L; 95% CI: -2.05, -0.84; P < 0.001), IL-8 (WMD = -2.56 pg/ml; 95% CI: -3.89, -1.23; P < 0.001) and homocysteine (WMD = -1.45 pg/ml; 95% CI: -2.74, -0.17; P = 0.027) levels.	Acetylcysteine	0-3	C-X-C motif chemokine ligand 8	Homo sapiens	106-110
32726657-13	2020	However, NAC effects were significant in ameliorating TNF-alpha and IL-6 using sensitivity analysis.	Acetylcysteine	9-12	tumor necrosis factor	Homo sapiens	54-63
32726657-13	2020	However, NAC effects were significant in ameliorating TNF-alpha and IL-6 using sensitivity analysis.	Acetylcysteine	9-12	interleukin 6	Homo sapiens	68-72
32726657-14	2020	NAC significantly decreased MDA, IL-8, and homocysteine levels.	Acetylcysteine	0-3	C-X-C motif chemokine ligand 8	Homo sapiens	33-37
32726657-15	2020	The effects of NAC on amending TNF-alpha and IL-6 levels were significant after sensitivity analysis.	Acetylcysteine	15-18	tumor necrosis factor	Homo sapiens	31-40
32726657-15	2020	The effects of NAC on amending TNF-alpha and IL-6 levels were significant after sensitivity analysis.	Acetylcysteine	15-18	interleukin 6	Homo sapiens	45-49
32706497-7	2020	Inhibiting NO production and ROS generation using N-acetylcysteine (NAC) and L-NG-monomethyl arginine acetate (L-NMMA), respectively, accelerated the influence of simvastatin on NF-kappaB activity.	Acetylcysteine	50-66	nuclear factor kappa B subunit 1	Homo sapiens	178-187
32706497-7	2020	Inhibiting NO production and ROS generation using N-acetylcysteine (NAC) and L-NG-monomethyl arginine acetate (L-NMMA), respectively, accelerated the influence of simvastatin on NF-kappaB activity.	Acetylcysteine	68-71	nuclear factor kappa B subunit 1	Homo sapiens	178-187
32706497-8	2020	In addition, NAC blocked SNP and simvastatin-mediated COX-2 production and NF-kappaB activity but did not alter IL-1beta and simvastatin-mediated COX-2 expression.	Acetylcysteine	13-16	prostaglandin-endoperoxide synthase 2	Homo sapiens	54-59
32706497-8	2020	In addition, NAC blocked SNP and simvastatin-mediated COX-2 production and NF-kappaB activity but did not alter IL-1beta and simvastatin-mediated COX-2 expression.	Acetylcysteine	13-16	nuclear factor kappa B subunit 1	Homo sapiens	75-84
32705396-6	2020	In further experiments investigating the protection conferred by melatonin, incubating HT22 cells with conditioned medium (CM) from thrombin-stimulated microglia induced HT22 cell apoptosis, and this effect was reversed after treating CM with either melatonin or N-acetyl-L-cysteine (NAC).	Acetylcysteine	263-282	coagulation factor II	Mus musculus	132-140
32705396-6	2020	In further experiments investigating the protection conferred by melatonin, incubating HT22 cells with conditioned medium (CM) from thrombin-stimulated microglia induced HT22 cell apoptosis, and this effect was reversed after treating CM with either melatonin or N-acetyl-L-cysteine (NAC).	Acetylcysteine	284-287	coagulation factor II	Mus musculus	132-140
32438104-4	2020	RESULTS: Pretreatment of NAC significantly alleviated pathologic damage of kidney tissues in septic rats; decreased the levels of serum creatinine, blood urea nitrogen, plasma neutrophil gelatinase-associated lipocalin, and kidney injury molecule-1; and reduced the expression of tumor necrosis factor a, interleukin [IL]-1beta, IL-6, and IL-8.	Acetylcysteine	25-28	interleukin 6	Rattus norvegicus	329-333
32438104-5	2020	Furthermore, NAC pretreatment reduced the level of protein-nitrotyrosine adducts and malondialdehyde in CLP-induced kidney tissues, while elevated the levels of superoxide dismutase, glutathione peroxidase, and catalase.	Acetylcysteine	13-16	catalase	Rattus norvegicus	211-219
32438104-6	2020	Moreover, pretreatment of NAC reduced the number of apoptosis in kidney tissues induced by CLP, decreased the mRNA levels of caspase-3, caspase-9, cytochrome c, and poly ADP-ribose polymerase, and increased mitochondrial membrane activity in renal cortical cells (complex I/II/III/IV).	Acetylcysteine	26-29	caspase 9	Rattus norvegicus	136-145
33312063-0	2020	Effect of propolis and N-acetylcysteine supplementation on lipoprotein subclasses distribution and paraoxonase 1 activity in subjects with acute respiratory infection.	Acetylcysteine	23-39	paraoxonase 1	Homo sapiens	99-112
32599978-13	2020	In vitro, NAC treatment significantly reduced the expression of NRF2, LC3B, p62, and Beclin-1 in keratinocytes compared with that after radiation treatment.	Acetylcysteine	10-13	NFE2 like bZIP transcription factor 2	Rattus norvegicus	64-68
32707089-5	2020	NAC blocked hemolysis and elevation of liver enzymes, C-reactive protein (CRP), and ferritin and allowed removal from respirator and veno-venous extracorporeal membrane oxygenator and full recovery of the G6PD-deficient patient.	Acetylcysteine	0-3	C-reactive protein	Homo sapiens	54-72
32707089-5	2020	NAC blocked hemolysis and elevation of liver enzymes, C-reactive protein (CRP), and ferritin and allowed removal from respirator and veno-venous extracorporeal membrane oxygenator and full recovery of the G6PD-deficient patient.	Acetylcysteine	0-3	C-reactive protein	Homo sapiens	74-77
32707089-7	2020	NAC elicited clinical improvement and markedly reduced CRP in all patients and ferritin in 9/10 patients.	Acetylcysteine	0-3	C-reactive protein	Homo sapiens	55-58
33098382-0	2020	The Effect of N-Acetyl-Cysteine on NRF2 Antioxidant Gene Expression in Asthenoteratozoospermia Men: A Clinical Trial Study.	Acetylcysteine	14-31	NFE2 like bZIP transcription factor 2	Homo sapiens	35-39
33098382-3	2020	The purpose of this study was to evaluate the effect of N-acetyl-L-cysteine (NAC), as an antioxidant drug, on NRF2 Gene Expression in Asthenoteratozoospermia Men.	Acetylcysteine	56-75	NFE2 like bZIP transcription factor 2	Homo sapiens	110-114
33098382-3	2020	The purpose of this study was to evaluate the effect of N-acetyl-L-cysteine (NAC), as an antioxidant drug, on NRF2 Gene Expression in Asthenoteratozoospermia Men.	Acetylcysteine	77-80	NFE2 like bZIP transcription factor 2	Homo sapiens	110-114
33098382-8	2020	A significant improvement in expression of NRF2 gene and antioxidant enzyme levels were observed compared to pre-treatment by NAC (P<0.05).	Acetylcysteine	126-129	NFE2 like bZIP transcription factor 2	Homo sapiens	43-47
33098382-10	2020	Conclusion: The results demonstrated that NAC oral supplementation protected against oxidative stress by enhancing NRF2 expression.	Acetylcysteine	42-45	NFE2 like bZIP transcription factor 2	Homo sapiens	115-119
32504923-8	2020	NAC has also been shown to inhibit the NLRP3 inflammasome pathway (IL1beta and IL18) in vitro, and decrease plasma TNF-alpha in human clinical trials.	Acetylcysteine	0-3	tumor necrosis factor	Homo sapiens	115-124
32534175-10	2020	A randomized controlled trial of blocking NF-kappaB and cytokine formation using glutathione precursors (N-acetyl-cysteine [NAC] and alpha lipoic acid) and PO/IV glutathione with associated anti-viral effects should be performed, along with an evaluation of Nrf2 activators (curcumin, sulforaphane glucosinolate) which have been scientifically proven to lower inflammation.	Acetylcysteine	105-122	nuclear factor kappa B subunit 1	Homo sapiens	42-51
33007928-0	2020	Supplementing Glycine and N-acetylcysteine (GlyNAC) in Aging HIV Patients Improves Oxidative Stress, Mitochondrial Dysfunction, Inflammation, Endothelial Dysfunction, Insulin Resistance, Genotoxicity, Strength, and Cognition: Results of an Open-Label Clinical Trial.	Acetylcysteine	26-42	insulin	Homo sapiens	167-174
32945495-0	2020	N-acetyl cysteine inhibits the lipopolysaccharide-induced inflammatory response in bone marrow mesenchymal stem cells by suppressing the TXNIP/NLRP3/IL-1beta signaling pathway.	Acetylcysteine	0-17	thioredoxin interacting protein	Homo sapiens	137-142
32945495-0	2020	N-acetyl cysteine inhibits the lipopolysaccharide-induced inflammatory response in bone marrow mesenchymal stem cells by suppressing the TXNIP/NLRP3/IL-1beta signaling pathway.	Acetylcysteine	0-17	NLR family pyrin domain containing 3	Homo sapiens	143-148
32945475-14	2020	Changes in the expression of PCNA, and Bcl-xL and in the levels of cleaved-caspase 3 were partly reversed by N-acetyl-L-cysteine, a reactive oxygen species (ROS) scavenger.	Acetylcysteine	109-128	BCL2 like 1	Homo sapiens	39-45
32945495-9	2020	Furthermore, NAC reduced the expression of ASC, NLRP3, caspase-1 and TXNIP, but enhanced that of TRX.	Acetylcysteine	13-16	PYD and CARD domain containing	Homo sapiens	43-46
32945495-9	2020	Furthermore, NAC reduced the expression of ASC, NLRP3, caspase-1 and TXNIP, but enhanced that of TRX.	Acetylcysteine	13-16	NLR family pyrin domain containing 3	Homo sapiens	48-53
32945495-9	2020	Furthermore, NAC reduced the expression of ASC, NLRP3, caspase-1 and TXNIP, but enhanced that of TRX.	Acetylcysteine	13-16	caspase 1	Homo sapiens	55-64
32945495-9	2020	Furthermore, NAC reduced the expression of ASC, NLRP3, caspase-1 and TXNIP, but enhanced that of TRX.	Acetylcysteine	13-16	thioredoxin interacting protein	Homo sapiens	69-74
32945495-10	2020	To conclude, NAC had anti-inflammatory effects on LPS-stimulated BMSCs, which was closely associated with the TXNIP/NLRP3/IL-1beta signaling pathway.	Acetylcysteine	13-16	thioredoxin interacting protein	Homo sapiens	110-115
32945495-10	2020	To conclude, NAC had anti-inflammatory effects on LPS-stimulated BMSCs, which was closely associated with the TXNIP/NLRP3/IL-1beta signaling pathway.	Acetylcysteine	13-16	NLR family pyrin domain containing 3	Homo sapiens	116-121
32929153-7	2020	Treatment of pancreatic cancer cells with the antioxidant N-acetyl-L-cysteine decreased ROS activity and expression level of NRF2 and ITGB7.	Acetylcysteine	58-77	NFE2 like bZIP transcription factor 2	Homo sapiens	125-129
32985606-7	2020	Notably, all these events were reverted by N-acetyl-L-cysteine and JNK inhibitor SP600125 furnishing evidence that APE exerted its effects through the activation of ROS/JNK signaling.	Acetylcysteine	43-62	mitogen-activated protein kinase 8	Homo sapiens	169-172
33162896-9	2020	The pretreatments of antioxidant N-acetylcysteine (NAC) and apocynin (APO) abolished the drop of the levels of PP2Ac Tyr307 and eNOS Ser1177 induced by AngII in HUVECs.	Acetylcysteine	33-49	angiotensinogen	Rattus norvegicus	152-157
33162896-9	2020	The pretreatments of antioxidant N-acetylcysteine (NAC) and apocynin (APO) abolished the drop of the levels of PP2Ac Tyr307 and eNOS Ser1177 induced by AngII in HUVECs.	Acetylcysteine	51-54	angiotensinogen	Rattus norvegicus	152-157
32999417-9	2020	The use of N-acetyl-L-cysteine as an EGFR inhibitor canceled urea-induced depletion of AAs.	Acetylcysteine	11-30	epidermal growth factor receptor	Homo sapiens	37-41
32916895-7	2020	In addition, well-known antioxidants, trolox and N-acetyl cysteine, significantly attenuated the BBB permeability increase, disruption of claudin-5 and ZO-1, and FoxO3a activation during hypoxia, suggesting that ROS are important mediators of BBB dysfunction during hypoxia.	Acetylcysteine	49-66	tight junction protein 1	Mus musculus	152-156
33029168-8	2020	In addition, CuD induced the activation of the p38 MAPK signaling pathway that regulates apoptosis, which was also inhibited by N-acetyl-L-cysteine and the p38 inhibitor SB203580.	Acetylcysteine	128-147	mitogen-activated protein kinase 14	Homo sapiens	47-50
32953569-8	2020	The upregulation of VEGF-A and CHOP induced by ATRA could be inhibited by NAC (antioxidant) and Salubrinal (ERS inhibitor) in vitro.	Acetylcysteine	74-77	vascular endothelial growth factor A	Homo sapiens	20-26
32953569-8	2020	The upregulation of VEGF-A and CHOP induced by ATRA could be inhibited by NAC (antioxidant) and Salubrinal (ERS inhibitor) in vitro.	Acetylcysteine	74-77	DNA damage inducible transcript 3	Homo sapiens	31-35
32933169-7	2020	Renal cystathionine beta-synthase (CBS) and 3-mercaptopyruvate sulphurtransferase (3MST) protein levels and H2S-releasing activity were increased in the SHR+NAC offspring.	Acetylcysteine	157-160	cystathionine beta synthase	Rattus norvegicus	6-33
32933169-7	2020	Renal cystathionine beta-synthase (CBS) and 3-mercaptopyruvate sulphurtransferase (3MST) protein levels and H2S-releasing activity were increased in the SHR+NAC offspring.	Acetylcysteine	157-160	cystathionine beta synthase	Rattus norvegicus	35-38
32339879-7	2020	Furthermore, N-acetylcysteine was applied as an enhancer for ATP synthesis, which reversed the downregulation of ATP5F, NDUF, and COX7A, and consequently alleviated the elevation of RELA, CAPN1, and RIP3.	Acetylcysteine	13-29	cytochrome c oxidase subunit 7A1	Homo sapiens	130-135
31330570-8	2020	NAC treatment rescued NAcore GLT-1 expression and attenuated cue-induced nicotine seeking, which was blocked by GLT-1 antisense.	Acetylcysteine	0-3	solute carrier family 1 member 2	Rattus norvegicus	29-34
32819581-7	2020	Our results showed that third-passage RSCs from WT mice had good stemness; Bmi-1 deficiency led to the decreased stemness, and the increased apoptosis for RSCs; NAC treatment or p16/p53 deletion ameliorated the decreased self-renewal of RSCs in Bmi-1 deficiency mice by maintaining redox balance or inhibiting cell cycle arrest respectively; Oxidative stress (OS) could negatively feedback regulate the mRNA expressions of Bmi-1, p16 and p53.	Acetylcysteine	161-164	Bmi1 polycomb ring finger oncogene	Mus musculus	75-80
32819581-7	2020	Our results showed that third-passage RSCs from WT mice had good stemness; Bmi-1 deficiency led to the decreased stemness, and the increased apoptosis for RSCs; NAC treatment or p16/p53 deletion ameliorated the decreased self-renewal of RSCs in Bmi-1 deficiency mice by maintaining redox balance or inhibiting cell cycle arrest respectively; Oxidative stress (OS) could negatively feedback regulate the mRNA expressions of Bmi-1, p16 and p53.	Acetylcysteine	161-164	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	430-433
33061803-7	2020	The activation of p38-MAPK/HSP27 induced by the p38-MAPK activator Anisomycin enhanced the apoptosis of lung SCC cells, while the ROS inhibitor N-acetyl-L-cysteine (NAC) and the p38-MAPK inhibitor SB203580 both attenuated dioscin-mediated cell apoptosis.	Acetylcysteine	144-163	mitogen-activated protein kinase 14	Homo sapiens	18-26
33061803-7	2020	The activation of p38-MAPK/HSP27 induced by the p38-MAPK activator Anisomycin enhanced the apoptosis of lung SCC cells, while the ROS inhibitor N-acetyl-L-cysteine (NAC) and the p38-MAPK inhibitor SB203580 both attenuated dioscin-mediated cell apoptosis.	Acetylcysteine	165-168	mitogen-activated protein kinase 14	Homo sapiens	18-26
33061803-8	2020	Moreover, NAC suppressed the activation of p38-MAPK/HSP27 that induced by dioscin.	Acetylcysteine	10-13	mitogen-activated protein kinase 14	Homo sapiens	43-51
31330570-8	2020	NAC treatment rescued NAcore GLT-1 expression and attenuated cue-induced nicotine seeking, which was blocked by GLT-1 antisense.	Acetylcysteine	0-3	solute carrier family 1 member 2	Rattus norvegicus	112-117
31330570-9	2020	NAC also reduced TNFalpha expression in the NAcore.	Acetylcysteine	0-3	tumor necrosis factor	Rattus norvegicus	17-25
32054204-10	2020	NAC decreased plasma malondialdehyde (MDA) level and cardiac total superoxide dismutase (T-SOD) activity in unstressed birds, but increased hepatic activities of T-SOD, catalase and glutathione peroxidase in stressed birds (P&lt;0.05).	Acetylcysteine	0-3	catalase	Homo sapiens	169-177
32736702-5	2020	TGF-beta1 treatment increased reactive oxygen species (ROS) via NOX4 upregulation, which acts downstream of ERK and mTORC1, as the ROS scavenger N-acetylcysteine and a pan-NADPH oxidase (NOX) inhibitor DPI dissipated excess ROS generation.	Acetylcysteine	145-161	transforming growth factor beta 1	Homo sapiens	0-9
32536618-9	2020	Furthermore, the suppression of cell viability and induction of Bax expression by the combination treatment were recovered by treatment with N-acetylcysteine.	Acetylcysteine	141-157	BCL2 associated X, apoptosis regulator	Homo sapiens	64-67
32098455-9	2020	Although treatment with NAC increased OVA-induced p-PDK1 protein levels, it decreased phosphorylated Akt (pAkt)/Akt levels.	Acetylcysteine	24-27	pyruvate dehydrogenase kinase, isoenzyme 1	Mus musculus	52-56
32098455-9	2020	Although treatment with NAC increased OVA-induced p-PDK1 protein levels, it decreased phosphorylated Akt (pAkt)/Akt levels.	Acetylcysteine	24-27	thymoma viral proto-oncogene 1	Mus musculus	101-104
32098455-9	2020	Although treatment with NAC increased OVA-induced p-PDK1 protein levels, it decreased phosphorylated Akt (pAkt)/Akt levels.	Acetylcysteine	24-27	thymoma viral proto-oncogene 1	Mus musculus	107-110
32534099-5	2020	While SFN significantly (p < 0.05) induced NRF2, KEAP1 and BACH1, NAC attenuated SFN-induced NRF2, KEAP1 and BACH1.	Acetylcysteine	66-69	nuclear factor, erythroid derived 2, like 2	Mus musculus	43-47
32534099-5	2020	While SFN significantly (p < 0.05) induced NRF2, KEAP1 and BACH1, NAC attenuated SFN-induced NRF2, KEAP1 and BACH1.	Acetylcysteine	66-69	nuclear factor, erythroid derived 2, like 2	Mus musculus	93-97
32512147-7	2020	Signaling activation of Akt and ERK was prevented by 5 mM N-Acetyl Cysteine (NAC) establishing the role of ROS as a key driver in the activation process.	Acetylcysteine	58-75	AKT serine/threonine kinase 1	Homo sapiens	24-27
32512147-7	2020	Signaling activation of Akt and ERK was prevented by 5 mM N-Acetyl Cysteine (NAC) establishing the role of ROS as a key driver in the activation process.	Acetylcysteine	58-75	mitogen-activated protein kinase 1	Homo sapiens	32-35
32512147-7	2020	Signaling activation of Akt and ERK was prevented by 5 mM N-Acetyl Cysteine (NAC) establishing the role of ROS as a key driver in the activation process.	Acetylcysteine	77-80	AKT serine/threonine kinase 1	Homo sapiens	24-27
32512147-7	2020	Signaling activation of Akt and ERK was prevented by 5 mM N-Acetyl Cysteine (NAC) establishing the role of ROS as a key driver in the activation process.	Acetylcysteine	77-80	mitogen-activated protein kinase 1	Homo sapiens	32-35
32983963-11	2020	In addition, NAC (low concentration) and CQ, previously considered to be tumor inhibitors, were shown to promote tumorigenesis in PTC with high SIRT6 expression by inducing the Warburg effect.	Acetylcysteine	13-16	sirtuin 6	Mus musculus	144-149
32681471-8	2020	NAC increased RUNX3 and alleviated EMT.	Acetylcysteine	0-3	RUNX family transcription factor 3	Rattus norvegicus	14-19
32640348-4	2020	Furthermore, RT-qPCR and immunofluorescence assay results indicated that NAC restored the expression of Gclc, reduced the expression of ATF4, JNK and Caspase-12, and decreased the expression of eNOS and IGF-1, in the placenta.	Acetylcysteine	73-76	activating transcription factor 4	Mus musculus	136-140
32634696-4	2020	In addition, SSA promoted apoptosis and suppressed phosphorylation of NF-kappaB in vitro, which were restored by the ROS scavenger N-acetylcysteine (NAC).	Acetylcysteine	131-147	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	70-79
32634696-4	2020	In addition, SSA promoted apoptosis and suppressed phosphorylation of NF-kappaB in vitro, which were restored by the ROS scavenger N-acetylcysteine (NAC).	Acetylcysteine	149-152	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	70-79
32736702-5	2020	TGF-beta1 treatment increased reactive oxygen species (ROS) via NOX4 upregulation, which acts downstream of ERK and mTORC1, as the ROS scavenger N-acetylcysteine and a pan-NADPH oxidase (NOX) inhibitor DPI dissipated excess ROS generation.	Acetylcysteine	145-161	mitogen-activated protein kinase 1	Homo sapiens	108-111
32922532-8	2020	ROS exclusive inhibitor antioxidant N-acetyl cysteine (NAC) weakens the phosphorylation of JNK proteins induced by Propranolol.	Acetylcysteine	36-53	mitogen-activated protein kinase 8	Homo sapiens	91-94
32825644-7	2020	The use of antioxidants such as N-acetylcysteine (NAC) and diallyl sulfide (DAS), which is also a CYP2E1 inhibitor, reverted cell death and oxidative stress, modulating also the upstream angiogenesis and inflammation regulators.	Acetylcysteine	32-48	cytochrome P450 family 2 subfamily E member 1	Homo sapiens	98-104
32825644-7	2020	The use of antioxidants such as N-acetylcysteine (NAC) and diallyl sulfide (DAS), which is also a CYP2E1 inhibitor, reverted cell death and oxidative stress, modulating also the upstream angiogenesis and inflammation regulators.	Acetylcysteine	50-53	cytochrome P450 family 2 subfamily E member 1	Homo sapiens	98-104
32526201-9	2020	It was also revealed by CM-H2DCF-DA assay and Western blottings that NEP can reduce the production of ultraviolet B (UVB)-induced reactive oxygen species (ROS) like with N-acetylcysteine (NAC), resulting in decreasing the expression levels of skin aging-related proteins, such as phospho-ERK (p-ERK), phospho-p38 (p-p38), and phospho-JNK (p-JNK).	Acetylcysteine	170-186	membrane metalloendopeptidase	Homo sapiens	69-72
32526201-9	2020	It was also revealed by CM-H2DCF-DA assay and Western blottings that NEP can reduce the production of ultraviolet B (UVB)-induced reactive oxygen species (ROS) like with N-acetylcysteine (NAC), resulting in decreasing the expression levels of skin aging-related proteins, such as phospho-ERK (p-ERK), phospho-p38 (p-p38), and phospho-JNK (p-JNK).	Acetylcysteine	188-191	membrane metalloendopeptidase	Homo sapiens	69-72
32922532-8	2020	ROS exclusive inhibitor antioxidant N-acetyl cysteine (NAC) weakens the phosphorylation of JNK proteins induced by Propranolol.	Acetylcysteine	55-58	mitogen-activated protein kinase 8	Homo sapiens	91-94
32782443-0	2020	N-acetylcysteine alleviates post-resuscitation myocardial dysfunction and improves survival outcomes via partly inhibiting NLRP3 inflammasome induced-pyroptosis.	Acetylcysteine	0-16	NLR family, pyrin domain containing 3	Rattus norvegicus	123-128
32222495-7	2020	Meanwhile, the activation of the NF-E2-related factor-2 (NRF2)-driven stress gene activation, a key element involved in HIC, was suppressed by NAC.	Acetylcysteine	143-146	NFE2 like bZIP transcription factor 2	Homo sapiens	33-55
32222495-7	2020	Meanwhile, the activation of the NF-E2-related factor-2 (NRF2)-driven stress gene activation, a key element involved in HIC, was suppressed by NAC.	Acetylcysteine	143-146	NFE2 like bZIP transcription factor 2	Homo sapiens	57-61
32782443-9	2020	Results: Results showed that after treatment with NAC, there was significantly better myocardial function and survival duration; protein expression levels of NLRP3, adaptor apoptosis-associated speck-like protein (ASC), Cleaved-Caspase-1 and gasdermin D (GSDMD) in myocardial tissues were significantly decreased; and inflammatory cytokines levels were reduced.	Acetylcysteine	50-53	NLR family, pyrin domain containing 3	Rattus norvegicus	158-163
32782443-9	2020	Results: Results showed that after treatment with NAC, there was significantly better myocardial function and survival duration; protein expression levels of NLRP3, adaptor apoptosis-associated speck-like protein (ASC), Cleaved-Caspase-1 and gasdermin D (GSDMD) in myocardial tissues were significantly decreased; and inflammatory cytokines levels were reduced.	Acetylcysteine	50-53	gasdermin D	Rattus norvegicus	242-253
32782443-9	2020	Results: Results showed that after treatment with NAC, there was significantly better myocardial function and survival duration; protein expression levels of NLRP3, adaptor apoptosis-associated speck-like protein (ASC), Cleaved-Caspase-1 and gasdermin D (GSDMD) in myocardial tissues were significantly decreased; and inflammatory cytokines levels were reduced.	Acetylcysteine	50-53	gasdermin D	Rattus norvegicus	255-260
32583517-3	2020	Bmi-1-/- mice were treated with the antioxidant NAC, supplied in drinking water (Bmi-1-/- +NAC).	Acetylcysteine	48-51	Bmi1 polycomb ring finger oncogene	Mus musculus	0-5
32402895-10	2020	Dietary NAC exerted its positive action against arsenic intoxication by up-regulation of Bcl-2 gene expression along with the suppression of pro-apoptotic Bax gene and p53 gene.	Acetylcysteine	8-11	BCL2, apoptosis regulator	Rattus norvegicus	89-94
32275808-11	2020	However, N-acetylcysteine as ROS scavengers inhibited ABA-induced apoptosis and autophagy and reversed these ABA-mediated effects on PI3K/AKT/mTOR pathway.	Acetylcysteine	9-25	AKT serine/threonine kinase 1	Homo sapiens	138-141
32275808-11	2020	However, N-acetylcysteine as ROS scavengers inhibited ABA-induced apoptosis and autophagy and reversed these ABA-mediated effects on PI3K/AKT/mTOR pathway.	Acetylcysteine	9-25	mechanistic target of rapamycin kinase	Homo sapiens	142-146
32583517-3	2020	Bmi-1-/- mice were treated with the antioxidant NAC, supplied in drinking water (Bmi-1-/- +NAC).	Acetylcysteine	48-51	Bmi1 polycomb ring finger oncogene	Mus musculus	81-86
32583517-7	2020	Bmi-1-/- mice showed significantly lower superoxide dismutase (SOD)-1, SOD-2, glutathione peroxidase (GPX)-1 and GPX-3 levels than their wild-type littermates and Bmi-1-/- + NAC mice.	Acetylcysteine	174-177	Bmi1 polycomb ring finger oncogene	Mus musculus	0-5
32583517-8	2020	Relative to Bmi-1-/- mice, the control and Bmi-1-/- +NAC mice showed significantly lower p16, p21, and p53 levels.	Acetylcysteine	53-56	Bmi1 polycomb ring finger oncogene	Mus musculus	43-48
32583517-8	2020	Relative to Bmi-1-/- mice, the control and Bmi-1-/- +NAC mice showed significantly lower p16, p21, and p53 levels.	Acetylcysteine	53-56	cyclin dependent kinase inhibitor 2A	Mus musculus	89-92
32253651-9	2020	Moreover, N-acetyl-L-cysteine, an ROS scavenger, suppressed the TRAF6 accumulation induced by oxygen-glucose deprivation via suppression of ROS bursts.	Acetylcysteine	10-29	TNF receptor-associated factor 6	Mus musculus	64-69
32745510-10	2020	After pretreatment with NAC, the phosphorylation levels of AKT and ERK, which are crucial for regulating the proliferation, pluripotency, and differentiation of hESC, were significantly attenuated compared with the non-NAC pretreated exposure group.	Acetylcysteine	24-27	mitogen-activated protein kinase 1	Homo sapiens	67-70
32329019-3	2020	A secondary objective of this study was to analyze positive and negative sentiments regarding symptoms and treatment effects post N-acetylcysteine (NAC) administration in individuals with RYR1-RM.	Acetylcysteine	130-146	ryanodine receptor 1	Homo sapiens	188-192
32329019-3	2020	A secondary objective of this study was to analyze positive and negative sentiments regarding symptoms and treatment effects post N-acetylcysteine (NAC) administration in individuals with RYR1-RM.	Acetylcysteine	148-151	ryanodine receptor 1	Homo sapiens	188-192
32745510-10	2020	After pretreatment with NAC, the phosphorylation levels of AKT and ERK, which are crucial for regulating the proliferation, pluripotency, and differentiation of hESC, were significantly attenuated compared with the non-NAC pretreated exposure group.	Acetylcysteine	24-27	AKT serine/threonine kinase 1	Homo sapiens	59-62
32236775-0	2020	Correction to: Mixed methods analysis of Health-Related Quality of Life in ambulant individuals affected with RYR1-related myopathies pre-post-N-acetylcysteine therapy.	Acetylcysteine	143-159	ryanodine receptor 1	Homo sapiens	110-114
32848653-7	2020	N-acetylcysteine administration: (a) induced the Nrf2-ARE system, lowering the hippocampal oxidative stress assessed as the ratio of oxidized glutathione (GSSG)/reduced glutathione (GSH); (b) reduced the neuroinflammation assessed by astrocyte and microglial activation by immunofluorescence; and (c) inhibited chronic and relapse ethanol intake.	Acetylcysteine	0-16	NFE2 like bZIP transcription factor 2	Rattus norvegicus	49-53
32745510-10	2020	After pretreatment with NAC, the phosphorylation levels of AKT and ERK, which are crucial for regulating the proliferation, pluripotency, and differentiation of hESC, were significantly attenuated compared with the non-NAC pretreated exposure group.	Acetylcysteine	219-222	AKT serine/threonine kinase 1	Homo sapiens	59-62
32745510-10	2020	After pretreatment with NAC, the phosphorylation levels of AKT and ERK, which are crucial for regulating the proliferation, pluripotency, and differentiation of hESC, were significantly attenuated compared with the non-NAC pretreated exposure group.	Acetylcysteine	219-222	mitogen-activated protein kinase 1	Homo sapiens	67-70
32361974-5	2020	The presence of NAC antagonized the ROS production, expressions of IRE1alpha and p-IRE1alpha; however, STF-083010 could decrease the expression levels of GRP78, XBP1, NF-kappaB, and p-NF-kappaB and attenuate IL-1beta, IL-6, TNF-alpha, VCAM-1, and ET-1 release induced by endosulfan.	Acetylcysteine	16-19	nuclear factor kappa B subunit 1	Homo sapiens	184-193
32722598-7	2020	Treatment of cancer cell lines with the antioxidant N-acetylcysteine reduces the extent of membrane dysfunction and the expression of both CHOP-DR5 and miR-425-PTEN axes, attenuating PAM/TRAIL-induced cancer cell apoptosis.	Acetylcysteine	52-68	DNA damage inducible transcript 3	Homo sapiens	139-143
32722598-7	2020	Treatment of cancer cell lines with the antioxidant N-acetylcysteine reduces the extent of membrane dysfunction and the expression of both CHOP-DR5 and miR-425-PTEN axes, attenuating PAM/TRAIL-induced cancer cell apoptosis.	Acetylcysteine	52-68	TNF superfamily member 10	Homo sapiens	187-192
32717964-0	2020	N-acetylcysteine Provides Cytoprotection in Murine Oligodendrocytes through Heme Oxygenase-1 Activity.	Acetylcysteine	0-16	heme oxygenase 1	Mus musculus	76-92
32717964-11	2020	Inhibition of HO-1 activity abolished the cytoprotective effect of NAC with a corresponding decrease in total antioxidant capacity.	Acetylcysteine	67-70	heme oxygenase 1	Mus musculus	14-18
32708634-7	2020	Both CBD-induced LC3A/B-II levels and caspase-3 cleavage were reduced by NAC.	Acetylcysteine	73-76	caspase 3	Homo sapiens	38-47
32724493-11	2020	Finally, N-acetyl-cysteine (NAC) was added and its regulatory effect on the MAPK-NF-kappaB-MUC5B pathway was examined in PQ-induced cell inflammation.	Acetylcysteine	9-26	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	81-90
32724493-11	2020	Finally, N-acetyl-cysteine (NAC) was added and its regulatory effect on the MAPK-NF-kappaB-MUC5B pathway was examined in PQ-induced cell inflammation.	Acetylcysteine	28-31	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	81-90
32724493-15	2020	As expected, the addition of NAC efficiently suppresses the TNF-alpha and IL-6 secretion stimulated from PQ and also downregulated ERK, JNK, and p65 phosphorylation (ERK/JNK MAPK and NF-kappaB pathways) as well as MUC5B expression.	Acetylcysteine	29-32	tumor necrosis factor	Mus musculus	60-69
32724493-15	2020	As expected, the addition of NAC efficiently suppresses the TNF-alpha and IL-6 secretion stimulated from PQ and also downregulated ERK, JNK, and p65 phosphorylation (ERK/JNK MAPK and NF-kappaB pathways) as well as MUC5B expression.	Acetylcysteine	29-32	interleukin 6	Mus musculus	74-78
32724493-15	2020	As expected, the addition of NAC efficiently suppresses the TNF-alpha and IL-6 secretion stimulated from PQ and also downregulated ERK, JNK, and p65 phosphorylation (ERK/JNK MAPK and NF-kappaB pathways) as well as MUC5B expression.	Acetylcysteine	29-32	mitogen-activated protein kinase 1	Mus musculus	131-134
32724493-15	2020	As expected, the addition of NAC efficiently suppresses the TNF-alpha and IL-6 secretion stimulated from PQ and also downregulated ERK, JNK, and p65 phosphorylation (ERK/JNK MAPK and NF-kappaB pathways) as well as MUC5B expression.	Acetylcysteine	29-32	mitogen-activated protein kinase 1	Mus musculus	166-169
32724493-15	2020	As expected, the addition of NAC efficiently suppresses the TNF-alpha and IL-6 secretion stimulated from PQ and also downregulated ERK, JNK, and p65 phosphorylation (ERK/JNK MAPK and NF-kappaB pathways) as well as MUC5B expression.	Acetylcysteine	29-32	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	183-192
32724493-17	2020	NAC can attenuate PQ-induced cell inflammation at least in part by suppressing the MAPK-NF-kappaB-MUC5B pathway.	Acetylcysteine	0-3	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	88-97
32658869-7	2020	Decrease of mtROS with N-acetyl-L-cysteine attenuated the activation of JNK and the increase of SOD2 transcription.	Acetylcysteine	23-42	mitogen-activated protein kinase 8	Homo sapiens	72-75
32409143-10	2020	Meanwhile, the GNP-induced Nrf2 translocation (activation) was also reduced by NAC, JNK and p38 MAPK inhibitors, and nuclear transport inhibitor.	Acetylcysteine	79-82	NFE2 like bZIP transcription factor 2	Rattus norvegicus	27-31
32848840-17	2020	The antioxidant N-acetyl cysteine significantly reduced ROS production and the increase in IL-8 and VEGF expression following CFTR inhibition.	Acetylcysteine	16-33	C-X-C motif chemokine ligand 8	Homo sapiens	91-95
32848840-17	2020	The antioxidant N-acetyl cysteine significantly reduced ROS production and the increase in IL-8 and VEGF expression following CFTR inhibition.	Acetylcysteine	16-33	vascular endothelial growth factor A	Homo sapiens	100-104
32848840-17	2020	The antioxidant N-acetyl cysteine significantly reduced ROS production and the increase in IL-8 and VEGF expression following CFTR inhibition.	Acetylcysteine	16-33	CF transmembrane conductance regulator	Homo sapiens	126-130
32353423-10	2020	Application of N-acetylcysteine blocked AKT/FOXO3a/Bim signaling.	Acetylcysteine	15-31	AKT serine/threonine kinase 1	Homo sapiens	40-43
32353423-10	2020	Application of N-acetylcysteine blocked AKT/FOXO3a/Bim signaling.	Acetylcysteine	15-31	forkhead box O3	Homo sapiens	44-50
32361974-5	2020	The presence of NAC antagonized the ROS production, expressions of IRE1alpha and p-IRE1alpha; however, STF-083010 could decrease the expression levels of GRP78, XBP1, NF-kappaB, and p-NF-kappaB and attenuate IL-1beta, IL-6, TNF-alpha, VCAM-1, and ET-1 release induced by endosulfan.	Acetylcysteine	16-19	interleukin 6	Homo sapiens	218-222
32361974-5	2020	The presence of NAC antagonized the ROS production, expressions of IRE1alpha and p-IRE1alpha; however, STF-083010 could decrease the expression levels of GRP78, XBP1, NF-kappaB, and p-NF-kappaB and attenuate IL-1beta, IL-6, TNF-alpha, VCAM-1, and ET-1 release induced by endosulfan.	Acetylcysteine	16-19	tumor necrosis factor	Homo sapiens	224-233
32361974-5	2020	The presence of NAC antagonized the ROS production, expressions of IRE1alpha and p-IRE1alpha; however, STF-083010 could decrease the expression levels of GRP78, XBP1, NF-kappaB, and p-NF-kappaB and attenuate IL-1beta, IL-6, TNF-alpha, VCAM-1, and ET-1 release induced by endosulfan.	Acetylcysteine	16-19	vascular cell adhesion molecule 1	Homo sapiens	235-241
32361974-5	2020	The presence of NAC antagonized the ROS production, expressions of IRE1alpha and p-IRE1alpha; however, STF-083010 could decrease the expression levels of GRP78, XBP1, NF-kappaB, and p-NF-kappaB and attenuate IL-1beta, IL-6, TNF-alpha, VCAM-1, and ET-1 release induced by endosulfan.	Acetylcysteine	16-19	endothelin 1	Homo sapiens	247-251
32303987-10	2020	Intraperitoneal injection of N-acetyl-cysteine, a source of cysteine that prevents the oxidation of cysteine residues on MMP-9, significantly relieved high estrogen-induced postoperative hyperalgesia via suppression of MMP-9 and IL-1beta activation in DRGs.	Acetylcysteine	29-46	interleukin 1 alpha	Rattus norvegicus	229-237
32604833-9	2020	Pre-treatment with the antioxidant N-acetyl-L-cysteine (NAC) significantly suppressed DWP05195-induced CHOP expression and p38 activation.	Acetylcysteine	35-54	DNA damage inducible transcript 3	Homo sapiens	103-107
32347295-0	2020	Mechanism of N-acetylcysteine in alleviating diabetic myocardial ischemia reperfusion injury by regulating PTEN/Akt pathway through promoting DJ-1.	Acetylcysteine	13-29	AKT serine/threonine kinase 1	Rattus norvegicus	112-115
32347295-0	2020	Mechanism of N-acetylcysteine in alleviating diabetic myocardial ischemia reperfusion injury by regulating PTEN/Akt pathway through promoting DJ-1.	Acetylcysteine	13-29	Parkinsonism associated deglycase	Rattus norvegicus	142-146
32347295-6	2020	However, in the groups of HG-N, DM, HG-N+I/R and DM+I/R, NAC can significantly reduce oxidative stress injury and apoptosis rate of myocytes, promote the Bcl-2 and DJ-1 molecules, inhibit BAX and c-caspase-3 protein and PTEN/Akt pathway.	Acetylcysteine	57-60	BCL2, apoptosis regulator	Rattus norvegicus	154-159
32347295-6	2020	However, in the groups of HG-N, DM, HG-N+I/R and DM+I/R, NAC can significantly reduce oxidative stress injury and apoptosis rate of myocytes, promote the Bcl-2 and DJ-1 molecules, inhibit BAX and c-caspase-3 protein and PTEN/Akt pathway.	Acetylcysteine	57-60	AKT serine/threonine kinase 1	Rattus norvegicus	225-228
32347295-8	2020	Taken together, the findings suggest that NAC can reduce ischemia reperfusion injury in diabetic myocardium by up-regulating the PTEN/Akt pathway through the level of DJ-1.	Acetylcysteine	42-45	AKT serine/threonine kinase 1	Rattus norvegicus	134-137
32604833-9	2020	Pre-treatment with the antioxidant N-acetyl-L-cysteine (NAC) significantly suppressed DWP05195-induced CHOP expression and p38 activation.	Acetylcysteine	35-54	mitogen-activated protein kinase 14	Homo sapiens	123-126
32604833-9	2020	Pre-treatment with the antioxidant N-acetyl-L-cysteine (NAC) significantly suppressed DWP05195-induced CHOP expression and p38 activation.	Acetylcysteine	56-59	DNA damage inducible transcript 3	Homo sapiens	103-107
32604833-9	2020	Pre-treatment with the antioxidant N-acetyl-L-cysteine (NAC) significantly suppressed DWP05195-induced CHOP expression and p38 activation.	Acetylcysteine	56-59	mitogen-activated protein kinase 14	Homo sapiens	123-126
32585852-11	2020	In addition, the results indicate that TDR cells can be re-sensitized to BRAF pathway inhibitors by the ROS scavenger, N-Acetyl Cysteine (NAC).	Acetylcysteine	119-136	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	73-77
32585852-11	2020	In addition, the results indicate that TDR cells can be re-sensitized to BRAF pathway inhibitors by the ROS scavenger, N-Acetyl Cysteine (NAC).	Acetylcysteine	138-141	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	73-77
31482411-9	2020	Treatment with the ROS scavenger NAC had differential effects on ROS/RNS production and NF-kappaB activation during acute and chronic DTHR.	Acetylcysteine	33-36	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	88-97
32560255-6	2020	We found that quadriceps and gastrocnemius muscles of Bla/J mice exhibit high levels of lipid peroxidation, protein carbonyls and superoxide dismutase and catalase activities, which were significantly reduced by NAC supplementation.	Acetylcysteine	212-215	catalase	Mus musculus	155-163
32545880-11	2020	Meanwhile, NAC pretreatment also blocked the phosphorylation of ERK1/2 and p38 induced by NEFA, and the nucleation of Nrf2 and p53, suggesting that ROS plays a crucial role in regulating the NEFA-induced apoptosis of GCs.	Acetylcysteine	11-14	NFE2 like bZIP transcription factor 2	Bos taurus	118-122
32551386-6	2020	NAC-related increase in glutathione was associated with significant alterations in tumor necrosis factor-alpha (TNF-alpha), interleukin (IL)-6, IL-8 and IL-10 levels secreted in the culture medium.	Acetylcysteine	0-3	tumor necrosis factor	Homo sapiens	83-110
32551386-6	2020	NAC-related increase in glutathione was associated with significant alterations in tumor necrosis factor-alpha (TNF-alpha), interleukin (IL)-6, IL-8 and IL-10 levels secreted in the culture medium.	Acetylcysteine	0-3	tumor necrosis factor	Homo sapiens	112-121
32551386-6	2020	NAC-related increase in glutathione was associated with significant alterations in tumor necrosis factor-alpha (TNF-alpha), interleukin (IL)-6, IL-8 and IL-10 levels secreted in the culture medium.	Acetylcysteine	0-3	interleukin 6	Homo sapiens	124-142
32551386-6	2020	NAC-related increase in glutathione was associated with significant alterations in tumor necrosis factor-alpha (TNF-alpha), interleukin (IL)-6, IL-8 and IL-10 levels secreted in the culture medium.	Acetylcysteine	0-3	C-X-C motif chemokine ligand 8	Homo sapiens	144-148
32551386-7	2020	A substantial decrease in the IL-6, IL-8 and TNF-alpha levels in the culture medium supplemented with NAC was obvious in hepatocytes recovered 14 days after differentiation.	Acetylcysteine	102-105	interleukin 6	Homo sapiens	30-34
32551386-7	2020	A substantial decrease in the IL-6, IL-8 and TNF-alpha levels in the culture medium supplemented with NAC was obvious in hepatocytes recovered 14 days after differentiation.	Acetylcysteine	102-105	C-X-C motif chemokine ligand 8	Homo sapiens	36-40
32551386-7	2020	A substantial decrease in the IL-6, IL-8 and TNF-alpha levels in the culture medium supplemented with NAC was obvious in hepatocytes recovered 14 days after differentiation.	Acetylcysteine	102-105	tumor necrosis factor	Homo sapiens	45-54
31482411-4	2020	Mice were treated with the ROS-scavenging and NF-kappaB inhibiting molecule N-acetylcysteine (NAC) or underwent sham treatment.	Acetylcysteine	76-92	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	46-55
31482411-4	2020	Mice were treated with the ROS-scavenging and NF-kappaB inhibiting molecule N-acetylcysteine (NAC) or underwent sham treatment.	Acetylcysteine	94-97	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	46-55
31837856-8	2020	Incidentally, both CH and NAC attenuated the EOM-induced changes in the mRNA expression of genes involved in cardiac development (nkx2.5, sox9b), oxidative stress (nrf2a, nrf2b, gstp1, gstp2, sod2, ho1, cat) and apoptosis (p53, bax).	Acetylcysteine	26-29	superoxide dismutase 2, mitochondrial	Danio rerio	192-196
32450865-10	2020	In the unfolded protein response (UPR) pathway, the expression of ECHS1, HSP60, and HSP70 was decreased in the HFD group (p < 0.05) and rescued by NAC therapy.	Acetylcysteine	147-150	heat shock protein 1B	Mus musculus	84-89
32566089-7	2020	N-Acetylcysteine (NAC) manifested similar effects as melatonin in scavenging ROS, maintaining prolyl-hydroxylase activity, and mitigating HIF-1alpha transcriptional activity in nickel-exposed cells.	Acetylcysteine	0-16	hypoxia inducible factor 1 subunit alpha	Homo sapiens	138-148
32566089-7	2020	N-Acetylcysteine (NAC) manifested similar effects as melatonin in scavenging ROS, maintaining prolyl-hydroxylase activity, and mitigating HIF-1alpha transcriptional activity in nickel-exposed cells.	Acetylcysteine	18-21	hypoxia inducible factor 1 subunit alpha	Homo sapiens	138-148
32432106-8	2020	In addition, suppressing ROS production by N-acetyl-L-cysteine down-regulated the number of intracellular autophagosomes and the expression of Beclin-1, ATG5, and cytokines IL-1beta, IL-6, and TNF-alpha.	Acetylcysteine	43-62	autophagy protein 5	Ovis aries	153-157
32670550-9	2020	Furthermore, hypoxia increased the expression of transforming growth factor-beta, and the activation of matrix metalloproteinases were suppressed by the treatment of beta-Es as well as pretreatment with N-acetylcysteine (NAC).	Acetylcysteine	203-219	tumor necrosis factor	Homo sapiens	49-80
32670550-9	2020	Furthermore, hypoxia increased the expression of transforming growth factor-beta, and the activation of matrix metalloproteinases were suppressed by the treatment of beta-Es as well as pretreatment with N-acetylcysteine (NAC).	Acetylcysteine	221-224	tumor necrosis factor	Homo sapiens	49-80
32432106-8	2020	In addition, suppressing ROS production by N-acetyl-L-cysteine down-regulated the number of intracellular autophagosomes and the expression of Beclin-1, ATG5, and cytokines IL-1beta, IL-6, and TNF-alpha.	Acetylcysteine	43-62	interleukin-6	Ovis aries	183-187
31957488-4	2020	The ROS scavenger N-acetyl-l-cysteine reduced Ang II-induced oxidative stress and apoptosis, indicating that ROS generation is involved in the Ang II-induced mitochondria-mediated apoptotic pathway.	Acetylcysteine	18-37	angiotensinogen	Homo sapiens	46-52
31957488-4	2020	The ROS scavenger N-acetyl-l-cysteine reduced Ang II-induced oxidative stress and apoptosis, indicating that ROS generation is involved in the Ang II-induced mitochondria-mediated apoptotic pathway.	Acetylcysteine	18-37	angiotensinogen	Homo sapiens	143-149
32568258-6	2020	N-acetylcysteine increased the number of immune cells and decreased TNF-alpha production after cyclophosphamide injection and decreased TNF-alpha, IFN-gamma, NF-kappaB, and IL-8 expression and increased IL-10 expression in peripheral blood mononuclear cells.	Acetylcysteine	0-16	IL10	Sus scrofa	203-208
32395078-6	2020	Pretreating cells with either NAC or DPI significantly enhanced the oncogenic H-Ras-mediated down-regulation of mdr1b expression and markedly prevented doxorubicin-induced cell death.	Acetylcysteine	30-33	ATP-binding cassette, sub-family B (MDR/TAP), member 1B	Mus musculus	112-117
32392918-6	2020	Pretreating cells with either NAC or DPI significantly enhanced the oncogenic H-Ras-mediated down-regulation of mdr1b expression and markedly prevented doxorubicin-induced cell death.	Acetylcysteine	30-33	ATP-binding cassette, sub-family B (MDR/TAP), member 1B	Mus musculus	112-117
32392918-7	2020	Moreover, NAC and DPI treatment led to a decrease in ERK activity, and the ERK inhibitors PD98059 or U0126 enhanced the mdr1b-Luc activity of H-RasV12-NIH3T3 and reduced doxorubicin-induced apoptosis.	Acetylcysteine	10-13	mitogen-activated protein kinase 1	Mus musculus	53-56
32395078-7	2020	Moreover, NAC and DPI treatment led to a decrease in ERK activity, and the ERK inhibitors PD98059 or U0126 enhanced the mdr1b-Luc activity of H-RasV12-NIH3T3 and reduced doxorubicin-induced apoptosis.	Acetylcysteine	10-13	mitogen-activated protein kinase 1	Mus musculus	53-56
32146648-6	2020	Corroborating the above observations, we found that the ROS scavenger N-acetylcysteine (NAC) countered caspase-3 activity and the cells were rescued from apoptosis.	Acetylcysteine	70-86	caspase 3	Homo sapiens	103-112
32146648-6	2020	Corroborating the above observations, we found that the ROS scavenger N-acetylcysteine (NAC) countered caspase-3 activity and the cells were rescued from apoptosis.	Acetylcysteine	88-91	caspase 3	Homo sapiens	103-112
32006234-9	2020	Thiol antioxidants such as N-acetyl cysteine and glutathione reduced the neurotoxicity of 15d-PGJ2 but enhanced that of the anti-NSE antibody.	Acetylcysteine	27-44	enolase 2	Homo sapiens	129-132
32378169-11	2020	There was decline of IKK-beta and NF-kappaB-P65 and elevation of IkappaB-alpha in the N-acetylcysteine group, which was even significantly in the Budesonide group (P < 0.01).	Acetylcysteine	86-102	nuclear factor of kappa light polypeptide gene enhancer in B cells inhibitor, alpha	Mus musculus	65-78
31587481-8	2020	The NAC therapy considerably attenuated the exacerbated effects of BPA, which was associated with increased AMP-activated protein kinase (AMPK), PGC-1alpha, silent information regulator 3 or sirtuin 3 (SIRT3), and mitofusin 2 (MFN2) expressions but decreased Phosphorylated dynamin-related protein 1 (p-DRP1)/Dynamin-related protein 1 (DRP1), PTEN-induced putative kinase (PINK), and PARKIN expressions.	Acetylcysteine	4-7	PPARG coactivator 1 alpha	Rattus norvegicus	145-155
32316268-7	2020	P2X7R deletion also increased expressions of GS and ASCT2 (a glutamine:cysteine exchanger), but diminished the efficacy of N-acetylcysteine (NAC, a GSH precursor) in the GSH level.	Acetylcysteine	123-139	purinergic receptor P2X, ligand-gated ion channel, 7	Mus musculus	0-5
32316268-7	2020	P2X7R deletion also increased expressions of GS and ASCT2 (a glutamine:cysteine exchanger), but diminished the efficacy of N-acetylcysteine (NAC, a GSH precursor) in the GSH level.	Acetylcysteine	141-144	purinergic receptor P2X, ligand-gated ion channel, 7	Mus musculus	0-5
32322478-7	2020	Conclusion: Oral and IV glutathione, glutathione precursors (N-acetyl-cysteine) and alpha lipoic acid may represent a novel treatment approach for blocking NF-kappaB and addressing "cytokine storm syndrome" and respiratory distress in patients with COVID-19 pneumonia.	Acetylcysteine	61-78	nuclear factor kappa B subunit 1	Homo sapiens	156-165
31587481-9	2020	These findings reveal the detrimental effect of repeated BPA exposure on the renal outcomes following the IR episode, and further demonstrate the protective efficacy of NAC by maintaining mitochondrial homeostasis, which is, partly, mediated through the AMPK-PGC-1alpha-SIRT3 axis.	Acetylcysteine	169-172	PPARG coactivator 1 alpha	Rattus norvegicus	259-269
32040762-3	2020	This study aims to investigate the expressions of IL-6, MIP-2, and MCP-5, as biomarkers in relation with MeHg-induced CNS impairment and N-acetyl-L-cysteine (NAC) treatment in mice, as well as histopathological changes of brain tissue and clinical symptom such as ataxia.	Acetylcysteine	137-156	interleukin 6	Mus musculus	50-54
32233142-10	2020	MS at 100 muM increased the generation of ROS, and MS-induced permeability increase was attenuated after co-exposure to 50 muM N-acetyl cysteine.	Acetylcysteine	127-144	latexin	Homo sapiens	123-126
32040762-8	2020	NAC significantly suppressed MeHg-induced IL-6 and MIP-2 expressions in the serum (p &lt; 0.05 for both), and slightly reduced MCP-5 expression in the cerebrum.	Acetylcysteine	0-3	interleukin 6	Mus musculus	42-46
32040762-8	2020	NAC significantly suppressed MeHg-induced IL-6 and MIP-2 expressions in the serum (p &lt; 0.05 for both), and slightly reduced MCP-5 expression in the cerebrum.	Acetylcysteine	0-3	chemokine (C-X-C motif) ligand 2	Mus musculus	51-56
31941795-0	2020	Randomized controlled trial of N-acetylcysteine therapy for RYR1-related myopathies.	Acetylcysteine	31-47	ryanodine receptor 1	Homo sapiens	60-64
31941795-1	2020	OBJECTIVE: To investigate the efficacy of N-acetylcysteine (NAC) for decreasing elevated oxidative stress and increasing physical endurance in individuals with ryanodine receptor 1-related myopathies (RYR1-RM).	Acetylcysteine	42-58	ryanodine receptor 1	Homo sapiens	160-180
31941795-1	2020	OBJECTIVE: To investigate the efficacy of N-acetylcysteine (NAC) for decreasing elevated oxidative stress and increasing physical endurance in individuals with ryanodine receptor 1-related myopathies (RYR1-RM).	Acetylcysteine	42-58	ryanodine receptor 1	Homo sapiens	201-205
31941795-1	2020	OBJECTIVE: To investigate the efficacy of N-acetylcysteine (NAC) for decreasing elevated oxidative stress and increasing physical endurance in individuals with ryanodine receptor 1-related myopathies (RYR1-RM).	Acetylcysteine	60-63	ryanodine receptor 1	Homo sapiens	160-180
31941795-1	2020	OBJECTIVE: To investigate the efficacy of N-acetylcysteine (NAC) for decreasing elevated oxidative stress and increasing physical endurance in individuals with ryanodine receptor 1-related myopathies (RYR1-RM).	Acetylcysteine	60-63	ryanodine receptor 1	Homo sapiens	201-205
31941795-10	2020	CLASSIFICATION OF EVIDENCE: This study provides Class I evidence that, for people with RYR1-RM, treatment with oral NAC does not decrease oxidative stress as measured by 15-F2t isoprostane.	Acetylcysteine	116-119	ryanodine receptor 1	Homo sapiens	87-91
32104284-11	2020	In conclusion, tetrandrine combined with acetylcysteine can improve pulmonary function and exercise tolerance of patients with silicosis by inhibiting the expressions of TGF-beta1 and MMP-7, thus improving clinical efficacy.	Acetylcysteine	41-55	transforming growth factor beta 1	Homo sapiens	170-179
32155766-8	2020	N-acetyl-L-cysteine (NAC) markedly decreased PCV2-induced ROS, down-regulated Drp1 phosphorylation, and lessened PINK1 expression and mitochondrial accumulation of Parkin.	Acetylcysteine	0-19	PTEN induced kinase 1	Sus scrofa	113-118
32155766-8	2020	N-acetyl-L-cysteine (NAC) markedly decreased PCV2-induced ROS, down-regulated Drp1 phosphorylation, and lessened PINK1 expression and mitochondrial accumulation of Parkin.	Acetylcysteine	21-24	PTEN induced kinase 1	Sus scrofa	113-118
31724279-7	2020	N-acetyl-L-cysteine, an ROS inhibitor, prevented p,p"-DDT-induced promotion of aerobic glycolysis, ERK1/2 activation, upregulation, and nucleus translocation of PKM2.	Acetylcysteine	0-19	mitogen-activated protein kinase 3	Homo sapiens	99-105
32131874-9	2020	RESULTS: Low-dose NAC (1000 muM) increased the expression of Nrf2 and phospho-p62 in MH7A cells, activating antioxidant genes, suppressing the expression of MMP-3, and inhibiting the phosphorylation of JNK.	Acetylcysteine	18-21	NFE2 like bZIP transcription factor 2	Homo sapiens	61-65
32131874-9	2020	RESULTS: Low-dose NAC (1000 muM) increased the expression of Nrf2 and phospho-p62 in MH7A cells, activating antioxidant genes, suppressing the expression of MMP-3, and inhibiting the phosphorylation of JNK.	Acetylcysteine	18-21	matrix metallopeptidase 3	Homo sapiens	157-162
32131874-9	2020	RESULTS: Low-dose NAC (1000 muM) increased the expression of Nrf2 and phospho-p62 in MH7A cells, activating antioxidant genes, suppressing the expression of MMP-3, and inhibiting the phosphorylation of JNK.	Acetylcysteine	18-21	mitogen-activated protein kinase 8	Homo sapiens	202-205
32440328-3	2020	Therefore, the present study was designed to explore the possible role of matrix metalloproteinases (MMP), tissue inhibitors of metalloproteinases (TIMP) and transforming growth factor-beta1 (TGF-beta1) pathway and their modulation by NAC in attenuating bleomycin-induced pulmonary fibrosis in rats.	Acetylcysteine	235-238	transforming growth factor, beta 1	Rattus norvegicus	192-201
32440328-10	2020	Moreover, NAC attenuated bleomycin-induced increased expression of TGF-beta1 and total lung collagen levels.	Acetylcysteine	10-13	transforming growth factor, beta 1	Rattus norvegicus	67-76
32036895-7	2020	Pretreatment with ROS scavenger N-acetyl cysteine (NAC) attenuated the impact of CWE on mitochondria-related apoptosis proteins, and partially recovered the inhibition of Akt phosphorylation.	Acetylcysteine	32-49	AKT serine/threonine kinase 1	Homo sapiens	171-174
32036895-7	2020	Pretreatment with ROS scavenger N-acetyl cysteine (NAC) attenuated the impact of CWE on mitochondria-related apoptosis proteins, and partially recovered the inhibition of Akt phosphorylation.	Acetylcysteine	51-54	AKT serine/threonine kinase 1	Homo sapiens	171-174
31883977-10	2020	The antioxidant N-acetylcysteine (NAC) reduces fumarate levels, protein succination and CHOP levels in adipocytes matured in high glucose.	Acetylcysteine	16-32	DNA damage inducible transcript 3	Homo sapiens	88-92
31945496-11	2020	Interestingly, mutation of redox sensitive cysteine residues at 124, 141 and 182 position in p53 significantly reduces mal C plus NAC mediated sensitization of cancer cells.	Acetylcysteine	130-133	tumor protein p53	Homo sapiens	93-96
32016465-15	2020	Finally, it was determined that combined treatment of LIUS and Dox induced anticancer effects by blocking the activation of the AKT/mTOR pathway, as demonstrated by the downregulation of phosphorylated (p-)AKT and p-mTOR; N-acetylcysteine, a general ROS inhibitor reversed the suppressive effects on the AKT/mTOR pathway mediated by LIUS and Dox.	Acetylcysteine	222-238	AKT serine/threonine kinase 1	Homo sapiens	128-131
32016465-15	2020	Finally, it was determined that combined treatment of LIUS and Dox induced anticancer effects by blocking the activation of the AKT/mTOR pathway, as demonstrated by the downregulation of phosphorylated (p-)AKT and p-mTOR; N-acetylcysteine, a general ROS inhibitor reversed the suppressive effects on the AKT/mTOR pathway mediated by LIUS and Dox.	Acetylcysteine	222-238	mechanistic target of rapamycin kinase	Homo sapiens	132-136
31883977-10	2020	The antioxidant N-acetylcysteine (NAC) reduces fumarate levels, protein succination and CHOP levels in adipocytes matured in high glucose.	Acetylcysteine	34-37	DNA damage inducible transcript 3	Homo sapiens	88-92
31883977-12	2020	NAC treatment restores adipocyte IL-13 secretion, confirming the redox-dependent regulation of a potent anti-inflammatory eotaxin.	Acetylcysteine	0-3	interleukin 13	Homo sapiens	33-38
31883977-12	2020	NAC treatment restores adipocyte IL-13 secretion, confirming the redox-dependent regulation of a potent anti-inflammatory eotaxin.	Acetylcysteine	0-3	C-C motif chemokine ligand 11	Homo sapiens	122-129
31995555-8	2020	Notably, the triple treatment-induced cytotoxic effects and the elevated expression of p53 and p21 proteins as well as the increased Bax/Bcl-2 ratio, all could be alleviated by the ROS scavenger, N-acetyl-cysteine (NAC).	Acetylcysteine	196-213	BCL2 associated X, apoptosis regulator	Homo sapiens	133-136
31838118-11	2020	Furthermore, NAC improved redox and inflammatory status; decreased levels of RIPK3, MLKL, NLRP3, IL-18; down-regulated ASC, iNOS, GFAP and MMP-9 expression; and decreased myeloperoxidase activity in cerebral cortex.	Acetylcysteine	13-16	mixed lineage kinase domain like pseudokinase	Rattus norvegicus	84-88
31838118-11	2020	Furthermore, NAC improved redox and inflammatory status; decreased levels of RIPK3, MLKL, NLRP3, IL-18; down-regulated ASC, iNOS, GFAP and MMP-9 expression; and decreased myeloperoxidase activity in cerebral cortex.	Acetylcysteine	13-16	NLR family, pyrin domain containing 3	Rattus norvegicus	90-95
31838118-11	2020	Furthermore, NAC improved redox and inflammatory status; decreased levels of RIPK3, MLKL, NLRP3, IL-18; down-regulated ASC, iNOS, GFAP and MMP-9 expression; and decreased myeloperoxidase activity in cerebral cortex.	Acetylcysteine	13-16	nitric oxide synthase 2	Rattus norvegicus	124-128
31891230-1	2020	We aimed to explore the molecular substrate underlying EGFR-TKI resistance and investigate the effects of N-acetylcysteine (NAC) on reversing EGFR-TKI resistance.	Acetylcysteine	124-127	epidermal growth factor receptor	Homo sapiens	142-146
31891230-3	2020	CCK8 assay showed that NAC plus gefitinib combination overcame EGFR-TKI resistance in non-small cell lung cancer (NSCLC) cells by lowering the value of half maximal inhibitory concentration (IC50).	Acetylcysteine	23-26	epidermal growth factor receptor	Homo sapiens	63-67
31891230-9	2020	Our findings suggest that NAC could restore the sensitivity of gefitinib-resistant NSCLC cells to gefitinib via suppressing Src activation and reversing epithelial-mesenchymal transition.	Acetylcysteine	26-29	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	124-127
31631367-17	2020	NAC or DEX administration can attenuate ALI by rebalancing Th1/Th2/Th17 cytokines.	Acetylcysteine	0-3	negative elongation factor complex member C/D, Th1l	Mus musculus	59-62
31631367-0	2020	Co-administration of N-acetylcysteine and dexmedetomidine plays a synergistic effect on protection of LPS-induced acute lung injury via correcting Th1/Th2/Th17 cytokines imbalance.	Acetylcysteine	21-37	negative elongation factor complex member C/D, Th1l	Mus musculus	147-150
31631367-15	2020	Combination of NAC with DEX obtained a maximum effect on decreasing Galectin-9/Tim-3 expression.	Acetylcysteine	15-18	lectin, galactose binding, soluble 9	Mus musculus	68-78
31857234-5	2020	NQO1 deficiency in vitro exacerbated the estrogen-DNA adduct formation and loss of cell viability, which was rescued by the supplementation of N-acetylcysteine, a ROS scavenger.	Acetylcysteine	143-159	NAD(P)H quinone dehydrogenase 1	Homo sapiens	0-4
31917283-7	2020	An anti-oxidant, N-acetylcysteine mimicked the effects of MS on ROS generation, RAGE gene expression, and lipid accumulation.	Acetylcysteine	17-33	advanced glycosylation end product-specific receptor	Rattus norvegicus	80-84
31978215-6	2020	In vitro analysis of platelet activation revealed that NAC reduced thrombin-induced platelet-leukocyte aggregate formation in JAK2V617F mice.	Acetylcysteine	55-58	coagulation factor II	Mus musculus	67-75
31995555-8	2020	Notably, the triple treatment-induced cytotoxic effects and the elevated expression of p53 and p21 proteins as well as the increased Bax/Bcl-2 ratio, all could be alleviated by the ROS scavenger, N-acetyl-cysteine (NAC).	Acetylcysteine	196-213	tumor protein p53	Homo sapiens	87-90
31995555-8	2020	Notably, the triple treatment-induced cytotoxic effects and the elevated expression of p53 and p21 proteins as well as the increased Bax/Bcl-2 ratio, all could be alleviated by the ROS scavenger, N-acetyl-cysteine (NAC).	Acetylcysteine	196-213	BCL2 apoptosis regulator	Homo sapiens	137-142
31995555-8	2020	Notably, the triple treatment-induced cytotoxic effects and the elevated expression of p53 and p21 proteins as well as the increased Bax/Bcl-2 ratio, all could be alleviated by the ROS scavenger, N-acetyl-cysteine (NAC).	Acetylcysteine	215-218	tumor protein p53	Homo sapiens	87-90
31995555-8	2020	Notably, the triple treatment-induced cytotoxic effects and the elevated expression of p53 and p21 proteins as well as the increased Bax/Bcl-2 ratio, all could be alleviated by the ROS scavenger, N-acetyl-cysteine (NAC).	Acetylcysteine	215-218	BCL2 associated X, apoptosis regulator	Homo sapiens	133-136
31995555-8	2020	Notably, the triple treatment-induced cytotoxic effects and the elevated expression of p53 and p21 proteins as well as the increased Bax/Bcl-2 ratio, all could be alleviated by the ROS scavenger, N-acetyl-cysteine (NAC).	Acetylcysteine	215-218	BCL2 apoptosis regulator	Homo sapiens	137-142
31991904-8	2020	Pre-treatment with N-acetyl-l-cysteine and antioxidant enzymes (superoxide dismutase and catalase) significantly suppressed AG-1-induced toxicity, suggesting that superoxide and hydrogen peroxide contribute to AG-1-induced toxicity in human cancer cells.	Acetylcysteine	19-38	catalase	Homo sapiens	89-97
32089786-6	2020	Interestingly, ET-1 significantly increased reactive oxygen species (ROS) production in association with SO2/AAT pathway downregulation in VSMCs compared with controls, while the ROS scavenger N-acetyl-L-cysteine (NAC) and the antioxidant glutathione (GSH) significantly abolished the ET-1-stimulated downregulation of the SO2/AAT pathway.	Acetylcysteine	193-212	endothelin 1	Rattus norvegicus	15-19
32089786-6	2020	Interestingly, ET-1 significantly increased reactive oxygen species (ROS) production in association with SO2/AAT pathway downregulation in VSMCs compared with controls, while the ROS scavenger N-acetyl-L-cysteine (NAC) and the antioxidant glutathione (GSH) significantly abolished the ET-1-stimulated downregulation of the SO2/AAT pathway.	Acetylcysteine	214-217	endothelin 1	Rattus norvegicus	15-19
32089786-7	2020	Moreover, the AAT activity was reduced in purified protein after the treatment for 2 h. However, NAC and GSH blocked the hydrogen peroxide-induced AAT activity reduction.	Acetylcysteine	97-100	glutamic-oxaloacetic transaminase 2	Rattus norvegicus	14-17
32089786-7	2020	Moreover, the AAT activity was reduced in purified protein after the treatment for 2 h. However, NAC and GSH blocked the hydrogen peroxide-induced AAT activity reduction.	Acetylcysteine	97-100	glutamic-oxaloacetic transaminase 2	Rattus norvegicus	147-150
31780563-9	2020	For arsenite, but not for sorbitol, quenching oxidative stress with N-acetylcysteine did suppress both SG formation and TDP-43 ubiquitylation and insolubility.	Acetylcysteine	68-84	TAR DNA binding protein	Homo sapiens	120-126
31845986-6	2020	The increased MN formation in irradiated OXR1-depleted cells was partially attenuated by the ROS inhibitor N-acetyl-L-cysteine, suggesting that OXR1-depeletion increases ROS-dependent genome instability.	Acetylcysteine	107-126	oxidation resistance 1	Homo sapiens	41-45
31845986-6	2020	The increased MN formation in irradiated OXR1-depleted cells was partially attenuated by the ROS inhibitor N-acetyl-L-cysteine, suggesting that OXR1-depeletion increases ROS-dependent genome instability.	Acetylcysteine	107-126	oxidation resistance 1	Homo sapiens	144-148
32064022-9	2020	The ROS scavenger N-acetyl cysteine (NAC) significantly attenuated hERG reduction induced by THIO and abolished the upregulation of ER stress marker proteins.	Acetylcysteine	18-35	ETS transcription factor ERG	Homo sapiens	67-71
32064022-9	2020	The ROS scavenger N-acetyl cysteine (NAC) significantly attenuated hERG reduction induced by THIO and abolished the upregulation of ER stress marker proteins.	Acetylcysteine	37-40	ETS transcription factor ERG	Homo sapiens	67-71
31790703-8	2020	Antioxidant N-acetylcysteine (NAC) or three MAPK inhibitors blocked the nuclear translocation of Nrf2 and HO-1 expression induced by Aureusidin, indicating that Aureusidin activated the Nrf2/HO-1 signaling pathway through ROS and MAPKs pathways.	Acetylcysteine	12-28	nuclear factor, erythroid derived 2, like 2	Mus musculus	97-101
31669540-11	2020	N-acetyl-l-cysteine treatment attenuated the 15-keto PGE2-induced phosphorylation of GSK3beta, transcriptional activity of Nrf2, and subsequently HO-1 expression.	Acetylcysteine	0-19	NFE2 like bZIP transcription factor 2	Homo sapiens	123-127
31812668-4	2020	We demonstrate that mutant p53 induces MnSOD expression, which is recovered by the ROS scavenger N-acetyl-l-cysteine.	Acetylcysteine	97-116	tumor protein p53	Homo sapiens	27-30
31790703-8	2020	Antioxidant N-acetylcysteine (NAC) or three MAPK inhibitors blocked the nuclear translocation of Nrf2 and HO-1 expression induced by Aureusidin, indicating that Aureusidin activated the Nrf2/HO-1 signaling pathway through ROS and MAPKs pathways.	Acetylcysteine	12-28	heme oxygenase 1	Mus musculus	106-110
31790703-8	2020	Antioxidant N-acetylcysteine (NAC) or three MAPK inhibitors blocked the nuclear translocation of Nrf2 and HO-1 expression induced by Aureusidin, indicating that Aureusidin activated the Nrf2/HO-1 signaling pathway through ROS and MAPKs pathways.	Acetylcysteine	12-28	nuclear factor, erythroid derived 2, like 2	Mus musculus	186-190
31790703-8	2020	Antioxidant N-acetylcysteine (NAC) or three MAPK inhibitors blocked the nuclear translocation of Nrf2 and HO-1 expression induced by Aureusidin, indicating that Aureusidin activated the Nrf2/HO-1 signaling pathway through ROS and MAPKs pathways.	Acetylcysteine	12-28	heme oxygenase 1	Mus musculus	191-195
31790703-8	2020	Antioxidant N-acetylcysteine (NAC) or three MAPK inhibitors blocked the nuclear translocation of Nrf2 and HO-1 expression induced by Aureusidin, indicating that Aureusidin activated the Nrf2/HO-1 signaling pathway through ROS and MAPKs pathways.	Acetylcysteine	30-33	nuclear factor, erythroid derived 2, like 2	Mus musculus	97-101
31790703-8	2020	Antioxidant N-acetylcysteine (NAC) or three MAPK inhibitors blocked the nuclear translocation of Nrf2 and HO-1 expression induced by Aureusidin, indicating that Aureusidin activated the Nrf2/HO-1 signaling pathway through ROS and MAPKs pathways.	Acetylcysteine	30-33	heme oxygenase 1	Mus musculus	106-110
32021099-13	2020	N-acetylcysteine treatment of gastric cancer cells inhibited ROS production and Akt-mTOR, Stat3, and IkappaBalpha phosphorylation.	Acetylcysteine	0-16	AKT serine/threonine kinase 1	Homo sapiens	80-83
31790703-8	2020	Antioxidant N-acetylcysteine (NAC) or three MAPK inhibitors blocked the nuclear translocation of Nrf2 and HO-1 expression induced by Aureusidin, indicating that Aureusidin activated the Nrf2/HO-1 signaling pathway through ROS and MAPKs pathways.	Acetylcysteine	30-33	nuclear factor, erythroid derived 2, like 2	Mus musculus	186-190
32021099-13	2020	N-acetylcysteine treatment of gastric cancer cells inhibited ROS production and Akt-mTOR, Stat3, and IkappaBalpha phosphorylation.	Acetylcysteine	0-16	mechanistic target of rapamycin kinase	Homo sapiens	84-88
32021099-13	2020	N-acetylcysteine treatment of gastric cancer cells inhibited ROS production and Akt-mTOR, Stat3, and IkappaBalpha phosphorylation.	Acetylcysteine	0-16	signal transducer and activator of transcription 3	Homo sapiens	90-95
31790703-8	2020	Antioxidant N-acetylcysteine (NAC) or three MAPK inhibitors blocked the nuclear translocation of Nrf2 and HO-1 expression induced by Aureusidin, indicating that Aureusidin activated the Nrf2/HO-1 signaling pathway through ROS and MAPKs pathways.	Acetylcysteine	30-33	heme oxygenase 1	Mus musculus	191-195
32021099-13	2020	N-acetylcysteine treatment of gastric cancer cells inhibited ROS production and Akt-mTOR, Stat3, and IkappaBalpha phosphorylation.	Acetylcysteine	0-16	NFKB inhibitor alpha	Homo sapiens	101-113
31707348-5	2020	In angiotensin II (Ang II)-treated cardiomyocytes, BRD4 decrease markedly blunted the prohypertrophic effect, which was further promoted by the combinational treatment of ROS scavenger (N-acetyl-cysteine, NAC).	Acetylcysteine	186-203	angiotensinogen (serpin peptidase inhibitor, clade A, member 8)	Mus musculus	3-17
31721616-10	2020	Furthermore, the induction of Pdk4 and Pck1 in WAT culture by CL316,243 was markedly reduced in the presence of antioxidants N-acetylcysteine or vitamin E.	Acetylcysteine	125-141	pyruvate dehydrogenase kinase, isoenzyme 4	Mus musculus	30-34
31906396-8	2020	Finally, TGF-beta1-induced proliferation and activation were also suppressed by N-acetylcysteine.	Acetylcysteine	80-96	transforming growth factor beta 1	Homo sapiens	9-18
33268712-3	2020	Renal expression of type III collagen and tumor necrosis factor (TNF)-alpha mRNAs was elevated in UUO mice and inhibited by NAC.	Acetylcysteine	124-127	tumor necrosis factor	Mus musculus	42-75
33268712-6	2020	Together, the results of this study suggest that renal interstitial fibrosis induced by UUO was ameliorated by NAC via several mechanisms including increased glutathione peroxidase activity, reduced phosphorylation of ERK1/2, and reduced expression of TNF-alpha and type III collagen mRNAs.	Acetylcysteine	111-114	tumor necrosis factor	Mus musculus	252-261
31931804-10	2020	RESULTS: In the present paper we showed how NAC supplementation affected parameters of oxidative stress (GSH, MDA, SOD), inflammation such as cytokines levels (IL-1beta, IL-6, TNFalpha) and mast cell activation and consequently on induced pain, during leishmaniosis in BALB\c mice.	Acetylcysteine	44-47	interleukin 1 beta	Mus musculus	160-168
31931804-10	2020	RESULTS: In the present paper we showed how NAC supplementation affected parameters of oxidative stress (GSH, MDA, SOD), inflammation such as cytokines levels (IL-1beta, IL-6, TNFalpha) and mast cell activation and consequently on induced pain, during leishmaniosis in BALB\c mice.	Acetylcysteine	44-47	interleukin 6	Mus musculus	170-174
31931804-10	2020	RESULTS: In the present paper we showed how NAC supplementation affected parameters of oxidative stress (GSH, MDA, SOD), inflammation such as cytokines levels (IL-1beta, IL-6, TNFalpha) and mast cell activation and consequently on induced pain, during leishmaniosis in BALB\c mice.	Acetylcysteine	44-47	tumor necrosis factor	Mus musculus	176-184
31940946-9	2020	The anti-oxidant N-acetyl cysteine (NAC) could overcome this AR-suppressive effect of CDDO-Me. Co-exposure of PC cells to CDDO-Me enhanced the efficacy of a clinically approved anti-androgen, enzalutamide (ENZ), as evident by decreased cell-viability along with migration and colony forming ability of PC cells.	Acetylcysteine	17-34	androgen receptor	Homo sapiens	61-63
31940946-9	2020	The anti-oxidant N-acetyl cysteine (NAC) could overcome this AR-suppressive effect of CDDO-Me. Co-exposure of PC cells to CDDO-Me enhanced the efficacy of a clinically approved anti-androgen, enzalutamide (ENZ), as evident by decreased cell-viability along with migration and colony forming ability of PC cells.	Acetylcysteine	36-39	androgen receptor	Homo sapiens	61-63
31668374-6	2020	Moreover, pre-treatment with N-acetyl-L cysteine (NAC), an ROS scavenger, blocked the effects of CGRP on Ang II-induced apoptosis.	Acetylcysteine	29-48	calcitonin related polypeptide alpha	Homo sapiens	97-101
31668374-6	2020	Moreover, pre-treatment with N-acetyl-L cysteine (NAC), an ROS scavenger, blocked the effects of CGRP on Ang II-induced apoptosis.	Acetylcysteine	50-53	calcitonin related polypeptide alpha	Homo sapiens	97-101
31707348-5	2020	In angiotensin II (Ang II)-treated cardiomyocytes, BRD4 decrease markedly blunted the prohypertrophic effect, which was further promoted by the combinational treatment of ROS scavenger (N-acetyl-cysteine, NAC).	Acetylcysteine	186-203	angiotensinogen (serpin peptidase inhibitor, clade A, member 8)	Mus musculus	19-25
31959867-7	2020	NAC treatment prolonged the lifespan and ameliorated pulmonary dysfunction and SAPF by downregulating TIME signaling more than p16INK4a deletion by inhibiting oxidative stress and DNA damage and promoting ubiquitin-proteasome degradation of p16INK4a and p53.	Acetylcysteine	0-3	cyclin dependent kinase inhibitor 2A	Homo sapiens	241-249
31519066-5	2020	The p38 MAP kinase activation promoted by voriconazole exposure can be mitigated by pretreating keratinocytes with N-acetylcysteine.Voriconazoleincreases oxidative stress in keratinocytes by directly inhibiting catalase leading to lower intracellular NADPH levels andthetriazole moieties in voriconazoleare critical for inhibiting catalase.	Acetylcysteine	115-131	mitogen-activated protein kinase 14	Homo sapiens	4-7
31959867-7	2020	NAC treatment prolonged the lifespan and ameliorated pulmonary dysfunction and SAPF by downregulating TIME signaling more than p16INK4a deletion by inhibiting oxidative stress and DNA damage and promoting ubiquitin-proteasome degradation of p16INK4a and p53.	Acetylcysteine	0-3	tumor protein p53	Homo sapiens	254-257
32423248-16	2020	More importantly, the reactive oxygen species (ROS) scavenger N-acetyl-L-cysteine (NAC) pretreatment significantly inhibited HS-induced RIPK1/RIPK3-dependent necroptosis formation both in vivo and in vitro, suggesting that preventing necroptosis via scavenging ROS production might alleviate HS-induced small intestinal tissue injury and cell death.Conclusion: This study provides strong evidence that HS causes damage to both the small intestine and intestinal epithelial cells, scavenging ROS production can significantly alleviate such RIPK1/RIPK3-dependent necroptosis, mediating HS-induced intestinal damage both in vitro and in vivo.	Acetylcysteine	62-81	receptor (TNFRSF)-interacting serine-threonine kinase 1	Mus musculus	136-141
32423248-16	2020	More importantly, the reactive oxygen species (ROS) scavenger N-acetyl-L-cysteine (NAC) pretreatment significantly inhibited HS-induced RIPK1/RIPK3-dependent necroptosis formation both in vivo and in vitro, suggesting that preventing necroptosis via scavenging ROS production might alleviate HS-induced small intestinal tissue injury and cell death.Conclusion: This study provides strong evidence that HS causes damage to both the small intestine and intestinal epithelial cells, scavenging ROS production can significantly alleviate such RIPK1/RIPK3-dependent necroptosis, mediating HS-induced intestinal damage both in vitro and in vivo.	Acetylcysteine	62-81	receptor (TNFRSF)-interacting serine-threonine kinase 1	Mus musculus	539-544
32423248-16	2020	More importantly, the reactive oxygen species (ROS) scavenger N-acetyl-L-cysteine (NAC) pretreatment significantly inhibited HS-induced RIPK1/RIPK3-dependent necroptosis formation both in vivo and in vitro, suggesting that preventing necroptosis via scavenging ROS production might alleviate HS-induced small intestinal tissue injury and cell death.Conclusion: This study provides strong evidence that HS causes damage to both the small intestine and intestinal epithelial cells, scavenging ROS production can significantly alleviate such RIPK1/RIPK3-dependent necroptosis, mediating HS-induced intestinal damage both in vitro and in vivo.	Acetylcysteine	83-86	receptor (TNFRSF)-interacting serine-threonine kinase 1	Mus musculus	136-141
32423248-16	2020	More importantly, the reactive oxygen species (ROS) scavenger N-acetyl-L-cysteine (NAC) pretreatment significantly inhibited HS-induced RIPK1/RIPK3-dependent necroptosis formation both in vivo and in vitro, suggesting that preventing necroptosis via scavenging ROS production might alleviate HS-induced small intestinal tissue injury and cell death.Conclusion: This study provides strong evidence that HS causes damage to both the small intestine and intestinal epithelial cells, scavenging ROS production can significantly alleviate such RIPK1/RIPK3-dependent necroptosis, mediating HS-induced intestinal damage both in vitro and in vivo.	Acetylcysteine	83-86	receptor (TNFRSF)-interacting serine-threonine kinase 1	Mus musculus	539-544
31697963-11	2020	Equally, administration of n-acetylcysteine to fasted WT mice prevented HFD-dependent learning impairment and caspase-1 activation in the BLp.	Acetylcysteine	27-43	gastrin releasing peptide	Mus musculus	138-141
31742908-0	2020	N-acetylcysteine prevents oxidized low-density lipoprotein-induced reduction of MG53 and enhances MG53 protective effect on bone marrow stem cells.	Acetylcysteine	0-16	tripartite motif-containing 72	Mus musculus	80-84
31742908-0	2020	N-acetylcysteine prevents oxidized low-density lipoprotein-induced reduction of MG53 and enhances MG53 protective effect on bone marrow stem cells.	Acetylcysteine	0-16	tripartite motif-containing 72	Mus musculus	98-102
31742908-6	2020	NAC treatment effectively prevented ox-LDL-induced reduction of Akt phosphorylation without protecting MAPCs against ox-LDL.	Acetylcysteine	0-3	thymoma viral proto-oncogene 1	Mus musculus	64-67
31742908-9	2020	NAC treatment prevented ox-LDL-induced MG53 reduction both in vitro and in vivo.	Acetylcysteine	0-3	tripartite motif-containing 72	Mus musculus	39-43
31742908-11	2020	These data suggested that NAC enhanced the protective effect of MG53 on MAPCs against ox-LDL through preventing ox-LDL-induced reduction of MG53.	Acetylcysteine	26-29	tripartite motif-containing 72	Mus musculus	64-68
31742908-11	2020	These data suggested that NAC enhanced the protective effect of MG53 on MAPCs against ox-LDL through preventing ox-LDL-induced reduction of MG53.	Acetylcysteine	26-29	tripartite motif-containing 72	Mus musculus	140-144
31617221-9	2020	In addition, ARG increased the generation of reactive oxygen species (ROS) in HepG2 cells, while the antioxidant N-acetyl cysteine almost reversed ARG-induced JNK and p38 activation, and dramatically decreased cell apoptosis.	Acetylcysteine	113-130	mitogen-activated protein kinase 8	Homo sapiens	159-162
31617221-9	2020	In addition, ARG increased the generation of reactive oxygen species (ROS) in HepG2 cells, while the antioxidant N-acetyl cysteine almost reversed ARG-induced JNK and p38 activation, and dramatically decreased cell apoptosis.	Acetylcysteine	113-130	mitogen-activated protein kinase 14	Homo sapiens	167-170
31751619-0	2020	N-acetylcysteine (NAC) alleviates the peripheral neuropathy associated with liver cirrhosis via modulation of neural MEG3/PAR2/ NF-kB axis.	Acetylcysteine	0-16	similar to GTL2, imprinted maternally expressed untranslated	Rattus norvegicus	117-121
32882411-5	2020	In a mouse model, N-acetyl-cysteine treatment significantly reduced the number of bacteria in the lungs and induced murine beta-defensin-3.	Acetylcysteine	18-35	defensin beta 3	Mus musculus	123-138
31751619-0	2020	N-acetylcysteine (NAC) alleviates the peripheral neuropathy associated with liver cirrhosis via modulation of neural MEG3/PAR2/ NF-kB axis.	Acetylcysteine	18-21	similar to GTL2, imprinted maternally expressed untranslated	Rattus norvegicus	117-121
31751619-3	2020	We aimed to investigate the role of this axis in cirrhotic neuropathy and whether an antioxidant compound such as N-acetylcysteine (NAC) could improve the peripheral nerve function through repression of MEG3/PAR2.	Acetylcysteine	114-130	similar to GTL2, imprinted maternally expressed untranslated	Rattus norvegicus	203-207
31751619-3	2020	We aimed to investigate the role of this axis in cirrhotic neuropathy and whether an antioxidant compound such as N-acetylcysteine (NAC) could improve the peripheral nerve function through repression of MEG3/PAR2.	Acetylcysteine	132-135	similar to GTL2, imprinted maternally expressed untranslated	Rattus norvegicus	203-207
31751619-11	2020	CONCLUSIONS: NAC could improve the peripheral neuropathy in cirrhotic rat through suppression of MEG3/PAR2 expression.	Acetylcysteine	13-16	similar to GTL2, imprinted maternally expressed untranslated	Rattus norvegicus	97-101
31885794-10	2019	NAC inhibited hypoxia-induced variations in the HIF-1alpha and NF-kappaB signaling pathway.	Acetylcysteine	0-3	hypoxia inducible factor 1 subunit alpha	Homo sapiens	48-58
31698002-5	2020	Further analysis indicated that mechanisms responsible for protecting GVBD oocytes from HS by NAC may include: (1) reversing disorganized spindle assembly and inhibited extracellular signal-regulated kinase (ERK) signaling; (2) correcting erroneous H3K27me3 modification and dysregulated expression of imprinted genes; (3) alleviating increased intraoocyte reactive oxygen species accumulation and apoptosis initiation.	Acetylcysteine	94-97	mitogen-activated protein kinase 1	Homo sapiens	169-206
31698002-5	2020	Further analysis indicated that mechanisms responsible for protecting GVBD oocytes from HS by NAC may include: (1) reversing disorganized spindle assembly and inhibited extracellular signal-regulated kinase (ERK) signaling; (2) correcting erroneous H3K27me3 modification and dysregulated expression of imprinted genes; (3) alleviating increased intraoocyte reactive oxygen species accumulation and apoptosis initiation.	Acetylcysteine	94-97	mitogen-activated protein kinase 1	Homo sapiens	208-211
31860682-0	2019	N-acetyl cysteine attenuates oxidative stress and glutathione-dependent redox imbalance caused by high glucose/high palmitic acid treatment in pancreatic Rin-5F cells.	Acetylcysteine	0-17	Ras-like without CAAX 2	Mus musculus	154-157
31756635-6	2020	The elevation of Drp1 phosphorylation was partly dependent on the reactive oxygen species (ROS)-mediated activation of c-Jun-N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (MAPK), as N-acetyl-l-cysteine (NAC) pretreatment inhibited the activation of JNK and p38 MAPK while attenuating Drp1 phosphorylation in acetaldehyde-treated cells.	Acetylcysteine	201-220	mitogen-activated protein kinase 8	Homo sapiens	119-142
31756635-6	2020	The elevation of Drp1 phosphorylation was partly dependent on the reactive oxygen species (ROS)-mediated activation of c-Jun-N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (MAPK), as N-acetyl-l-cysteine (NAC) pretreatment inhibited the activation of JNK and p38 MAPK while attenuating Drp1 phosphorylation in acetaldehyde-treated cells.	Acetylcysteine	222-225	mitogen-activated protein kinase 8	Homo sapiens	119-142
31735020-5	2019	ROS inhibitor NAC (N-acetyl cysteine) recovered SETDB1 expression decreased by PL.	Acetylcysteine	14-17	SET domain bifurcated histone lysine methyltransferase 1	Homo sapiens	48-54
31735020-5	2019	ROS inhibitor NAC (N-acetyl cysteine) recovered SETDB1 expression decreased by PL.	Acetylcysteine	19-36	SET domain bifurcated histone lysine methyltransferase 1	Homo sapiens	48-54
31934265-11	2019	After pretreatment with NAC, the phosphorylation of P38MAPK, JNK, and NF-kappaB and TGF-beta expressions in ECs under stretch was suppressed; similar results were observed in simvastatin-treated ECs.	Acetylcysteine	24-27	mitogen-activated protein kinase 14	Homo sapiens	52-59
31934265-11	2019	After pretreatment with NAC, the phosphorylation of P38MAPK, JNK, and NF-kappaB and TGF-beta expressions in ECs under stretch was suppressed; similar results were observed in simvastatin-treated ECs.	Acetylcysteine	24-27	mitogen-activated protein kinase 8	Homo sapiens	61-64
31934265-11	2019	After pretreatment with NAC, the phosphorylation of P38MAPK, JNK, and NF-kappaB and TGF-beta expressions in ECs under stretch was suppressed; similar results were observed in simvastatin-treated ECs.	Acetylcysteine	24-27	nuclear factor kappa B subunit 1	Homo sapiens	70-79
31934265-11	2019	After pretreatment with NAC, the phosphorylation of P38MAPK, JNK, and NF-kappaB and TGF-beta expressions in ECs under stretch was suppressed; similar results were observed in simvastatin-treated ECs.	Acetylcysteine	24-27	transforming growth factor beta 1	Homo sapiens	84-92
30873870-8	2019	Moreover, after pretreatment with N-acetyl-cysteine, Shikonin increased the production of reactive oxygen species that are involved in regulating ER stress-mediated apoptosis and p38-activated autophagy, as evidenced by the reversion of cell viability and apoptosis and a decrease in p-eIF2alpha, CHOP, p-p38, LC3B-II, and Beclin 1 levels.	Acetylcysteine	34-51	mitogen-activated protein kinase 14	Homo sapiens	179-182
31817202-6	2019	The anti-oxidant N-acetylcysteine (NAC) not only suppresses IL-6 production and VSMC pathological responses including migration and proliferation but also prevents atherosclerosis in ApoE-/- mice.	Acetylcysteine	17-33	interleukin 6	Mus musculus	60-64
31817202-6	2019	The anti-oxidant N-acetylcysteine (NAC) not only suppresses IL-6 production and VSMC pathological responses including migration and proliferation but also prevents atherosclerosis in ApoE-/- mice.	Acetylcysteine	17-33	apolipoprotein E	Mus musculus	183-187
31817202-6	2019	The anti-oxidant N-acetylcysteine (NAC) not only suppresses IL-6 production and VSMC pathological responses including migration and proliferation but also prevents atherosclerosis in ApoE-/- mice.	Acetylcysteine	35-38	interleukin 6	Mus musculus	60-64
31817202-6	2019	The anti-oxidant N-acetylcysteine (NAC) not only suppresses IL-6 production and VSMC pathological responses including migration and proliferation but also prevents atherosclerosis in ApoE-/- mice.	Acetylcysteine	35-38	apolipoprotein E	Mus musculus	183-187
31817202-7	2019	Inhibition experiments with NAC and pharmacological inhibitors demonstrated that NaVO3-induced IL-6 production is signaled by ROS-triggered p38-mediated NF-kappaB-dependent pathways.	Acetylcysteine	28-31	interleukin 6	Mus musculus	95-99
30873870-8	2019	Moreover, after pretreatment with N-acetyl-cysteine, Shikonin increased the production of reactive oxygen species that are involved in regulating ER stress-mediated apoptosis and p38-activated autophagy, as evidenced by the reversion of cell viability and apoptosis and a decrease in p-eIF2alpha, CHOP, p-p38, LC3B-II, and Beclin 1 levels.	Acetylcysteine	34-51	DNA damage inducible transcript 3	Homo sapiens	297-301
30873870-8	2019	Moreover, after pretreatment with N-acetyl-cysteine, Shikonin increased the production of reactive oxygen species that are involved in regulating ER stress-mediated apoptosis and p38-activated autophagy, as evidenced by the reversion of cell viability and apoptosis and a decrease in p-eIF2alpha, CHOP, p-p38, LC3B-II, and Beclin 1 levels.	Acetylcysteine	34-51	mitogen-activated protein kinase 14	Homo sapiens	305-308
32077040-2	2019	In rodenticide-induced hepatotoxicity patients, we analyzed if plasma VWF levels predicted survival and also the outcome of VWF lowering by N-acetyl cysteine (NAC), fresh frozen plasma (FFP) infusions, and plasma exchange (PLEX).	Acetylcysteine	140-157	von Willebrand factor	Homo sapiens	124-127
31180592-5	2019	DPI and NAC treatments reduced eosinophil peroxidase (EPO), goblet cells hyperplasia, proinflammatory cytokines, NFkappaB p65 immunocontent, and oxidative stress in lung.	Acetylcysteine	8-11	eosinophil peroxidase	Mus musculus	31-52
31180592-5	2019	DPI and NAC treatments reduced eosinophil peroxidase (EPO), goblet cells hyperplasia, proinflammatory cytokines, NFkappaB p65 immunocontent, and oxidative stress in lung.	Acetylcysteine	8-11	eosinophil peroxidase	Mus musculus	54-57
31578574-8	2019	Reduced ROS by using N-acetylcysteine led to a decrease in proteasome activity and sequentially inhibited the degradation of Twist.	Acetylcysteine	21-37	twist family bHLH transcription factor 1	Homo sapiens	125-130
31627175-6	2019	The binding of STAT3 inhibitors and NAC was analyzed by LC-MS.	Acetylcysteine	36-39	signal transducer and activator of transcription 3	Mus musculus	15-20
31627175-11	2019	CONCLUSIONS: NAC antagonizes the activities of Stattic and BP-1-102, which inhibit STAT3 activation by interacting with cysteine residues in STAT3.	Acetylcysteine	13-16	signal transducer and activator of transcription 3	Mus musculus	83-88
31627175-0	2019	N-Acetyl cysteine prevents activities of STAT3 inhibitors, Stattic and BP-1-102 independently of its antioxidant properties.	Acetylcysteine	0-17	signal transducer and activator of transcription 3	Mus musculus	41-46
31627175-2	2019	We found that the antioxidant reagent, N-acetyl cysteine (NAC) prevented the abilities of Stattic and BP-1-102, but not LLL12 to induce apoptosis in transformed cells expressing NPM-ALK, providing a novel problem in use of STAT3 inhibitors.	Acetylcysteine	39-56	signal transducer and activator of transcription 3	Mus musculus	223-228
31627175-11	2019	CONCLUSIONS: NAC antagonizes the activities of Stattic and BP-1-102, which inhibit STAT3 activation by interacting with cysteine residues in STAT3.	Acetylcysteine	13-16	signal transducer and activator of transcription 3	Mus musculus	141-146
31627175-2	2019	We found that the antioxidant reagent, N-acetyl cysteine (NAC) prevented the abilities of Stattic and BP-1-102, but not LLL12 to induce apoptosis in transformed cells expressing NPM-ALK, providing a novel problem in use of STAT3 inhibitors.	Acetylcysteine	58-61	signal transducer and activator of transcription 3	Mus musculus	223-228
31757605-8	2019	TNFalpha effect was not mediated by oxidative stress unlike NO, since the presence of N-acetyl-l-cysteine (2.5 and 5.0 mM) prevented NO induced cell cycle arrest and death.	Acetylcysteine	86-105	tumor necrosis factor	Homo sapiens	0-8
31771272-11	2019	The cytokines IL-1beta, IL-6 and KC/GRO were increased in mdx plasma and diaphragm compared with wild type; NAC decreased systemic IL-1beta and KC/GRO concentrations in mdx mice.	Acetylcysteine	108-111	interleukin 1 beta	Mus musculus	131-139
30676497-6	2019	NAC ameliorated the gentamicin-induced decreases in the levels of autophagy-related proteins, such as LC3 (microtubule-associated protein 1 light chain 3), PINK1 (phosphatase and tensin homologue deleted on chromosome10-induced kinase 1), phospho-parkin, AMBRA1 (activatingmolecule in Beclin 1-regulated autophagy), p62/SQSTM1 (sequestosome protein 1), and polyubiquitinated protein aggregates.	Acetylcysteine	0-3	PTEN induced kinase 1	Sus scrofa	156-161
30676497-6	2019	NAC ameliorated the gentamicin-induced decreases in the levels of autophagy-related proteins, such as LC3 (microtubule-associated protein 1 light chain 3), PINK1 (phosphatase and tensin homologue deleted on chromosome10-induced kinase 1), phospho-parkin, AMBRA1 (activatingmolecule in Beclin 1-regulated autophagy), p62/SQSTM1 (sequestosome protein 1), and polyubiquitinated protein aggregates.	Acetylcysteine	0-3	beclin 1	Sus scrofa	285-293
30676497-6	2019	NAC ameliorated the gentamicin-induced decreases in the levels of autophagy-related proteins, such as LC3 (microtubule-associated protein 1 light chain 3), PINK1 (phosphatase and tensin homologue deleted on chromosome10-induced kinase 1), phospho-parkin, AMBRA1 (activatingmolecule in Beclin 1-regulated autophagy), p62/SQSTM1 (sequestosome protein 1), and polyubiquitinated protein aggregates.	Acetylcysteine	0-3	sequestosome 1	Sus scrofa	320-326
31606392-9	2019	After NAC reduced the level of ROS, activation of the NLRP3 inflammasome was significantly inhibited.	Acetylcysteine	6-9	NLR family pyrin domain containing 3	Homo sapiens	54-59
31611307-7	2019	N-acetyl-L-cysteine and mito-TEMPO blocked the induction of IL-1beta by inhibiting reactive oxygen species (ROS) with SAA treatment.	Acetylcysteine	0-19	interleukin 1 beta	Mus musculus	60-68
31542478-3	2019	Antioxidants N-acetylcysteine and butylated hydroxyanisole suppressed MPP+-induced cytotoxicity, AMPK, and Akt activation.	Acetylcysteine	13-29	AKT serine/threonine kinase 1	Homo sapiens	107-110
31752383-10	2019	However, when intracellular ROS production was suppressed by N-acetyl-l-cysteine (NAC), the synergistic effects of ASH and TRAIL on hepatocellular carcinoma (HCC) cell apoptosis was abolished.	Acetylcysteine	61-80	TNF superfamily member 10	Homo sapiens	123-128
31752383-10	2019	However, when intracellular ROS production was suppressed by N-acetyl-l-cysteine (NAC), the synergistic effects of ASH and TRAIL on hepatocellular carcinoma (HCC) cell apoptosis was abolished.	Acetylcysteine	82-85	TNF superfamily member 10	Homo sapiens	123-128
31752383-11	2019	Furthermore, NAC could alleviate p53 and the p53 upregulated modulator of apoptosis (PUMA) expression induced by TRAIL and ASH.	Acetylcysteine	13-16	tumor protein p53	Homo sapiens	33-36
31752383-11	2019	Furthermore, NAC could alleviate p53 and the p53 upregulated modulator of apoptosis (PUMA) expression induced by TRAIL and ASH.	Acetylcysteine	13-16	tumor protein p53	Homo sapiens	45-48
31752383-11	2019	Furthermore, NAC could alleviate p53 and the p53 upregulated modulator of apoptosis (PUMA) expression induced by TRAIL and ASH.	Acetylcysteine	13-16	TNF superfamily member 10	Homo sapiens	113-118
31827376-9	2019	Pretreatment of THP-1 cells with the antioxidant N-acetyl-L-cysteine (NAC) markedly blunted DEP-induced EGFR phosphorylation, indicating that oxidative stress was involved in DEP-induced EGFR activation.	Acetylcysteine	49-68	epidermal growth factor receptor	Homo sapiens	104-108
31827376-9	2019	Pretreatment of THP-1 cells with the antioxidant N-acetyl-L-cysteine (NAC) markedly blunted DEP-induced EGFR phosphorylation, indicating that oxidative stress was involved in DEP-induced EGFR activation.	Acetylcysteine	49-68	epidermal growth factor receptor	Homo sapiens	187-191
31827376-9	2019	Pretreatment of THP-1 cells with the antioxidant N-acetyl-L-cysteine (NAC) markedly blunted DEP-induced EGFR phosphorylation, indicating that oxidative stress was involved in DEP-induced EGFR activation.	Acetylcysteine	70-73	epidermal growth factor receptor	Homo sapiens	104-108
31827376-9	2019	Pretreatment of THP-1 cells with the antioxidant N-acetyl-L-cysteine (NAC) markedly blunted DEP-induced EGFR phosphorylation, indicating that oxidative stress was involved in DEP-induced EGFR activation.	Acetylcysteine	70-73	epidermal growth factor receptor	Homo sapiens	187-191
31827376-10	2019	Furthermore, the pretreatment of THP-1 cells with either NAC or a selective EGFR inhibitor significantly blocked DEP-induced IL-8 expression, implying that oxidative stress and subsequent EGFR activation mediated DEP-induced inflammatory response.	Acetylcysteine	57-60	C-X-C motif chemokine ligand 8	Homo sapiens	125-129
31827376-10	2019	Furthermore, the pretreatment of THP-1 cells with either NAC or a selective EGFR inhibitor significantly blocked DEP-induced IL-8 expression, implying that oxidative stress and subsequent EGFR activation mediated DEP-induced inflammatory response.	Acetylcysteine	57-60	epidermal growth factor receptor	Homo sapiens	188-192
30953354-7	2019	The levels of fibrotic proteins in CFs stimulated with high concentrations of the recombinant FGF23 protein were reversed by N-acetylcysteine (NAC, a ROS inhibitor), ship information system 3 (a SMAD3 inhibitor), and Stattic (a STAT3 inhibitor).	Acetylcysteine	143-146	signal transducer and activator of transcription 3	Homo sapiens	228-233
31386885-10	2019	The apoptotic process was probably mediated via ROS overproduction and MAPK (ERK and JNK) activation as N-acetylcysteine, or specific inhibitors of these kinases prevented the XN-induced caspase-3 activity and, hence, apoptosis.	Acetylcysteine	104-120	mitogen-activated protein kinase 1	Homo sapiens	71-75
31386885-10	2019	The apoptotic process was probably mediated via ROS overproduction and MAPK (ERK and JNK) activation as N-acetylcysteine, or specific inhibitors of these kinases prevented the XN-induced caspase-3 activity and, hence, apoptosis.	Acetylcysteine	104-120	mitogen-activated protein kinase 1	Homo sapiens	77-80
31386885-10	2019	The apoptotic process was probably mediated via ROS overproduction and MAPK (ERK and JNK) activation as N-acetylcysteine, or specific inhibitors of these kinases prevented the XN-induced caspase-3 activity and, hence, apoptosis.	Acetylcysteine	104-120	mitogen-activated protein kinase 8	Homo sapiens	85-88
31386885-10	2019	The apoptotic process was probably mediated via ROS overproduction and MAPK (ERK and JNK) activation as N-acetylcysteine, or specific inhibitors of these kinases prevented the XN-induced caspase-3 activity and, hence, apoptosis.	Acetylcysteine	104-120	caspase 3	Homo sapiens	187-196
31419475-6	2019	Importantly, TCE exposure resulted in the activation of hepatic inflammasome (NLRP3 and caspase-1) and up-regulation of pro-inflammatory cytokine IL-1beta, and these changes were attenuated by NAC supplementation.	Acetylcysteine	193-196	interleukin 1 beta	Mus musculus	146-154
31368586-10	2019	NAC-pretreated cells showed increased anti-apoptotic protein Bcl-2 and decreased pro-apoptotic protein Bax expression.	Acetylcysteine	0-3	B cell leukemia/lymphoma 2	Mus musculus	61-66
31717992-9	2019	Finally, TGF-beta1-stimulated EMT was also inhibited by the antioxidant N-acetylcysteine.	Acetylcysteine	72-88	transforming growth factor beta 1	Homo sapiens	9-18
31521245-7	2019	Additionally, we also observed that N-Acetylcysteine (NAC, a ROS scavenger) pretreatment inhibited NLRP3 inflammasome activation as evidenced by suppressing the upregulation of NLRP3, ASC, cleaved-caspase-1, GSDMD-N, IL-1beta and IL-18 protein levels in CSE-treated ECs.	Acetylcysteine	36-52	NLR family pyrin domain containing 3	Homo sapiens	99-104
31521245-7	2019	Additionally, we also observed that N-Acetylcysteine (NAC, a ROS scavenger) pretreatment inhibited NLRP3 inflammasome activation as evidenced by suppressing the upregulation of NLRP3, ASC, cleaved-caspase-1, GSDMD-N, IL-1beta and IL-18 protein levels in CSE-treated ECs.	Acetylcysteine	36-52	NLR family pyrin domain containing 3	Homo sapiens	177-182
31521245-7	2019	Additionally, we also observed that N-Acetylcysteine (NAC, a ROS scavenger) pretreatment inhibited NLRP3 inflammasome activation as evidenced by suppressing the upregulation of NLRP3, ASC, cleaved-caspase-1, GSDMD-N, IL-1beta and IL-18 protein levels in CSE-treated ECs.	Acetylcysteine	36-52	PYD and CARD domain containing	Homo sapiens	184-187
31521245-7	2019	Additionally, we also observed that N-Acetylcysteine (NAC, a ROS scavenger) pretreatment inhibited NLRP3 inflammasome activation as evidenced by suppressing the upregulation of NLRP3, ASC, cleaved-caspase-1, GSDMD-N, IL-1beta and IL-18 protein levels in CSE-treated ECs.	Acetylcysteine	36-52	interleukin 1 beta	Homo sapiens	217-225
31521245-7	2019	Additionally, we also observed that N-Acetylcysteine (NAC, a ROS scavenger) pretreatment inhibited NLRP3 inflammasome activation as evidenced by suppressing the upregulation of NLRP3, ASC, cleaved-caspase-1, GSDMD-N, IL-1beta and IL-18 protein levels in CSE-treated ECs.	Acetylcysteine	54-57	NLR family pyrin domain containing 3	Homo sapiens	99-104
31521245-7	2019	Additionally, we also observed that N-Acetylcysteine (NAC, a ROS scavenger) pretreatment inhibited NLRP3 inflammasome activation as evidenced by suppressing the upregulation of NLRP3, ASC, cleaved-caspase-1, GSDMD-N, IL-1beta and IL-18 protein levels in CSE-treated ECs.	Acetylcysteine	54-57	NLR family pyrin domain containing 3	Homo sapiens	177-182
31521245-7	2019	Additionally, we also observed that N-Acetylcysteine (NAC, a ROS scavenger) pretreatment inhibited NLRP3 inflammasome activation as evidenced by suppressing the upregulation of NLRP3, ASC, cleaved-caspase-1, GSDMD-N, IL-1beta and IL-18 protein levels in CSE-treated ECs.	Acetylcysteine	54-57	PYD and CARD domain containing	Homo sapiens	184-187
31521245-7	2019	Additionally, we also observed that N-Acetylcysteine (NAC, a ROS scavenger) pretreatment inhibited NLRP3 inflammasome activation as evidenced by suppressing the upregulation of NLRP3, ASC, cleaved-caspase-1, GSDMD-N, IL-1beta and IL-18 protein levels in CSE-treated ECs.	Acetylcysteine	54-57	interleukin 1 beta	Homo sapiens	217-225
29735977-8	2019	Exogenous administration of N-Acetyl-L-cysteine (NAC), a small molecular inhibitor of ROS, remarkably suppressed caspase-1 p20 expression and IL-1beta and IL-18 production in livers of Tim-3 KO mice, thus significantly reducing the severity of steatohepatitis induced by MCD.	Acetylcysteine	28-47	demilune cell and parotid protein 1	Mus musculus	123-126
29735977-8	2019	Exogenous administration of N-Acetyl-L-cysteine (NAC), a small molecular inhibitor of ROS, remarkably suppressed caspase-1 p20 expression and IL-1beta and IL-18 production in livers of Tim-3 KO mice, thus significantly reducing the severity of steatohepatitis induced by MCD.	Acetylcysteine	28-47	interleukin 1 beta	Mus musculus	142-150
29735977-8	2019	Exogenous administration of N-Acetyl-L-cysteine (NAC), a small molecular inhibitor of ROS, remarkably suppressed caspase-1 p20 expression and IL-1beta and IL-18 production in livers of Tim-3 KO mice, thus significantly reducing the severity of steatohepatitis induced by MCD.	Acetylcysteine	49-52	demilune cell and parotid protein 1	Mus musculus	123-126
29735977-8	2019	Exogenous administration of N-Acetyl-L-cysteine (NAC), a small molecular inhibitor of ROS, remarkably suppressed caspase-1 p20 expression and IL-1beta and IL-18 production in livers of Tim-3 KO mice, thus significantly reducing the severity of steatohepatitis induced by MCD.	Acetylcysteine	49-52	interleukin 1 beta	Mus musculus	142-150
31310363-4	2019	The effects of H2 O2 and N-acetylcysteine (NAC) on the levels of HIF1-alpha and HIF2-alpha after overexpression of GPX3 were studied.	Acetylcysteine	25-41	hypoxia inducible factor 1 subunit alpha	Homo sapiens	65-75
31310363-4	2019	The effects of H2 O2 and N-acetylcysteine (NAC) on the levels of HIF1-alpha and HIF2-alpha after overexpression of GPX3 were studied.	Acetylcysteine	43-46	hypoxia inducible factor 1 subunit alpha	Homo sapiens	65-75
31310363-12	2019	The addition of H2 O2 increased while NAC reduced the protein levels of HIF1-alpha and HIF2-alpha in the cells overexpressing GPX3.	Acetylcysteine	38-41	hypoxia inducible factor 1 subunit alpha	Homo sapiens	72-82
31310363-12	2019	The addition of H2 O2 increased while NAC reduced the protein levels of HIF1-alpha and HIF2-alpha in the cells overexpressing GPX3.	Acetylcysteine	38-41	glutathione peroxidase 3	Homo sapiens	126-130
31640182-8	2019	NAC also mitigated the abnormalities in mitochondrial functions, dynamics, mitophagy, and ultrastructure of the liver by improving the mitochondrial homeostasis regulatory signaling AMPK-PGC-1alpha-SIRT3.	Acetylcysteine	0-3	PPARG coactivator 1 alpha	Rattus norvegicus	187-197
31545445-0	2019	N-acetyl cysteine protects HUVECs against lipopolysaccharide-mediated inflammatory reaction by blocking the NF-kappaB signaling pathway.	Acetylcysteine	0-17	nuclear factor kappa B subunit 1	Homo sapiens	108-117
31545445-10	2019	However, pretreatment of HUVECs with NAC significantly attenuated the increase in the expression of inflammatory factors and the level of phosphorylated p65; this indicated that NAC prevented the activation of the NF-kappaB signaling pathway.	Acetylcysteine	37-40	nuclear factor kappa B subunit 1	Homo sapiens	214-223
31545445-10	2019	However, pretreatment of HUVECs with NAC significantly attenuated the increase in the expression of inflammatory factors and the level of phosphorylated p65; this indicated that NAC prevented the activation of the NF-kappaB signaling pathway.	Acetylcysteine	178-181	nuclear factor kappa B subunit 1	Homo sapiens	214-223
31425726-13	2019	Alpha smooth muscle actin (alpha-SMA) increased in PAE neonatal hearts, and this increase was prevented by NAC treatment.	Acetylcysteine	107-110	actin alpha 2, smooth muscle, aorta	Mus musculus	0-25
31425726-13	2019	Alpha smooth muscle actin (alpha-SMA) increased in PAE neonatal hearts, and this increase was prevented by NAC treatment.	Acetylcysteine	107-110	actin alpha 2, smooth muscle, aorta	Mus musculus	27-36
31288199-6	2019	Detailed analysis indicated that the protective effect of NAC was mediated by its ability to form stable complex with cadmium [Cd(NAC)2].	Acetylcysteine	58-61	NACC family member 2	Homo sapiens	130-135
32041914-9	2019	RESULTS: HsCRP, MPO, and Gal-3 levels between NAC and control groups at admission were not significantly different; while intergroup differences after 72 h of NAC supplementation were significant (p values of HsCRP, MPO, and Gal-3 levels were 0.0001, 0.001, and 0.017, respectively).	Acetylcysteine	159-162	myeloperoxidase	Homo sapiens	216-219
32041914-10	2019	Furthermore, in the NAC group, HsCRP, MPO, and Gal-3 levels at 72 h after treatment were significantly different from the corresponding levels at admission (p values: 0.0001, 0.0001, and 0.0001, respectively); the control group did not show these differences.	Acetylcysteine	20-23	myeloperoxidase	Homo sapiens	38-41
32041914-11	2019	There were also significant intergroup differences between the NAC and control groups regarding HsCRP, MPO, and Gal-3 levels (p values: 0.011, 0.022, and 0.014, respectively).	Acetylcysteine	63-66	myeloperoxidase	Homo sapiens	103-106
32041914-12	2019	CONCLUSION: oral supplementation of 600 mg NAC every 8 h for 72 h can reduce HsCRP, MPO, and Gal-3 levels in AMI patients receiving fibrinolytic therapy.	Acetylcysteine	43-46	myeloperoxidase	Homo sapiens	84-87
31390228-6	2019	Selective angiotensin II type 1 receptor (AT1R) blocker losartan suppressed ROS production and ROS scavenger N-Acetyl-L-cysteine (NAC) prevented p38 MAPK phosphorylation.	Acetylcysteine	109-128	mitogen-activated protein kinase 14	Homo sapiens	145-148
31569917-9	2019	Regarding biochemical markers, NAC and verapamil significantly decreased serum nitric oxide synthase, C-reactive protein, and cyclooxygenase- 2 levels compared to the edema control value.	Acetylcysteine	31-34	C-reactive protein	Rattus norvegicus	102-120
31273783-10	2019	N-Acetylcysteine treatment led to significantly greater improvement in free testosterone and insulin resistance parameters as compared with l-carnitine (all P&lt;0.05).	Acetylcysteine	0-16	insulin	Homo sapiens	93-100
31422095-10	2019	In high glucose-cultured cardiomyocytes, Klotho and N-acetylcysteine significantly downregulated intracellular reactive oxygen species generation and TXNIP/NLRP3 inflammasome activation.	Acetylcysteine	52-68	NLR family, pyrin domain containing 3	Rattus norvegicus	156-161
28969526-12	2019	Pretreatment with N-acetylcysteine significantly decreased the mRNA levels of TLR4/IRF5 and its downstream cytokines 3 hours after reperfusion and subsequently improved the previously mentioned hepatic damages 168 hours after reperfusion.	Acetylcysteine	18-34	toll-like receptor 4	Mus musculus	78-82
28969526-12	2019	Pretreatment with N-acetylcysteine significantly decreased the mRNA levels of TLR4/IRF5 and its downstream cytokines 3 hours after reperfusion and subsequently improved the previously mentioned hepatic damages 168 hours after reperfusion.	Acetylcysteine	18-34	interferon regulatory factor 5	Mus musculus	83-87
31273783-12	2019	However, N-acetylcysteine was superior in ameliorating insulin resistance and only l-carnitine improved lipid profile.	Acetylcysteine	9-25	insulin	Homo sapiens	55-62
31332969-6	2019	The ROS inhibitor N-acetylcysteine and MAPK inhibitors significantly reduced the expression of IL-6 and IL-24 induced by T. forsythia.	Acetylcysteine	18-34	interleukin 6	Homo sapiens	95-99
31577702-0	2019	N-acetyl cysteine inhibits lipopolysaccharide-mediated synthesis of interleukin-1beta and tumor necrosis factor-alpha in human periodontal ligament fibroblast cells through nuclear factor-kappa B signaling.	Acetylcysteine	0-17	interleukin 1 beta	Homo sapiens	68-85
31577702-0	2019	N-acetyl cysteine inhibits lipopolysaccharide-mediated synthesis of interleukin-1beta and tumor necrosis factor-alpha in human periodontal ligament fibroblast cells through nuclear factor-kappa B signaling.	Acetylcysteine	0-17	tumor necrosis factor	Homo sapiens	90-117
31577702-0	2019	N-acetyl cysteine inhibits lipopolysaccharide-mediated synthesis of interleukin-1beta and tumor necrosis factor-alpha in human periodontal ligament fibroblast cells through nuclear factor-kappa B signaling.	Acetylcysteine	0-17	nuclear factor kappa B subunit 1	Homo sapiens	173-195
31577702-1	2019	BACKGROUND: The aim of this study was to investigate the role of n-acetyl cysteine (NAC) in the lipopolysaccharide (LPS)-mediated induction of tumor necrosis factor-alpha (TNF-alpha) and interleukin-1beta (IL-1beta) synthesis by human periodontal ligament fibroblast cells (hPDLFs).	Acetylcysteine	65-82	tumor necrosis factor	Homo sapiens	143-170
31577702-1	2019	BACKGROUND: The aim of this study was to investigate the role of n-acetyl cysteine (NAC) in the lipopolysaccharide (LPS)-mediated induction of tumor necrosis factor-alpha (TNF-alpha) and interleukin-1beta (IL-1beta) synthesis by human periodontal ligament fibroblast cells (hPDLFs).	Acetylcysteine	65-82	tumor necrosis factor	Homo sapiens	172-181
31577702-1	2019	BACKGROUND: The aim of this study was to investigate the role of n-acetyl cysteine (NAC) in the lipopolysaccharide (LPS)-mediated induction of tumor necrosis factor-alpha (TNF-alpha) and interleukin-1beta (IL-1beta) synthesis by human periodontal ligament fibroblast cells (hPDLFs).	Acetylcysteine	65-82	interleukin 1 beta	Homo sapiens	187-204
31577702-1	2019	BACKGROUND: The aim of this study was to investigate the role of n-acetyl cysteine (NAC) in the lipopolysaccharide (LPS)-mediated induction of tumor necrosis factor-alpha (TNF-alpha) and interleukin-1beta (IL-1beta) synthesis by human periodontal ligament fibroblast cells (hPDLFs).	Acetylcysteine	84-87	tumor necrosis factor	Homo sapiens	143-170
31577702-1	2019	BACKGROUND: The aim of this study was to investigate the role of n-acetyl cysteine (NAC) in the lipopolysaccharide (LPS)-mediated induction of tumor necrosis factor-alpha (TNF-alpha) and interleukin-1beta (IL-1beta) synthesis by human periodontal ligament fibroblast cells (hPDLFs).	Acetylcysteine	84-87	tumor necrosis factor	Homo sapiens	172-181
31577702-1	2019	BACKGROUND: The aim of this study was to investigate the role of n-acetyl cysteine (NAC) in the lipopolysaccharide (LPS)-mediated induction of tumor necrosis factor-alpha (TNF-alpha) and interleukin-1beta (IL-1beta) synthesis by human periodontal ligament fibroblast cells (hPDLFs).	Acetylcysteine	84-87	interleukin 1 beta	Homo sapiens	187-204
31577702-2	2019	In addition, we aimed to determine the involvement of the nuclear factor-kappa B (NF-kappaB) pathway in any changes in IL-1beta and TNF-alpha expression observed in response to LPS and NAC.	Acetylcysteine	185-188	nuclear factor kappa B subunit 1	Homo sapiens	58-80
31577702-2	2019	In addition, we aimed to determine the involvement of the nuclear factor-kappa B (NF-kappaB) pathway in any changes in IL-1beta and TNF-alpha expression observed in response to LPS and NAC.	Acetylcysteine	185-188	nuclear factor kappa B subunit 1	Homo sapiens	82-91
31577702-2	2019	In addition, we aimed to determine the involvement of the nuclear factor-kappa B (NF-kappaB) pathway in any changes in IL-1beta and TNF-alpha expression observed in response to LPS and NAC.	Acetylcysteine	185-188	tumor necrosis factor	Homo sapiens	132-141
31577702-12	2019	Pretreatment with both NAC (1 mmol/L) and BAY11-7082 (10 mumol/L) significantly inhibited the NF-kappaB activity induced by LPS.	Acetylcysteine	23-26	nuclear factor kappa B subunit 1	Homo sapiens	94-103
31577702-13	2019	CONCLUSION: NAC inhibits the LPS-mediated synthesis of tumor TNF-alpha and IL-1beta in hPDLFs, through the NF-kappaB pathway.	Acetylcysteine	12-15	tumor necrosis factor	Homo sapiens	61-70
31577702-13	2019	CONCLUSION: NAC inhibits the LPS-mediated synthesis of tumor TNF-alpha and IL-1beta in hPDLFs, through the NF-kappaB pathway.	Acetylcysteine	12-15	nuclear factor kappa B subunit 1	Homo sapiens	107-116
31322268-7	2019	Cell survival of antioxidant [N-acetylcysteine (NAC)]-treated NQO1-overexpressing 231 cells was significantly recovered, and NQO1-negative 231 cells did not respond to beta-Lap.	Acetylcysteine	30-46	NAD(P)H quinone dehydrogenase 1	Homo sapiens	62-66
31432125-13	2019	The antioxidant N-acetylcysteine was identified to antagonize 2,5-HD-stimulated cleaved-caspase-3 and Bax upregulation, and Bcl-2 downregulation.	Acetylcysteine	16-32	BCL2, apoptosis regulator	Rattus norvegicus	124-129
31322268-7	2019	Cell survival of antioxidant [N-acetylcysteine (NAC)]-treated NQO1-overexpressing 231 cells was significantly recovered, and NQO1-negative 231 cells did not respond to beta-Lap.	Acetylcysteine	48-51	NAD(P)H quinone dehydrogenase 1	Homo sapiens	62-66
31381934-12	2019	N-Acetylcysteine (NAC), a classic antioxidant pretreatment decreased the phosphorylated p38 MAPK level and intracellular ROS production, alleviated cell injury, and inhibited apoptosis.	Acetylcysteine	0-16	mitogen-activated protein kinase 14	Homo sapiens	88-91
30273693-5	2019	The transactivation of the EGFR and HER2 was inhibited by gefitinib or lapatinib (tyrosine kinase inhibitors), PACAP (6-38) (PAC1 antagonist), N-acetylcysteine (NAC is an anti-oxidant) or dipheyleneiodonium (DPI is an inhibitor of Nox and Duox enzymes).	Acetylcysteine	143-159	epidermal growth factor receptor	Homo sapiens	27-31
30273693-5	2019	The transactivation of the EGFR and HER2 was inhibited by gefitinib or lapatinib (tyrosine kinase inhibitors), PACAP (6-38) (PAC1 antagonist), N-acetylcysteine (NAC is an anti-oxidant) or dipheyleneiodonium (DPI is an inhibitor of Nox and Duox enzymes).	Acetylcysteine	143-159	erb-b2 receptor tyrosine kinase 2	Homo sapiens	36-40
31381934-12	2019	N-Acetylcysteine (NAC), a classic antioxidant pretreatment decreased the phosphorylated p38 MAPK level and intracellular ROS production, alleviated cell injury, and inhibited apoptosis.	Acetylcysteine	18-21	mitogen-activated protein kinase 14	Homo sapiens	88-91
31533227-9	2019	In addition, both reactive oxygen species (ROS) scavenger N-acetyl-L-cysteine (NAC) and VAC abolished HG-evoked dephosphorylation of AMPK and eNOS, increased miRNA-34a expression, and decreased NO production.	Acetylcysteine	58-77	nitric oxide synthase 3	Homo sapiens	142-146
31533227-9	2019	In addition, both reactive oxygen species (ROS) scavenger N-acetyl-L-cysteine (NAC) and VAC abolished HG-evoked dephosphorylation of AMPK and eNOS, increased miRNA-34a expression, and decreased NO production.	Acetylcysteine	79-82	nitric oxide synthase 3	Homo sapiens	142-146
31510052-7	2019	Cytochrome c and caspase 3/9 activities were significantly induced in the mouse KECs after a high-dose rmC5a (50 ng/mL) treatment, and this was rescued by pretreatment with the C5a receptor (C5aR) inhibitor (W-54011) and N-acetylcysteine (NAC).	Acetylcysteine	221-237	complement component 5a receptor 1	Mus musculus	177-189
31315024-9	2019	Nicotine exposure directly inhibited Nrf2 and increased ERK phosphorylation in cardiomyocytes, which were obstructed by NAC.	Acetylcysteine	120-123	nuclear factor, erythroid derived 2, like 2	Mus musculus	37-41
31315024-9	2019	Nicotine exposure directly inhibited Nrf2 and increased ERK phosphorylation in cardiomyocytes, which were obstructed by NAC.	Acetylcysteine	120-123	mitogen-activated protein kinase 1	Mus musculus	56-59
31510052-7	2019	Cytochrome c and caspase 3/9 activities were significantly induced in the mouse KECs after a high-dose rmC5a (50 ng/mL) treatment, and this was rescued by pretreatment with the C5a receptor (C5aR) inhibitor (W-54011) and N-acetylcysteine (NAC).	Acetylcysteine	221-237	complement component 5a receptor 1	Mus musculus	191-195
31510052-7	2019	Cytochrome c and caspase 3/9 activities were significantly induced in the mouse KECs after a high-dose rmC5a (50 ng/mL) treatment, and this was rescued by pretreatment with the C5a receptor (C5aR) inhibitor (W-54011) and N-acetylcysteine (NAC).	Acetylcysteine	239-242	complement component 5a receptor 1	Mus musculus	177-189
31510052-7	2019	Cytochrome c and caspase 3/9 activities were significantly induced in the mouse KECs after a high-dose rmC5a (50 ng/mL) treatment, and this was rescued by pretreatment with the C5a receptor (C5aR) inhibitor (W-54011) and N-acetylcysteine (NAC).	Acetylcysteine	239-242	complement component 5a receptor 1	Mus musculus	191-195
31583053-6	2019	Similarly, NAC could restore RPC protection from high glucose and hypoxia/reoxygenation-induced injury evidenced by decreased levels of LDH release, 15-F2t-isoprostane, O2 -, and JC-1 monomeric cells, which were reversed by caveolae disrupter methyl-beta-cyclodextrin, wortmannin, or AG490 in isolated primary cardiomyocytes or siRNAs of Cav-3, Akt, or STAT3 in H9C2 cells.	Acetylcysteine	11-14	caveolin 3	Rattus norvegicus	338-343
31583053-5	2019	Pretreatment with the antioxidant N-acetylcysteine (NAC) attenuated hyperglycemia-induced reduction of Cav-3 expression and Akt and STAT3 activation and restored RPC-mediated cardioprotection in diabetes, which was abolished by cardiac-specific knockdown of Cav-3 by AAV9-shRNA-Cav-3, PI3K/Akt inhibitor wortmannin, or JAK2/STAT3 inhibitor AG490, respectively.	Acetylcysteine	34-50	caveolin 3	Rattus norvegicus	103-108
31583053-5	2019	Pretreatment with the antioxidant N-acetylcysteine (NAC) attenuated hyperglycemia-induced reduction of Cav-3 expression and Akt and STAT3 activation and restored RPC-mediated cardioprotection in diabetes, which was abolished by cardiac-specific knockdown of Cav-3 by AAV9-shRNA-Cav-3, PI3K/Akt inhibitor wortmannin, or JAK2/STAT3 inhibitor AG490, respectively.	Acetylcysteine	34-50	AKT serine/threonine kinase 1	Rattus norvegicus	124-127
31506575-6	2019	APE downregulated Dusp-1 and induced a significant increase in JNK/c-Jun phosphorylation that were both prevented by NAC.	Acetylcysteine	117-120	mitogen-activated protein kinase 8	Homo sapiens	63-66
31136867-1	2019	This study describes synthesis of N-acetyl-l-cysteine-capped CdTe quantum dots (QDs) and investigates their interaction with plasma protein fibrinogen (FIB) and the structural changes of FIB.	Acetylcysteine	34-53	fibrinogen beta chain	Homo sapiens	140-150
31136867-1	2019	This study describes synthesis of N-acetyl-l-cysteine-capped CdTe quantum dots (QDs) and investigates their interaction with plasma protein fibrinogen (FIB) and the structural changes of FIB.	Acetylcysteine	34-53	fibrinogen beta chain	Homo sapiens	152-155
31136867-1	2019	This study describes synthesis of N-acetyl-l-cysteine-capped CdTe quantum dots (QDs) and investigates their interaction with plasma protein fibrinogen (FIB) and the structural changes of FIB.	Acetylcysteine	34-53	fibrinogen beta chain	Homo sapiens	187-190
31583053-5	2019	Pretreatment with the antioxidant N-acetylcysteine (NAC) attenuated hyperglycemia-induced reduction of Cav-3 expression and Akt and STAT3 activation and restored RPC-mediated cardioprotection in diabetes, which was abolished by cardiac-specific knockdown of Cav-3 by AAV9-shRNA-Cav-3, PI3K/Akt inhibitor wortmannin, or JAK2/STAT3 inhibitor AG490, respectively.	Acetylcysteine	34-50	caveolin 3	Rattus norvegicus	258-263
31583053-5	2019	Pretreatment with the antioxidant N-acetylcysteine (NAC) attenuated hyperglycemia-induced reduction of Cav-3 expression and Akt and STAT3 activation and restored RPC-mediated cardioprotection in diabetes, which was abolished by cardiac-specific knockdown of Cav-3 by AAV9-shRNA-Cav-3, PI3K/Akt inhibitor wortmannin, or JAK2/STAT3 inhibitor AG490, respectively.	Acetylcysteine	34-50	caveolin 3	Rattus norvegicus	258-263
31583053-6	2019	Similarly, NAC could restore RPC protection from high glucose and hypoxia/reoxygenation-induced injury evidenced by decreased levels of LDH release, 15-F2t-isoprostane, O2 -, and JC-1 monomeric cells, which were reversed by caveolae disrupter methyl-beta-cyclodextrin, wortmannin, or AG490 in isolated primary cardiomyocytes or siRNAs of Cav-3, Akt, or STAT3 in H9C2 cells.	Acetylcysteine	11-14	AKT serine/threonine kinase 1	Rattus norvegicus	345-348
31583053-5	2019	Pretreatment with the antioxidant N-acetylcysteine (NAC) attenuated hyperglycemia-induced reduction of Cav-3 expression and Akt and STAT3 activation and restored RPC-mediated cardioprotection in diabetes, which was abolished by cardiac-specific knockdown of Cav-3 by AAV9-shRNA-Cav-3, PI3K/Akt inhibitor wortmannin, or JAK2/STAT3 inhibitor AG490, respectively.	Acetylcysteine	34-50	AKT serine/threonine kinase 1	Rattus norvegicus	290-293
31583053-5	2019	Pretreatment with the antioxidant N-acetylcysteine (NAC) attenuated hyperglycemia-induced reduction of Cav-3 expression and Akt and STAT3 activation and restored RPC-mediated cardioprotection in diabetes, which was abolished by cardiac-specific knockdown of Cav-3 by AAV9-shRNA-Cav-3, PI3K/Akt inhibitor wortmannin, or JAK2/STAT3 inhibitor AG490, respectively.	Acetylcysteine	52-55	caveolin 3	Rattus norvegicus	103-108
31583053-10	2019	Antioxidant treatment with NAC could restore RPC-induced cardioprotection in diabetes by improving Cav-3-dependent Akt and STAT3 activation and by facilitating the cross talk between PI3K/Akt and JAK2/STAT3 signaling pathways.	Acetylcysteine	27-30	caveolin 3	Rattus norvegicus	99-104
31583053-5	2019	Pretreatment with the antioxidant N-acetylcysteine (NAC) attenuated hyperglycemia-induced reduction of Cav-3 expression and Akt and STAT3 activation and restored RPC-mediated cardioprotection in diabetes, which was abolished by cardiac-specific knockdown of Cav-3 by AAV9-shRNA-Cav-3, PI3K/Akt inhibitor wortmannin, or JAK2/STAT3 inhibitor AG490, respectively.	Acetylcysteine	52-55	AKT serine/threonine kinase 1	Rattus norvegicus	124-127
31583053-5	2019	Pretreatment with the antioxidant N-acetylcysteine (NAC) attenuated hyperglycemia-induced reduction of Cav-3 expression and Akt and STAT3 activation and restored RPC-mediated cardioprotection in diabetes, which was abolished by cardiac-specific knockdown of Cav-3 by AAV9-shRNA-Cav-3, PI3K/Akt inhibitor wortmannin, or JAK2/STAT3 inhibitor AG490, respectively.	Acetylcysteine	52-55	caveolin 3	Rattus norvegicus	258-263
31583053-5	2019	Pretreatment with the antioxidant N-acetylcysteine (NAC) attenuated hyperglycemia-induced reduction of Cav-3 expression and Akt and STAT3 activation and restored RPC-mediated cardioprotection in diabetes, which was abolished by cardiac-specific knockdown of Cav-3 by AAV9-shRNA-Cav-3, PI3K/Akt inhibitor wortmannin, or JAK2/STAT3 inhibitor AG490, respectively.	Acetylcysteine	52-55	caveolin 3	Rattus norvegicus	258-263
31583053-5	2019	Pretreatment with the antioxidant N-acetylcysteine (NAC) attenuated hyperglycemia-induced reduction of Cav-3 expression and Akt and STAT3 activation and restored RPC-mediated cardioprotection in diabetes, which was abolished by cardiac-specific knockdown of Cav-3 by AAV9-shRNA-Cav-3, PI3K/Akt inhibitor wortmannin, or JAK2/STAT3 inhibitor AG490, respectively.	Acetylcysteine	52-55	AKT serine/threonine kinase 1	Rattus norvegicus	290-293
31583053-10	2019	Antioxidant treatment with NAC could restore RPC-induced cardioprotection in diabetes by improving Cav-3-dependent Akt and STAT3 activation and by facilitating the cross talk between PI3K/Akt and JAK2/STAT3 signaling pathways.	Acetylcysteine	27-30	AKT serine/threonine kinase 1	Rattus norvegicus	115-118
31583053-10	2019	Antioxidant treatment with NAC could restore RPC-induced cardioprotection in diabetes by improving Cav-3-dependent Akt and STAT3 activation and by facilitating the cross talk between PI3K/Akt and JAK2/STAT3 signaling pathways.	Acetylcysteine	27-30	AKT serine/threonine kinase 1	Rattus norvegicus	188-191
30867543-13	2019	We further showed that Akt signaling was impaired in diabetic CEC, which was partially improved by NAC treatment.	Acetylcysteine	99-102	AKT serine/threonine kinase 1	Homo sapiens	23-26
30861304-5	2019	Pre-treatment with the ROS inhibitors N-acetyl cysteine (NAC) and diphenyleneiodonium (DPI) partially attenuated CXCL8 and IL-6 responses to 200 microg/mL, but not to 100 microg/mL Si50.	Acetylcysteine	38-55	C-X-C motif chemokine ligand 8	Homo sapiens	113-118
30861304-5	2019	Pre-treatment with the ROS inhibitors N-acetyl cysteine (NAC) and diphenyleneiodonium (DPI) partially attenuated CXCL8 and IL-6 responses to 200 microg/mL, but not to 100 microg/mL Si50.	Acetylcysteine	38-55	interleukin 6	Homo sapiens	123-127
30861304-5	2019	Pre-treatment with the ROS inhibitors N-acetyl cysteine (NAC) and diphenyleneiodonium (DPI) partially attenuated CXCL8 and IL-6 responses to 200 microg/mL, but not to 100 microg/mL Si50.	Acetylcysteine	57-60	C-X-C motif chemokine ligand 8	Homo sapiens	113-118
30861304-5	2019	Pre-treatment with the ROS inhibitors N-acetyl cysteine (NAC) and diphenyleneiodonium (DPI) partially attenuated CXCL8 and IL-6 responses to 200 microg/mL, but not to 100 microg/mL Si50.	Acetylcysteine	57-60	interleukin 6	Homo sapiens	123-127
31228582-8	2019	Moreover, the antioxidant N-acetylcysteine attenuated Sb-induced Akt/mTOR inhibition and decreased autophagy and apoptosis, with autophagy inhibition also playing a cytoprotective role.	Acetylcysteine	26-42	AKT serine/threonine kinase 1	Homo sapiens	65-68
31176737-10	2019	In addition, the activation of JNK signaling pathway prompted by WZ26 and cisplatin was also reversed by NAC pretreatment.	Acetylcysteine	105-108	mitogen-activated protein kinase 8	Homo sapiens	31-34
31228582-8	2019	Moreover, the antioxidant N-acetylcysteine attenuated Sb-induced Akt/mTOR inhibition and decreased autophagy and apoptosis, with autophagy inhibition also playing a cytoprotective role.	Acetylcysteine	26-42	mechanistic target of rapamycin kinase	Homo sapiens	69-73
31356540-10	2019	Eliminating ROS with N-acetylcysteine or preinject CY into rat jugular vein reduces the expression of IL-6, TNF-a, and, especially, IL-1b in an in vivo I/R model.	Acetylcysteine	21-37	interleukin 6	Rattus norvegicus	102-106
31356540-10	2019	Eliminating ROS with N-acetylcysteine or preinject CY into rat jugular vein reduces the expression of IL-6, TNF-a, and, especially, IL-1b in an in vivo I/R model.	Acetylcysteine	21-37	interleukin 1 beta	Rattus norvegicus	132-137
31044464-5	2019	After 24-hour MPA-CdTe QD exposure, the activation level of extracellular regulated protein kinase (ERK) signaling pathway and cysteinyl-directed aspartate-specific proteases (Caspases) significantly increased, which led to the increasing level of reactive oxygen species (ROS) and cell apoptosis; the group pretreated with ROS scavenger N-acetyl-L-cysteine (NAC) significantly reduced the apoptotic cell percentage, indicating that ROS played a critical role in QD-induced cytotoxicity.	Acetylcysteine	338-357	mitogen-activated protein kinase 1	Mus musculus	60-98
31044464-5	2019	After 24-hour MPA-CdTe QD exposure, the activation level of extracellular regulated protein kinase (ERK) signaling pathway and cysteinyl-directed aspartate-specific proteases (Caspases) significantly increased, which led to the increasing level of reactive oxygen species (ROS) and cell apoptosis; the group pretreated with ROS scavenger N-acetyl-L-cysteine (NAC) significantly reduced the apoptotic cell percentage, indicating that ROS played a critical role in QD-induced cytotoxicity.	Acetylcysteine	338-357	mitogen-activated protein kinase 1	Mus musculus	100-103
31044464-5	2019	After 24-hour MPA-CdTe QD exposure, the activation level of extracellular regulated protein kinase (ERK) signaling pathway and cysteinyl-directed aspartate-specific proteases (Caspases) significantly increased, which led to the increasing level of reactive oxygen species (ROS) and cell apoptosis; the group pretreated with ROS scavenger N-acetyl-L-cysteine (NAC) significantly reduced the apoptotic cell percentage, indicating that ROS played a critical role in QD-induced cytotoxicity.	Acetylcysteine	359-362	mitogen-activated protein kinase 1	Mus musculus	60-98
31044464-5	2019	After 24-hour MPA-CdTe QD exposure, the activation level of extracellular regulated protein kinase (ERK) signaling pathway and cysteinyl-directed aspartate-specific proteases (Caspases) significantly increased, which led to the increasing level of reactive oxygen species (ROS) and cell apoptosis; the group pretreated with ROS scavenger N-acetyl-L-cysteine (NAC) significantly reduced the apoptotic cell percentage, indicating that ROS played a critical role in QD-induced cytotoxicity.	Acetylcysteine	359-362	mitogen-activated protein kinase 1	Mus musculus	100-103
31456939-6	2019	We show that blockade of proteasome activity, by MG-132 and bortezomib, or ROS accumulation, by N-acetylcysteine (NAC), restored the level of STAT3 protein.	Acetylcysteine	96-112	signal transducer and activator of transcription 3	Homo sapiens	142-147
31524245-0	2019	N-acetyl cysteine inhibits lipopolysaccharide-induced apoptosis of human umbilical vein endothelial cells via the p38MAPK signaling pathway.	Acetylcysteine	0-17	mitogen-activated protein kinase 14	Homo sapiens	114-117
31330229-8	2019	Pretreatment with the antioxidant N-acetylcysteine (NAC) effectively prevented MeHg-induced neuronal cell reactive oxygen species (ROS) generation, apoptotic and ER stress-related signals, and Akt inactivation.	Acetylcysteine	34-50	thymoma viral proto-oncogene 1	Mus musculus	193-196
31330229-8	2019	Pretreatment with the antioxidant N-acetylcysteine (NAC) effectively prevented MeHg-induced neuronal cell reactive oxygen species (ROS) generation, apoptotic and ER stress-related signals, and Akt inactivation.	Acetylcysteine	52-55	thymoma viral proto-oncogene 1	Mus musculus	193-196
31158660-6	2019	FD exposure impaired vasorelaxation in response to bradykinin and activated the local angiotensin system (LAS), which was inhibited by treatment with the antioxidant N-acetyl cysteine (NAC) and angiotensin II receptor type 1 (AT1) antagonist losartan (LOS).	Acetylcysteine	166-183	kininogen 1	Homo sapiens	51-61
31158660-7	2019	NAC and LOS also suppressed FD-induced SA-beta-gal activity, increased EC proliferation and eNOS expression, and improved endothelial function.	Acetylcysteine	0-3	nitric oxide synthase 3	Homo sapiens	92-96
31012781-7	2019	MWCNT-induced lipid accumulation in THP-1 macrophages was decreased modestly by antioxidant N-acetyl-l-cysteine and more effectively by ER stress inhibitor 4-phenylbutyric acid.	Acetylcysteine	92-111	GLI family zinc finger 2	Homo sapiens	36-41
31524245-12	2019	RT-qPCR and western blotting showed that LPS promoted caspase-3 and Bax expression, but inhibited that of Bcl-2 in HUVECs; however, these effects were attenuated by pretreatment with NAC or SB203580.	Acetylcysteine	183-186	caspase 3	Homo sapiens	54-63
31524245-12	2019	RT-qPCR and western blotting showed that LPS promoted caspase-3 and Bax expression, but inhibited that of Bcl-2 in HUVECs; however, these effects were attenuated by pretreatment with NAC or SB203580.	Acetylcysteine	183-186	BCL2 associated X, apoptosis regulator	Homo sapiens	68-71
31524245-12	2019	RT-qPCR and western blotting showed that LPS promoted caspase-3 and Bax expression, but inhibited that of Bcl-2 in HUVECs; however, these effects were attenuated by pretreatment with NAC or SB203580.	Acetylcysteine	183-186	BCL2 apoptosis regulator	Homo sapiens	106-111
31560470-7	2019	According to the serologic results (CRP test), C-reactive protein was at highest level in 150 mg/kg Nano-NAC and control groups and at lowest level in 50 mg/kg Nano-NAC and 75 mg/kg Nano-NAC groups (p(0.001).	Acetylcysteine	105-108	C-reactive protein	Rattus norvegicus	47-65
31560470-7	2019	According to the serologic results (CRP test), C-reactive protein was at highest level in 150 mg/kg Nano-NAC and control groups and at lowest level in 50 mg/kg Nano-NAC and 75 mg/kg Nano-NAC groups (p(0.001).	Acetylcysteine	165-168	C-reactive protein	Rattus norvegicus	47-65
31560470-7	2019	According to the serologic results (CRP test), C-reactive protein was at highest level in 150 mg/kg Nano-NAC and control groups and at lowest level in 50 mg/kg Nano-NAC and 75 mg/kg Nano-NAC groups (p(0.001).	Acetylcysteine	165-168	C-reactive protein	Rattus norvegicus	47-65
31560470-10	2019	Nano-NAC administration was proved feasible, safe and effective in reduction of the C-reactive protein level.	Acetylcysteine	5-8	C-reactive protein	Rattus norvegicus	84-102
31054874-6	2019	Whereas the antioxidants N-acetylcysteine (NAC) and Tempol significantly suppressed the expression of BiP and CHOP, suggesting that ROS generation is an early trigger of Cd-activated ER stress.	Acetylcysteine	25-41	growth differentiation factor 10	Homo sapiens	102-105
31054874-6	2019	Whereas the antioxidants N-acetylcysteine (NAC) and Tempol significantly suppressed the expression of BiP and CHOP, suggesting that ROS generation is an early trigger of Cd-activated ER stress.	Acetylcysteine	25-41	DNA damage inducible transcript 3	Homo sapiens	110-114
31054874-6	2019	Whereas the antioxidants N-acetylcysteine (NAC) and Tempol significantly suppressed the expression of BiP and CHOP, suggesting that ROS generation is an early trigger of Cd-activated ER stress.	Acetylcysteine	43-46	growth differentiation factor 10	Homo sapiens	102-105
31054874-6	2019	Whereas the antioxidants N-acetylcysteine (NAC) and Tempol significantly suppressed the expression of BiP and CHOP, suggesting that ROS generation is an early trigger of Cd-activated ER stress.	Acetylcysteine	43-46	DNA damage inducible transcript 3	Homo sapiens	110-114
31438633-8	2019	Genistein further increased the accumulation of reactive oxygen species (ROS), which was significantly suppressed by N-acetyl cysteine (NAC), a ROS scavenger, and in particular, NAC prevented genistein-mediated inactivation of PI3K/Akt signaling, G2/M arrest and apoptosis.	Acetylcysteine	117-134	AKT serine/threonine kinase 1	Homo sapiens	232-235
31438633-8	2019	Genistein further increased the accumulation of reactive oxygen species (ROS), which was significantly suppressed by N-acetyl cysteine (NAC), a ROS scavenger, and in particular, NAC prevented genistein-mediated inactivation of PI3K/Akt signaling, G2/M arrest and apoptosis.	Acetylcysteine	136-139	AKT serine/threonine kinase 1	Homo sapiens	232-235
31438633-8	2019	Genistein further increased the accumulation of reactive oxygen species (ROS), which was significantly suppressed by N-acetyl cysteine (NAC), a ROS scavenger, and in particular, NAC prevented genistein-mediated inactivation of PI3K/Akt signaling, G2/M arrest and apoptosis.	Acetylcysteine	178-181	AKT serine/threonine kinase 1	Homo sapiens	232-235
31266772-6	2019	Reduced expression of HIF2alpha inhibited the self-renewal of Sca-1+ cells; this effect was blocked through suppression of ROS by N-acetyl cysteine or the knockdown of p53, Nanog, or Sox2.	Acetylcysteine	130-147	ataxin 1	Homo sapiens	62-67
31456939-6	2019	We show that blockade of proteasome activity, by MG-132 and bortezomib, or ROS accumulation, by N-acetylcysteine (NAC), restored the level of STAT3 protein.	Acetylcysteine	114-117	signal transducer and activator of transcription 3	Homo sapiens	142-147
31646013-5	2019	Mechanistically, prolonged activation of Akt signaling caused an accumulation of reactive oxygen species and triggered chondrocyte senescence as well as a senescence-associated secretory phenotype, whereas chronic administration of the antioxidant N-acetylcysteine suppressed chondrocyte senescence and mitigated OA progression in PTEN-deficient mice.	Acetylcysteine	248-264	thymoma viral proto-oncogene 1	Mus musculus	41-44
31396402-8	2019	Inhibition of ROS with N-acetyl cysteine (NAC) significantly decreased pristimerin-induced cell death by inhibiting the phosphorylation of ASK1 and JNK.	Acetylcysteine	23-40	mitogen-activated protein kinase 8	Homo sapiens	148-151
31396402-8	2019	Inhibition of ROS with N-acetyl cysteine (NAC) significantly decreased pristimerin-induced cell death by inhibiting the phosphorylation of ASK1 and JNK.	Acetylcysteine	42-45	mitogen-activated protein kinase 8	Homo sapiens	148-151
31646013-5	2019	Mechanistically, prolonged activation of Akt signaling caused an accumulation of reactive oxygen species and triggered chondrocyte senescence as well as a senescence-associated secretory phenotype, whereas chronic administration of the antioxidant N-acetylcysteine suppressed chondrocyte senescence and mitigated OA progression in PTEN-deficient mice.	Acetylcysteine	248-264	phosphatase and tensin homolog	Mus musculus	331-335
30793306-10	2019	Furthermore, N-acetyl- l-cysteine markedly abrogated VEGF-A-increased ROS production, IRE-1, GRP78/Bip, beclin-1 expression, and LC3-II/LC3-I in the HUVECs.	Acetylcysteine	13-33	heat shock protein 5	Mus musculus	93-98
31398338-5	2019	N-acetyl cysteine treatment partially rescues the effects of FN3K loss on NRF2 driven tumor phenotypes indicating a key role for NRF2-mediated redox balance.	Acetylcysteine	0-17	fructosamine 3 kinase	Homo sapiens	61-65
31398338-5	2019	N-acetyl cysteine treatment partially rescues the effects of FN3K loss on NRF2 driven tumor phenotypes indicating a key role for NRF2-mediated redox balance.	Acetylcysteine	0-17	NFE2 like bZIP transcription factor 2	Homo sapiens	74-78
31398338-5	2019	N-acetyl cysteine treatment partially rescues the effects of FN3K loss on NRF2 driven tumor phenotypes indicating a key role for NRF2-mediated redox balance.	Acetylcysteine	0-17	NFE2 like bZIP transcription factor 2	Homo sapiens	129-133
30916421-8	2019	Furthermore, the MAPK signaling pathway regulated the expression levels of STAT3 and NF-kappaB upon treatment with MAPK inhibitor and N-acetyl-L-cysteine (NAC).	Acetylcysteine	134-153	signal transducer and activator of transcription 3	Homo sapiens	75-80
30916421-8	2019	Furthermore, the MAPK signaling pathway regulated the expression levels of STAT3 and NF-kappaB upon treatment with MAPK inhibitor and N-acetyl-L-cysteine (NAC).	Acetylcysteine	134-153	nuclear factor kappa B subunit 1	Homo sapiens	85-94
30916421-8	2019	Furthermore, the MAPK signaling pathway regulated the expression levels of STAT3 and NF-kappaB upon treatment with MAPK inhibitor and N-acetyl-L-cysteine (NAC).	Acetylcysteine	155-158	signal transducer and activator of transcription 3	Homo sapiens	75-80
30916421-8	2019	Furthermore, the MAPK signaling pathway regulated the expression levels of STAT3 and NF-kappaB upon treatment with MAPK inhibitor and N-acetyl-L-cysteine (NAC).	Acetylcysteine	155-158	nuclear factor kappa B subunit 1	Homo sapiens	85-94
31447555-5	2019	NAC can effectively mitigate iron-induced oxidative injury of cardiomyocytes, evidenced by reduced production of MDA, 8-iso-PGF2alpha, and 8-OHDG and maintained concentrations of SOD, CAT, GSH-Px, and GSH in ELISA and biochemical tests; downregulated expression of CHOP, GRP78, p62, and LC3-II proteins in Western Blot, and less cardiomyocytes apoptosis in flow cytometric analysis.	Acetylcysteine	0-3	catalase	Rattus norvegicus	184-187
31102529-4	2019	OBJECTIVES: To test whether physiological concentrations of N-acetylcysteine, a clinically safe antioxidant drug currently used in human therapy, is able to reduce ROS production, SOS induction and mutagenesis in ciprofloxacin-treated bacteria without affecting antibiotic activity.	Acetylcysteine	60-76	xylosyltransferase 2	Homo sapiens	180-183
31102529-7	2019	RESULTS: Treatment with N-acetylcysteine reduced intracellular ROS levels (by ~40%), as well as SOS induction (by up to 75%) and bacterial filamentation caused by subinhibitory concentrations of ciprofloxacin, without affecting ciprofloxacin antibacterial activity.	Acetylcysteine	24-40	xylosyltransferase 2	Homo sapiens	96-99
31102529-8	2019	Remarkably, N-acetylcysteine completely abolished SOS-mediated mutagenesis.	Acetylcysteine	12-28	xylosyltransferase 2	Homo sapiens	50-53
31102529-9	2019	CONCLUSIONS: Collectively, our data strongly support the notion that ROS are a key factor in antibiotic-induced SOS mutagenesis and open the possibility of using N-acetylcysteine in combination with antibiotic therapy to hinder the development of antibiotic resistance.	Acetylcysteine	162-178	xylosyltransferase 2	Homo sapiens	112-115
30825206-9	2019	Moreover, NAC blocked cholesterol-induced phosphorylation of IkappaBalpha and p65.	Acetylcysteine	10-13	nuclear factor of kappa light polypeptide gene enhancer in B cells inhibitor, alpha	Mus musculus	61-73
30793306-10	2019	Furthermore, N-acetyl- l-cysteine markedly abrogated VEGF-A-increased ROS production, IRE-1, GRP78/Bip, beclin-1 expression, and LC3-II/LC3-I in the HUVECs.	Acetylcysteine	13-33	heat shock protein 5	Mus musculus	99-102
31233063-6	2019	SP600125, a JNK inhibitor, and N-acetylcysteine (NAC), a ROS inhibitor, attenuated Slp-induced autophagic cell death in HCT116 cells.	Acetylcysteine	31-47	surface layer protein	Lactobacillus acidophilus NCFM	83-86
30633345-8	2019	NAC, TTFA, DPI, inhibitors of ERK1/2, p38, and NF-kappaB all downregulated FPA-induced CRP expression.	Acetylcysteine	0-3	C-reactive protein	Homo sapiens	87-90
31206177-14	2019	We also found that treatment with the antioxidant N-acetylcysteine (NAC) improved fetal survival in DHT+insulin-treated pregnant rats, an effect related to changes in Keap1/Nrf2 and nuclear factor-kappaB signalling.	Acetylcysteine	50-66	NFE2 like bZIP transcription factor 2	Rattus norvegicus	173-177
31206177-14	2019	We also found that treatment with the antioxidant N-acetylcysteine (NAC) improved fetal survival in DHT+insulin-treated pregnant rats, an effect related to changes in Keap1/Nrf2 and nuclear factor-kappaB signalling.	Acetylcysteine	68-71	NFE2 like bZIP transcription factor 2	Rattus norvegicus	173-177
31423251-9	2019	Exposure to ROS scavenger N-acetyl-cysteine or NF-kappaB inhibitor PDTC inhibited the activation of the above pathway and the expression of VEGF induced by acute hypoxia.	Acetylcysteine	26-43	vascular endothelial growth factor A	Homo sapiens	140-144
31254666-6	2019	In addition to attenuating an abnormal pro-inflammatory response and limiting oxidative damage, NAC could inhibit lipid accumulation by targeting adipogenic transcription factors such as peroxisome proliferator-activated receptor gamma (PPARgamma) and CCAAT/enhancer binding protein beta (C/EBPbeta), and improve insulin sensitivity through augmenting phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT) pathway.	Acetylcysteine	96-99	peroxisome proliferator activated receptor gamma	Homo sapiens	187-235
31254666-6	2019	In addition to attenuating an abnormal pro-inflammatory response and limiting oxidative damage, NAC could inhibit lipid accumulation by targeting adipogenic transcription factors such as peroxisome proliferator-activated receptor gamma (PPARgamma) and CCAAT/enhancer binding protein beta (C/EBPbeta), and improve insulin sensitivity through augmenting phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT) pathway.	Acetylcysteine	96-99	peroxisome proliferator activated receptor gamma	Homo sapiens	237-246
31254666-6	2019	In addition to attenuating an abnormal pro-inflammatory response and limiting oxidative damage, NAC could inhibit lipid accumulation by targeting adipogenic transcription factors such as peroxisome proliferator-activated receptor gamma (PPARgamma) and CCAAT/enhancer binding protein beta (C/EBPbeta), and improve insulin sensitivity through augmenting phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT) pathway.	Acetylcysteine	96-99	AKT serine/threonine kinase 1	Homo sapiens	403-406
31273057-12	2019	We also found the down-regulation of oxidising enzymes (NOX2, iNOS, SOD2, and XO) after NAC treatment.	Acetylcysteine	88-91	nitric oxide synthase 2, inducible	Mus musculus	62-66
31273057-12	2019	We also found the down-regulation of oxidising enzymes (NOX2, iNOS, SOD2, and XO) after NAC treatment.	Acetylcysteine	88-91	superoxide dismutase 2, mitochondrial	Mus musculus	68-72
31273057-13	2019	Moreover, E-cadherin expression was increased while vimentin and Cytochrome C expressions were decreased by NAC.	Acetylcysteine	108-111	cadherin 1	Mus musculus	10-20
31233063-6	2019	SP600125, a JNK inhibitor, and N-acetylcysteine (NAC), a ROS inhibitor, attenuated Slp-induced autophagic cell death in HCT116 cells.	Acetylcysteine	49-52	surface layer protein	Lactobacillus acidophilus NCFM	83-86
31233063-7	2019	Furthermore, NAC was found to prevent Slp-induced p70 and JNK phosphorylation.	Acetylcysteine	13-16	surface layer protein	Lactobacillus acidophilus NCFM	38-41
31233063-7	2019	Furthermore, NAC was found to prevent Slp-induced p70 and JNK phosphorylation.	Acetylcysteine	13-16	ubiquitin associated and SH3 domain containing B	Homo sapiens	50-53
31233063-7	2019	Furthermore, NAC was found to prevent Slp-induced p70 and JNK phosphorylation.	Acetylcysteine	13-16	mitogen-activated protein kinase 8	Homo sapiens	58-61
30511398-7	2019	Furthermore, Mad-induced reactive oxygen species (ROS) activated PTEN and inactivated Akt-Erk1/2 contributing to cell death, as N-acetyl- L-cysteine ameliorated the event.	Acetylcysteine	128-148	AKT serine/threonine kinase 1	Rattus norvegicus	86-89
31360201-12	2019	UII also enhanced Akt phosphorylation significantly, and this effect was potently inhibited by urantide, N-acetylcysteine, diphenyliodonium and LY294002.	Acetylcysteine	105-121	urotensin 2	Mus musculus	0-3
30737888-11	2019	CD31 immunohistology results revealed relatively more new vessels in the PCL-Col/NAC group than the control groups.	Acetylcysteine	81-84	platelet and endothelial cell adhesion molecule 1	Rattus norvegicus	0-4
31084929-7	2019	Furthermore, we found that superoxide anion levels were significantly increased in AngII-treated endothelial cells compared with controls and that the ROS scavenger N-acetyl-l-cysteine (NAC) significantly abolished CSE ubiquitination.	Acetylcysteine	165-184	angiotensinogen	Homo sapiens	83-88
30628067-6	2019	On the basis of time and dose-dependent manner, our data demonstrated that GEM-induced PTX3 expression was dependent on ROS generation as it was abrogated by pretreatment of lung cancer cells with the free radical scavenger N-acetyl-l-cysteine.	Acetylcysteine	224-243	pentraxin 3	Homo sapiens	87-91
31084929-7	2019	Furthermore, we found that superoxide anion levels were significantly increased in AngII-treated endothelial cells compared with controls and that the ROS scavenger N-acetyl-l-cysteine (NAC) significantly abolished CSE ubiquitination.	Acetylcysteine	186-189	angiotensinogen	Homo sapiens	83-88
31148586-8	2019	NAC inhibited the induction and nuclear localization of phospho-Smad2 protein in bladder tissues and the upregulation of genes related to fibrosis, such as Tgfb2, Tgfb3, Smad2, Smad3, Cxcl10, and Card10.	Acetylcysteine	0-3	transforming growth factor, beta 3	Rattus norvegicus	163-168
31293646-6	2019	Cisplatin exposure induced ROS stress in Hep-2 cells in a time-dependent manner and was accompanied by increased Nrf2 and SENP3 protein accumulations, an effect reversed by the addition of the antioxidant N-acetyl-cysteine (NAC).	Acetylcysteine	205-222	NFE2 like bZIP transcription factor 2	Homo sapiens	113-117
31360690-17	2019	The inhibition of ROS by treatment with N-acetylcysteine, a radical scavenger, abrogated Z-ajoene-induced expression of NQO1 as well as activation of ERK and Nrf2, suggesting that Z-ajoene augments the Nrf2-dependent antioxidant defense via ROS generation and ERK activation.	Acetylcysteine	40-56	NAD(P)H quinone dehydrogenase 1	Homo sapiens	120-124
31360690-17	2019	The inhibition of ROS by treatment with N-acetylcysteine, a radical scavenger, abrogated Z-ajoene-induced expression of NQO1 as well as activation of ERK and Nrf2, suggesting that Z-ajoene augments the Nrf2-dependent antioxidant defense via ROS generation and ERK activation.	Acetylcysteine	40-56	mitogen-activated protein kinase 1	Homo sapiens	150-153
31360690-17	2019	The inhibition of ROS by treatment with N-acetylcysteine, a radical scavenger, abrogated Z-ajoene-induced expression of NQO1 as well as activation of ERK and Nrf2, suggesting that Z-ajoene augments the Nrf2-dependent antioxidant defense via ROS generation and ERK activation.	Acetylcysteine	40-56	NFE2 like bZIP transcription factor 2	Homo sapiens	158-162
31360690-17	2019	The inhibition of ROS by treatment with N-acetylcysteine, a radical scavenger, abrogated Z-ajoene-induced expression of NQO1 as well as activation of ERK and Nrf2, suggesting that Z-ajoene augments the Nrf2-dependent antioxidant defense via ROS generation and ERK activation.	Acetylcysteine	40-56	NFE2 like bZIP transcription factor 2	Homo sapiens	202-206
31360690-17	2019	The inhibition of ROS by treatment with N-acetylcysteine, a radical scavenger, abrogated Z-ajoene-induced expression of NQO1 as well as activation of ERK and Nrf2, suggesting that Z-ajoene augments the Nrf2-dependent antioxidant defense via ROS generation and ERK activation.	Acetylcysteine	40-56	mitogen-activated protein kinase 1	Homo sapiens	260-263
31186685-9	2019	In addition, ALT induced apoptosis via the inhibition of RAC-alpha serine/threonine-protein kinase (AKT) signaling and ROS generation, which was effectively inhibited by the ROS scavenger, N-acetyl cysteine.	Acetylcysteine	189-206	AKT serine/threonine kinase 1	Homo sapiens	100-103
30617744-8	2019	In fatty acid-treated HepG2 cells, knockdown of catalase accelerated cellular lipid accumulation and depressed mitochondrial biogenesis, which was recovered by co-treatment with N-acetyl cysteine or melatonin.	Acetylcysteine	178-195	catalase	Homo sapiens	48-56
31196186-15	2019	Treatment of leukemic cell lines with NAC prevented the DFX-mediated phosphorylation of STAT1 as well as the expression of the IFN-stimulated genes.	Acetylcysteine	38-41	interferon alpha 1	Homo sapiens	127-130
31041622-13	2019	Rapamycin and NAC, which impact on the MTOR pathway, both reduced both pools of progerin without increasing prelamin A in HGPS cell nuclei.	Acetylcysteine	14-17	mechanistic target of rapamycin kinase	Homo sapiens	39-43
30796177-6	2019	And ROS scavenger N-acetyl-cysteine attenuated the activation of caspase-1 induced by MST1 and the effect of MST1 in PDAC cell death, proliferation, migration, and invasion.	Acetylcysteine	18-35	caspase 1	Homo sapiens	65-74
31148586-8	2019	NAC inhibited the induction and nuclear localization of phospho-Smad2 protein in bladder tissues and the upregulation of genes related to fibrosis, such as Tgfb2, Tgfb3, Smad2, Smad3, Cxcl10, and Card10.	Acetylcysteine	0-3	SMAD family member 3	Rattus norvegicus	177-182
31148586-8	2019	NAC inhibited the induction and nuclear localization of phospho-Smad2 protein in bladder tissues and the upregulation of genes related to fibrosis, such as Tgfb2, Tgfb3, Smad2, Smad3, Cxcl10, and Card10.	Acetylcysteine	0-3	caspase recruitment domain family, member 10	Rattus norvegicus	196-202
30818202-0	2019	N-acetylcysteine attenuates PM2.5-induced apoptosis by ROS-mediated Nrf2 pathway in human embryonic stem cells.	Acetylcysteine	0-16	NFE2 like bZIP transcription factor 2	Homo sapiens	68-72
30818202-8	2019	Interestingly, scavenging of PM2.5-induced ROS by N-acetylcysteine (NAC) could block cell apoptosis and rescue the activity of Nrf2 signaling pathway.	Acetylcysteine	50-66	NFE2 like bZIP transcription factor 2	Homo sapiens	127-131
30818202-8	2019	Interestingly, scavenging of PM2.5-induced ROS by N-acetylcysteine (NAC) could block cell apoptosis and rescue the activity of Nrf2 signaling pathway.	Acetylcysteine	68-71	NFE2 like bZIP transcription factor 2	Homo sapiens	127-131
30624620-8	2019	Finally, tumor number decreased 7-fold in the lungs of XPC-/- mice by concurrent treatment with the antioxidant, N-acetylcysteine.	Acetylcysteine	113-129	xeroderma pigmentosum, complementation group C	Mus musculus	55-58
30926546-5	2019	Interestingly, systemic administration of N-acetylcysteine (NAC), a drug that both upregulates GLT-1 and promotes glial-glutamate release, reduced cued methamphetamine seeking.	Acetylcysteine	42-58	solute carrier family 1 member 2	Homo sapiens	95-100
30926546-5	2019	Interestingly, systemic administration of N-acetylcysteine (NAC), a drug that both upregulates GLT-1 and promotes glial-glutamate release, reduced cued methamphetamine seeking.	Acetylcysteine	60-63	solute carrier family 1 member 2	Homo sapiens	95-100
31223283-10	2019	Furthermore, treatment with antioxidant, N-acetyl-cysteine (NAC) in offspring reversed GDM-mediated DNA hypermethylation, Sirt1 repression and autophagy-related gene protein overexpression in the hearts, and rescued GDM-induced deterioration in heart ischemic injury and LV dysfunction.	Acetylcysteine	41-58	sirtuin 1	Rattus norvegicus	122-127
31223283-10	2019	Furthermore, treatment with antioxidant, N-acetyl-cysteine (NAC) in offspring reversed GDM-mediated DNA hypermethylation, Sirt1 repression and autophagy-related gene protein overexpression in the hearts, and rescued GDM-induced deterioration in heart ischemic injury and LV dysfunction.	Acetylcysteine	60-63	sirtuin 1	Rattus norvegicus	122-127
30849338-4	2019	Elevated oxidative stress and mitogen-activated protein kinase (MAPKs) phosphorylation were observed after IS stimulation for 1 and 24 h. After N-acetylcysteine (NAC) treatment as antioxidants, the recovery in IS-induced decrease myotube diameter and ERK phosphorylation was observed.	Acetylcysteine	144-160	mitogen-activated protein kinase 1	Mus musculus	251-254
30677238-7	2019	Furthermore, application of N-acetylcysteine protected hypothalamic AVP neurons from ER stress-induced apoptosis through blocking the PI3K/Akt and ERK pathways.	Acetylcysteine	28-44	AKT serine/threonine kinase 1	Homo sapiens	139-142
30677238-7	2019	Furthermore, application of N-acetylcysteine protected hypothalamic AVP neurons from ER stress-induced apoptosis through blocking the PI3K/Akt and ERK pathways.	Acetylcysteine	28-44	mitogen-activated protein kinase 1	Homo sapiens	147-150
31141608-11	2019	In the retina of diabetic mice and cells exposed to hyperglycemic conditions, NAC normalized ROS and prevented an increase in REDD1 expression.	Acetylcysteine	78-81	DNA-damage-inducible transcript 4	Mus musculus	126-131
30894323-7	2019	Only LPS induction of HMOX1 was inhibited by NAC while that of TXNRD1 and PRDX1 was unaffected.	Acetylcysteine	45-48	heme oxygenase 1	Mus musculus	22-27
30843602-13	2019	After training, NAC increased resting muscle GSH concentration and thigh net K+ release during Ex2 only in BFR-leg (P < 0.05), whereas the abundance of Na+ ,K+ -ATPase-isoform alpha1 in type II (51%), beta1 in type I (33%), and FXYD1 in type I (108%) and type II (60%) fibres was higher in BFR-leg than in CON-leg (P < 0.05).	Acetylcysteine	16-19	FXYD domain containing ion transport regulator 1	Homo sapiens	228-233
30951973-8	2019	NAC and LA supplementation prevented GSH and total non-enzymatic antioxidants depletion as well as restored GPx and GR activities, TNF-alpha, IL6 and cholesterol in OVX rats.	Acetylcysteine	0-3	tumor necrosis factor	Rattus norvegicus	131-140
30951973-8	2019	NAC and LA supplementation prevented GSH and total non-enzymatic antioxidants depletion as well as restored GPx and GR activities, TNF-alpha, IL6 and cholesterol in OVX rats.	Acetylcysteine	0-3	interleukin 6	Rattus norvegicus	142-145
30865562-6	2019	Blocking ROS generation by N-acetylcysteine (NAC) or overexpressing constitutively active AKT vector (CA-AKT) inhibited HMS-incurred p53 mitochondrial translocation and promoted its nuclear targeting.	Acetylcysteine	45-48	tumor protein p53	Homo sapiens	133-136
30971398-7	2019	Importantly, treatment of GMFG-knockdown macrophages with the antioxidant N-acetylcysteine reversed the altered expression of iron metabolism proteins and significantly inhibited the enhanced gene expression of M2 macrophage markers, suggesting that mtROS is mechanistically linked to cellular iron metabolism and macrophage phenotype.	Acetylcysteine	74-90	glia maturation factor, gamma	Mus musculus	26-30
30865562-6	2019	Blocking ROS generation by N-acetylcysteine (NAC) or overexpressing constitutively active AKT vector (CA-AKT) inhibited HMS-incurred p53 mitochondrial translocation and promoted its nuclear targeting.	Acetylcysteine	27-43	tumor protein p53	Homo sapiens	133-136
30896878-6	2019	Mechanistically, CsA treatment increased reactive oxygen species (ROS) generation, and the intracellular ROS scavenger N-acetyl-cysteine (NAC) attenuated CsA-induced cell proliferation as well as the activation of Akt/Cyclin D1 signaling.	Acetylcysteine	119-136	AKT serine/threonine kinase 1	Homo sapiens	214-217
30896878-6	2019	Mechanistically, CsA treatment increased reactive oxygen species (ROS) generation, and the intracellular ROS scavenger N-acetyl-cysteine (NAC) attenuated CsA-induced cell proliferation as well as the activation of Akt/Cyclin D1 signaling.	Acetylcysteine	138-141	AKT serine/threonine kinase 1	Homo sapiens	214-217
30684762-7	2019	Among those genes, N-acetyl-L-cysteine (NAC) treatment blocked the H2S-triggered expression of FOS and IL8.	Acetylcysteine	19-38	Fos proto-oncogene, AP-1 transcription factor subunit	Gallus gallus	95-98
30684762-7	2019	Among those genes, N-acetyl-L-cysteine (NAC) treatment blocked the H2S-triggered expression of FOS and IL8.	Acetylcysteine	40-43	Fos proto-oncogene, AP-1 transcription factor subunit	Gallus gallus	95-98
30652495-12	2019	The antioxidant N-acetylcysteine prevents CSE-induced miR-29b downregulation and BRD4 and IL-8 upregulation.	Acetylcysteine	16-32	bromodomain containing 4	Homo sapiens	81-85
30797898-8	2019	Pretreatment with the pan-caspase inhibitor Z-VAD-FMK, PI3K/Akt pathway activator insulin or ROS scavenger N-acetylcysteine (NAC) further demonstrated that ROS/PI3K/Akt pathway was responsible for Rk1-induced apoptosis.	Acetylcysteine	107-123	AKT serine/threonine kinase 1	Homo sapiens	165-168
30797898-8	2019	Pretreatment with the pan-caspase inhibitor Z-VAD-FMK, PI3K/Akt pathway activator insulin or ROS scavenger N-acetylcysteine (NAC) further demonstrated that ROS/PI3K/Akt pathway was responsible for Rk1-induced apoptosis.	Acetylcysteine	125-128	AKT serine/threonine kinase 1	Homo sapiens	165-168
30652495-12	2019	The antioxidant N-acetylcysteine prevents CSE-induced miR-29b downregulation and BRD4 and IL-8 upregulation.	Acetylcysteine	16-32	C-X-C motif chemokine ligand 8	Homo sapiens	90-94
30799090-10	2019	The highest concentrations of eluted NAC were 42.99 muM (1 day; Filtek  Supreme XTE-1 wt% NAC; 1 day; methanol) and 108.11 muM (Filtek  Supreme XTE-1 wt% NAC; 7 day; water).	Acetylcysteine	37-40	latexin	Homo sapiens	52-55
30810066-6	2019	The antioxidants diphenyleneiodonium and N-acetylcysteine blocked IGFBP-5-stimulated ECM production in normal, SSc, and IPF human primary lung fibroblasts.	Acetylcysteine	41-57	insulin like growth factor binding protein 5	Homo sapiens	66-73
30847537-9	2019	Induction of IL-1beta is dependent on the activation of the NLRP3 (NOD-like receptor family, pyrin domain containing 3) inflammasome and ROS (reactive oxygen species) production in macrophages, as inhibition of NLRP3 by MCC950 and reduction of ROS production by N-acetylcysteine blocked NLRP3 activation, IL-1beta induction, and fibroblast activation and differentiation.	Acetylcysteine	262-278	interleukin 1 beta	Homo sapiens	13-21
30847537-9	2019	Induction of IL-1beta is dependent on the activation of the NLRP3 (NOD-like receptor family, pyrin domain containing 3) inflammasome and ROS (reactive oxygen species) production in macrophages, as inhibition of NLRP3 by MCC950 and reduction of ROS production by N-acetylcysteine blocked NLRP3 activation, IL-1beta induction, and fibroblast activation and differentiation.	Acetylcysteine	262-278	NLR family pyrin domain containing 3	Homo sapiens	60-65
30799090-10	2019	The highest concentrations of eluted NAC were 42.99 muM (1 day; Filtek  Supreme XTE-1 wt% NAC; 1 day; methanol) and 108.11 muM (Filtek  Supreme XTE-1 wt% NAC; 7 day; water).	Acetylcysteine	37-40	latexin	Homo sapiens	123-126
30496017-9	2019	Expressions of Brca2, Xpc, Mlh3, Rad51, Xrcc2, Hus1, Rad9a, Cdkn1a, Gadd45a which are the DNA-repair genes were found to be significantly higher in NAC + ALC + IR group than those in individual treatment of ALC or NAC.	Acetylcysteine	148-151	cyclin dependent kinase inhibitor 1A	Homo sapiens	60-66
30317657-5	2019	Furthermore, the antioxidant compound N-acetyl-cysteine eliminated the nicotine-activated production of reactive oxygen species (ROS) and inhibited signal transducer and activator of transcription 3 (STAT-3) phosphorylation; these two mechanisms mediated the upregulation of IL-6 expression by nicotine.	Acetylcysteine	38-55	signal transducer and activator of transcription 3	Homo sapiens	148-198
30317657-5	2019	Furthermore, the antioxidant compound N-acetyl-cysteine eliminated the nicotine-activated production of reactive oxygen species (ROS) and inhibited signal transducer and activator of transcription 3 (STAT-3) phosphorylation; these two mechanisms mediated the upregulation of IL-6 expression by nicotine.	Acetylcysteine	38-55	signal transducer and activator of transcription 3	Homo sapiens	200-206
30317657-5	2019	Furthermore, the antioxidant compound N-acetyl-cysteine eliminated the nicotine-activated production of reactive oxygen species (ROS) and inhibited signal transducer and activator of transcription 3 (STAT-3) phosphorylation; these two mechanisms mediated the upregulation of IL-6 expression by nicotine.	Acetylcysteine	38-55	interleukin 6	Homo sapiens	275-279
31037153-9	2019	N-acetylcysteine blocked the downregulation of PD-L1 suggesting the involvement of reactive oxygen species.	Acetylcysteine	0-16	CD274 antigen	Mus musculus	47-52
30742845-10	2019	N-Acetyl-cysteine and SB203580 pretreatment essentially abolished arsenic-induced phosphorylation of p38 and reversed arsenic-induced increased osteoclast differentiation in Nrf2 deficiency.	Acetylcysteine	0-17	nuclear factor, erythroid derived 2, like 2	Mus musculus	174-178
30590262-10	2019	Treatment with N-acetyl cysteine attenuated the suppression of SOD1.	Acetylcysteine	15-32	superoxide dismutase 1	Homo sapiens	63-67
30540918-10	2019	Antioxidant N-acetylcysteine and recombinant ALR (rALR) both inhibited ALR depletion-induced miR-540 expression and lipid accumulation in hepatocytes.	Acetylcysteine	12-28	growth factor, augmenter of liver regeneration	Mus musculus	51-54
30540918-10	2019	Antioxidant N-acetylcysteine and recombinant ALR (rALR) both inhibited ALR depletion-induced miR-540 expression and lipid accumulation in hepatocytes.	Acetylcysteine	12-28	microRNA 540	Mus musculus	93-100
30948926-5	2019	Secondly, the influence of ROS content on the activity of the JNK1/Sirt1/FoxO3a signaling pathway was explored through the application of NAC, sp600125 (a JNK1 inhibitor), and nicotinamide (a Sirt1 inhibitor).	Acetylcysteine	138-141	sirtuin 1	Rattus norvegicus	67-72
30146791-10	2019	NAC significantly prevented A. salmonea-induced HER-2/neu depletion and PI3K/AKT inactivation, indicating that A. salmonea-triggered apoptosis is mediated by ROS-inhibited HER-2/neu signaling cascades.	Acetylcysteine	0-3	AKT serine/threonine kinase 1	Homo sapiens	77-80
30146791-10	2019	NAC significantly prevented A. salmonea-induced HER-2/neu depletion and PI3K/AKT inactivation, indicating that A. salmonea-triggered apoptosis is mediated by ROS-inhibited HER-2/neu signaling cascades.	Acetylcysteine	0-3	erb-b2 receptor tyrosine kinase 2	Homo sapiens	48-53
30146791-10	2019	NAC significantly prevented A. salmonea-induced HER-2/neu depletion and PI3K/AKT inactivation, indicating that A. salmonea-triggered apoptosis is mediated by ROS-inhibited HER-2/neu signaling cascades.	Acetylcysteine	0-3	erb-b2 receptor tyrosine kinase 2	Homo sapiens	54-57
30548974-7	2019	The role of TLR9/NF-kappaB dependent activity was confirmed by HEK-Blue hTLR9 reporter cell line analysis after coincubation with TLF specimens with predetermined concentrations of NAC or CQ alone or TLR9 inhibitory oligodeoxynucleotide (iODN).	Acetylcysteine	181-184	TLR9	Sus scrofa	12-16
31127990-10	2019	N-acetylcysteine (NAC) treatment almost completely eliminated the reactive oxygen species (ROS) produced by TGF-beta1 and ERK activation.	Acetylcysteine	0-16	transforming growth factor beta 1	Homo sapiens	108-117
31127990-10	2019	N-acetylcysteine (NAC) treatment almost completely eliminated the reactive oxygen species (ROS) produced by TGF-beta1 and ERK activation.	Acetylcysteine	0-16	mitogen-activated protein kinase 1	Homo sapiens	122-125
31127990-10	2019	N-acetylcysteine (NAC) treatment almost completely eliminated the reactive oxygen species (ROS) produced by TGF-beta1 and ERK activation.	Acetylcysteine	18-21	transforming growth factor beta 1	Homo sapiens	108-117
31127990-10	2019	N-acetylcysteine (NAC) treatment almost completely eliminated the reactive oxygen species (ROS) produced by TGF-beta1 and ERK activation.	Acetylcysteine	18-21	mitogen-activated protein kinase 1	Homo sapiens	122-125
30633885-5	2019	The ROS scavenger N-acetylcysteine (NAC) and the specific p38 inhibitor SB203580 reversed the effects of A-macB on the p38 network and thus rescued ESCC cells from apoptosis.	Acetylcysteine	18-34	mitogen-activated protein kinase 14	Homo sapiens	119-122
30597356-8	2019	N-acetylcysteine, a well-known antioxidant, abrogated D-glucose-induced NFkappaB and Egr1 activation in BV2 cells.	Acetylcysteine	0-16	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	72-80
30660392-7	2019	In contrast, total glutathione, superoxide dismutase and catalase were markedly increased after treatment with BMSCs or NAC.	Acetylcysteine	120-123	catalase	Rattus norvegicus	57-65
30633982-0	2019	N-acetylcysteine alleviates fluoride-induced testicular apoptosis by modulating IRE1alpha/JNK signaling and nuclear Nrf2 activation.	Acetylcysteine	0-16	NFE2 like bZIP transcription factor 2	Rattus norvegicus	116-120
30911553-12	2019	Meanwhile, Ac-YVAD-CMK, BAY11-7082, or NAC attenuated HG- and H/R-induced H9C2 cell injury with LPS stimulated by reversing the activation of NLRP3 inflammasome-mediated pyroptosis.	Acetylcysteine	39-42	NLR family, pyrin domain containing 3	Rattus norvegicus	142-147
30707992-10	2019	Importantly, dampening oxidative stress with N-acetylcysteine (NAC) lowered hypertrophy in MTG1 KO to WT levels.	Acetylcysteine	45-61	mitochondrial ribosome-associated GTPase 1	Mus musculus	91-95
30707992-10	2019	Importantly, dampening oxidative stress with N-acetylcysteine (NAC) lowered hypertrophy in MTG1 KO to WT levels.	Acetylcysteine	63-66	mitochondrial ribosome-associated GTPase 1	Mus musculus	91-95
30508555-6	2019	alphaNF also induced accumulation of reactive oxygen species (ROS) and an antioxidant, N-acetylcysteine, reduced alphaNF-induced MAPK phosphorylation, CHOP expression, and cell death.	Acetylcysteine	87-103	mitogen-activated protein kinase 1	Mus musculus	129-133
30633982-8	2019	Antioxidant NAC, however, prevented NaF-induced testicular apoptosis accompanied by activating Nrf2-mediated antioxidant potential.	Acetylcysteine	12-15	NFE2 like bZIP transcription factor 2	Rattus norvegicus	95-99
30633982-10	2019	Collectively, the present results suggested that prolonged administration of NAC preserved testicular function and normalized sex hormonal disruption induced by NaF via the inhibition of Nrf2-associated oxidative damage and Ire1alpha-JNK-mediated apoptosis in rat testis.	Acetylcysteine	77-80	NFE2 like bZIP transcription factor 2	Rattus norvegicus	187-191
30633885-5	2019	The ROS scavenger N-acetylcysteine (NAC) and the specific p38 inhibitor SB203580 reversed the effects of A-macB on the p38 network and thus rescued ESCC cells from apoptosis.	Acetylcysteine	36-39	mitogen-activated protein kinase 14	Homo sapiens	119-122
30396020-5	2019	Moreover, the detection of intracellular pH fluctuation induced by redox species such as NAC (N-acetylcysteine) and H2O2 was also achieved by both one- and two-photon excitation of the PFV/PSMA-DA NPs probe.	Acetylcysteine	89-92	folate hydrolase 1	Homo sapiens	189-193
30520466-4	2019	First, N-acetyl-l-cysteine was used to decrease the viscosity of HSF samples and consequently enhance bacterial isolation with vancomycin-coated nano-magnetic beads.	Acetylcysteine	7-26	interleukin 6	Homo sapiens	65-68
30765703-5	2019	Treatment with the antioxidant N-acetylcysteine disrupts ROS-induced interaction of Mst1/2 with phagosomes or mitochondria, and thereby diminishes the Mst-Nrf2 signal.	Acetylcysteine	31-47	serine/threonine kinase 3	Homo sapiens	84-90
30765703-5	2019	Treatment with the antioxidant N-acetylcysteine disrupts ROS-induced interaction of Mst1/2 with phagosomes or mitochondria, and thereby diminishes the Mst-Nrf2 signal.	Acetylcysteine	31-47	NFE2 like bZIP transcription factor 2	Homo sapiens	155-159
30396020-5	2019	Moreover, the detection of intracellular pH fluctuation induced by redox species such as NAC (N-acetylcysteine) and H2O2 was also achieved by both one- and two-photon excitation of the PFV/PSMA-DA NPs probe.	Acetylcysteine	94-110	folate hydrolase 1	Homo sapiens	189-193
30549180-9	2019	TGF-beta1-induced excessive ROS production was remarkably reversed by FKA treatment in A7r5 cells, and inhibition by FKA or N-acetylcysteine (NAC) substantially diminished TGF-beta1-induced p-Smad3 activation and wound-healing migration.	Acetylcysteine	124-140	transforming growth factor, beta 1	Rattus norvegicus	172-181
30289994-10	2019	Moreover, NAC combined with sildenafil inhibited the expression of MCP-1 and p-p38 MAPK.	Acetylcysteine	10-13	corticostatin-3	Oryctolagus cuniculus	67-72
30741054-8	2019	N-acetylcysteine, a substrate of GSH synthesis, also stimulated osteoclast formation and NFATc1 nuclear localisation.	Acetylcysteine	0-16	nuclear factor of activated T cells, cytoplasmic, calcineurin dependent 1	Mus musculus	89-95
30483736-4	2019	Treatment with N-acetyl-L-cysteine reversed these effects, restoring the MTP and attenuated ROS production and p53 expression.	Acetylcysteine	15-34	tumor protein p53	Homo sapiens	111-114
30549180-9	2019	TGF-beta1-induced excessive ROS production was remarkably reversed by FKA treatment in A7r5 cells, and inhibition by FKA or N-acetylcysteine (NAC) substantially diminished TGF-beta1-induced p-Smad3 activation and wound-healing migration.	Acetylcysteine	142-145	SMAD family member 3	Rattus norvegicus	192-197
30289994-11	2019	Thus, NAC potentiates the haemodynamic-improving effect of sildenafil in a rabbit model of acute pulmonary thromboembolism via the MCP-1 and p38 MAPK signalling pathway.	Acetylcysteine	6-9	corticostatin-3	Oryctolagus cuniculus	131-136
30549180-9	2019	TGF-beta1-induced excessive ROS production was remarkably reversed by FKA treatment in A7r5 cells, and inhibition by FKA or N-acetylcysteine (NAC) substantially diminished TGF-beta1-induced p-Smad3 activation and wound-healing migration.	Acetylcysteine	124-140	SMAD family member 3	Rattus norvegicus	192-197
30549180-9	2019	TGF-beta1-induced excessive ROS production was remarkably reversed by FKA treatment in A7r5 cells, and inhibition by FKA or N-acetylcysteine (NAC) substantially diminished TGF-beta1-induced p-Smad3 activation and wound-healing migration.	Acetylcysteine	142-145	transforming growth factor, beta 1	Rattus norvegicus	0-9
30549180-9	2019	TGF-beta1-induced excessive ROS production was remarkably reversed by FKA treatment in A7r5 cells, and inhibition by FKA or N-acetylcysteine (NAC) substantially diminished TGF-beta1-induced p-Smad3 activation and wound-healing migration.	Acetylcysteine	142-145	transforming growth factor, beta 1	Rattus norvegicus	172-181
30761138-12	2019	Inhibition of ROS by N-Acetyl Cysteine inhibited TLR2-induced priming of the NLRP3 inflammasome, but had no effect on MSU-induced activation.	Acetylcysteine	21-38	toll like receptor 2	Homo sapiens	49-53
30814814-9	2019	The biochemical marker of insulin resistance like fasting insulin, fasting glucose/insulin ratio improved significantly in group N. Greater reduction of total testosterone was observed in group N. ConclusionS: Better improvement of metabolic and hormonal profile was observed in N acetylcysteine group.	Acetylcysteine	281-295	insulin	Homo sapiens	26-90
30761138-12	2019	Inhibition of ROS by N-Acetyl Cysteine inhibited TLR2-induced priming of the NLRP3 inflammasome, but had no effect on MSU-induced activation.	Acetylcysteine	21-38	NLR family pyrin domain containing 3	Homo sapiens	77-82
31527329-7	2019	Cordycepin further enhanced the intracellular levels of reactive oxygen species (ROS), while the addition of N-acetyl cysteine (NAC), a ROS inhibitor, significantly diminished cordycepin-induced mitochondrial dysfunction and growth inhibition, and also blocked the inactivation of PI3K/Akt signaling pathway.	Acetylcysteine	109-126	AKT serine/threonine kinase 1	Homo sapiens	286-289
30606241-0	2019	N-acetylcysteine decreases malignant characteristics of glioblastoma cells by inhibiting Notch2 signaling.	Acetylcysteine	0-16	notch receptor 2	Homo sapiens	89-95
30606241-11	2019	RESULTS: Our data showed that NAC could decrease the protein level of Notch2.	Acetylcysteine	30-33	notch receptor 2	Homo sapiens	70-76
30606241-12	2019	Meanwhile, NAC had a decreasing effect on the mRNA and protein levels of its downstream targets Hes1 and Hey1.	Acetylcysteine	11-14	hes related family bHLH transcription factor with YRPW motif 1	Homo sapiens	105-109
30606241-14	2019	The mechanism of NAC-mediated Notch2 reduction was elucidated by promoting Notch2 degradation through Itch-dependent lysosome pathway.	Acetylcysteine	17-20	notch receptor 2	Homo sapiens	30-36
30606241-14	2019	The mechanism of NAC-mediated Notch2 reduction was elucidated by promoting Notch2 degradation through Itch-dependent lysosome pathway.	Acetylcysteine	17-20	notch receptor 2	Homo sapiens	75-81
30606241-14	2019	The mechanism of NAC-mediated Notch2 reduction was elucidated by promoting Notch2 degradation through Itch-dependent lysosome pathway.	Acetylcysteine	17-20	itchy E3 ubiquitin protein ligase	Homo sapiens	102-106
30606241-15	2019	Furthermore, NAC could prevent proliferation, migration, and invasion and might induce apoptosis in GBM cells via targeting Notch2.	Acetylcysteine	13-16	notch receptor 2	Homo sapiens	124-130
30606241-17	2019	CONCLUSIONS: NAC could facilitate Notch2 degradation through lysosomal pathway in an antioxidant-independent manner, thus attenuating Notch2 malignant signaling in GBM cells.	Acetylcysteine	13-16	notch receptor 2	Homo sapiens	34-40
30606241-17	2019	CONCLUSIONS: NAC could facilitate Notch2 degradation through lysosomal pathway in an antioxidant-independent manner, thus attenuating Notch2 malignant signaling in GBM cells.	Acetylcysteine	13-16	notch receptor 2	Homo sapiens	134-140
30641872-7	2019	The benefits of NAC were associated with enhanced AMPK-PGC-1alpha-SIRT3 signaling protein expressions, which led to decreased acetylation of superoxide dismutase 2 (SOD2) and increased expression of mitochondrial antioxidant manganese superoxide dismutase (MnSOD).	Acetylcysteine	16-19	PPARG coactivator 1 alpha	Rattus norvegicus	55-65
31527329-7	2019	Cordycepin further enhanced the intracellular levels of reactive oxygen species (ROS), while the addition of N-acetyl cysteine (NAC), a ROS inhibitor, significantly diminished cordycepin-induced mitochondrial dysfunction and growth inhibition, and also blocked the inactivation of PI3K/Akt signaling pathway.	Acetylcysteine	128-131	AKT serine/threonine kinase 1	Homo sapiens	286-289
31120230-10	2019	Importantly, Cd-induced COX-2 expression and migration were significantly abolished by N-Acetyl-Cysteine (NAC), a ROS scavenger, or SB202190, a specific p38 inhibitor.	Acetylcysteine	87-104	prostaglandin-endoperoxide synthase 2	Homo sapiens	24-29
30375708-7	2019	We also found that reactive oxygen species (ROS) were involved in the HCA-induced inhibition of STAT3 activation and cell proliferation because the suppressed p-STAT3 level was rescued by glutathione or N-acetyl-L-cysteine treatment, which are general ROS inhibitors.	Acetylcysteine	203-222	signal transducer and activator of transcription 3	Homo sapiens	96-101
30375708-7	2019	We also found that reactive oxygen species (ROS) were involved in the HCA-induced inhibition of STAT3 activation and cell proliferation because the suppressed p-STAT3 level was rescued by glutathione or N-acetyl-L-cysteine treatment, which are general ROS inhibitors.	Acetylcysteine	203-222	signal transducer and activator of transcription 3	Homo sapiens	161-166
31050281-14	2019	The expression of autophagy related-protein and inflammatory cytokines iNOS, IL-12, and TNF-alpha were inhibited by the ROS inhibitor N-acetyl cysteine.	Acetylcysteine	134-151	tumor necrosis factor	Mus musculus	88-97
31120230-10	2019	Importantly, Cd-induced COX-2 expression and migration were significantly abolished by N-Acetyl-Cysteine (NAC), a ROS scavenger, or SB202190, a specific p38 inhibitor.	Acetylcysteine	106-109	prostaglandin-endoperoxide synthase 2	Homo sapiens	24-29
31120230-11	2019	Furthermore, Cd-induced p38 phosphorylation was inhibited by NAC.	Acetylcysteine	61-64	mitogen-activated protein kinase 14	Homo sapiens	24-27
29672839-7	2019	Inhibition of cyclooxygenase 1 by aspirin, supplementation of PGI2 by beraprost, and inhibition of PGIS S-nitrosylation by N-acetyl-cysteine improved GTN-induced nitrate cross-tolerance in rats.	Acetylcysteine	123-140	prostaglandin I2 synthase	Rattus norvegicus	99-103
29672839-5	2019	Clearance of nitric oxide by carboxy-PTIO or inhibition of S-nitrosylation by N-acetyl-cysteine decreased GTN-induced PGIS S-nitrosylation.	Acetylcysteine	78-95	prostaglandin I2 synthase	Homo sapiens	118-122
30447351-0	2019	N-acetylcysteine ameliorates cisplatin-induced renal senescence and renal interstitial fibrosis through sirtuin1 activation and p53 deacetylation.	Acetylcysteine	0-16	tumor protein p53	Homo sapiens	128-131
30255760-6	2019	RESULTS: Results showed that in the NAC group, the serum levels of MDA, NO, IL-6, TNF-alpha, ESR and CRP were significantly lower than the baseline.	Acetylcysteine	36-39	interleukin 6	Homo sapiens	76-80
30255760-6	2019	RESULTS: Results showed that in the NAC group, the serum levels of MDA, NO, IL-6, TNF-alpha, ESR and CRP were significantly lower than the baseline.	Acetylcysteine	36-39	tumor necrosis factor	Homo sapiens	82-91
30255760-6	2019	RESULTS: Results showed that in the NAC group, the serum levels of MDA, NO, IL-6, TNF-alpha, ESR and CRP were significantly lower than the baseline.	Acetylcysteine	36-39	C-reactive protein	Homo sapiens	101-104
30252537-12	2019	QPaa-NAC complexes with insulin are the most promising formulation for future work, given their ability to offer protection against intestinal enzymes.	Acetylcysteine	5-8	insulin	Homo sapiens	24-31
30447351-10	2019	N-acetylcysteine (NAC), an antioxidant, attenuated premature senescence and decreased renal fibrosis, and its effects were dependent on sirtuin1 (SIRT1) activation and p53 deacetylation.	Acetylcysteine	0-16	tumor protein p53	Homo sapiens	168-171
30447351-10	2019	N-acetylcysteine (NAC), an antioxidant, attenuated premature senescence and decreased renal fibrosis, and its effects were dependent on sirtuin1 (SIRT1) activation and p53 deacetylation.	Acetylcysteine	18-21	tumor protein p53	Homo sapiens	168-171
30415189-9	2019	Further, we found that N-acetylcysteine (NAC), an ROS scavenger, could inhibit the PPL-stimulated activation of these pathways and the release of IL-1beta.	Acetylcysteine	23-39	interleukin 1 beta	Mus musculus	146-154
30415189-9	2019	Further, we found that N-acetylcysteine (NAC), an ROS scavenger, could inhibit the PPL-stimulated activation of these pathways and the release of IL-1beta.	Acetylcysteine	41-44	interleukin 1 beta	Mus musculus	146-154
29923087-9	2019	Moreover, a published report showed treatment of a transaldolase-deficient patient with N-acetylcysteine was associated with a decrease in alpha-fetoprotein levels.	Acetylcysteine	88-104	alpha fetoprotein	Homo sapiens	139-156
30387809-8	2019	Furthermore, NAC pretreatment decreased H2O2-induced phosphorylation of apoptosis signal-regulating kinase 1, which depends on the redox state of Trx1, and increased H2O2-induced phosphorylation of protein kinase B, which is essential to cell survival.	Acetylcysteine	13-16	mitogen-activated protein kinase kinase kinase 5	Rattus norvegicus	72-108
30387809-8	2019	Furthermore, NAC pretreatment decreased H2O2-induced phosphorylation of apoptosis signal-regulating kinase 1, which depends on the redox state of Trx1, and increased H2O2-induced phosphorylation of protein kinase B, which is essential to cell survival.	Acetylcysteine	13-16	thioredoxin 1	Rattus norvegicus	146-150
30338935-5	2019	In vitro and in vivo experiments showed that Ang II increased intracellular reactive oxygen species (ROS) production and cardiomyocyte apoptosis; these were reversed by administration of the ROS scavenger N-acetylcysteine and by Mst1 deficiency, which suppressed c-Jun N-terminal kinase (JNK) phosphorylation and downstream signaling.	Acetylcysteine	205-221	angiotensinogen	Homo sapiens	45-51
30338935-5	2019	In vitro and in vivo experiments showed that Ang II increased intracellular reactive oxygen species (ROS) production and cardiomyocyte apoptosis; these were reversed by administration of the ROS scavenger N-acetylcysteine and by Mst1 deficiency, which suppressed c-Jun N-terminal kinase (JNK) phosphorylation and downstream signaling.	Acetylcysteine	205-221	mitogen-activated protein kinase 8	Homo sapiens	263-286
30338935-5	2019	In vitro and in vivo experiments showed that Ang II increased intracellular reactive oxygen species (ROS) production and cardiomyocyte apoptosis; these were reversed by administration of the ROS scavenger N-acetylcysteine and by Mst1 deficiency, which suppressed c-Jun N-terminal kinase (JNK) phosphorylation and downstream signaling.	Acetylcysteine	205-221	mitogen-activated protein kinase 8	Homo sapiens	288-291
29845722-9	2019	Further, NAC upregulated occludin and mucin glycoprotein levels in the proximal colon of HFD-treated mice.	Acetylcysteine	9-12	occludin	Mus musculus	25-33
31068539-9	2019	Pretreatment of cells with ROS scavenger N-acetyl cysteine (NAC) abrogated the stimulatory effect of TiO2-NPs on p65, p50, and COX-2 expression.	Acetylcysteine	41-58	nuclear factor kappa B subunit 1	Homo sapiens	118-121
31068539-9	2019	Pretreatment of cells with ROS scavenger N-acetyl cysteine (NAC) abrogated the stimulatory effect of TiO2-NPs on p65, p50, and COX-2 expression.	Acetylcysteine	41-58	prostaglandin-endoperoxide synthase 2	Homo sapiens	127-132
31068539-9	2019	Pretreatment of cells with ROS scavenger N-acetyl cysteine (NAC) abrogated the stimulatory effect of TiO2-NPs on p65, p50, and COX-2 expression.	Acetylcysteine	60-63	nuclear factor kappa B subunit 1	Homo sapiens	118-121
31068539-9	2019	Pretreatment of cells with ROS scavenger N-acetyl cysteine (NAC) abrogated the stimulatory effect of TiO2-NPs on p65, p50, and COX-2 expression.	Acetylcysteine	60-63	prostaglandin-endoperoxide synthase 2	Homo sapiens	127-132
29923087-10	2019	After discontinuation of acetaminophen and prior to initiation of N-acetylcysteine treatment, our patient demonstrated resolving alpha-fetoprotein levels suggesting acetaminophen incited the liver failure.	Acetylcysteine	66-82	alpha fetoprotein	Homo sapiens	129-146
30971653-8	2019	Strikingly, NAC canceled these taxodione-caused inhibition of BCR-ABL, STAT5 and Akt.	Acetylcysteine	12-15	AKT serine/threonine kinase 1	Homo sapiens	81-84
30959503-10	2019	Also, secretion of the studied solutes, with the exception of ICAM-1, was reduced in the presence of NAC: IL6 -34%, p &lt; 0.01; VEGF -40%, p &lt; 0.005; vWF -25%, p &lt; 0.001; t-PA -47%, p &lt; 0.01, and MMP9 -37%, p &lt; 0.001.	Acetylcysteine	101-104	interleukin 6	Homo sapiens	106-109
30959503-10	2019	Also, secretion of the studied solutes, with the exception of ICAM-1, was reduced in the presence of NAC: IL6 -34%, p &lt; 0.01; VEGF -40%, p &lt; 0.005; vWF -25%, p &lt; 0.001; t-PA -47%, p &lt; 0.01, and MMP9 -37%, p &lt; 0.001.	Acetylcysteine	101-104	vascular endothelial growth factor A	Homo sapiens	129-133
30959503-10	2019	Also, secretion of the studied solutes, with the exception of ICAM-1, was reduced in the presence of NAC: IL6 -34%, p &lt; 0.01; VEGF -40%, p &lt; 0.005; vWF -25%, p &lt; 0.001; t-PA -47%, p &lt; 0.01, and MMP9 -37%, p &lt; 0.001.	Acetylcysteine	101-104	von Willebrand factor	Homo sapiens	154-157
30394176-6	2019	N-acetylcysteine also restored the effects of Zn-CuONPs on protein expressions related to apoptosis, autophagy and NF-kappaB pathways.	Acetylcysteine	0-16	nuclear factor kappa B subunit 1	Homo sapiens	115-124
30597845-8	2018	Moreover, the apoptotic effect of MHY440 was reactive oxygen species (ROS)-dependent, as evidenced by the inhibition of MHY440-induced PARP cleavage and ROS generation via N-acetylcysteine-induced ROS scavenging.	Acetylcysteine	172-188	poly(ADP-ribose) polymerase 1	Homo sapiens	135-139
30362123-6	2019	Moreover, the participation of oxidative stress is supported by the antioxidant action of N-acetylcysteine (NAC), which significantly protects XP-V cells from UVA light, even in the presence of the ATR inhibitor.	Acetylcysteine	90-106	ATR serine/threonine kinase	Homo sapiens	198-201
30362123-6	2019	Moreover, the participation of oxidative stress is supported by the antioxidant action of N-acetylcysteine (NAC), which significantly protects XP-V cells from UVA light, even in the presence of the ATR inhibitor.	Acetylcysteine	108-111	ATR serine/threonine kinase	Homo sapiens	198-201
29206074-6	2019	The ROS scavenger N-acetylcysteine (NAC) abolished superoxide anion generation in response to all tested stimuli, but the pan-NADPH oxidase (NOX) inhibitor VAS2870 only inhibited superoxide anion formation in response to thrombin and CRP.	Acetylcysteine	36-39	coagulation factor II, thrombin	Homo sapiens	221-229
30574085-7	2018	Rats fed with NAC for 3-weeks prior to AbetaOs injections displayed comparable redox potential, RyR2 and Arc protein contents, similar ERK1/2 phosphorylation and RyR2 single channel activation by Ca2+ as saline-injected (control) rats.	Acetylcysteine	14-17	carbonic anhydrase 2	Rattus norvegicus	196-199
30547092-5	2018	Furthermore, administration of acetylsalicylic acid (aspirin) or N-acetylcysteine (NAC) to juvenile ptk7 mutants significantly reduces the incidence and/or severity of scoliosis phenotypes.	Acetylcysteine	65-81	protein tyrosine kinase 7b	Danio rerio	100-104
30547092-5	2018	Furthermore, administration of acetylsalicylic acid (aspirin) or N-acetylcysteine (NAC) to juvenile ptk7 mutants significantly reduces the incidence and/or severity of scoliosis phenotypes.	Acetylcysteine	83-86	protein tyrosine kinase 7b	Danio rerio	100-104
30571738-8	2018	Finally, anti-Sm mAb still up-regulated the IL-6 production of monocytes in the presence of anti-RNP mAb under the influence of N-acetyl cysteine or pyrrolidine dithiocarbamate that totally abrogated the IL-6 production provoked by anti-Sm mAb alone in the absence of anti-RNP mAb.	Acetylcysteine	128-145	interleukin 6	Homo sapiens	44-48
30571738-8	2018	Finally, anti-Sm mAb still up-regulated the IL-6 production of monocytes in the presence of anti-RNP mAb under the influence of N-acetyl cysteine or pyrrolidine dithiocarbamate that totally abrogated the IL-6 production provoked by anti-Sm mAb alone in the absence of anti-RNP mAb.	Acetylcysteine	128-145	interleukin 6	Homo sapiens	204-208
30168649-5	2018	TXNIP-/- MEF cells showed greater induced glucose uptake and ROS levels than wild-type cells, and N-acetylcysteine (NAC) treatment rescued the cellular senescence of TXNIP-/- MEF cells.	Acetylcysteine	98-114	thioredoxin interacting protein	Mus musculus	166-171
30168649-5	2018	TXNIP-/- MEF cells showed greater induced glucose uptake and ROS levels than wild-type cells, and N-acetylcysteine (NAC) treatment rescued the cellular senescence of TXNIP-/- MEF cells.	Acetylcysteine	116-119	thioredoxin interacting protein	Mus musculus	166-171
30107137-9	2018	NAC supplementation also downregulated the expression of inflammatory markers (TNF-alpha, IL-1beta, IL-6) and upregulated the expression of marker genes associated with aging (sirtuin-1) and neurodegeneration (neuron-specific enolase, neuroglobin, synapsin-I, myelin basic protein 2) in old rats.	Acetylcysteine	0-3	tumor necrosis factor	Rattus norvegicus	79-88
29364751-6	2018	Furthermore, HG could promote the generation of reactive oxygen species (ROS), while N-acetyl cysteine, a ROS scavenger, had an inhibitory effect on the expression of TNF-alpha, IL-6 and PAI-1 in HG-treated cells.	Acetylcysteine	85-102	tumor necrosis factor	Homo sapiens	167-176
29364751-6	2018	Furthermore, HG could promote the generation of reactive oxygen species (ROS), while N-acetyl cysteine, a ROS scavenger, had an inhibitory effect on the expression of TNF-alpha, IL-6 and PAI-1 in HG-treated cells.	Acetylcysteine	85-102	interleukin 6	Homo sapiens	178-182
30107137-9	2018	NAC supplementation also downregulated the expression of inflammatory markers (TNF-alpha, IL-1beta, IL-6) and upregulated the expression of marker genes associated with aging (sirtuin-1) and neurodegeneration (neuron-specific enolase, neuroglobin, synapsin-I, myelin basic protein 2) in old rats.	Acetylcysteine	0-3	interleukin 1 alpha	Rattus norvegicus	90-98
30107137-9	2018	NAC supplementation also downregulated the expression of inflammatory markers (TNF-alpha, IL-1beta, IL-6) and upregulated the expression of marker genes associated with aging (sirtuin-1) and neurodegeneration (neuron-specific enolase, neuroglobin, synapsin-I, myelin basic protein 2) in old rats.	Acetylcysteine	0-3	interleukin 6	Rattus norvegicus	100-104
30107137-9	2018	NAC supplementation also downregulated the expression of inflammatory markers (TNF-alpha, IL-1beta, IL-6) and upregulated the expression of marker genes associated with aging (sirtuin-1) and neurodegeneration (neuron-specific enolase, neuroglobin, synapsin-I, myelin basic protein 2) in old rats.	Acetylcysteine	0-3	sirtuin 1	Rattus norvegicus	176-185
30107137-9	2018	NAC supplementation also downregulated the expression of inflammatory markers (TNF-alpha, IL-1beta, IL-6) and upregulated the expression of marker genes associated with aging (sirtuin-1) and neurodegeneration (neuron-specific enolase, neuroglobin, synapsin-I, myelin basic protein 2) in old rats.	Acetylcysteine	0-3	neuroglobin	Rattus norvegicus	235-246
30584464-5	2018	When treating PC cells with N-acetyl-L-cysteine (NAC), the intracellular ROS generation is repressed, but the expression of phosphorylation of JNK and c-Jun increased.	Acetylcysteine	28-47	mitogen-activated protein kinase 8	Homo sapiens	143-146
30603674-11	2018	Compared to cells treated without NAC under hypoxia, the Bcl-2/Bax ratio increased significantly in cells treated with NAC.	Acetylcysteine	34-37	BCL2 apoptosis regulator	Homo sapiens	57-62
30603674-11	2018	Compared to cells treated without NAC under hypoxia, the Bcl-2/Bax ratio increased significantly in cells treated with NAC.	Acetylcysteine	34-37	BCL2 associated X, apoptosis regulator	Homo sapiens	63-66
30603674-11	2018	Compared to cells treated without NAC under hypoxia, the Bcl-2/Bax ratio increased significantly in cells treated with NAC.	Acetylcysteine	119-122	BCL2 apoptosis regulator	Homo sapiens	57-62
30603674-11	2018	Compared to cells treated without NAC under hypoxia, the Bcl-2/Bax ratio increased significantly in cells treated with NAC.	Acetylcysteine	119-122	BCL2 associated X, apoptosis regulator	Homo sapiens	63-66
30037745-12	2018	N-acetylcysteine (NAC), a ROS scavenger, partly restrained the combined treatment induced cell proliferation inhibition, Caspase3 and NF-kappaB compared to doxorubicin treatment (all P&lt;0.05).	Acetylcysteine	0-16	caspase 3	Homo sapiens	121-129
30037745-12	2018	N-acetylcysteine (NAC), a ROS scavenger, partly restrained the combined treatment induced cell proliferation inhibition, Caspase3 and NF-kappaB compared to doxorubicin treatment (all P&lt;0.05).	Acetylcysteine	0-16	nuclear factor kappa B subunit 1	Homo sapiens	134-143
30037745-12	2018	N-acetylcysteine (NAC), a ROS scavenger, partly restrained the combined treatment induced cell proliferation inhibition, Caspase3 and NF-kappaB compared to doxorubicin treatment (all P&lt;0.05).	Acetylcysteine	18-21	caspase 3	Homo sapiens	121-129
30037745-12	2018	N-acetylcysteine (NAC), a ROS scavenger, partly restrained the combined treatment induced cell proliferation inhibition, Caspase3 and NF-kappaB compared to doxorubicin treatment (all P&lt;0.05).	Acetylcysteine	18-21	nuclear factor kappa B subunit 1	Homo sapiens	134-143
30196390-8	2018	The ROS scavenger N-acetylcysteine (NAC) and the ROS formation inhibitor diphenyleneiodonium (DPI) also inhibited TNFalpha expression in stimulated macrophages, but unlike 3-AB, NAC and DPI were unable to abolish NFkappaB activity.	Acetylcysteine	18-34	tumor necrosis factor	Mus musculus	114-122
30196390-8	2018	The ROS scavenger N-acetylcysteine (NAC) and the ROS formation inhibitor diphenyleneiodonium (DPI) also inhibited TNFalpha expression in stimulated macrophages, but unlike 3-AB, NAC and DPI were unable to abolish NFkappaB activity.	Acetylcysteine	36-39	tumor necrosis factor	Mus musculus	114-122
30584464-5	2018	When treating PC cells with N-acetyl-L-cysteine (NAC), the intracellular ROS generation is repressed, but the expression of phosphorylation of JNK and c-Jun increased.	Acetylcysteine	49-52	mitogen-activated protein kinase 8	Homo sapiens	143-146
30194941-14	2018	NAC prevented the increases in LC3 II protein, LC3 scores, Beclin1, Atg12 and ERK activity in AAC rats.	Acetylcysteine	0-3	Eph receptor B1	Rattus norvegicus	78-81
30662622-7	2018	Furthermore, H2O2-induced proliferation inhibition, apoptosis, and inflammation in HK-2 cells were ameliorated by NAC (N-acetyl cysteine, the ROS scavenger) and SP600125 (the JNK inhibitor).	Acetylcysteine	114-117	mitogen-activated protein kinase 8	Homo sapiens	175-178
30662622-7	2018	Furthermore, H2O2-induced proliferation inhibition, apoptosis, and inflammation in HK-2 cells were ameliorated by NAC (N-acetyl cysteine, the ROS scavenger) and SP600125 (the JNK inhibitor).	Acetylcysteine	119-136	mitogen-activated protein kinase 8	Homo sapiens	175-178
30407312-7	2018	The primary endpoint indicators were the changes in oxidative stress parameters (MDA, TAOC, SOD) and TNF-alpha after treatment in the NAC group compared with those in the non-NAC group.	Acetylcysteine	134-137	tumor necrosis factor	Homo sapiens	101-110
30533170-9	2018	Coincubation with N-acetylcysteine or L-ascorbate improves impaired osteogenesis caused by cigarette smoke exposure by both activation of nuclear factor erythroid 2-related factor 2 (Nrf2) signaling and scavenging of ROS, which thus might represent therapeutic targets to support fracture healing in smokers.	Acetylcysteine	18-34	NFE2 like bZIP transcription factor 2	Homo sapiens	138-181
30533170-9	2018	Coincubation with N-acetylcysteine or L-ascorbate improves impaired osteogenesis caused by cigarette smoke exposure by both activation of nuclear factor erythroid 2-related factor 2 (Nrf2) signaling and scavenging of ROS, which thus might represent therapeutic targets to support fracture healing in smokers.	Acetylcysteine	18-34	NFE2 like bZIP transcription factor 2	Homo sapiens	183-187
30257333-10	2018	IL-17A-induced oxidative stress/IL-6 expression and neutrophilic inflammation was attenuated by NAC treatment, whereas there was no effect on chemokines.	Acetylcysteine	96-99	interleukin 6	Mus musculus	32-36
30257333-11	2018	This suggests that antioxidant NAC attenuates IL-17A-induced pulmonary inflammation by restoring oxidant-antioxidant balance and attenuation of IL-6 in the lung.	Acetylcysteine	31-34	interleukin 6	Mus musculus	144-148
29423685-4	2018	Catalase, superoxide dismutase, and acetylcholinesterase activities were increased by Cys and NAC.	Acetylcysteine	94-97	catalase	Rattus norvegicus	0-8
30407312-9	2018	Plasma levels of MDA and TNF-alpha decreased more (P &lt; .05 MDA:p 0.004, TNF-alpha:p &lt;0.001) in the NAC group than the non-NAC group, and there was a reliable increase in TAOC content (p 0.005).	Acetylcysteine	105-108	tumor necrosis factor	Homo sapiens	25-34
30407312-9	2018	Plasma levels of MDA and TNF-alpha decreased more (P &lt; .05 MDA:p 0.004, TNF-alpha:p &lt;0.001) in the NAC group than the non-NAC group, and there was a reliable increase in TAOC content (p 0.005).	Acetylcysteine	105-108	tumor necrosis factor	Homo sapiens	75-84
29964331-7	2018	Moreover, inhibition of reactive oxygen species by N-acetyl-L-cysteine efficiently blocked BIX-01294-induced DR5 upregulation by inhibiting ATF4/CHOP expression, leading to diminished sensitization to TRAIL.	Acetylcysteine	51-70	DNA damage inducible transcript 3	Homo sapiens	145-149
30407312-11	2018	No NAC-related adverse effects were observed.Addition of NAC therapy for CAP patients reduced MDA and TNF-alpha and increased TAOC.	Acetylcysteine	57-60	tumor necrosis factor	Homo sapiens	102-111
29964331-7	2018	Moreover, inhibition of reactive oxygen species by N-acetyl-L-cysteine efficiently blocked BIX-01294-induced DR5 upregulation by inhibiting ATF4/CHOP expression, leading to diminished sensitization to TRAIL.	Acetylcysteine	51-70	TNF superfamily member 10	Homo sapiens	201-206
30037311-9	2018	NAC administration decreased the mRNA levels of both iNOS and NOX4 with a concomitant increase in Gpx1 expression.	Acetylcysteine	0-3	nitric oxide synthase 2	Homo sapiens	53-57
30296076-5	2018	HPO-DAEE-elicited CHOP expression and cell death were markedly suppressed by pretreatment with N-acetylcysteine (NAC), an antioxidant, by 2.40 +- 1.57-fold and 5.7 +- 1.6%, respectively.	Acetylcysteine	95-111	DNA damage inducible transcript 3	Homo sapiens	18-22
30359319-9	2018	Pre-treatment with SP600125 or N-acetylcysteine reversed the effects of high glucose on the JNK signaling pathway and autophagy-related proteins.	Acetylcysteine	31-47	mitogen-activated protein kinase 8	Homo sapiens	92-95
30243728-6	2018	We found that pre-incubation of cultures with inhibitory ryanodine to suppress RyR-mediated Ca2+ release, with the reducing agent N-acetylcysteine or with inhibitors of ERK or PI3K activity, prevented the nuclear translocation of Nrf2 induced by incubation for 6 h with BFNF.	Acetylcysteine	130-146	ryanodine receptor 2	Homo sapiens	79-82
30243728-6	2018	We found that pre-incubation of cultures with inhibitory ryanodine to suppress RyR-mediated Ca2+ release, with the reducing agent N-acetylcysteine or with inhibitors of ERK or PI3K activity, prevented the nuclear translocation of Nrf2 induced by incubation for 6 h with BFNF.	Acetylcysteine	130-146	NFE2 like bZIP transcription factor 2	Homo sapiens	230-234
29357673-5	2018	RyR2 downregulation or inhibitors of N-methyl-d-aspartate (NMDA) receptors, or NOS or of NADPH oxidase type-2 (NOX2) prevented RyR2 upregulation and the spine remodeling induced by BDNF, as did incubation with the antioxidant agent N-acetyl l-cysteine.	Acetylcysteine	232-251	ryanodine receptor 2	Homo sapiens	0-4
30296076-5	2018	HPO-DAEE-elicited CHOP expression and cell death were markedly suppressed by pretreatment with N-acetylcysteine (NAC), an antioxidant, by 2.40 +- 1.57-fold and 5.7 +- 1.6%, respectively.	Acetylcysteine	113-116	DNA damage inducible transcript 3	Homo sapiens	18-22
30114659-7	2018	The antioxidant N-acetyl-L-cysteine (NAC) can significantly reduce TiO2-NPs-induced ERS characterized by the down-regulation of GRP78 and cleaved caspase-12 levels, which indicates that oxidative stress is participated in TiO2-NPs-induced ERS.	Acetylcysteine	16-35	heat shock protein 5	Mus musculus	128-133
30279524-7	2018	Furthermore, human HL cells exposed to taSMG underwent autophagy via AMPK/Akt/mTOR and MAPK pathway modulation; such autophagy was inhibited by the ROS scavenger N-acetylcysteine (NAC).	Acetylcysteine	162-178	AKT serine/threonine kinase 1	Homo sapiens	74-77
30279524-7	2018	Furthermore, human HL cells exposed to taSMG underwent autophagy via AMPK/Akt/mTOR and MAPK pathway modulation; such autophagy was inhibited by the ROS scavenger N-acetylcysteine (NAC).	Acetylcysteine	162-178	mechanistic target of rapamycin kinase	Homo sapiens	78-82
30020826-9	2018	Antioxidant N-acetylcysteine and mammalian target of rapamycin (mTOR) inhibitor blocked ID-induced HIF-1alpha protein increase and VEGF transcription.	Acetylcysteine	12-28	vascular endothelial growth factor A	Homo sapiens	131-135
30119245-9	2018	Thymoquinone, silymarin, and N-acetylcysteine improved the levels of alanine aminotransferase, tumor necrosis factor-alpha, platelet-derived growth factor-BB, and interleukin-6, which were increased by CCl4.	Acetylcysteine	29-45	interleukin 6	Rattus norvegicus	163-176
30119245-9	2018	Thymoquinone, silymarin, and N-acetylcysteine improved the levels of alanine aminotransferase, tumor necrosis factor-alpha, platelet-derived growth factor-BB, and interleukin-6, which were increased by CCl4.	Acetylcysteine	29-45	C-C motif chemokine ligand 4	Rattus norvegicus	202-206
30088830-7	2018	Rosiglitazone-induced HO-1 expression was significantly attenuated by NADPH oxidase (NOX) inhibitors (apocynin and diphenyleneiodonium) or ROS scavenger (N-acetyl cysteine).	Acetylcysteine	154-171	heme oxygenase 1	Mus musculus	22-26
30416532-5	2018	Additionally, exposure of bone marrow stromal cells (HS-5) to NAC increased adiponectin, PPARgamma, HO-1, and SIRT-1 and increased beta-oxidation markers such as PPARalpha and PPARdelta mRNA levels.	Acetylcysteine	62-65	adiponectin, C1Q and collagen domain containing	Homo sapiens	76-87
30416532-5	2018	Additionally, exposure of bone marrow stromal cells (HS-5) to NAC increased adiponectin, PPARgamma, HO-1, and SIRT-1 and increased beta-oxidation markers such as PPARalpha and PPARdelta mRNA levels.	Acetylcysteine	62-65	peroxisome proliferator activated receptor gamma	Homo sapiens	89-98
30055241-9	2018	In addition, NAC also inhibited JNK and ERK activation by Sb exposure.	Acetylcysteine	13-16	mitogen-activated protein kinase 8	Homo sapiens	32-35
30055241-9	2018	In addition, NAC also inhibited JNK and ERK activation by Sb exposure.	Acetylcysteine	13-16	mitogen-activated protein kinase 1	Homo sapiens	40-43
30318520-6	2018	The restoration of the mitochondrial uncoupling protein 2 (UCP2) expression, as well as the addition of the radical scavenger N-acetyl-L-cysteine, reversed the oncogenic effects of mutant p53 as cellular hyper-proliferation, antiapoptotic effect, and resistance to drugs.	Acetylcysteine	126-145	tumor protein p53	Homo sapiens	188-191
30114659-7	2018	The antioxidant N-acetyl-L-cysteine (NAC) can significantly reduce TiO2-NPs-induced ERS characterized by the down-regulation of GRP78 and cleaved caspase-12 levels, which indicates that oxidative stress is participated in TiO2-NPs-induced ERS.	Acetylcysteine	37-40	heat shock protein 5	Mus musculus	128-133
30307163-9	2018	Besides, TGFB1 induced the activation of NLRP3 inflammasome and the generation of ROS, which were blocked by NLRP3 interference or NAC.	Acetylcysteine	131-134	transforming growth factor beta 1	Homo sapiens	9-14
30307163-9	2018	Besides, TGFB1 induced the activation of NLRP3 inflammasome and the generation of ROS, which were blocked by NLRP3 interference or NAC.	Acetylcysteine	131-134	NLR family pyrin domain containing 3	Homo sapiens	41-46
30307163-10	2018	Tubular cells exposed to TGFB1 also underwent EMT, and this could be inhibited by NLRP3 shRNA or NAC.	Acetylcysteine	97-100	transforming growth factor beta 1	Homo sapiens	25-30
29876988-6	2018	Of note, Tan I generated reactive oxygen species (ROS) and conversely an ROS scavenger, N-acetyl-L -cysteine, reversed ROS production, PARP cleavage, caspase-3 activation, and p38 MAPK phosphorylation induced by Tan I in HCT116 cells.	Acetylcysteine	88-108	poly(ADP-ribose) polymerase 1	Homo sapiens	135-139
29876988-6	2018	Of note, Tan I generated reactive oxygen species (ROS) and conversely an ROS scavenger, N-acetyl-L -cysteine, reversed ROS production, PARP cleavage, caspase-3 activation, and p38 MAPK phosphorylation induced by Tan I in HCT116 cells.	Acetylcysteine	88-108	caspase 3	Homo sapiens	150-159
29876988-6	2018	Of note, Tan I generated reactive oxygen species (ROS) and conversely an ROS scavenger, N-acetyl-L -cysteine, reversed ROS production, PARP cleavage, caspase-3 activation, and p38 MAPK phosphorylation induced by Tan I in HCT116 cells.	Acetylcysteine	88-108	mitogen-activated protein kinase 14	Homo sapiens	176-179
30217943-9	2018	The levels of TNF-alpha, IL-8, CC16, and ICAM-1 in EBC were significantly lower, and SOD activity was higher, at T2 in the NAC group; similar data were found in serum at T2, T3, and T4.	Acetylcysteine	123-126	superoxide dismutase 1	Homo sapiens	85-88
29894800-10	2018	In addition, SiO2-NPs generated reactive oxygen species (ROS) and treatment of N-acetyl cysteine (NAC) attenuated the phosphorylation of JAK2, Src, Akt and STAT3, as well as the expression of COX-2 in SiO2-NPs-treated HaCaT cells.	Acetylcysteine	79-96	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	143-146
29894800-10	2018	In addition, SiO2-NPs generated reactive oxygen species (ROS) and treatment of N-acetyl cysteine (NAC) attenuated the phosphorylation of JAK2, Src, Akt and STAT3, as well as the expression of COX-2 in SiO2-NPs-treated HaCaT cells.	Acetylcysteine	79-96	AKT serine/threonine kinase 1	Homo sapiens	148-151
29894800-10	2018	In addition, SiO2-NPs generated reactive oxygen species (ROS) and treatment of N-acetyl cysteine (NAC) attenuated the phosphorylation of JAK2, Src, Akt and STAT3, as well as the expression of COX-2 in SiO2-NPs-treated HaCaT cells.	Acetylcysteine	79-96	signal transducer and activator of transcription 3	Homo sapiens	156-161
29894800-10	2018	In addition, SiO2-NPs generated reactive oxygen species (ROS) and treatment of N-acetyl cysteine (NAC) attenuated the phosphorylation of JAK2, Src, Akt and STAT3, as well as the expression of COX-2 in SiO2-NPs-treated HaCaT cells.	Acetylcysteine	79-96	prostaglandin-endoperoxide synthase 2	Homo sapiens	192-197
29894800-10	2018	In addition, SiO2-NPs generated reactive oxygen species (ROS) and treatment of N-acetyl cysteine (NAC) attenuated the phosphorylation of JAK2, Src, Akt and STAT3, as well as the expression of COX-2 in SiO2-NPs-treated HaCaT cells.	Acetylcysteine	98-101	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	143-146
29894800-10	2018	In addition, SiO2-NPs generated reactive oxygen species (ROS) and treatment of N-acetyl cysteine (NAC) attenuated the phosphorylation of JAK2, Src, Akt and STAT3, as well as the expression of COX-2 in SiO2-NPs-treated HaCaT cells.	Acetylcysteine	98-101	AKT serine/threonine kinase 1	Homo sapiens	148-151
29894800-10	2018	In addition, SiO2-NPs generated reactive oxygen species (ROS) and treatment of N-acetyl cysteine (NAC) attenuated the phosphorylation of JAK2, Src, Akt and STAT3, as well as the expression of COX-2 in SiO2-NPs-treated HaCaT cells.	Acetylcysteine	98-101	signal transducer and activator of transcription 3	Homo sapiens	156-161
29894800-10	2018	In addition, SiO2-NPs generated reactive oxygen species (ROS) and treatment of N-acetyl cysteine (NAC) attenuated the phosphorylation of JAK2, Src, Akt and STAT3, as well as the expression of COX-2 in SiO2-NPs-treated HaCaT cells.	Acetylcysteine	98-101	prostaglandin-endoperoxide synthase 2	Homo sapiens	192-197
30217943-9	2018	The levels of TNF-alpha, IL-8, CC16, and ICAM-1 in EBC were significantly lower, and SOD activity was higher, at T2 in the NAC group; similar data were found in serum at T2, T3, and T4.	Acetylcysteine	123-126	tumor necrosis factor	Homo sapiens	14-23
30217943-9	2018	The levels of TNF-alpha, IL-8, CC16, and ICAM-1 in EBC were significantly lower, and SOD activity was higher, at T2 in the NAC group; similar data were found in serum at T2, T3, and T4.	Acetylcysteine	123-126	C-X-C motif chemokine ligand 8	Homo sapiens	25-29
29655793-9	2018	Pre-treatment of MLE-12 cells with ROS scavenger of N-acetylcysteine (NAC) remarkably decreased lipopolysaccharide (LPS)- and rMuNLRP9-induced production of ROS, and the secretion of inflammatory cytokines or chemokine, as well as the activity of IkappaBalpha/NF-kappaB, ASC/Casapse-1 and Caspase-3/PARP signaling pathways.	Acetylcysteine	52-68	nuclear factor of kappa light polypeptide gene enhancer in B cells inhibitor, alpha	Mus musculus	247-259
30279737-8	2018	However, NAC restored the dysregulation of RGS4-mediated functional deficits of glutamate.	Acetylcysteine	9-12	regulator of G-protein signaling 4	Mus musculus	43-47
30279737-11	2018	RGS4 knockdown mice that received NAC treatment had improved glutamatergic dysfunction and schizophrenia behaviors.	Acetylcysteine	34-37	regulator of G-protein signaling 4	Mus musculus	0-4
29655793-9	2018	Pre-treatment of MLE-12 cells with ROS scavenger of N-acetylcysteine (NAC) remarkably decreased lipopolysaccharide (LPS)- and rMuNLRP9-induced production of ROS, and the secretion of inflammatory cytokines or chemokine, as well as the activity of IkappaBalpha/NF-kappaB, ASC/Casapse-1 and Caspase-3/PARP signaling pathways.	Acetylcysteine	70-73	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	260-269
29655793-9	2018	Pre-treatment of MLE-12 cells with ROS scavenger of N-acetylcysteine (NAC) remarkably decreased lipopolysaccharide (LPS)- and rMuNLRP9-induced production of ROS, and the secretion of inflammatory cytokines or chemokine, as well as the activity of IkappaBalpha/NF-kappaB, ASC/Casapse-1 and Caspase-3/PARP signaling pathways.	Acetylcysteine	52-68	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	260-269
29655793-9	2018	Pre-treatment of MLE-12 cells with ROS scavenger of N-acetylcysteine (NAC) remarkably decreased lipopolysaccharide (LPS)- and rMuNLRP9-induced production of ROS, and the secretion of inflammatory cytokines or chemokine, as well as the activity of IkappaBalpha/NF-kappaB, ASC/Casapse-1 and Caspase-3/PARP signaling pathways.	Acetylcysteine	70-73	nuclear factor of kappa light polypeptide gene enhancer in B cells inhibitor, alpha	Mus musculus	247-259
30271093-11	2018	In addition, the ROS scavenger N-acetyl-L-cysteine markedly inhibited increased phosphorylation levels of P38 and HSP27 under H/R.	Acetylcysteine	31-50	mitogen-activated protein kinase 14	Homo sapiens	106-109
30203714-6	2018	N-acetylcysteine attenuated ROS production and nuclear translocation of Nrf2.	Acetylcysteine	0-16	NFE2 like bZIP transcription factor 2	Homo sapiens	72-76
30069915-8	2018	D-NAC treatment dose-dependently reduced TNFalpha and glutamate secretion and replenished total intracellular glutathione levels in cALD patient macrophages, more efficiently than NAC.	Acetylcysteine	2-5	tumor necrosis factor	Homo sapiens	41-49
29960031-6	2018	ROS scavenger N-acetyl cysteine abrogated the effects of XTT on ERK/p38 MAPK activation and JAK2/STAT3 inhibition, and rescued HCC cells from XTT-induced apoptosis.	Acetylcysteine	14-31	signal transducer and activator of transcription 3	Homo sapiens	97-102
29929056-0	2018	N-acetyl cysteine inhibits lipopolysaccharide-mediated induction of interleukin-6 synthesis in MC3T3-E1 cells through the NF-kB signaling pathway.	Acetylcysteine	0-17	interleukin 6	Mus musculus	68-81
29929056-5	2018	However, whether NAC can affect the LPS-mediated reduction of IL-6 synthesis in MC3T3-E1 cells is still unknown.	Acetylcysteine	17-20	interleukin 6	Mus musculus	62-66
29929056-6	2018	AIMS: The aim of this study was to investigate the role of NAC in the LPS -mediated reduction of IL-6 synthesis by MC3T3-E1 cells and to explore the underlying molecular mechanisms.	Acetylcysteine	59-62	interleukin 6	Mus musculus	97-101
29929056-7	2018	In addition, we aimed to determine the involvement of the NF-kB pathway in any changes in IL-6 expression observed in response to LPS and NAC.	Acetylcysteine	138-141	interleukin 6	Mus musculus	90-94
29929056-16	2018	CONCLUSION: NAC inhibits the LPS-mediated induction of IL-6 synthesis in MC3T3-E1 cells through the NF-kB pathway.	Acetylcysteine	12-15	interleukin 6	Mus musculus	55-59
29960031-6	2018	ROS scavenger N-acetyl cysteine abrogated the effects of XTT on ERK/p38 MAPK activation and JAK2/STAT3 inhibition, and rescued HCC cells from XTT-induced apoptosis.	Acetylcysteine	14-31	mitogen-activated protein kinase 1	Homo sapiens	64-67
29960031-6	2018	ROS scavenger N-acetyl cysteine abrogated the effects of XTT on ERK/p38 MAPK activation and JAK2/STAT3 inhibition, and rescued HCC cells from XTT-induced apoptosis.	Acetylcysteine	14-31	mitogen-activated protein kinase 14	Homo sapiens	68-71
29960031-6	2018	ROS scavenger N-acetyl cysteine abrogated the effects of XTT on ERK/p38 MAPK activation and JAK2/STAT3 inhibition, and rescued HCC cells from XTT-induced apoptosis.	Acetylcysteine	14-31	mitogen-activated protein kinase 1	Homo sapiens	72-76
29704590-0	2018	Protective influences of N-acetylcysteine against alcohol abstinence-induced depression by regulating biochemical and GRIN2A, GRIN2B gene expression of NMDA receptor signaling pathway in rats.	Acetylcysteine	25-41	glutamate ionotropic receptor NMDA type subunit 2A	Rattus norvegicus	118-124
29722447-8	2018	Furthermore, gamma-H2AX induced by TCE was also attenuated by CYP2E1 inhibitors and the antioxidant N-acetylcysteine.	Acetylcysteine	100-116	H2A.X variant histone	Mus musculus	13-23
30570876-11	2018	Hydrogen peroxide stimulated mTOR pathway, iNOS and nitrotyrosine quantities, the last one prevented by the antioxidant n-acetyl-cysteine (NAC) in the granulocytes of MPN.	Acetylcysteine	139-142	mechanistic target of rapamycin kinase	Homo sapiens	29-33
29704590-15	2018	The increased expression levels of GRIN2A and GRIN2B following ethanol abstinence were reversed with a higher dose of NAC (100 mg/kg) treatment.	Acetylcysteine	118-121	glutamate ionotropic receptor NMDA type subunit 2A	Rattus norvegicus	35-41
29704590-16	2018	In conclusion, the results of the study reveal that NAC has remarkable protective effects in the alcohol abstinence-induced depression by modulating alcohol markers, serotonin levels and GRIN2A, GRIN2B gene expression of NMDAR signaling pathway in rats.	Acetylcysteine	52-55	glutamate ionotropic receptor NMDA type subunit 2A	Rattus norvegicus	187-193
29890337-7	2018	Pretreatment with the thiol reducing agents, N-acetylcysteine (NAC) or dithiothreitol (DTT), attenuated Nrf2 activation and HO-1 expression.	Acetylcysteine	45-61	NFE2 like bZIP transcription factor 2	Rattus norvegicus	104-108
29986212-8	2018	Moreover, N-acetyl-cysteine abrogated mir-34(gk437)-induced longevity.	Acetylcysteine	10-27	mir-34	Caenorhabditis elegans	38-44
29783176-9	2018	NAC, folic acid and omega-3 increased superoxide dismutase and catalase activities in the rat brain subjected to early or late life stress.	Acetylcysteine	0-3	catalase	Rattus norvegicus	63-71
29890337-7	2018	Pretreatment with the thiol reducing agents, N-acetylcysteine (NAC) or dithiothreitol (DTT), attenuated Nrf2 activation and HO-1 expression.	Acetylcysteine	63-66	NFE2 like bZIP transcription factor 2	Rattus norvegicus	104-108
29935984-7	2018	These results indicate that NAC could prevent toluene-induced reward facilitation and behavioral disturbances and its beneficial effects, at least for cognitive function and social interaction, are associated with activation of the xCT and mGluR2/3.	Acetylcysteine	28-31	glutamate receptor, metabotropic 2	Mus musculus	240-248
30116167-1	2018	This study is designed to evaluate the potential impact of N-acetyl cysteine (NAC) and coenzyme Q10 (CoQ10) each alone or in combination against carbon tetrachloride (CCl4)-induced cardiac damage in rats.	Acetylcysteine	59-76	C-C motif chemokine ligand 4	Rattus norvegicus	167-171
30180452-9	2018	Co-treatment with NAC, an antioxidant, inhibited hIAPP-induced ROS generation, and the expression of LC3-II/LC3-I and p-AMPK in the INS-1 cells (all P&lt;0.05).	Acetylcysteine	18-21	protein kinase AMP-activated catalytic subunit alpha 2	Rattus norvegicus	120-124
30161099-10	2018	RESULTS Suppression of oxidative stress by NAC reduced NF-kappaB and GSDMD activation and increased pyroptosis, characterized by LDH release and NLRP3 inflammasome activation in H9C2 cells under OGD.	Acetylcysteine	43-46	gasdermin D	Rattus norvegicus	69-74
30161099-10	2018	RESULTS Suppression of oxidative stress by NAC reduced NF-kappaB and GSDMD activation and increased pyroptosis, characterized by LDH release and NLRP3 inflammasome activation in H9C2 cells under OGD.	Acetylcysteine	43-46	NLR family, pyrin domain containing 3	Rattus norvegicus	145-150
30116167-1	2018	This study is designed to evaluate the potential impact of N-acetyl cysteine (NAC) and coenzyme Q10 (CoQ10) each alone or in combination against carbon tetrachloride (CCl4)-induced cardiac damage in rats.	Acetylcysteine	78-81	C-C motif chemokine ligand 4	Rattus norvegicus	167-171
29582209-8	2018	These traits and the overall senescent phenotype were significantly reversed using the known anti-oxidant N-acetyl-L-cysteine or a specific p38 MAPK inhibitor, suggesting the participation of oxidative stress and of the p38 MAPK pathway in TNF-alpha-triggered premature senescence.	Acetylcysteine	106-125	mitogen-activated protein kinase 14	Homo sapiens	220-223
29513056-0	2018	l-N-acetylcysteine protects outer hair cells against TNFalpha initiated ototoxicity in vitro.	Acetylcysteine	0-18	tumor necrosis factor	Rattus norvegicus	53-61
29513056-1	2018	OBJECTIVE: The present study is aimed at determining the efficacy and exploring the mechanisms by which l-N-acetylcysteine (l-NAC) provides protection against tumor necrosis factor-alpha (TNFalpha)-induced oxidative stress damage and hair cell loss in 3-day-old rat organ of Corti (OC) explants.	Acetylcysteine	104-122	tumor necrosis factor	Rattus norvegicus	159-186
29513056-1	2018	OBJECTIVE: The present study is aimed at determining the efficacy and exploring the mechanisms by which l-N-acetylcysteine (l-NAC) provides protection against tumor necrosis factor-alpha (TNFalpha)-induced oxidative stress damage and hair cell loss in 3-day-old rat organ of Corti (OC) explants.	Acetylcysteine	104-122	tumor necrosis factor	Rattus norvegicus	188-196
29513056-1	2018	OBJECTIVE: The present study is aimed at determining the efficacy and exploring the mechanisms by which l-N-acetylcysteine (l-NAC) provides protection against tumor necrosis factor-alpha (TNFalpha)-induced oxidative stress damage and hair cell loss in 3-day-old rat organ of Corti (OC) explants.	Acetylcysteine	124-129	tumor necrosis factor	Rattus norvegicus	159-186
29513056-1	2018	OBJECTIVE: The present study is aimed at determining the efficacy and exploring the mechanisms by which l-N-acetylcysteine (l-NAC) provides protection against tumor necrosis factor-alpha (TNFalpha)-induced oxidative stress damage and hair cell loss in 3-day-old rat organ of Corti (OC) explants.	Acetylcysteine	124-129	tumor necrosis factor	Rattus norvegicus	188-196
29807795-6	2018	Notably, we used drug affinity responsive target stability (DARTS) to show that CG-06 binds directly to STAT3, and the reactive oxygen species (ROS) scavenger N-acetyl cysteine (NAC) rescued the CG-06-induced suppression p-STAT3.	Acetylcysteine	159-176	signal transducer and activator of transcription 3	Homo sapiens	223-228
29786746-12	2018	Notably, the inhibition of ROS generation by the antioxidant N-acetyl-L-cysteine significantly attenuated the luteolin-induced loss of DeltaPsim and activities of caspase-3, -8 and -9.	Acetylcysteine	61-80	caspase 3	Homo sapiens	163-183
30415238-8	2018	Pretreatment of thiol antioxidants GSH and NAC reduced ROS levels and attenuated the increase in ROS, the activation of NF-kappaB, AP-1, and STAT-3, and the expression of COX-2 in LPS-treated A549 cells.	Acetylcysteine	43-46	nuclear factor kappa B subunit 1	Homo sapiens	120-129
30415238-8	2018	Pretreatment of thiol antioxidants GSH and NAC reduced ROS levels and attenuated the increase in ROS, the activation of NF-kappaB, AP-1, and STAT-3, and the expression of COX-2 in LPS-treated A549 cells.	Acetylcysteine	43-46	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	131-135
30415238-8	2018	Pretreatment of thiol antioxidants GSH and NAC reduced ROS levels and attenuated the increase in ROS, the activation of NF-kappaB, AP-1, and STAT-3, and the expression of COX-2 in LPS-treated A549 cells.	Acetylcysteine	43-46	signal transducer and activator of transcription 3	Homo sapiens	141-147
30415238-8	2018	Pretreatment of thiol antioxidants GSH and NAC reduced ROS levels and attenuated the increase in ROS, the activation of NF-kappaB, AP-1, and STAT-3, and the expression of COX-2 in LPS-treated A549 cells.	Acetylcysteine	43-46	prostaglandin-endoperoxide synthase 2	Homo sapiens	171-176
30415238-9	2018	In conclusion, GSH and NAC suppress COX-2 expression by reducing ROS levels and inhibiting the activation of NF-kappaB, AP-1, and STAT-3 in pulmonary epithelial A549 cells exposed to LPS.	Acetylcysteine	23-26	prostaglandin-endoperoxide synthase 2	Homo sapiens	36-41
30415238-9	2018	In conclusion, GSH and NAC suppress COX-2 expression by reducing ROS levels and inhibiting the activation of NF-kappaB, AP-1, and STAT-3 in pulmonary epithelial A549 cells exposed to LPS.	Acetylcysteine	23-26	nuclear factor kappa B subunit 1	Homo sapiens	109-118
30415238-9	2018	In conclusion, GSH and NAC suppress COX-2 expression by reducing ROS levels and inhibiting the activation of NF-kappaB, AP-1, and STAT-3 in pulmonary epithelial A549 cells exposed to LPS.	Acetylcysteine	23-26	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	120-124
30415238-9	2018	In conclusion, GSH and NAC suppress COX-2 expression by reducing ROS levels and inhibiting the activation of NF-kappaB, AP-1, and STAT-3 in pulmonary epithelial A549 cells exposed to LPS.	Acetylcysteine	23-26	signal transducer and activator of transcription 3	Homo sapiens	130-136
30105036-8	2018	NPYR antagonists as well as antioxidant N-acetylcysteine showed anti-adipogenic effects by reducing the ROS levels, indicating that PTX3 mediates adipogenesis through NPY-dependent ROS production.	Acetylcysteine	40-56	pentraxin related gene	Mus musculus	132-136
29972798-4	2018	This transition is reversed by N-acetylcysteine and mediated by activation of the AMPK-HIF1alpha axis.	Acetylcysteine	31-47	hypoxia inducible factor 1 subunit alpha	Homo sapiens	87-96
29698568-11	2018	Inflammatory markers tumor necrosis factor-alpha, interferon-gamma, and interleukin-6 were significantly decreased in serum and callus following NAC treatment.	Acetylcysteine	145-148	tumor necrosis factor	Rattus norvegicus	21-48
29698568-11	2018	Inflammatory markers tumor necrosis factor-alpha, interferon-gamma, and interleukin-6 were significantly decreased in serum and callus following NAC treatment.	Acetylcysteine	145-148	interleukin 6	Rattus norvegicus	72-85
29635121-0	2018	N-Acetylcysteine protects human bronchi by modulating the release of neurokinin A in an ex vivo model of COPD exacerbation.	Acetylcysteine	0-16	tachykinin precursor 1	Homo sapiens	69-81
29635121-6	2018	KEY FINDINGS: NAC at high concentrations normalized the peroxidase activity, H2O2, malondialdehyde (MDA), nitric oxide, glutathione (GSH), total antioxidant capacity (TAC), and interleukin 6 (IL-6) (overall change 34.32% +- 4.22%, P &lt; 0.05 vs. LPS-treated).	Acetylcysteine	14-17	interleukin 6	Homo sapiens	177-190
29635121-6	2018	KEY FINDINGS: NAC at high concentrations normalized the peroxidase activity, H2O2, malondialdehyde (MDA), nitric oxide, glutathione (GSH), total antioxidant capacity (TAC), and interleukin 6 (IL-6) (overall change 34.32% +- 4.22%, P &lt; 0.05 vs. LPS-treated).	Acetylcysteine	14-17	interleukin 6	Homo sapiens	192-196
29635121-7	2018	NAC at low concentrations modulated peroxidase activity, H2O2, MDA, GSH, TAC, and IL-6 (overall change 34.88% +- 7.39%, P &lt; 0.05 vs. LPS-treated).	Acetylcysteine	0-3	interleukin 6	Homo sapiens	82-86
29635121-8	2018	NAC at very-low concentrations was effective on peroxidase activity, H2O2, GSH, and IL-6 (overall change 35.05 +- 7.71%, P &lt; 0.05 vs. LPS-treated).	Acetylcysteine	0-3	interleukin 6	Homo sapiens	84-88
29635121-9	2018	Binary logistic regression analysis indicated that the modulatory effect of NAC on NKA levels was associated with a reduction of pro-oxidant factors and IL-6, and selectively blocking the NK2 receptor abolished such an association.	Acetylcysteine	76-79	tachykinin precursor 1	Homo sapiens	83-86
29635121-9	2018	Binary logistic regression analysis indicated that the modulatory effect of NAC on NKA levels was associated with a reduction of pro-oxidant factors and IL-6, and selectively blocking the NK2 receptor abolished such an association.	Acetylcysteine	76-79	interleukin 6	Homo sapiens	153-157
29635121-10	2018	SIGNIFICANCE: This study demonstrates that, along with its well-known antioxidant activity, the protective effect of NAC against the detrimental effect of LPS is due to the modulation of NKA and IL-6 levels.	Acetylcysteine	117-120	tachykinin precursor 1	Homo sapiens	187-190
29635121-10	2018	SIGNIFICANCE: This study demonstrates that, along with its well-known antioxidant activity, the protective effect of NAC against the detrimental effect of LPS is due to the modulation of NKA and IL-6 levels.	Acetylcysteine	117-120	interleukin 6	Homo sapiens	195-199
30131715-6	2018	Furthermore, NAC pretreatment partly inhibited MC-LR-induced ERs and autophagy via the PERK/ATG12 and XBP1/Beclin1 pathways.	Acetylcysteine	13-16	X-box binding protein 1	Mus musculus	102-106
29513056-7	2018	RESULTS: l-NAC (5 and 10 mM) provided protection for OHCs from ototoxic level of TNFalpha in OC explants.	Acetylcysteine	9-14	tumor necrosis factor	Rattus norvegicus	81-89
29513056-8	2018	Groups treated with TNFalpha+l-NAC (5 mM) showed a highly significant reduction of both ROS (p &lt; 0.01) and 4-hydroxy-2-nonenal immunostaining (p &lt; 0.001) compared to TNFalpha-challenged explants.	Acetylcysteine	29-34	tumor necrosis factor	Rattus norvegicus	20-28
29513056-8	2018	Groups treated with TNFalpha+l-NAC (5 mM) showed a highly significant reduction of both ROS (p &lt; 0.01) and 4-hydroxy-2-nonenal immunostaining (p &lt; 0.001) compared to TNFalpha-challenged explants.	Acetylcysteine	29-34	tumor necrosis factor	Rattus norvegicus	172-180
29513056-10	2018	CONCLUSIONS: l-NAC is a promising treatment for protecting auditory HCs from TNFalpha-induced oxidative stress and subsequent loss via programmed cell death.	Acetylcysteine	13-18	tumor necrosis factor	Rattus norvegicus	77-85
29985009-8	2018	We found that both doses of NAC blocked 5-HT1B agonist-induced deficits on the DAT.	Acetylcysteine	28-31	5-hydroxytryptamine (serotonin) receptor 1B	Mus musculus	40-46
29985009-10	2018	We found that blockade of 5-HT1B agonist-induced OCD-like behavior is present at 3 weeks, but not 1 week, of NAC treatment.	Acetylcysteine	109-112	5-hydroxytryptamine (serotonin) receptor 1B	Mus musculus	26-32
29668110-8	2018	Pre-incubation with ROS scavenger N-acetyl-l-cysteine preserved AR and PSA abundance, markedly reduced ISC-4-induced apoptosis and attenuated p53 Ser phosphorylation, p21Cip1, and p-H2A.X.	Acetylcysteine	34-53	androgen receptor	Homo sapiens	64-66
29668110-8	2018	Pre-incubation with ROS scavenger N-acetyl-l-cysteine preserved AR and PSA abundance, markedly reduced ISC-4-induced apoptosis and attenuated p53 Ser phosphorylation, p21Cip1, and p-H2A.X.	Acetylcysteine	34-53	tumor protein p53	Homo sapiens	142-145
29668110-8	2018	Pre-incubation with ROS scavenger N-acetyl-l-cysteine preserved AR and PSA abundance, markedly reduced ISC-4-induced apoptosis and attenuated p53 Ser phosphorylation, p21Cip1, and p-H2A.X.	Acetylcysteine	34-53	cyclin dependent kinase inhibitor 1A	Homo sapiens	167-174
30026883-10	2018	The antioxidant N-acetyl-L-cysteine significantly inhibited the increases in interleukin-8 induced by solutions with particulate matter, regardless of ozone exposure.	Acetylcysteine	16-35	C-X-C motif chemokine ligand 8	Homo sapiens	77-90
30011295-6	2018	Pre-treatment with the antioxidant, N-acetylcysteine, prevented the actions of arecoline on cell viability, G2/M growth arrest, reactive oxygen species (ROS) production, and the levels of CDK1, p21, p27, p53, cyclin B1, and phospho-AMPK proteins.	Acetylcysteine	36-52	cyclin dependent kinase inhibitor 1A	Homo sapiens	194-197
30011295-6	2018	Pre-treatment with the antioxidant, N-acetylcysteine, prevented the actions of arecoline on cell viability, G2/M growth arrest, reactive oxygen species (ROS) production, and the levels of CDK1, p21, p27, p53, cyclin B1, and phospho-AMPK proteins.	Acetylcysteine	36-52	tumor protein p53	Homo sapiens	204-207
29582209-8	2018	These traits and the overall senescent phenotype were significantly reversed using the known anti-oxidant N-acetyl-L-cysteine or a specific p38 MAPK inhibitor, suggesting the participation of oxidative stress and of the p38 MAPK pathway in TNF-alpha-triggered premature senescence.	Acetylcysteine	106-125	tumor necrosis factor	Homo sapiens	240-249
29080256-9	2018	Anti-oxidant N-acetylcysteine, PI3K and NF-kappaB-specific pathway inhibitors can abolish the secretion of these inflammatory factors; pretreatment with anti-oxidant N-acetylcysteine significantly decreased PI3K expression, the level of phosphorylated AKT and nuclear NF-kappaB; pretreatment of LY294002 can significantly decrease the NF-kappaB level in nuclei.	Acetylcysteine	166-182	AKT serine/threonine kinase 1	Rattus norvegicus	252-255
29659325-9	2018	However, pretreatment with NAC or PDTC, the scavenger of ROS, not only counteracted the effects of a 50-Hz MF on ROS level and AMS activity, but also inhibited the EGFR clustering induced by MF exposure.	Acetylcysteine	27-30	epidermal growth factor receptor	Homo sapiens	164-168
30045259-1	2018	OBJECTIVES: This study assessed the efficacy of oral consumption of N-acetyl cysteine (NAC) and melatonin (ML) in reducing early reperfusion injury and acute oxidative stress in patients undergoing coronary artery bypass grafting (CABG) with respect to the measurements of cardiac troponin I, lactate, malondealdehyde (MDA), and tumor necrosis factor-alpha (TNF-alpha) levels in the blood.	Acetylcysteine	68-85	tumor necrosis factor	Homo sapiens	329-356
29684820-6	2018	Importantly, antioxidant N-acetylcysteine (NAC) significantly attenuated the induction of DNA damage and the perturbation of proliferation by PARP inhibition or depletion.	Acetylcysteine	25-41	poly(ADP-ribose) polymerase 1	Homo sapiens	142-146
29684820-6	2018	Importantly, antioxidant N-acetylcysteine (NAC) significantly attenuated the induction of DNA damage and the perturbation of proliferation by PARP inhibition or depletion.	Acetylcysteine	43-46	poly(ADP-ribose) polymerase 1	Homo sapiens	142-146
30045259-1	2018	OBJECTIVES: This study assessed the efficacy of oral consumption of N-acetyl cysteine (NAC) and melatonin (ML) in reducing early reperfusion injury and acute oxidative stress in patients undergoing coronary artery bypass grafting (CABG) with respect to the measurements of cardiac troponin I, lactate, malondealdehyde (MDA), and tumor necrosis factor-alpha (TNF-alpha) levels in the blood.	Acetylcysteine	68-85	tumor necrosis factor	Homo sapiens	358-367
30045259-1	2018	OBJECTIVES: This study assessed the efficacy of oral consumption of N-acetyl cysteine (NAC) and melatonin (ML) in reducing early reperfusion injury and acute oxidative stress in patients undergoing coronary artery bypass grafting (CABG) with respect to the measurements of cardiac troponin I, lactate, malondealdehyde (MDA), and tumor necrosis factor-alpha (TNF-alpha) levels in the blood.	Acetylcysteine	87-90	tumor necrosis factor	Homo sapiens	329-356
30045259-1	2018	OBJECTIVES: This study assessed the efficacy of oral consumption of N-acetyl cysteine (NAC) and melatonin (ML) in reducing early reperfusion injury and acute oxidative stress in patients undergoing coronary artery bypass grafting (CABG) with respect to the measurements of cardiac troponin I, lactate, malondealdehyde (MDA), and tumor necrosis factor-alpha (TNF-alpha) levels in the blood.	Acetylcysteine	87-90	tumor necrosis factor	Homo sapiens	358-367
29679655-8	2018	In fact, NAC allows the anti-apoptotic molecule Bcl-2 to reduce the cell death caused by pro-necrotic concentrations of cisplatin, to a significantly greater extent than in the absence of NAC.	Acetylcysteine	9-12	BCL2 apoptosis regulator	Homo sapiens	48-53
29660332-11	2018	Intriguingly, pre-treatment of ROS scavenger, N-acetylcysteine (NAC), markedly abolished DUSP14-KD-augmented NF-kappaB and MAPKs activation in HR-stimulated primary cardiomyocytes.	Acetylcysteine	46-62	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	109-118
29660332-11	2018	Intriguingly, pre-treatment of ROS scavenger, N-acetylcysteine (NAC), markedly abolished DUSP14-KD-augmented NF-kappaB and MAPKs activation in HR-stimulated primary cardiomyocytes.	Acetylcysteine	64-67	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	109-118
29799741-7	2018	However, the ERK but not p38 or JNK pathway was involved in the protection of SeMet and NAC against the immunotoxicity.	Acetylcysteine	88-91	mitogen-activated protein kinase 1	Homo sapiens	13-16
30025127-9	2018	Although there was no significant difference in MUC16 gene expression, the MUC16 concentration of the tear film and ocular surface tissue was significantly increased in the NAC group versus in the control group (P &lt; 0.01 and P &lt; 0.05, respectively).	Acetylcysteine	173-176	mucin 16, cell surface associated	Rattus norvegicus	75-80
29627441-9	2018	Additionally, AFN-induced Nrf2 activation was inhibited by N-acetyl cysteine.	Acetylcysteine	59-76	NFE2 like bZIP transcription factor 2	Homo sapiens	26-30
30025127-11	2018	Conclusions: Topical administration of 10% NAC induced ocular surface damage and tear film instability by prompting MUC16 disruption and release from the ocular surface.	Acetylcysteine	43-46	mucin 16, cell surface associated	Rattus norvegicus	116-121
29348462-9	2018	Ectopic expression of GSTP1 or pre-treatment with antioxidant N-acetyl-L-cysteine (NAC) abrogates the ROS elevation and decreases DNA damage, apoptosis, and autophagic cell death prompted by PL/APR-246.	Acetylcysteine	62-81	phorbol-12-myristate-13-acetate-induced protein 1	Homo sapiens	194-197
29573703-4	2018	The aim of this work was to study the extent of the protective effect of the antioxidant N-acetylcysteine (NAC) over the proinflammatory state (IL-6 and IL-8), oxidative stress (reactive oxygen species, ROS), and CFTR levels, caused by Cigarette Smoke Extract (CSE) in Calu-3 airway epithelial cells.	Acetylcysteine	89-105	interleukin 6	Homo sapiens	144-148
29573703-4	2018	The aim of this work was to study the extent of the protective effect of the antioxidant N-acetylcysteine (NAC) over the proinflammatory state (IL-6 and IL-8), oxidative stress (reactive oxygen species, ROS), and CFTR levels, caused by Cigarette Smoke Extract (CSE) in Calu-3 airway epithelial cells.	Acetylcysteine	89-105	C-X-C motif chemokine ligand 8	Homo sapiens	153-157
29573703-4	2018	The aim of this work was to study the extent of the protective effect of the antioxidant N-acetylcysteine (NAC) over the proinflammatory state (IL-6 and IL-8), oxidative stress (reactive oxygen species, ROS), and CFTR levels, caused by Cigarette Smoke Extract (CSE) in Calu-3 airway epithelial cells.	Acetylcysteine	89-105	CF transmembrane conductance regulator	Homo sapiens	213-217
29573703-4	2018	The aim of this work was to study the extent of the protective effect of the antioxidant N-acetylcysteine (NAC) over the proinflammatory state (IL-6 and IL-8), oxidative stress (reactive oxygen species, ROS), and CFTR levels, caused by Cigarette Smoke Extract (CSE) in Calu-3 airway epithelial cells.	Acetylcysteine	107-110	interleukin 6	Homo sapiens	144-148
29573703-4	2018	The aim of this work was to study the extent of the protective effect of the antioxidant N-acetylcysteine (NAC) over the proinflammatory state (IL-6 and IL-8), oxidative stress (reactive oxygen species, ROS), and CFTR levels, caused by Cigarette Smoke Extract (CSE) in Calu-3 airway epithelial cells.	Acetylcysteine	107-110	C-X-C motif chemokine ligand 8	Homo sapiens	153-157
29573703-4	2018	The aim of this work was to study the extent of the protective effect of the antioxidant N-acetylcysteine (NAC) over the proinflammatory state (IL-6 and IL-8), oxidative stress (reactive oxygen species, ROS), and CFTR levels, caused by Cigarette Smoke Extract (CSE) in Calu-3 airway epithelial cells.	Acetylcysteine	107-110	CF transmembrane conductance regulator	Homo sapiens	213-217
29754474-7	2018	Pre-treatment with Z-VAD-fmk, JNK inhibitor SP600125 and N-acetyl-l-cysteine (NAC), a ROS scavenger, partly improved the survival rates and restored OMT-induced cellular damage, and reduced caspase-3 cleavage.	Acetylcysteine	57-76	caspase 3	Homo sapiens	190-199
29754474-8	2018	SP600125 or NAC reduced OMT-induced p-JNK and NAC significantly lowered caspase-4.	Acetylcysteine	12-15	mitogen-activated protein kinase 8	Homo sapiens	38-41
29754474-7	2018	Pre-treatment with Z-VAD-fmk, JNK inhibitor SP600125 and N-acetyl-l-cysteine (NAC), a ROS scavenger, partly improved the survival rates and restored OMT-induced cellular damage, and reduced caspase-3 cleavage.	Acetylcysteine	78-81	caspase 3	Homo sapiens	190-199
29754474-8	2018	SP600125 or NAC reduced OMT-induced p-JNK and NAC significantly lowered caspase-4.	Acetylcysteine	12-15	caspase 4	Homo sapiens	72-81
29754474-8	2018	SP600125 or NAC reduced OMT-induced p-JNK and NAC significantly lowered caspase-4.	Acetylcysteine	46-49	caspase 4	Homo sapiens	72-81
29351404-11	2018	These insulin-induced effects were reversed by N-acetylcysteine antioxidant treatment.	Acetylcysteine	47-63	insulin	Homo sapiens	6-13
29604266-8	2018	N-acetyl-l-cysteine (NAC), a ROS inhibitor, protected against PAT-induced cytotoxicity, decreased the protein expression of LC3-II, and up-regulated the level of p-Akt1 and p-MTOR.	Acetylcysteine	0-19	AKT serine/threonine kinase 1	Homo sapiens	164-168
29604266-8	2018	N-acetyl-l-cysteine (NAC), a ROS inhibitor, protected against PAT-induced cytotoxicity, decreased the protein expression of LC3-II, and up-regulated the level of p-Akt1 and p-MTOR.	Acetylcysteine	0-19	mechanistic target of rapamycin kinase	Homo sapiens	175-179
29649567-10	2018	Antioxidants, N-acetyl cysteine and glutathione also protect these cells during glucose deprivation, leading us to conclude that Nrf2 signaling via its antioxidant activity has a critical and previously undescribed role of protecting cells during glucose deprivation-induced autophagy.	Acetylcysteine	14-31	NFE2 like bZIP transcription factor 2	Homo sapiens	129-133
29746502-7	2018	PK11195 and NAC also reduced SDT-induced mitochondrial membrane potential (DeltaPsim) loss, the translocation of cytochrome c and cell apoptosis.	Acetylcysteine	12-15	cytochrome c, somatic	Homo sapiens	113-125
28515173-10	2018	Cotreatment with ferrostatin-1 (ferroptosis inhibitor), deferoxamine (iron chelator), or N-acetyl-l-cysteine (glutathione replenisher) significantly increased cell viability and attenuated erastin-induced ferroptosis in both HO-1+/+ and HO-1-/- PTCs.	Acetylcysteine	89-108	heme oxygenase 1	Mus musculus	225-229
28515173-10	2018	Cotreatment with ferrostatin-1 (ferroptosis inhibitor), deferoxamine (iron chelator), or N-acetyl-l-cysteine (glutathione replenisher) significantly increased cell viability and attenuated erastin-induced ferroptosis in both HO-1+/+ and HO-1-/- PTCs.	Acetylcysteine	89-108	heme oxygenase 1	Mus musculus	237-241
29426002-0	2018	Acrylamide-induced oxidative stress and inflammatory response are alleviated by N-acetylcysteine in PC12 cells: Involvement of the crosstalk between Nrf2 and NF-kappaB pathways regulated by MAPKs.	Acetylcysteine	80-96	NFE2 like bZIP transcription factor 2	Rattus norvegicus	149-153
29426002-6	2018	NAC attenuated ACR-induced enhancement of MDA and ROS levels and TNF-alpha generation.	Acetylcysteine	0-3	tumor necrosis factor	Rattus norvegicus	65-74
29426002-10	2018	NAC treatment increased Nrf2 expression and suppressed NF-kappaB p65 expression to ameliorate oxidative stress and inflammatory response caused by ACR.	Acetylcysteine	0-3	NFE2 like bZIP transcription factor 2	Rattus norvegicus	24-28
29426002-10	2018	NAC treatment increased Nrf2 expression and suppressed NF-kappaB p65 expression to ameliorate oxidative stress and inflammatory response caused by ACR.	Acetylcysteine	0-3	synaptotagmin 1	Rattus norvegicus	65-68
29426002-15	2018	NAC protected against oxidative damage and inflammatory response induced by ACR by activating Nrf2 and inhibiting NF-kappaB pathways in PC12 cells.	Acetylcysteine	0-3	NFE2 like bZIP transcription factor 2	Rattus norvegicus	94-98
29734752-6	2018	Moreover, putative protective drugs, namely the antioxidants N-acetyl-l-cysteine (NAC; 1 mM) and 100 &amp;mu;M tiron, the inhibitor of caspase-3/7, Ac-DEVD-CHO (100 &amp;mu;M), and a protein synthesis inhibitor, cycloheximide (CHX; 10 nM), were tested to prevent DOX- or MTX-induced toxicity.	Acetylcysteine	61-80	caspase 3	Homo sapiens	135-144
29317200-11	2018	These uric acid-induced changes of BCRP and Akt were reversed in the presence of the antioxidant N-acetylcysteine.	Acetylcysteine	97-113	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	35-39
29317200-11	2018	These uric acid-induced changes of BCRP and Akt were reversed in the presence of the antioxidant N-acetylcysteine.	Acetylcysteine	97-113	AKT serine/threonine kinase 1	Homo sapiens	44-47
29908644-13	2018	N-acetylcysteine (NAC), an antioxidant and a glutathione precursor, blocked CdCl2-evoked Akt phosphorylation in mouse placenta and human trophoblast cells.	Acetylcysteine	0-16	thymoma viral proto-oncogene 1	Mus musculus	89-92
29565452-8	2018	Furthermore, pretreatment of Caki cells with ROS scavengers (N-acetylcysteine and glutathione) prevented the downregulation of cFLIP(L), the upregulation of cFLIP(S) and apoptosis induced by FasL.	Acetylcysteine	61-77	CASP8 and FADD like apoptosis regulator	Homo sapiens	127-135
29565452-8	2018	Furthermore, pretreatment of Caki cells with ROS scavengers (N-acetylcysteine and glutathione) prevented the downregulation of cFLIP(L), the upregulation of cFLIP(S) and apoptosis induced by FasL.	Acetylcysteine	61-77	CASP8 and FADD like apoptosis regulator	Homo sapiens	127-132
29908644-13	2018	N-acetylcysteine (NAC), an antioxidant and a glutathione precursor, blocked CdCl2-evoked Akt phosphorylation in mouse placenta and human trophoblast cells.	Acetylcysteine	18-21	thymoma viral proto-oncogene 1	Mus musculus	89-92
29731195-8	2018	Cellular ROS production was increased by PM treatment, and antioxidant N-acetyl cysteine pretreatment prevented induction of inflammatory cytokines IL-8 and MMP-1.	Acetylcysteine	71-88	C-X-C motif chemokine ligand 8	Homo sapiens	148-152
28770700-10	2018	Interestingly, FasL-induced RIP1/3 binding was significantly suppressed by the antioxidants Trolox and N-acetyl cysteine (NAC), suggesting the involvement of reactive oxygen species (ROS) in FasL-induced necroptotic cellular processes.	Acetylcysteine	103-120	receptor (TNFRSF)-interacting serine-threonine kinase 1	Mus musculus	28-32
30701862-5	2018	Biological and pharmacological effects of NAC include improvement in rheological properties of mucus, reduction of excess mucin production, restoration of mucociliary clearance and production of sIgA, suppression of excess production of IgE and IgG4, destruction of biofilms and inhibition of their formation, suppression of adhesion of pathogenic bacteria to epithelial cells, antioxidant activity, regulation of the production of pro-inflammatory and profibrotic cytokines.	Acetylcysteine	42-45	immunoglobulin heavy constant epsilon	Homo sapiens	237-240
29510199-10	2018	ROS scavenger N-acetyl-L-cysteine partially rescued HepG2 cell growth and prevented MPP depolarization, ERK and JNK activation.	Acetylcysteine	14-33	mitogen-activated protein kinase 1	Homo sapiens	104-107
29510199-10	2018	ROS scavenger N-acetyl-L-cysteine partially rescued HepG2 cell growth and prevented MPP depolarization, ERK and JNK activation.	Acetylcysteine	14-33	mitogen-activated protein kinase 8	Homo sapiens	112-115
29649125-7	2018	On the other hand, N-acetylcysteine (NAC) pretreatment prevented the phosphorylation of p38 but not that of JNK.	Acetylcysteine	19-35	mitogen-activated protein kinase 14	Homo sapiens	88-91
29649125-7	2018	On the other hand, N-acetylcysteine (NAC) pretreatment prevented the phosphorylation of p38 but not that of JNK.	Acetylcysteine	37-40	mitogen-activated protein kinase 14	Homo sapiens	88-91
29522769-5	2018	KEY FINDINGS: Chronic NAC treatment in MSG rats efficiently decreased the high circulating levels of triglycerides, UA, transaminases and TBARS, as well as peripheral (high insulinemia and HOMA indexes) and liver (LISI and the P-AKT:AKT and P-eNOS:eNOS protein ratio values) insulin-resistance.	Acetylcysteine	22-25	AKT serine/threonine kinase 1	Rattus norvegicus	229-232
29522769-5	2018	KEY FINDINGS: Chronic NAC treatment in MSG rats efficiently decreased the high circulating levels of triglycerides, UA, transaminases and TBARS, as well as peripheral (high insulinemia and HOMA indexes) and liver (LISI and the P-AKT:AKT and P-eNOS:eNOS protein ratio values) insulin-resistance.	Acetylcysteine	22-25	AKT serine/threonine kinase 1	Rattus norvegicus	233-236
28770700-10	2018	Interestingly, FasL-induced RIP1/3 binding was significantly suppressed by the antioxidants Trolox and N-acetyl cysteine (NAC), suggesting the involvement of reactive oxygen species (ROS) in FasL-induced necroptotic cellular processes.	Acetylcysteine	122-125	receptor (TNFRSF)-interacting serine-threonine kinase 1	Mus musculus	28-32
29642488-6	2018	These caspases and PARP activations were suppressed by N-acetylcysteine (NAC) pretreatment.	Acetylcysteine	55-71	poly(ADP-ribose) polymerase 1	Homo sapiens	19-23
29396710-0	2018	N-acetyl cysteine protects anti-melanoma cytotoxic T cells from exhaustion induced by rapid expansion via the downmodulation of Foxo1 in an Akt-dependent manner.	Acetylcysteine	0-17	forkhead box O1	Homo sapiens	128-133
29642488-6	2018	These caspases and PARP activations were suppressed by N-acetylcysteine (NAC) pretreatment.	Acetylcysteine	73-76	poly(ADP-ribose) polymerase 1	Homo sapiens	19-23
30788945-8	2018	Compared with TCP group, serum levels of TNF-alpha, IL-1beta and IL-6, and osteolysis area were decreased markedly in NAC group (P&lt;0.05), serum level of T-AOC and SOD activity were increased obviously in NAC group (P&lt;0.05), and GRP78 expression, the ratio of p-PERK/PERK and p-eIF2alpha/eIF2alpha were obviously down-regulated.	Acetylcysteine	118-121	tumor necrosis factor	Mus musculus	41-50
30788945-8	2018	Compared with TCP group, serum levels of TNF-alpha, IL-1beta and IL-6, and osteolysis area were decreased markedly in NAC group (P&lt;0.05), serum level of T-AOC and SOD activity were increased obviously in NAC group (P&lt;0.05), and GRP78 expression, the ratio of p-PERK/PERK and p-eIF2alpha/eIF2alpha were obviously down-regulated.	Acetylcysteine	118-121	interleukin 1 beta	Mus musculus	52-60
30788945-8	2018	Compared with TCP group, serum levels of TNF-alpha, IL-1beta and IL-6, and osteolysis area were decreased markedly in NAC group (P&lt;0.05), serum level of T-AOC and SOD activity were increased obviously in NAC group (P&lt;0.05), and GRP78 expression, the ratio of p-PERK/PERK and p-eIF2alpha/eIF2alpha were obviously down-regulated.	Acetylcysteine	118-121	interleukin 6	Mus musculus	65-69
30788945-8	2018	Compared with TCP group, serum levels of TNF-alpha, IL-1beta and IL-6, and osteolysis area were decreased markedly in NAC group (P&lt;0.05), serum level of T-AOC and SOD activity were increased obviously in NAC group (P&lt;0.05), and GRP78 expression, the ratio of p-PERK/PERK and p-eIF2alpha/eIF2alpha were obviously down-regulated.	Acetylcysteine	118-121	heat shock protein 5	Mus musculus	234-239
29849896-2	2018	We previously demonstrated that administration of exogenous antioxidants (N-acetylcysteine and trolox) reduces CASQ1-null mortality during exposure to heat.	Acetylcysteine	74-90	calsequestrin 1	Mus musculus	111-116
29396710-7	2018	Interestingly, NAC did not affect memory subsets, but diminished up-regulation of senescence (CD57) and exhaustion (PD-1) markers and significantly decreased expression of the transcription factors EOMES and Foxo1.	Acetylcysteine	15-18	beta-1,3-glucuronyltransferase 1	Homo sapiens	94-98
29396710-7	2018	Interestingly, NAC did not affect memory subsets, but diminished up-regulation of senescence (CD57) and exhaustion (PD-1) markers and significantly decreased expression of the transcription factors EOMES and Foxo1.	Acetylcysteine	15-18	forkhead box O1	Homo sapiens	208-213
29396710-8	2018	Pharmacological inhibition of the PI3K/Akt pathway ablates the decrease in Foxo1 induced by NAC treatment of activated T cells.	Acetylcysteine	92-95	AKT serine/threonine kinase 1	Homo sapiens	39-42
29396710-8	2018	Pharmacological inhibition of the PI3K/Akt pathway ablates the decrease in Foxo1 induced by NAC treatment of activated T cells.	Acetylcysteine	92-95	forkhead box O1	Homo sapiens	75-80
29396710-0	2018	N-acetyl cysteine protects anti-melanoma cytotoxic T cells from exhaustion induced by rapid expansion via the downmodulation of Foxo1 in an Akt-dependent manner.	Acetylcysteine	0-17	AKT serine/threonine kinase 1	Homo sapiens	140-143
29396710-9	2018	This suggests a model in which NAC through PI3K/Akt activation suppresses Foxo1 expression, thereby impacting its transcriptional targets EOMES, PD-1, and granzyme B.	Acetylcysteine	31-34	AKT serine/threonine kinase 1	Homo sapiens	48-51
29396710-9	2018	This suggests a model in which NAC through PI3K/Akt activation suppresses Foxo1 expression, thereby impacting its transcriptional targets EOMES, PD-1, and granzyme B.	Acetylcysteine	31-34	forkhead box O1	Homo sapiens	74-79
28961512-18	2018	NAC, given after the establishment of diabetes, may offer protection against the risk for stroke by altering both systemic and vascular prothrombotic responses via enhancing platelet GSH, and GSH-dependent MG elimination, as well as correcting levels of antioxidants such as SOD1 and GPx-1.	Acetylcysteine	0-3	superoxide dismutase 1, soluble	Mus musculus	275-279
29367760-5	2018	The pre-treatment of FSPCre-Pparb/d-/- and Pparb/dfl/fl with antioxidant N-acetyl-cysteine prior DSS-induced tumorigenesis resulted in lower tumor load.	Acetylcysteine	73-90	peroxisome proliferator activator receptor delta	Mus musculus	21-48
29137484-10	2018	In vivo studies in rats, NAC treatment increased the LC3 II/I ratio and p-Akt protein expression in myocardium.	Acetylcysteine	25-28	AKT serine/threonine kinase 1	Rattus norvegicus	74-77
29215273-5	2018	In vitro alkylation experiments with the natural product and N-acetyl-l-cysteine suggest that honaucin A activates this pathway through covalent interaction with the sulfhydryl residues of the cytosolic repressor protein Keap1.	Acetylcysteine	61-80	kelch like ECH associated protein 1	Homo sapiens	221-226
29673449-3	2018	Both NAC and AA eliminated transient increased ROS levels after hemin treatment, inhibited hemin-induced hemoglobin synthesis, and decreased mRNA expression levels of beta-globin, gamma-globin, and GATA-1 genes significantly.	Acetylcysteine	5-8	GATA binding protein 1	Homo sapiens	198-204
29288670-10	2018	Notably, reducing ROS production by its scavenger, N-acetyl cysteine (NAC), could down-regulate p-AMPK levels, while up-regulate the phosphorylated mechanistic target of rapamycin (p-mTOR) expressions, accompanied with the restored cell viability, as well as the reduced apoptosis and autophagy in Bri-treated liver cancer cells.	Acetylcysteine	51-68	mechanistic target of rapamycin kinase	Homo sapiens	183-187
29288670-10	2018	Notably, reducing ROS production by its scavenger, N-acetyl cysteine (NAC), could down-regulate p-AMPK levels, while up-regulate the phosphorylated mechanistic target of rapamycin (p-mTOR) expressions, accompanied with the restored cell viability, as well as the reduced apoptosis and autophagy in Bri-treated liver cancer cells.	Acetylcysteine	70-73	mechanistic target of rapamycin kinase	Homo sapiens	183-187
29193446-9	2018	Antioxidant NAC inhibited p38MAPK activation by TNF-alpha.	Acetylcysteine	12-15	tumor necrosis factor	Homo sapiens	48-57
29326072-5	2018	Western blot results indicated that BSNQ and OSNQ up-regulated the phosphorylation of p38 and JNK, and down-regulated the phosphorylation of ERK, Akt and STAT3, and that these effects were blocked by N-acetyl-l-cysteine.	Acetylcysteine	200-219	mitogen-activated protein kinase 14	Homo sapiens	86-89
29392716-5	2018	Antioxidant (N-acetyl-L-cysteine, NAC) treatment in vitro not only quantitatively and functionally improved BM MSCs derived from PT patients through down-regulation of the p38 (also termed MAPK14) and p53 (also termed TP53) pathways but also partially rescued the impaired ability of BM MSCs to support megakaryocytopoiesis.	Acetylcysteine	13-32	mitogen-activated protein kinase 14	Homo sapiens	172-175
29392716-5	2018	Antioxidant (N-acetyl-L-cysteine, NAC) treatment in vitro not only quantitatively and functionally improved BM MSCs derived from PT patients through down-regulation of the p38 (also termed MAPK14) and p53 (also termed TP53) pathways but also partially rescued the impaired ability of BM MSCs to support megakaryocytopoiesis.	Acetylcysteine	13-32	mitogen-activated protein kinase 14	Homo sapiens	189-195
29392716-5	2018	Antioxidant (N-acetyl-L-cysteine, NAC) treatment in vitro not only quantitatively and functionally improved BM MSCs derived from PT patients through down-regulation of the p38 (also termed MAPK14) and p53 (also termed TP53) pathways but also partially rescued the impaired ability of BM MSCs to support megakaryocytopoiesis.	Acetylcysteine	13-32	tumor protein p53	Homo sapiens	201-204
29392716-5	2018	Antioxidant (N-acetyl-L-cysteine, NAC) treatment in vitro not only quantitatively and functionally improved BM MSCs derived from PT patients through down-regulation of the p38 (also termed MAPK14) and p53 (also termed TP53) pathways but also partially rescued the impaired ability of BM MSCs to support megakaryocytopoiesis.	Acetylcysteine	13-32	tumor protein p53	Homo sapiens	218-222
29326072-5	2018	Western blot results indicated that BSNQ and OSNQ up-regulated the phosphorylation of p38 and JNK, and down-regulated the phosphorylation of ERK, Akt and STAT3, and that these effects were blocked by N-acetyl-l-cysteine.	Acetylcysteine	200-219	mitogen-activated protein kinase 8	Homo sapiens	94-97
29326072-5	2018	Western blot results indicated that BSNQ and OSNQ up-regulated the phosphorylation of p38 and JNK, and down-regulated the phosphorylation of ERK, Akt and STAT3, and that these effects were blocked by N-acetyl-l-cysteine.	Acetylcysteine	200-219	mitogen-activated protein kinase 1	Homo sapiens	141-144
29326072-5	2018	Western blot results indicated that BSNQ and OSNQ up-regulated the phosphorylation of p38 and JNK, and down-regulated the phosphorylation of ERK, Akt and STAT3, and that these effects were blocked by N-acetyl-l-cysteine.	Acetylcysteine	200-219	AKT serine/threonine kinase 1	Homo sapiens	146-149
29326072-5	2018	Western blot results indicated that BSNQ and OSNQ up-regulated the phosphorylation of p38 and JNK, and down-regulated the phosphorylation of ERK, Akt and STAT3, and that these effects were blocked by N-acetyl-l-cysteine.	Acetylcysteine	200-219	signal transducer and activator of transcription 3	Homo sapiens	154-159
29458843-7	2018	The growth inhibition of elo2  and elo3  could be partially rescued by two commonly used antioxidant agents N-acetyl cysteine (NAC) and Ascorbic acid (VC).	Acetylcysteine	108-125	fatty acid elongase ELO2	Saccharomyces cerevisiae S288C	25-29
29458843-7	2018	The growth inhibition of elo2  and elo3  could be partially rescued by two commonly used antioxidant agents N-acetyl cysteine (NAC) and Ascorbic acid (VC).	Acetylcysteine	108-125	fatty acid elongase ELO3	Saccharomyces cerevisiae S288C	35-39
29458843-7	2018	The growth inhibition of elo2  and elo3  could be partially rescued by two commonly used antioxidant agents N-acetyl cysteine (NAC) and Ascorbic acid (VC).	Acetylcysteine	127-130	fatty acid elongase ELO2	Saccharomyces cerevisiae S288C	25-29
29458843-7	2018	The growth inhibition of elo2  and elo3  could be partially rescued by two commonly used antioxidant agents N-acetyl cysteine (NAC) and Ascorbic acid (VC).	Acetylcysteine	127-130	fatty acid elongase ELO3	Saccharomyces cerevisiae S288C	35-39
29328400-6	2018	Nacetylcysteine, a Nox4 inhibitor, was demonstrated to inhibit ROS generation, suppress VCAM-1 and ICAM-1 protein expression, and decrease oxidative stress and inflammation in HK-2 cells following overexpression of miR-146a.	Acetylcysteine	0-15	vascular cell adhesion molecule 1	Homo sapiens	88-94
28849708-8	2018	We also demonstrated that cell death mediated by z-L-CMK was associated with oxidative stress via the depletion of intracellular glutathione (GSH) and increase in reactive oxygen species (ROS), which was blocked by N-acetyl cysteine.	Acetylcysteine	215-232	C-X-C motif chemokine ligand 9	Homo sapiens	53-56
29408318-7	2018	Conversely, pretreatment with NAC reduced Cd-induced ROS production and disruption of HIF, MT and TGFbeta pathway signaling.	Acetylcysteine	30-33	transforming growth factor beta 1	Homo sapiens	98-105
29174818-7	2018	In vitro study revealed that methylglyoxal-derived AGE (MG-AGE) incubation in isolated cardiomyocytes promoted oxidation of sarco(endo)plasmic reticulum Ca2+-ATPase (SERCA2a) and production of superoxide, the effects of which were negated by the autophagy inducer rapamycin, the ER stress chaperone TUDCA or the antioxidant N-acetylcysteine.	Acetylcysteine	324-340	ATPase, Ca++ transporting, ubiquitous	Mus musculus	124-164
28815354-12	2018	Moreover, scavenging ROS by N-acetyl cysteine could inhibit the increasing expression of TGF-beta1 promoted by Nrf2 knockdown.	Acetylcysteine	28-45	transforming growth factor beta 1	Homo sapiens	89-98
29294389-9	2018	Given that NAC inhibits Snail-mediated EMT, this may be a potential therapeutic intervention for FECD.	Acetylcysteine	11-14	snail family transcriptional repressor 1	Homo sapiens	24-29
29416034-8	2018	Further experiments revealed that the nicotine-NLRP3-ASC-pyroptosis pathway was activated by reactive oxygen species (ROS), since ROS scavenger (N-acetyl-cysteine, NAC) prevented endothelial cell pyroptosis.	Acetylcysteine	145-162	NLR family pyrin domain containing 3	Homo sapiens	47-52
29416034-8	2018	Further experiments revealed that the nicotine-NLRP3-ASC-pyroptosis pathway was activated by reactive oxygen species (ROS), since ROS scavenger (N-acetyl-cysteine, NAC) prevented endothelial cell pyroptosis.	Acetylcysteine	145-162	PYD and CARD domain containing	Homo sapiens	53-56
28993908-7	2018	To investigate the crosstalk between different signaling pathways, pretreatment of HepG2 with N-acetylcysteine, an ROS scavenger, attenuated 4-methoxy-TEMPO-induced DNA damage, suppressed JNK activation, and diminished autophagy induction.	Acetylcysteine	94-110	mitogen-activated protein kinase 8	Homo sapiens	188-191
28815354-12	2018	Moreover, scavenging ROS by N-acetyl cysteine could inhibit the increasing expression of TGF-beta1 promoted by Nrf2 knockdown.	Acetylcysteine	28-45	NFE2 like bZIP transcription factor 2	Homo sapiens	111-115
29291542-3	2018	Protocatechuic acid, Akt inhibitor, Bay 11-7085 and N-acetylcysteine reduced the lipopolysaccharide-caused production of cytokines and chemokines, expression of cyclooxygenase, increase in the levels and activities of Toll-like receptor-4, p-Akt and mTOR, activation of NF-kappaB, phosphorylation of the JNK and p38-MAPK, and production of reactive oxygen species in keratinocytes.	Acetylcysteine	52-68	AKT serine/threonine kinase 1	Homo sapiens	21-24
28898446-7	2018	In diethylnitrosamine (DEN)-treated primary hepatocytes, NAC and Trolox alleviated DNA damage by activating ataxia-telangiectasia mutated (ATM)/ATM and Rad3-related (ATR) for DNA repair whereas SS-31 and Mito-Q aggravated damage by inactivating them.	Acetylcysteine	57-60	ataxia telangiectasia and Rad3 related	Mus musculus	166-169
28898446-10	2018	Furthermore, blockage of phospho-ATR (p-ATR) led to the recurrence of NAC-ameliorated DEN HCC.	Acetylcysteine	70-73	ataxia telangiectasia and Rad3 related	Mus musculus	33-36
28898446-10	2018	Furthermore, blockage of phospho-ATR (p-ATR) led to the recurrence of NAC-ameliorated DEN HCC.	Acetylcysteine	70-73	ataxia telangiectasia and Rad3 related	Mus musculus	40-43
29258000-8	2018	Moreover, NAC, or SB203580 (a p38 MAPK inhibitor), blocked the OMF-induced nuclear translocation of Nrf2 and HO-1 expression, suggesting that OMF induces HO-1 expression by activating Nrf2 through the p38 MAPK pathway.	Acetylcysteine	10-13	nuclear factor, erythroid derived 2, like 2	Mus musculus	100-104
29258000-8	2018	Moreover, NAC, or SB203580 (a p38 MAPK inhibitor), blocked the OMF-induced nuclear translocation of Nrf2 and HO-1 expression, suggesting that OMF induces HO-1 expression by activating Nrf2 through the p38 MAPK pathway.	Acetylcysteine	10-13	nuclear factor, erythroid derived 2, like 2	Mus musculus	184-188
29291542-3	2018	Protocatechuic acid, Akt inhibitor, Bay 11-7085 and N-acetylcysteine reduced the lipopolysaccharide-caused production of cytokines and chemokines, expression of cyclooxygenase, increase in the levels and activities of Toll-like receptor-4, p-Akt and mTOR, activation of NF-kappaB, phosphorylation of the JNK and p38-MAPK, and production of reactive oxygen species in keratinocytes.	Acetylcysteine	52-68	mitogen-activated protein kinase 8	Homo sapiens	304-307
29291542-3	2018	Protocatechuic acid, Akt inhibitor, Bay 11-7085 and N-acetylcysteine reduced the lipopolysaccharide-caused production of cytokines and chemokines, expression of cyclooxygenase, increase in the levels and activities of Toll-like receptor-4, p-Akt and mTOR, activation of NF-kappaB, phosphorylation of the JNK and p38-MAPK, and production of reactive oxygen species in keratinocytes.	Acetylcysteine	52-68	mitogen-activated protein kinase 14	Homo sapiens	312-320
29291542-3	2018	Protocatechuic acid, Akt inhibitor, Bay 11-7085 and N-acetylcysteine reduced the lipopolysaccharide-caused production of cytokines and chemokines, expression of cyclooxygenase, increase in the levels and activities of Toll-like receptor-4, p-Akt and mTOR, activation of NF-kappaB, phosphorylation of the JNK and p38-MAPK, and production of reactive oxygen species in keratinocytes.	Acetylcysteine	52-68	AKT serine/threonine kinase 1	Homo sapiens	242-245
29291542-3	2018	Protocatechuic acid, Akt inhibitor, Bay 11-7085 and N-acetylcysteine reduced the lipopolysaccharide-caused production of cytokines and chemokines, expression of cyclooxygenase, increase in the levels and activities of Toll-like receptor-4, p-Akt and mTOR, activation of NF-kappaB, phosphorylation of the JNK and p38-MAPK, and production of reactive oxygen species in keratinocytes.	Acetylcysteine	52-68	mechanistic target of rapamycin kinase	Homo sapiens	250-254
29291542-3	2018	Protocatechuic acid, Akt inhibitor, Bay 11-7085 and N-acetylcysteine reduced the lipopolysaccharide-caused production of cytokines and chemokines, expression of cyclooxygenase, increase in the levels and activities of Toll-like receptor-4, p-Akt and mTOR, activation of NF-kappaB, phosphorylation of the JNK and p38-MAPK, and production of reactive oxygen species in keratinocytes.	Acetylcysteine	52-68	nuclear factor kappa B subunit 1	Homo sapiens	270-279
28782153-8	2018	The combined NAC/prednisolone treatment was well tolerated and led to significant ALT, AST and INR improvements within 2 weeks.	Acetylcysteine	13-16	solute carrier family 17 member 5	Homo sapiens	87-90
28600879-10	2018	After N-acetyl cysteine treatment ROS level was partly abolished providing additional enhancement of IL-6 and suppression of IL-8 and VEGF production.	Acetylcysteine	6-23	interleukin 6	Homo sapiens	101-105
28600879-10	2018	After N-acetyl cysteine treatment ROS level was partly abolished providing additional enhancement of IL-6 and suppression of IL-8 and VEGF production.	Acetylcysteine	6-23	C-X-C motif chemokine ligand 8	Homo sapiens	125-129
28600879-10	2018	After N-acetyl cysteine treatment ROS level was partly abolished providing additional enhancement of IL-6 and suppression of IL-8 and VEGF production.	Acetylcysteine	6-23	vascular endothelial growth factor A	Homo sapiens	134-138
28656526-10	2018	N-acetyl-L-cysteine reduced proliferation and IFNgamma in GO, and HA and IL1beta in both GO and control fibroblasts.	Acetylcysteine	0-19	interferon gamma	Homo sapiens	46-54
29207064-11	2018	The ROS scavenger N-acetyl-L-cysteine restored quinalizarin-induced cell apoptosis, and inactivated the MAPK and STAT3 signalling pathways.	Acetylcysteine	18-37	signal transducer and activator of transcription 3	Homo sapiens	113-118
29207099-9	2018	Three weeks after obstruction relief, UUO+iohexol+NAC rats exhibited a lower apoptosis rate, lower Bax mRNA expression, higher expression of Bcl-2 mRNA and higher ratio of Bcl-2/Bax (all P&lt;0.05) compared with day 1 following drug administration.	Acetylcysteine	50-53	BCL2, apoptosis regulator	Rattus norvegicus	141-146
29207099-9	2018	Three weeks after obstruction relief, UUO+iohexol+NAC rats exhibited a lower apoptosis rate, lower Bax mRNA expression, higher expression of Bcl-2 mRNA and higher ratio of Bcl-2/Bax (all P&lt;0.05) compared with day 1 following drug administration.	Acetylcysteine	50-53	BCL2, apoptosis regulator	Rattus norvegicus	172-177
29207099-10	2018	The prophylactic use of NAC reduced the apoptotic rate of renal tubular cells following contrast exposition, which was accompanied by changes in the expression of Bcl-2/Bax mRNA.	Acetylcysteine	24-27	BCL2, apoptosis regulator	Rattus norvegicus	163-168
29364969-8	2018	In addition, N-acetyl cysteine (NAC), a scavenger of O2-, inhibitors of growth factor receptors and of c-Src, all inhibited the overexpression of cell cycle proteins cyclin D1 and cdk4 in VSMC from SHR.	Acetylcysteine	13-30	cyclin D1	Rattus norvegicus	166-175
29389802-9	2018	N-acetyl-L-cysteine, a scavenger of ROS, significantly reversed dioscin-induced cell death and activation of JNK and p38.	Acetylcysteine	0-19	mitogen-activated protein kinase 8	Homo sapiens	109-112
29389802-9	2018	N-acetyl-L-cysteine, a scavenger of ROS, significantly reversed dioscin-induced cell death and activation of JNK and p38.	Acetylcysteine	0-19	mitogen-activated protein kinase 14	Homo sapiens	117-120
29364969-8	2018	In addition, N-acetyl cysteine (NAC), a scavenger of O2-, inhibitors of growth factor receptors and of c-Src, all inhibited the overexpression of cell cycle proteins cyclin D1 and cdk4 in VSMC from SHR.	Acetylcysteine	13-30	cyclin-dependent kinase 4	Rattus norvegicus	180-184
29364969-8	2018	In addition, N-acetyl cysteine (NAC), a scavenger of O2-, inhibitors of growth factor receptors and of c-Src, all inhibited the overexpression of cell cycle proteins cyclin D1 and cdk4 in VSMC from SHR.	Acetylcysteine	32-35	cyclin D1	Rattus norvegicus	166-175
29364969-8	2018	In addition, N-acetyl cysteine (NAC), a scavenger of O2-, inhibitors of growth factor receptors and of c-Src, all inhibited the overexpression of cell cycle proteins cyclin D1 and cdk4 in VSMC from SHR.	Acetylcysteine	32-35	cyclin-dependent kinase 4	Rattus norvegicus	180-184
29375377-7	2017	We also showed that cisplatin and pemetrexed induce the phosphorylation of AXL and Akt, which was also blocked by BGB324 as well as by N-acetylcysteine antioxidant.	Acetylcysteine	135-151	AKT serine/threonine kinase 1	Homo sapiens	83-86
29113965-9	2018	Furthermore, treatment of atherosclerotic-MSCs with the reactive oxygen species scavenger N-acetyl-l-cysteine reduced the levels of interleukin-6, interleukin-8/C-X-C motif chemokine ligand 8, and monocyte chemoattractant protein-1/chemokine ligand 2 in the MSC secretome and improved MSCs immunosuppressive capacity (P=0.03).	Acetylcysteine	90-109	interleukin 6	Homo sapiens	132-145
29113965-9	2018	Furthermore, treatment of atherosclerotic-MSCs with the reactive oxygen species scavenger N-acetyl-l-cysteine reduced the levels of interleukin-6, interleukin-8/C-X-C motif chemokine ligand 8, and monocyte chemoattractant protein-1/chemokine ligand 2 in the MSC secretome and improved MSCs immunosuppressive capacity (P=0.03).	Acetylcysteine	90-109	C-X-C motif chemokine ligand 8	Homo sapiens	147-160
29113965-9	2018	Furthermore, treatment of atherosclerotic-MSCs with the reactive oxygen species scavenger N-acetyl-l-cysteine reduced the levels of interleukin-6, interleukin-8/C-X-C motif chemokine ligand 8, and monocyte chemoattractant protein-1/chemokine ligand 2 in the MSC secretome and improved MSCs immunosuppressive capacity (P=0.03).	Acetylcysteine	90-109	C-X-C motif chemokine ligand 8	Homo sapiens	161-191
29278702-8	2018	Finally, the role of the ROS-TXNIP axis in mediating the activation of the NLRP3 inflammasome and cell death was characterized by pretreating with the ROS scavenger N-acetylcysteine (NAC) and performing TXNIP knockdown experiments in MIN6.	Acetylcysteine	165-181	thioredoxin interacting protein	Mus musculus	29-34
29278702-8	2018	Finally, the role of the ROS-TXNIP axis in mediating the activation of the NLRP3 inflammasome and cell death was characterized by pretreating with the ROS scavenger N-acetylcysteine (NAC) and performing TXNIP knockdown experiments in MIN6.	Acetylcysteine	183-186	thioredoxin interacting protein	Mus musculus	29-34
29278702-8	2018	Finally, the role of the ROS-TXNIP axis in mediating the activation of the NLRP3 inflammasome and cell death was characterized by pretreating with the ROS scavenger N-acetylcysteine (NAC) and performing TXNIP knockdown experiments in MIN6.	Acetylcysteine	183-186	thioredoxin interacting protein	Mus musculus	203-208
29139022-14	2018	ROS uptake was observed in PAL-treated cells, and the antitumor effect was inhibited by NAC.	Acetylcysteine	88-91	Shc SH2-domain binding protein 1	Mus musculus	27-30
29315209-8	2018	Pin-activated ERK/JNK were significantly reduced after the administration of NAC; however, the inhibition of ERK/JNK failed to change the Pin-induced ROS production.	Acetylcysteine	77-80	Eph receptor B1	Rattus norvegicus	14-17
30384368-10	2018	However, platelet activation and autophagy were aggravated by the Rapamycin treatment, and decreased following treatment with NAC, 3-MA, or NAC and 3-MA, together with increased activity of the PI3K/AKT/mTOR pathway.	Acetylcysteine	140-143	AKT serine/threonine kinase 1	Homo sapiens	199-202
29359681-8	2018	In vitro, antioxidant N-acetyl-l-cysteine significantly prevented the active effects of high Na or oxidant Rosup on NLRP3 inflammasome, so did K. Our study indicates that oxidative stress modulation of NLRP3 inflammasome may be involved in the impacts of Na and K on insulin resistance.	Acetylcysteine	22-41	NLR family pyrin domain containing 3	Homo sapiens	116-121
29359681-8	2018	In vitro, antioxidant N-acetyl-l-cysteine significantly prevented the active effects of high Na or oxidant Rosup on NLRP3 inflammasome, so did K. Our study indicates that oxidative stress modulation of NLRP3 inflammasome may be involved in the impacts of Na and K on insulin resistance.	Acetylcysteine	22-41	NLR family pyrin domain containing 3	Homo sapiens	202-207
29359681-8	2018	In vitro, antioxidant N-acetyl-l-cysteine significantly prevented the active effects of high Na or oxidant Rosup on NLRP3 inflammasome, so did K. Our study indicates that oxidative stress modulation of NLRP3 inflammasome may be involved in the impacts of Na and K on insulin resistance.	Acetylcysteine	22-41	insulin	Homo sapiens	267-274
30071509-14	2018	The expression of autophagy related-protein and inflammatory cytokines iNOS, IL-12, and TNF-alpha were inhibited by the ROS inhibitor N-acetyl cysteine.	Acetylcysteine	134-151	tumor necrosis factor	Mus musculus	88-97
30384368-10	2018	However, platelet activation and autophagy were aggravated by the Rapamycin treatment, and decreased following treatment with NAC, 3-MA, or NAC and 3-MA, together with increased activity of the PI3K/AKT/mTOR pathway.	Acetylcysteine	140-143	mechanistic target of rapamycin kinase	Homo sapiens	203-207
30504711-10	2018	ROS-AKT-mTOR pathway was associated with Cr(VI)-induced autophagy, and ROS scavenger N-acetylcysteine (NAC) pretreatment inhibited Cr(VI)-induced autophagy by alleviating the inhibition of the AKT-mTOR pathway.	Acetylcysteine	85-101	AKT serine/threonine kinase 1	Homo sapiens	193-196
30504711-10	2018	ROS-AKT-mTOR pathway was associated with Cr(VI)-induced autophagy, and ROS scavenger N-acetylcysteine (NAC) pretreatment inhibited Cr(VI)-induced autophagy by alleviating the inhibition of the AKT-mTOR pathway.	Acetylcysteine	85-101	mechanistic target of rapamycin kinase	Homo sapiens	197-201
30504711-10	2018	ROS-AKT-mTOR pathway was associated with Cr(VI)-induced autophagy, and ROS scavenger N-acetylcysteine (NAC) pretreatment inhibited Cr(VI)-induced autophagy by alleviating the inhibition of the AKT-mTOR pathway.	Acetylcysteine	103-106	AKT serine/threonine kinase 1	Homo sapiens	193-196
30504711-10	2018	ROS-AKT-mTOR pathway was associated with Cr(VI)-induced autophagy, and ROS scavenger N-acetylcysteine (NAC) pretreatment inhibited Cr(VI)-induced autophagy by alleviating the inhibition of the AKT-mTOR pathway.	Acetylcysteine	103-106	mechanistic target of rapamycin kinase	Homo sapiens	197-201
29462817-13	2018	The potentiation of biofilm formation is due mainly to interaction between NAC and transferrin.	Acetylcysteine	75-78	transferrin	Homo sapiens	83-94
28992480-5	2018	However, ROS inhibitor N-acetyl-l-cysteine (NAC) reduced IL-1beta and IL-18 release to 45 pg mL-1 and 108 pg mL-1.	Acetylcysteine	23-42	interleukin 1 beta	Mus musculus	57-65
29462817-0	2018	The Interaction of N-Acetylcysteine and Serum Transferrin Promotes Bacterial Biofilm Formation.	Acetylcysteine	19-35	transferrin	Homo sapiens	46-57
29550818-11	2018	In TCMK-1 cells, Klotho and NAC attenuated the elevation in RIP1, RIP3, and LDH release induced by H/R or H2O2.	Acetylcysteine	28-31	receptor (TNFRSF)-interacting serine-threonine kinase 1	Mus musculus	60-64
28992480-5	2018	However, ROS inhibitor N-acetyl-l-cysteine (NAC) reduced IL-1beta and IL-18 release to 45 pg mL-1 and 108 pg mL-1.	Acetylcysteine	44-47	interleukin 1 beta	Mus musculus	57-65
29223039-0	2018	N-acetyl-l-cysteine ameliorates the PM2.5-induced oxidative stress by regulating SIRT-1 in rats.	Acetylcysteine	0-19	sirtuin 1	Rattus norvegicus	81-87
29079704-13	2018	Finally, administration of the antioxidant N-acetyl-l-cysteine to Ucp2-/- pregnant mice alleviated the effect of knocking out UCP2 on pancreas development.	Acetylcysteine	43-62	uncoupling protein 2 (mitochondrial, proton carrier)	Mus musculus	66-70
29079704-13	2018	Finally, administration of the antioxidant N-acetyl-l-cysteine to Ucp2-/- pregnant mice alleviated the effect of knocking out UCP2 on pancreas development.	Acetylcysteine	43-62	uncoupling protein 2 (mitochondrial, proton carrier)	Mus musculus	126-130
29223039-8	2018	NAC can activate SIRT1 and exert an anti-oxidative role in PM2.5-induced oxidative injury.	Acetylcysteine	0-3	sirtuin 1	Rattus norvegicus	17-22
29043702-11	2018	The c-kit expression in unfertilized mature oocytes were significantly lower in the NAC group compared to the other groups (P&lt;0.001).	Acetylcysteine	84-87	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	4-9
29155359-4	2018	Reactive oxygen species (ROS) tended to increase when Het-1A cells were treated with MTBITC, and the increases in ROS and Nrf2 expression in the cells treated with MTBITC were completely abolished by treatment with N-acetyl-l-cysteine.	Acetylcysteine	215-234	NFE2 like bZIP transcription factor 2	Homo sapiens	122-126
29339659-9	2018	RESULTS: The second airway challenge increased CK2alpha phosphorylation and protein expression in airway epithelial cells as well as nuclear translocation of the p50 and p65 subunits of NF-kappaB, all of which were inhibited by the CK2alpha inhibitor 4,5,6,7-tetrabromobenzotriazole and the antioxidant N-acetyl-L-cysteine.	Acetylcysteine	303-322	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	186-195
29043702-0	2018	N-Acetylcysteine Compared to Metformin, Improves The Expression Profile of Growth Differentiation Factor-9 and Receptor Tyrosine Kinase c-Kit in The Oocytes of Patients with Polycystic Ovarian Syndrome.	Acetylcysteine	0-16	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	136-141
29043702-2	2018	The aim of this study was to investigate the effects of metformin (MET), N-acetylcysteine (NAC) and their combination on the hormonal levels and expression profile of GDF-9, BMP-15 and c-kit, as hallmarks of oocyte quality, in PCOS patients.	Acetylcysteine	73-89	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	185-190
29043702-2	2018	The aim of this study was to investigate the effects of metformin (MET), N-acetylcysteine (NAC) and their combination on the hormonal levels and expression profile of GDF-9, BMP-15 and c-kit, as hallmarks of oocyte quality, in PCOS patients.	Acetylcysteine	91-94	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	185-190
29043702-3	2018	MATERIALS AND METHODS: This prospective randomized, double-blind, placebo controlled trial aims to study the effects of MET, NAC and their combination (MET+NAC) on expression of GDF-9, BMP-15 and c-kit mRNA in oocytes [10 at the germinal vesicle (GV) stage, 10 at the MI stage, and 10 at the MII stage from per group] derived following ovulation induction in PCOS.	Acetylcysteine	125-128	bone morphogenetic protein 15	Homo sapiens	185-191
29043702-3	2018	MATERIALS AND METHODS: This prospective randomized, double-blind, placebo controlled trial aims to study the effects of MET, NAC and their combination (MET+NAC) on expression of GDF-9, BMP-15 and c-kit mRNA in oocytes [10 at the germinal vesicle (GV) stage, 10 at the MI stage, and 10 at the MII stage from per group] derived following ovulation induction in PCOS.	Acetylcysteine	156-159	bone morphogenetic protein 15	Homo sapiens	185-191
29043702-7	2018	RESULTS: The follicular fluid (FF) level of c-kit protein significantly decreased in the NAC group compared to the other groups.	Acetylcysteine	89-92	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	44-49
28681938-6	2018	Moreover, pretreatment of the cells with antioxidant N-acetyl cysteine (NAC) inhibited omega-HUA-induced increased reactive oxygen species (ROS) levels, cleaved caspase-3 and cleaved PARP, and phosphorylated JNK, phosphorylated p38, and increased cell viability and colony-forming ability.	Acetylcysteine	53-70	poly(ADP-ribose) polymerase 1	Homo sapiens	183-187
28681938-6	2018	Moreover, pretreatment of the cells with antioxidant N-acetyl cysteine (NAC) inhibited omega-HUA-induced increased reactive oxygen species (ROS) levels, cleaved caspase-3 and cleaved PARP, and phosphorylated JNK, phosphorylated p38, and increased cell viability and colony-forming ability.	Acetylcysteine	53-70	mitogen-activated protein kinase 8	Homo sapiens	208-211
28681938-6	2018	Moreover, pretreatment of the cells with antioxidant N-acetyl cysteine (NAC) inhibited omega-HUA-induced increased reactive oxygen species (ROS) levels, cleaved caspase-3 and cleaved PARP, and phosphorylated JNK, phosphorylated p38, and increased cell viability and colony-forming ability.	Acetylcysteine	53-70	mitogen-activated protein kinase 14	Homo sapiens	228-231
28681938-6	2018	Moreover, pretreatment of the cells with antioxidant N-acetyl cysteine (NAC) inhibited omega-HUA-induced increased reactive oxygen species (ROS) levels, cleaved caspase-3 and cleaved PARP, and phosphorylated JNK, phosphorylated p38, and increased cell viability and colony-forming ability.	Acetylcysteine	72-75	poly(ADP-ribose) polymerase 1	Homo sapiens	183-187
28681938-6	2018	Moreover, pretreatment of the cells with antioxidant N-acetyl cysteine (NAC) inhibited omega-HUA-induced increased reactive oxygen species (ROS) levels, cleaved caspase-3 and cleaved PARP, and phosphorylated JNK, phosphorylated p38, and increased cell viability and colony-forming ability.	Acetylcysteine	72-75	mitogen-activated protein kinase 8	Homo sapiens	208-211
28681938-6	2018	Moreover, pretreatment of the cells with antioxidant N-acetyl cysteine (NAC) inhibited omega-HUA-induced increased reactive oxygen species (ROS) levels, cleaved caspase-3 and cleaved PARP, and phosphorylated JNK, phosphorylated p38, and increased cell viability and colony-forming ability.	Acetylcysteine	72-75	mitogen-activated protein kinase 14	Homo sapiens	228-231
29115506-6	2018	The results of the present study ndicated that Ang II upregulated MCP-1 expression in osteoblasts, which was mitigated by agonists of the AT1R, including olmesartan, a ROS scavenger N-acetylcysteine (NAC), ammonium pyrrolidinethiocarbamate (PDTC) and nuclear factor (NF)-kappaB, but not by the Ang II type 2 receptor antagonist, PD123319.	Acetylcysteine	182-198	angiotensinogen	Homo sapiens	47-53
28322443-7	2018	Notably, we showed that TXNIP-mediated HSC activation was suppressed by antioxidant N-acetylcysteine.	Acetylcysteine	84-100	thioredoxin interacting protein	Homo sapiens	24-29
28834244-7	2018	IGF-1, which possessed only moderate cell protective and no chondroprotective qualities after cartilage trauma, even reduced NAC-mediated cell and chondroprotection.	Acetylcysteine	125-128	insulin like growth factor 1	Homo sapiens	0-5
30191979-5	2018	This interaction was accompanied by increased expression of the mitochondrial master regulator, proliferator-activated receptor gamma coactivator alpha, and a cytoprotective effect of the agent N-acetylcysteine suppressing ROS production, transforming growth factor-beta1, and tissue inhibitor of metalloproteinase-1.	Acetylcysteine	194-210	transforming growth factor beta 1	Homo sapiens	239-271
29479036-8	2018	An antioxidant N-acetylcysteine pretreatment diminished the apoptosis-inducing effect of NaAsO2 and TNF-alpha combination and also inhibited MAPK signaling.	Acetylcysteine	15-31	tumor necrosis factor	Homo sapiens	100-109
29479036-8	2018	An antioxidant N-acetylcysteine pretreatment diminished the apoptosis-inducing effect of NaAsO2 and TNF-alpha combination and also inhibited MAPK signaling.	Acetylcysteine	15-31	mitogen-activated protein kinase 1	Homo sapiens	141-145
29115506-6	2018	The results of the present study ndicated that Ang II upregulated MCP-1 expression in osteoblasts, which was mitigated by agonists of the AT1R, including olmesartan, a ROS scavenger N-acetylcysteine (NAC), ammonium pyrrolidinethiocarbamate (PDTC) and nuclear factor (NF)-kappaB, but not by the Ang II type 2 receptor antagonist, PD123319.	Acetylcysteine	200-203	angiotensinogen	Homo sapiens	47-53
29115506-8	2018	These effects of Ang II were blocked by olmesartan, NAC and PDTC, but not by PD1123319 in osteoblasts.	Acetylcysteine	52-55	angiotensinogen	Homo sapiens	17-23
29535810-7	2018	Antioxidants such as N-acetyl-L-cysteine and glutathione reversed the apoptosis-inducing effects of TRAIL.	Acetylcysteine	21-40	TNF superfamily member 10	Homo sapiens	100-105
29085973-3	2018	The toxicity of z-FA-CMK in Jurkat T cells was completely abrogated by N-acetylcysteine (NAC), suggesting that the toxicity mediated by z-FA-CMK is due to oxidative stress.	Acetylcysteine	71-87	C-X-C motif chemokine ligand 9	Homo sapiens	21-24
29085973-3	2018	The toxicity of z-FA-CMK in Jurkat T cells was completely abrogated by N-acetylcysteine (NAC), suggesting that the toxicity mediated by z-FA-CMK is due to oxidative stress.	Acetylcysteine	71-87	C-X-C motif chemokine ligand 9	Homo sapiens	141-144
29085973-3	2018	The toxicity of z-FA-CMK in Jurkat T cells was completely abrogated by N-acetylcysteine (NAC), suggesting that the toxicity mediated by z-FA-CMK is due to oxidative stress.	Acetylcysteine	89-92	C-X-C motif chemokine ligand 9	Homo sapiens	21-24
29085973-3	2018	The toxicity of z-FA-CMK in Jurkat T cells was completely abrogated by N-acetylcysteine (NAC), suggesting that the toxicity mediated by z-FA-CMK is due to oxidative stress.	Acetylcysteine	89-92	C-X-C motif chemokine ligand 9	Homo sapiens	141-144
29085973-5	2018	However, NAC was still able to block z-FA-CMK toxicity in Jurkat T cells in the presence of BSO, indicating that the protective effect of NAC does not involve GSH biosynthesis.	Acetylcysteine	9-12	C-X-C motif chemokine ligand 9	Homo sapiens	42-45
29116368-10	2018	Decreased IL-10 in the LPS, MA and LPS + MA animals, and increased TNF-alpha in the LPS and MA animals, was reversed with NAC.	Acetylcysteine	122-125	tumor necrosis factor	Rattus norvegicus	67-76
28823537-13	2018	Moreover, ROS generation occurred upon treatment of SH-SY5Y cells with HPO-DAEE, and the antioxidants N-acetylcysteine and glutathione suppressed HPO-DAEE-induced activation of the Nrf2-ARE and eIF2alpha-ATF4 pathways.	Acetylcysteine	102-118	NFE2 like bZIP transcription factor 2	Homo sapiens	181-185
29267310-16	2017	Impaired Akt phosphorylation partially normalized after antioxidant N-acetyl-L-cysteine treatment.	Acetylcysteine	68-87	AKT serine/threonine kinase 1	Rattus norvegicus	9-12
29375391-13	2017	Phenotypic changes induced by thrombin were prevented by NAC pretreatment.	Acetylcysteine	57-60	coagulation factor II, thrombin	Homo sapiens	30-38
29435131-5	2018	The expression of HIF-1alpha and YAP1 was concomitantly decreased by PD-L1 silencing or by ROS scavenger treatment (N-acetylcysteine, NAC); however, a ROS inducer treatment (pyocyanin) completely reversed the decreased expression of both genes in EGFR-mutated and -wild-type (WT) NSCLC cells.	Acetylcysteine	116-132	hypoxia inducible factor 1 subunit alpha	Homo sapiens	18-28
29399204-6	2017	VWF was detected in clots at low and high shear, but when N-acetylcysteine was added to the whole blood, both platelet and VWF deposition were markedly decreased at either low or high flow.	Acetylcysteine	58-74	von Willebrand factor	Homo sapiens	123-126
29106990-10	2017	N-Acetylcysteine, a ROS scavenger, protected the cells from LED light-induced cellular damage, with rescued cell viability and restored mRNA expression of IGF-1 and TNF-alpha.	Acetylcysteine	0-16	tumor necrosis factor	Mus musculus	165-174
28271166-8	2017	The adverse effects of LPS on porcine intestinal function and redox status were mitigated by NAC supplementation through the activation of multiple signaling pathways involving PI3K/Akt/mTOR, EGFR, TLR4/NF-kappaB, AMPK, and type I IFN.	Acetylcysteine	93-96	AKT serine/threonine kinase 1	Homo sapiens	182-185
28271166-8	2017	The adverse effects of LPS on porcine intestinal function and redox status were mitigated by NAC supplementation through the activation of multiple signaling pathways involving PI3K/Akt/mTOR, EGFR, TLR4/NF-kappaB, AMPK, and type I IFN.	Acetylcysteine	93-96	mechanistic target of rapamycin kinase	Homo sapiens	186-190
28271166-8	2017	The adverse effects of LPS on porcine intestinal function and redox status were mitigated by NAC supplementation through the activation of multiple signaling pathways involving PI3K/Akt/mTOR, EGFR, TLR4/NF-kappaB, AMPK, and type I IFN.	Acetylcysteine	93-96	epidermal growth factor receptor	Homo sapiens	192-196
28271166-8	2017	The adverse effects of LPS on porcine intestinal function and redox status were mitigated by NAC supplementation through the activation of multiple signaling pathways involving PI3K/Akt/mTOR, EGFR, TLR4/NF-kappaB, AMPK, and type I IFN.	Acetylcysteine	93-96	nuclear factor kappa B subunit 1	Homo sapiens	203-212
28966297-7	2017	In addition, NAC (N-acetylcysteine, a reactive oxygen species (ROS) scavenger) treatment dramatically decreased ROS generation in H1299 cells; both of NAC and 4-PBA (4-phenylbutyrate, a specific endoplasmic reticulum (ER) stress inhibitor) administration impaired apoptosis and expression levels of ATF4, CHOP and caspase-4 in G-Rh2 incubated H1299 cells.	Acetylcysteine	18-34	DNA damage inducible transcript 3	Homo sapiens	305-309
28966297-7	2017	In addition, NAC (N-acetylcysteine, a reactive oxygen species (ROS) scavenger) treatment dramatically decreased ROS generation in H1299 cells; both of NAC and 4-PBA (4-phenylbutyrate, a specific endoplasmic reticulum (ER) stress inhibitor) administration impaired apoptosis and expression levels of ATF4, CHOP and caspase-4 in G-Rh2 incubated H1299 cells.	Acetylcysteine	18-34	caspase 4	Homo sapiens	314-323
28880428-7	2017	Pretreatment with N-Acetyl L-Cysteine, a ROS scavenger, could fully reverse SZC017-induced ROS and increase the expression of Akt, p-STAT3, and procaspase-3, while decrease the ratio of LC3-II/I and the expression of Beclin-1.	Acetylcysteine	18-37	AKT serine/threonine kinase 1	Homo sapiens	126-129
28880428-7	2017	Pretreatment with N-Acetyl L-Cysteine, a ROS scavenger, could fully reverse SZC017-induced ROS and increase the expression of Akt, p-STAT3, and procaspase-3, while decrease the ratio of LC3-II/I and the expression of Beclin-1.	Acetylcysteine	18-37	signal transducer and activator of transcription 3	Homo sapiens	133-138
28880428-7	2017	Pretreatment with N-Acetyl L-Cysteine, a ROS scavenger, could fully reverse SZC017-induced ROS and increase the expression of Akt, p-STAT3, and procaspase-3, while decrease the ratio of LC3-II/I and the expression of Beclin-1.	Acetylcysteine	18-37	caspase 3	Homo sapiens	144-156
28804952-7	2017	Furthermore, propofol induced oxygen stresses by increasing O2- and H2 O2 levels but treatment with the antioxidant N-acetylcysteine (NAC) partially reversed propofol-regulated antioxidative enzyme levels (superoxide dismutase, catalase, and glutathione peroxidase).	Acetylcysteine	116-132	catalase	Homo sapiens	228-236
28804952-7	2017	Furthermore, propofol induced oxygen stresses by increasing O2- and H2 O2 levels but treatment with the antioxidant N-acetylcysteine (NAC) partially reversed propofol-regulated antioxidative enzyme levels (superoxide dismutase, catalase, and glutathione peroxidase).	Acetylcysteine	134-137	catalase	Homo sapiens	228-236
28804952-8	2017	Most significantly, propofol induced apoptotic effects by decreasing Bcl-2 but increasing Bax, cleaved caspase-9/caspase-3 levels, which were partially reversed by NAC.	Acetylcysteine	164-167	BCL2 associated X, apoptosis regulator	Homo sapiens	90-93
28804952-8	2017	Most significantly, propofol induced apoptotic effects by decreasing Bcl-2 but increasing Bax, cleaved caspase-9/caspase-3 levels, which were partially reversed by NAC.	Acetylcysteine	164-167	caspase 3	Homo sapiens	113-122
28983599-8	2017	Butylated hydroxyanisole and N-acetyl-cysteine, known reactive oxygen species (ROS) scavengers, significantly suppressed the potentiated cytotoxicity induced by baicalin and TRAIL co-treatment.	Acetylcysteine	29-46	TNF superfamily member 10	Homo sapiens	174-179
29039537-9	2017	Pretreatment with N-acetyl cysteine, a ROS scavenger, significantly reduced the cytotoxicity of juglone in combination with TRAIL, which further supported that ROS was involved in the juglone-induced sensitization of TRAIL.	Acetylcysteine	18-35	TNF superfamily member 10	Homo sapiens	124-129
28902442-0	2017	Spectroscopic investigations on the conformational changes of lysozyme effected by different sizes of N-acetyl-l-cysteine-capped CdTe quantum dots.	Acetylcysteine	102-121	lysozyme	Homo sapiens	62-70
28902442-1	2017	The effect of N-acetyl-l-cysteine-capped CdTe quantum dots (NAC-CdTe QDs) with different sizes on lysozyme was investigated by isothermal titration calorimetry (ITC), enzyme activity assays, and multi-spectroscopic methods.	Acetylcysteine	14-33	lysozyme	Homo sapiens	98-106
28905500-11	2017	Furthermore, the pharmacological effect of Sal associated with the ROS-mediated PI3K/Akt/mTOR pathway was proved by the use of ROS scavenger, N-acetyl-l-cysteine, in LPS-stimulated H9C2 cells.	Acetylcysteine	142-161	AKT serine/threonine kinase 1	Rattus norvegicus	85-88
29039537-9	2017	Pretreatment with N-acetyl cysteine, a ROS scavenger, significantly reduced the cytotoxicity of juglone in combination with TRAIL, which further supported that ROS was involved in the juglone-induced sensitization of TRAIL.	Acetylcysteine	18-35	TNF superfamily member 10	Homo sapiens	217-222
29122013-0	2017	Suppression of methylmercury-induced MIP-2 expression by N-acetyl-L-cysteine in murine RAW264.7 macrophage cell line.	Acetylcysteine	57-76	chemokine (C-X-C motif) ligand 2	Mus musculus	37-42
29019035-5	2017	Furthermore, the mRNA levels of TNF-alpha, IL-1beta, and IL-6 were elevated in astrocytes and cortical neurons treated with Con A. Intracellular reactive oxygen species (ROS) levels were increased in Con A-treated cortical neurons, and N-acetyl-cysteine (NAC, an antioxidant) and diphenyleneiodonium (DPI, a NADPH oxidase inhibitor) reduced intracellular ROS accumulation.	Acetylcysteine	236-253	tumor necrosis factor	Rattus norvegicus	32-41
29019035-5	2017	Furthermore, the mRNA levels of TNF-alpha, IL-1beta, and IL-6 were elevated in astrocytes and cortical neurons treated with Con A. Intracellular reactive oxygen species (ROS) levels were increased in Con A-treated cortical neurons, and N-acetyl-cysteine (NAC, an antioxidant) and diphenyleneiodonium (DPI, a NADPH oxidase inhibitor) reduced intracellular ROS accumulation.	Acetylcysteine	236-253	interleukin 6	Rattus norvegicus	57-61
29019035-5	2017	Furthermore, the mRNA levels of TNF-alpha, IL-1beta, and IL-6 were elevated in astrocytes and cortical neurons treated with Con A. Intracellular reactive oxygen species (ROS) levels were increased in Con A-treated cortical neurons, and N-acetyl-cysteine (NAC, an antioxidant) and diphenyleneiodonium (DPI, a NADPH oxidase inhibitor) reduced intracellular ROS accumulation.	Acetylcysteine	255-258	tumor necrosis factor	Rattus norvegicus	32-41
29019035-5	2017	Furthermore, the mRNA levels of TNF-alpha, IL-1beta, and IL-6 were elevated in astrocytes and cortical neurons treated with Con A. Intracellular reactive oxygen species (ROS) levels were increased in Con A-treated cortical neurons, and N-acetyl-cysteine (NAC, an antioxidant) and diphenyleneiodonium (DPI, a NADPH oxidase inhibitor) reduced intracellular ROS accumulation.	Acetylcysteine	255-258	interleukin 6	Rattus norvegicus	57-61
27937011-12	2017	DISCUSSION AND CONCLUSION: Pirfenidone, prednisone and acetylcysteine can inhibit airsacculitis and pulmonary fibrosis in rat IPF models, which may be related with enhanced caveolin-1, reduced TNF-alpha, TGF-beta1, PDGF.	Acetylcysteine	55-69	caveolin 1	Rattus norvegicus	173-183
27937011-12	2017	DISCUSSION AND CONCLUSION: Pirfenidone, prednisone and acetylcysteine can inhibit airsacculitis and pulmonary fibrosis in rat IPF models, which may be related with enhanced caveolin-1, reduced TNF-alpha, TGF-beta1, PDGF.	Acetylcysteine	55-69	tumor necrosis factor	Rattus norvegicus	193-202
27937011-12	2017	DISCUSSION AND CONCLUSION: Pirfenidone, prednisone and acetylcysteine can inhibit airsacculitis and pulmonary fibrosis in rat IPF models, which may be related with enhanced caveolin-1, reduced TNF-alpha, TGF-beta1, PDGF.	Acetylcysteine	55-69	transforming growth factor, beta 1	Rattus norvegicus	204-213
29123322-4	2017	Treatment of cells with NAC also attenuated hypoxia-mediated activation of EGFR, but did not have any effect on hypoxia-mediated induction of HIF1alpha.	Acetylcysteine	24-27	epidermal growth factor receptor	Homo sapiens	75-79
29039574-6	2017	NAC, the NOX4 inhibitor diphenylene iodonium or small interfering RNA (siRNA) to NOX4, and the NOX2 inhibitor apocynin all suppressed TGF-beta1-induced chemokinesis of Panc1 and Colo357 cells as did various inhibitors of RAC1 used as control.	Acetylcysteine	0-3	transforming growth factor beta 1	Homo sapiens	134-143
28739487-9	2017	Notably, treatment with the ROS scavenger N-acetylcysteine (NAC) markedly blocked 27HC-induced ROS production and activation of IL-6/STAT3 signaling pathway.	Acetylcysteine	42-58	interleukin 6	Rattus norvegicus	128-132
28739487-9	2017	Notably, treatment with the ROS scavenger N-acetylcysteine (NAC) markedly blocked 27HC-induced ROS production and activation of IL-6/STAT3 signaling pathway.	Acetylcysteine	60-63	interleukin 6	Rattus norvegicus	128-132
28986255-7	2017	Analysis of mTORC2, the complex responsible for phosphorylating Akt at S473, reveals increased cysteine oxidation of Rictor in Prdx3 KD cells that can be rescued with NAC.	Acetylcysteine	167-170	AKT serine/threonine kinase 1	Homo sapiens	64-67
29070760-9	2017	However, N-acetyl cysteine, a general ROS scavenger, completely reversed the EECU-induced dephosphorylation of PI3K and Akt, as well as cell apoptosis.	Acetylcysteine	9-26	AKT serine/threonine kinase 1	Homo sapiens	120-123
29122013-10	2017	Effect of MeHg on MIP-2 expressions was suppressed by pre-, co-, and post-treatment with NAC.	Acetylcysteine	89-92	chemokine (C-X-C motif) ligand 2	Mus musculus	18-23
28901511-5	2017	The activation of caspase-9 and -3, and cleavage of procaspase-9 and -3, but not of caspase-8, were involved in NAC-induced apoptosis.	Acetylcysteine	112-115	caspase 9	Rattus norvegicus	18-34
28901421-6	2017	The antioxidant, N-acetylcysteine, eliminated the uric acid-induced expression of TNF-alpha.	Acetylcysteine	17-33	tumor necrosis factor	Rattus norvegicus	82-91
28963372-9	2017	However, all these effects in Ftmt knockout mice were markedly mitigated by pharmacological inhibition of oxidative stress using an antioxidant, N-acetylcysteine.	Acetylcysteine	145-161	ferritin mitochondrial	Mus musculus	30-34
28418588-8	2017	We also found that a decrease in cellular ROS level by ROS scavenger, N-acetylcysteine (NAC), resulting in the abolishment of QDs-induced AKT de-phosphorylation and cellular apoptosis.	Acetylcysteine	70-86	AKT serine/threonine kinase 1	Homo sapiens	138-141
28418588-8	2017	We also found that a decrease in cellular ROS level by ROS scavenger, N-acetylcysteine (NAC), resulting in the abolishment of QDs-induced AKT de-phosphorylation and cellular apoptosis.	Acetylcysteine	88-91	AKT serine/threonine kinase 1	Homo sapiens	138-141
28901448-7	2017	Pretreatment of cells with an antioxidant, N-acetyl cysteine (NAC), prior to plasma exposure suppressed the formation of 8-oxoG and restored the expression levels of OGG1 and Nrf2.	Acetylcysteine	43-60	NFE2 like bZIP transcription factor 2	Homo sapiens	175-179
28901448-7	2017	Pretreatment of cells with an antioxidant, N-acetyl cysteine (NAC), prior to plasma exposure suppressed the formation of 8-oxoG and restored the expression levels of OGG1 and Nrf2.	Acetylcysteine	62-65	NFE2 like bZIP transcription factor 2	Homo sapiens	175-179
28691995-10	2017	In vitro, Ang II significantly increased autophagy flux in cultured cardiomyocytes, which could be partly inhibited by N-acetylcysteine.	Acetylcysteine	119-135	angiotensinogen (serpin peptidase inhibitor, clade A, member 8)	Mus musculus	10-16
29045497-13	2017	Moreover, our results suggest that CEF and NAC may induce brain tolerance to ischemia by influencing GLT-1 and system xc- expression levels.	Acetylcysteine	43-46	solute carrier family 1 member 2	Rattus norvegicus	101-106
28887131-9	2017	The mechanisms behind the benefit of PGI2 mimetics in reducing LPS/GalN-induced liver injury involved, in part, their suppressive effects on increased generation of reactive oxygen species (ROS), since their ability to prevent LPS/GalN-induced hepatic apoptosis was mimicked by the antioxidant N-acetyl-l-cysteine.	Acetylcysteine	294-313	toll-like receptor 4	Mus musculus	63-66
28335665-8	2017	Inhibition of ROS by N-acetyl-l-cysteine (NAC) attenuated the activation of Akt, ASK1, p38 MAPK, and down-regulation of ZO-1 and occludin.	Acetylcysteine	21-40	tight junction protein 1	Canis lupus familiaris	120-137
28335665-8	2017	Inhibition of ROS by N-acetyl-l-cysteine (NAC) attenuated the activation of Akt, ASK1, p38 MAPK, and down-regulation of ZO-1 and occludin.	Acetylcysteine	42-45	tight junction protein 1	Canis lupus familiaris	120-137
29089038-4	2017	Patients in the treatment group (NacA, n = 60) received intravenously N-acetylcysteine (1200 mg) and ascorbic acid (2 g) dissolved separately in 100 ml of normal saline 2 hours before, and at 10 hours and 18 hours following the infusion of contrast agent, while control group patients (CG, n = 64) received only normal saline.	Acetylcysteine	70-86	nascent polypeptide associated complex subunit alpha	Homo sapiens	33-37
29049376-5	2017	We use real-time polymerase chain reaction and Western blot analysis to evaluate whether NAC and DPI impair the ability of TGFbeta1 to induce expression of fibrogenic genes in fibroblasts.	Acetylcysteine	89-92	transforming growth factor beta 1	Homo sapiens	123-131
29049376-7	2017	In HDF and HGF, TGFbeta1 induces CCN2, CCN1, endothelin-1 and alpha-smooth muscle actin (SMA) in a fashion sensitive to NAC.	Acetylcysteine	120-123	transforming growth factor beta 1	Homo sapiens	16-24
29049376-7	2017	In HDF and HGF, TGFbeta1 induces CCN2, CCN1, endothelin-1 and alpha-smooth muscle actin (SMA) in a fashion sensitive to NAC.	Acetylcysteine	120-123	cyclin A2	Homo sapiens	39-43
29049376-7	2017	In HDF and HGF, TGFbeta1 induces CCN2, CCN1, endothelin-1 and alpha-smooth muscle actin (SMA) in a fashion sensitive to NAC.	Acetylcysteine	120-123	endothelin 1	Homo sapiens	45-57
29049376-10	2017	NAC and DPI impaired the ability of TGFbeta1 to induce protein expression of CCN2 and alpha-SMA in HDF and HGF.	Acetylcysteine	0-3	transforming growth factor beta 1	Homo sapiens	36-44
28798231-6	2017	Also, using the reactive oxygen species (ROS) scavengers N-acetyl cysteine and Mito-TEMPO, we determined that mitochondrial reactive oxygen species are required for P2X7R-mediated IL-1beta release.	Acetylcysteine	57-74	purinergic receptor P2X, ligand-gated ion channel, 7	Mus musculus	165-170
29254201-8	2017	Radiation enhanced the protein level of TGF-beta1, which was blocked by N-acetylcysteine, an antioxidant.	Acetylcysteine	72-88	transforming growth factor, beta 1	Rattus norvegicus	40-49
28798231-6	2017	Also, using the reactive oxygen species (ROS) scavengers N-acetyl cysteine and Mito-TEMPO, we determined that mitochondrial reactive oxygen species are required for P2X7R-mediated IL-1beta release.	Acetylcysteine	57-74	interleukin 1 beta	Mus musculus	180-188
28623559-5	2017	Importantly, the ROS scavenger N-acetyl cysteine (NAC) prevented mitochondrial dysfunctions, type I IFN-stimulated transcript levels, inflammatory cell infiltrate, and muscle weakness in an experimental autoimmune myositis mouse model.	Acetylcysteine	31-48	interferon alpha 1	Homo sapiens	100-103
29056901-7	2017	Combination of hydrogen peroxide and myeloperoxidase augmented cisplatin cytotoxicity, and this synergism was inhibited by N-Acetyl-L-cysteine and ML-171.	Acetylcysteine	123-142	myeloperoxidase	Homo sapiens	37-52
28981107-10	2017	Importantly, re-supply of GSH or its precursor NAC completely prevents AUR/ERA- and AUR/BSO-induced accumulation of ubiquitinated proteins, NOXA upregulation and cell death, indicating that GSH depletion rather than ROS production is critical for AUR/BSO- or AUR/ERA-mediated cell death.	Acetylcysteine	47-50	phorbol-12-myristate-13-acetate-induced protein 1	Homo sapiens	140-144
28901751-4	2017	Hypoxia-inducible factor 1alpha (HIF-1alpha)-Snail signaling, regulated by the generation of reactive oxygen species (ROS), was involved in the (NH4)2SO4-induced EMT, and the potent antioxidant N-acetylcysteine (NAC) inhibited the activation of HIF-1alpha-Snail and blocked the EMT, cell invasion, and migration in response to (NH4)2SO4.	Acetylcysteine	194-210	hypoxia inducible factor 1 subunit alpha	Homo sapiens	0-31
28901751-4	2017	Hypoxia-inducible factor 1alpha (HIF-1alpha)-Snail signaling, regulated by the generation of reactive oxygen species (ROS), was involved in the (NH4)2SO4-induced EMT, and the potent antioxidant N-acetylcysteine (NAC) inhibited the activation of HIF-1alpha-Snail and blocked the EMT, cell invasion, and migration in response to (NH4)2SO4.	Acetylcysteine	194-210	hypoxia inducible factor 1 subunit alpha	Homo sapiens	33-43
28901751-4	2017	Hypoxia-inducible factor 1alpha (HIF-1alpha)-Snail signaling, regulated by the generation of reactive oxygen species (ROS), was involved in the (NH4)2SO4-induced EMT, and the potent antioxidant N-acetylcysteine (NAC) inhibited the activation of HIF-1alpha-Snail and blocked the EMT, cell invasion, and migration in response to (NH4)2SO4.	Acetylcysteine	212-215	hypoxia inducible factor 1 subunit alpha	Homo sapiens	0-31
28901751-4	2017	Hypoxia-inducible factor 1alpha (HIF-1alpha)-Snail signaling, regulated by the generation of reactive oxygen species (ROS), was involved in the (NH4)2SO4-induced EMT, and the potent antioxidant N-acetylcysteine (NAC) inhibited the activation of HIF-1alpha-Snail and blocked the EMT, cell invasion, and migration in response to (NH4)2SO4.	Acetylcysteine	212-215	hypoxia inducible factor 1 subunit alpha	Homo sapiens	33-43
28623559-5	2017	Importantly, the ROS scavenger N-acetyl cysteine (NAC) prevented mitochondrial dysfunctions, type I IFN-stimulated transcript levels, inflammatory cell infiltrate, and muscle weakness in an experimental autoimmune myositis mouse model.	Acetylcysteine	50-53	interferon alpha 1	Homo sapiens	100-103
28946937-6	2017	The ROS scavenger N-acetylcysteine inhibited CLB2.0-induced IL-6 secretion, thereby decreasing the CLB2.0-induced MUC5AC expression, whereas CLB2.0-induced MUC1 expression increased.	Acetylcysteine	18-34	interleukin 6	Homo sapiens	60-64
28628905-7	2017	Additionally, NAC and the p38 mitogen activated protein kinase (MAPK) signaling pathway inhibitor SB 203580 greatly reduced Nrf2 and HO-1 induction.	Acetylcysteine	14-17	nuclear factor, erythroid derived 2, like 2	Mus musculus	124-128
28843610-8	2017	In contrast, inhibitors of the MAP kinases p38 and JNK as well as the antioxidant N-acetylcysteine attenuated the LPS-stimulated TNF-alpha expression both in the absence and presence of OGG1.	Acetylcysteine	82-98	tumor necrosis factor	Mus musculus	129-138
28555929-5	2017	PM2.5 induced heme oxygenase-1 (HO-1) gene, which was attenuated by N-acetylcysteine (NAC).	Acetylcysteine	68-84	heme oxygenase 1	Mus musculus	14-30
28555929-5	2017	PM2.5 induced heme oxygenase-1 (HO-1) gene, which was attenuated by N-acetylcysteine (NAC).	Acetylcysteine	68-84	heme oxygenase 1	Mus musculus	32-36
28555929-5	2017	PM2.5 induced heme oxygenase-1 (HO-1) gene, which was attenuated by N-acetylcysteine (NAC).	Acetylcysteine	86-89	heme oxygenase 1	Mus musculus	14-30
28555929-5	2017	PM2.5 induced heme oxygenase-1 (HO-1) gene, which was attenuated by N-acetylcysteine (NAC).	Acetylcysteine	86-89	heme oxygenase 1	Mus musculus	32-36
28934876-8	2017	Both HA and NAC produced comparable reductions in TOS and MMP-3.	Acetylcysteine	12-15	matrix metallopeptidase 3	Homo sapiens	58-63
28807874-9	2017	N-Acetyl-l-cysteine, a ROS scavenger, abrogated the DHA-induced increases in Akt phosphorylation, Nrf2 nuclear accumulation, and OSGIN1 expression.	Acetylcysteine	0-19	AKT serine/threonine kinase 1	Homo sapiens	77-80
28807874-9	2017	N-Acetyl-l-cysteine, a ROS scavenger, abrogated the DHA-induced increases in Akt phosphorylation, Nrf2 nuclear accumulation, and OSGIN1 expression.	Acetylcysteine	0-19	NFE2 like bZIP transcription factor 2	Homo sapiens	98-102
29416235-8	2017	Results: ALT and AST were significantly elevated after surgery, but to a less extent with NAC versus C (day 3; 118.3 +- 18.6 vs. 145.4 +- 14.0 U/L.	Acetylcysteine	90-93	solute carrier family 17 member 5	Homo sapiens	17-20
29416235-10	2017	Lower serum CRP and ICAM 1 with NAC versus C on day 3 (44.2 +- 13.4 vs. 68.7 +- 48.2 mg/l, P = 0.003), (308.8 +- 38.2 vs. 352.8 +- 59.4 ng/ml, P = 0.002), respectively.	Acetylcysteine	32-35	C-reactive protein	Homo sapiens	12-15
29416235-13	2017	Conclusion: Prophylactic NAC in hepatic patients undergoing liver surgery attenuated postoperative increase in transaminases, ICAM 1, and CRP blood levels.	Acetylcysteine	25-28	C-reactive protein	Homo sapiens	138-141
28628905-7	2017	Additionally, NAC and the p38 mitogen activated protein kinase (MAPK) signaling pathway inhibitor SB 203580 greatly reduced Nrf2 and HO-1 induction.	Acetylcysteine	14-17	heme oxygenase 1	Mus musculus	133-137
28432555-3	2017	Rotundarpene, Akt inhibitor, Bay 11-7085, rapamycin, and N-acetylcysteine inhibited the TNF-alpha-stimulated production of cytokines and chemokines, increase in the levels of p-Akt and mTOR, activation of NF-kappaB, and production of reactive oxygen species in keratinocytes.	Acetylcysteine	57-73	nuclear factor kappa B subunit 1	Homo sapiens	205-214
28432555-3	2017	Rotundarpene, Akt inhibitor, Bay 11-7085, rapamycin, and N-acetylcysteine inhibited the TNF-alpha-stimulated production of cytokines and chemokines, increase in the levels of p-Akt and mTOR, activation of NF-kappaB, and production of reactive oxygen species in keratinocytes.	Acetylcysteine	57-73	tumor necrosis factor	Homo sapiens	88-97
28432555-3	2017	Rotundarpene, Akt inhibitor, Bay 11-7085, rapamycin, and N-acetylcysteine inhibited the TNF-alpha-stimulated production of cytokines and chemokines, increase in the levels of p-Akt and mTOR, activation of NF-kappaB, and production of reactive oxygen species in keratinocytes.	Acetylcysteine	57-73	AKT serine/threonine kinase 1	Homo sapiens	177-180
28432555-3	2017	Rotundarpene, Akt inhibitor, Bay 11-7085, rapamycin, and N-acetylcysteine inhibited the TNF-alpha-stimulated production of cytokines and chemokines, increase in the levels of p-Akt and mTOR, activation of NF-kappaB, and production of reactive oxygen species in keratinocytes.	Acetylcysteine	57-73	mechanistic target of rapamycin kinase	Homo sapiens	185-189
28782507-3	2017	Exposing YD8 cells to Cd reduced the expression levels of catalase and superoxide dismutase 1/2 and induced the expression of HO-1 as well as autophagy and apoptosis, which were reversed by N-acetyl-l-cysteine (NAC).	Acetylcysteine	190-209	catalase	Homo sapiens	58-66
28535741-11	2017	This study confirmed the protective effect of NAC on diclofenac-induced hepatotoxicity in rats due to not only reduces liver inflammatory cells, TNF-alpha, serum MDA, and PC but also through increases liver vitamin C, catalase, and superoxide dismutase activities.	Acetylcysteine	46-49	tumor necrosis factor	Rattus norvegicus	145-154
28535741-11	2017	This study confirmed the protective effect of NAC on diclofenac-induced hepatotoxicity in rats due to not only reduces liver inflammatory cells, TNF-alpha, serum MDA, and PC but also through increases liver vitamin C, catalase, and superoxide dismutase activities.	Acetylcysteine	46-49	catalase	Rattus norvegicus	218-226
28782507-3	2017	Exposing YD8 cells to Cd reduced the expression levels of catalase and superoxide dismutase 1/2 and induced the expression of HO-1 as well as autophagy and apoptosis, which were reversed by N-acetyl-l-cysteine (NAC).	Acetylcysteine	190-209	superoxide dismutase 1	Homo sapiens	71-95
28778520-4	2017	Additionally, N-acetylcysteine (NAC), a glutathione (GSH) provider and a direct scavenger of reactive oxygen species (ROS), clearly decreases Mn-induced ROS accumulation, caspase-3 activation and TUNEL staining, which indicate increased cell survival.	Acetylcysteine	14-30	caspase 3	Homo sapiens	171-180
28592194-6	2017	In addition, scavenging of reactive oxygen species (ROS) by 10 muM N-acetyl-l-cysteine (NAC) partly rescued impaired insulin-induced eNOS activities and NO productions induced by PCB-118 in HUVECs.	Acetylcysteine	67-86	pyruvate carboxylase	Homo sapiens	179-182
28592194-6	2017	In addition, scavenging of reactive oxygen species (ROS) by 10 muM N-acetyl-l-cysteine (NAC) partly rescued impaired insulin-induced eNOS activities and NO productions induced by PCB-118 in HUVECs.	Acetylcysteine	88-91	pyruvate carboxylase	Homo sapiens	179-182
29416738-9	2018	Overexpression of TrxR1 or application of antioxidant N-acetyl-L-cysteine (NAC) depletes the ROS increase, reduces DNA damage, and decreases cell death triggered by APR-246/PHEN in HNSCC cells.	Acetylcysteine	54-73	phorbol-12-myristate-13-acetate-induced protein 1	Homo sapiens	165-168
28924345-8	2017	Inhibition was characterized by significant elevation of intracellular reactive oxygen species and subsequent inhibition of Akt and regulation of apoptotic proteins, which could be partly reversed by pretreatment with the antioxidant N-acetylcysteine.	Acetylcysteine	234-250	AKT serine/threonine kinase 1	Homo sapiens	124-127
28778520-4	2017	Additionally, N-acetylcysteine (NAC), a glutathione (GSH) provider and a direct scavenger of reactive oxygen species (ROS), clearly decreases Mn-induced ROS accumulation, caspase-3 activation and TUNEL staining, which indicate increased cell survival.	Acetylcysteine	32-35	caspase 3	Homo sapiens	171-180
28180948-11	2017	Similarly, islets treated with TBT significantly increased glucose-stimulated insulin secretion, which could be reversed by ICI182780, NAC, and PKC inhibitor.	Acetylcysteine	135-138	insulin	Homo sapiens	78-85
28455747-8	2017	After intervention of ROS scavenger N-acetyl cysteine (NAC) and NADPH inhibitor apocynin (Apo) in 6-month-old dTH mice for 4 weeks, myocardial oxidative stress level was reduced and KCa3.1 channel protein expression was decreased.	Acetylcysteine	36-53	potassium intermediate/small conductance calcium-activated channel, subfamily N, member 4	Mus musculus	182-188
28705740-5	2017	Especially, the glutamine metabolic process related molecules, GPX1, GPX3, SMS, GGCT, GSTK1, NFkappaB, GSTT2, SOD1 and GCLM, are involved in the switching process from oxidized glutathione (GSSG) conversion to the reduced glutathione (GSH) by glutathione, mercapturic acid and arginine metabolism process.	Acetylcysteine	256-272	glutathione peroxidase 3	Homo sapiens	69-73
28705740-5	2017	Especially, the glutamine metabolic process related molecules, GPX1, GPX3, SMS, GGCT, GSTK1, NFkappaB, GSTT2, SOD1 and GCLM, are involved in the switching process from oxidized glutathione (GSSG) conversion to the reduced glutathione (GSH) by glutathione, mercapturic acid and arginine metabolism process.	Acetylcysteine	256-272	nuclear factor kappa B subunit 1	Homo sapiens	93-101
28705740-5	2017	Especially, the glutamine metabolic process related molecules, GPX1, GPX3, SMS, GGCT, GSTK1, NFkappaB, GSTT2, SOD1 and GCLM, are involved in the switching process from oxidized glutathione (GSSG) conversion to the reduced glutathione (GSH) by glutathione, mercapturic acid and arginine metabolism process.	Acetylcysteine	256-272	superoxide dismutase 1	Homo sapiens	110-114
28705740-5	2017	Especially, the glutamine metabolic process related molecules, GPX1, GPX3, SMS, GGCT, GSTK1, NFkappaB, GSTT2, SOD1 and GCLM, are involved in the switching process from oxidized glutathione (GSSG) conversion to the reduced glutathione (GSH) by glutathione, mercapturic acid and arginine metabolism process.	Acetylcysteine	256-272	glutamate-cysteine ligase modifier subunit	Homo sapiens	119-123
28710022-4	2017	Taxifolin, N-acetylcysteine, trolox, Akt inhibitor and Bay11-7085 attenuated the cholesterol oxidation product-induced changes in the apoptosis-related protein levels, activation of the Akt and NF-kappaB, reactive oxygen species production, GSH depletion and cell death.	Acetylcysteine	11-27	AKT serine/threonine kinase 1	Homo sapiens	186-189
28059488-9	2017	N-acetyl cysteine (NAC), a known scavenger of ROS, could protect palmitate-induced expression of TNF-alpha and IL-6.	Acetylcysteine	0-17	tumor necrosis factor	Mus musculus	97-106
28059488-9	2017	N-acetyl cysteine (NAC), a known scavenger of ROS, could protect palmitate-induced expression of TNF-alpha and IL-6.	Acetylcysteine	0-17	interleukin 6	Mus musculus	111-115
28059488-9	2017	N-acetyl cysteine (NAC), a known scavenger of ROS, could protect palmitate-induced expression of TNF-alpha and IL-6.	Acetylcysteine	19-22	tumor necrosis factor	Mus musculus	97-106
28059488-9	2017	N-acetyl cysteine (NAC), a known scavenger of ROS, could protect palmitate-induced expression of TNF-alpha and IL-6.	Acetylcysteine	19-22	interleukin 6	Mus musculus	111-115
28180948-12	2017	Mice exposed to TBT for 3 weeks significantly increased blood glucose and plasma insulin and induced glucose intolerance and insulin resistance, which could be reversed by NAC.	Acetylcysteine	172-175	insulin	Homo sapiens	81-88
28180948-12	2017	Mice exposed to TBT for 3 weeks significantly increased blood glucose and plasma insulin and induced glucose intolerance and insulin resistance, which could be reversed by NAC.	Acetylcysteine	172-175	insulin	Homo sapiens	125-132
28528167-4	2017	We administered CXCL1 neutralizing antibody or the antioxidant agent, N-acetylcysteine, to Xpa-deficient mice after UVB irradiation and found significant suppression of blood levels of CXCL1, ear swelling and erythema, the hallmarks of inflammation and neutrophil chemotaxis.	Acetylcysteine	70-86	chemokine (C-X-C motif) ligand 1	Mus musculus	185-190
28814068-4	2017	RESULTS: NAC and caspase-1 inhibitor suppressed CSE- and DEP-induced secretion of IL-1beta in RAW 264.7 cells.	Acetylcysteine	9-12	interleukin 1 beta	Mus musculus	82-90
28814068-8	2017	NAC inhibited CSE- and DEP-induced IL-1beta secretion in both the normal and elastase-induced emphysema groups.	Acetylcysteine	0-3	interleukin 1 beta	Mus musculus	35-43
28731136-10	2017	Moreover, the apoptotic effect of MHY451 was reactive oxygen species (ROS)-dependent, evidenced by the inhibition of MHY451-induced PARP cleavage and ROS generation by N-acetylcysteine-induced ROS scavenging.	Acetylcysteine	168-184	poly(ADP-ribose) polymerase 1	Homo sapiens	132-136
28583366-8	2017	Pre-treatment with n-acetyl-l-cysteine (NAC), a ROS scavenger, enhanced PTX-mediated cell cycle arrest, apoptosis and the JNK and ERK MAPK activation, while pre-treatment with SP600125 or PD98509 attenuated PTX-mediated effects in HepG2 cells.	Acetylcysteine	19-38	mitogen-activated protein kinase 8	Homo sapiens	122-125
28487393-9	2017	RESULTS: We demonstrated that intravenous NAC administration promotes lysis of arterial thrombi that are resistant to conventional approaches such as recombinant tissue-type plasminogen activator, direct thrombin inhibitors, and antiplatelet treatments.	Acetylcysteine	42-45	coagulation factor II	Mus musculus	204-212
29179463-7	2017	Pre-treatment with antioxidant N-acetylcysteine effectively ameliorated olaquindox-induced exhaustion of ZO-1 and N-Cadherin proteins, DNA damage and apoptosis.	Acetylcysteine	31-47	tight junction protein 1	Homo sapiens	105-109
28583366-8	2017	Pre-treatment with n-acetyl-l-cysteine (NAC), a ROS scavenger, enhanced PTX-mediated cell cycle arrest, apoptosis and the JNK and ERK MAPK activation, while pre-treatment with SP600125 or PD98509 attenuated PTX-mediated effects in HepG2 cells.	Acetylcysteine	19-38	mitogen-activated protein kinase 1	Homo sapiens	130-133
28583366-8	2017	Pre-treatment with n-acetyl-l-cysteine (NAC), a ROS scavenger, enhanced PTX-mediated cell cycle arrest, apoptosis and the JNK and ERK MAPK activation, while pre-treatment with SP600125 or PD98509 attenuated PTX-mediated effects in HepG2 cells.	Acetylcysteine	19-38	mitogen-activated protein kinase 3	Homo sapiens	134-138
28704996-9	2017	N-Acetyl cysteine also partially reversed the effects of imidacloprid on reduced phosphorylation of protein kinase B (AKT) in C2C12 myotubes.	Acetylcysteine	0-17	thymoma viral proto-oncogene 1	Mus musculus	118-121
28218905-7	2017	Inhibition of LDH activity by small hairpin ribonucleic acid or expression of phospho-deficient LDHA Y10F sensitized the cancer cells to anoikis induction and resulted in attenuated cell invasion and elevated reactive oxygen species, whereas such phenotypes were reversed by its product lactate or antioxidant N-acetylcysteine, suggesting that Y10 phosphorylation-mediated LDHA activity promotes cancer cell invasion and anoikis resistance through redox homeostasis.	Acetylcysteine	310-326	lactate dehydrogenase A	Homo sapiens	14-17
27783328-5	2017	We found that systemic administration of NAC or PBN significantly alleviated compound 48/80- and chloroquine-induced acute itch in a dose-dependent manner, attenuated dry skin-induced chronic itch, and suppressed oxidative stress in the affected skin.	Acetylcysteine	41-44	itchy, E3 ubiquitin protein ligase	Mus musculus	123-127
28577450-9	2017	mRNA expression level of ABCC8 subunit significantly increased in all NAC groups compared to the control group.	Acetylcysteine	70-73	ATP binding cassette subfamily C member 8	Rattus norvegicus	25-30
28577450-11	2017	CONCLUSION: Our findings suggest that NAC relaxes vascular smooth muscle cells through a direct effect on KATP channels, by increasing outward K+ flux, partly by increasing mRNA expression of KATP subunit ABCC8, by decreasing in intracellular calcium and by decreasing in Na+/K+-ATPase activity.	Acetylcysteine	38-41	ATP binding cassette subfamily C member 8	Rattus norvegicus	205-210
29050275-8	2017	Moreover, NAC was able to eliminate AB23A-induced JNK phosphorylation.	Acetylcysteine	10-13	mitogen-activated protein kinase 8	Homo sapiens	50-53
28730106-10	2017	H2O2 up-regulated P-gp in D407 cells, which could be reversed by NAC treatment.	Acetylcysteine	65-68	ATP binding cassette subfamily B member 1	Homo sapiens	18-22
29404485-7	2017	EV CYP2E1 amounts depended on increased oxidative and endoplasmic reticulum (ER) stress because their levels were decreased by cotreatment with the antioxidant N-acetylcysteine or the CYP2E1 inhibitor chlormethiazole but increased by ER stress-inducer thapsigargin, which was blocked by 4-phenylbutyric acid.	Acetylcysteine	160-176	cytochrome P450 family 2 subfamily E member 1	Homo sapiens	3-9
27650197-7	2017	On the other hand, the increased phosphorylation of mitogen-activated protein kinase (MAPK) proteins (c-Jun N-terminal kinase [JNK], p38, and extracellular signal-regulated kinase [ERK]) by JDA-202 was suppressed by N-acetylcysteine (NAC) or catalase, a known reactive oxygen species (ROS) or H2O2 scavenger.	Acetylcysteine	216-232	mitogen-activated protein kinase 8	Homo sapiens	102-125
27650197-7	2017	On the other hand, the increased phosphorylation of mitogen-activated protein kinase (MAPK) proteins (c-Jun N-terminal kinase [JNK], p38, and extracellular signal-regulated kinase [ERK]) by JDA-202 was suppressed by N-acetylcysteine (NAC) or catalase, a known reactive oxygen species (ROS) or H2O2 scavenger.	Acetylcysteine	216-232	mitogen-activated protein kinase 8	Homo sapiens	127-130
27650197-7	2017	On the other hand, the increased phosphorylation of mitogen-activated protein kinase (MAPK) proteins (c-Jun N-terminal kinase [JNK], p38, and extracellular signal-regulated kinase [ERK]) by JDA-202 was suppressed by N-acetylcysteine (NAC) or catalase, a known reactive oxygen species (ROS) or H2O2 scavenger.	Acetylcysteine	234-237	mitogen-activated protein kinase 8	Homo sapiens	102-125
27650197-7	2017	On the other hand, the increased phosphorylation of mitogen-activated protein kinase (MAPK) proteins (c-Jun N-terminal kinase [JNK], p38, and extracellular signal-regulated kinase [ERK]) by JDA-202 was suppressed by N-acetylcysteine (NAC) or catalase, a known reactive oxygen species (ROS) or H2O2 scavenger.	Acetylcysteine	234-237	mitogen-activated protein kinase 8	Homo sapiens	127-130
28915557-8	2017	One biological consequence of elevated ROS in p16-deficient PMFs was enhanced migration, which was reduced by the ROS scavenger N-acetylcysteine.	Acetylcysteine	128-144	cyclin dependent kinase inhibitor 2A	Homo sapiens	46-49
28341391-8	2017	Addition of NAC to drinking water protected KO +Fe from hepatic steatosis, injury and fibrosis, and prevented activation of AKT, ERK, NF-kappaB and reappearance of beta-catenin.	Acetylcysteine	12-15	thymoma viral proto-oncogene 1	Mus musculus	124-127
28341391-8	2017	Addition of NAC to drinking water protected KO +Fe from hepatic steatosis, injury and fibrosis, and prevented activation of AKT, ERK, NF-kappaB and reappearance of beta-catenin.	Acetylcysteine	12-15	mitogen-activated protein kinase 1	Mus musculus	129-132
28341391-8	2017	Addition of NAC to drinking water protected KO +Fe from hepatic steatosis, injury and fibrosis, and prevented activation of AKT, ERK, NF-kappaB and reappearance of beta-catenin.	Acetylcysteine	12-15	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	134-143
28499252-8	2017	N-acetyl cysteine, diphenyl iodonium, and apocynin suppressed HIV-1 Tat-induced expression of HDAC6 and the pro-inflammatory chemokines CCL2, CXCL8, and CXCL10.	Acetylcysteine	0-17	histone deacetylase 6	Homo sapiens	94-99
28758971-9	2017	Moreover, an ROS scavenger, N-acetylcysteine (NAC), reversed tricetin-induced JNK activation and subsequent cell apoptosis.	Acetylcysteine	28-44	mitogen-activated protein kinase 8	Homo sapiens	78-81
28758971-9	2017	Moreover, an ROS scavenger, N-acetylcysteine (NAC), reversed tricetin-induced JNK activation and subsequent cell apoptosis.	Acetylcysteine	46-49	mitogen-activated protein kinase 8	Homo sapiens	78-81
28218905-7	2017	Inhibition of LDH activity by small hairpin ribonucleic acid or expression of phospho-deficient LDHA Y10F sensitized the cancer cells to anoikis induction and resulted in attenuated cell invasion and elevated reactive oxygen species, whereas such phenotypes were reversed by its product lactate or antioxidant N-acetylcysteine, suggesting that Y10 phosphorylation-mediated LDHA activity promotes cancer cell invasion and anoikis resistance through redox homeostasis.	Acetylcysteine	310-326	lactate dehydrogenase A	Homo sapiens	96-100
28915658-10	2017	Interventions by Cyp1A2 and Mek2siRNA, MEK inhibitor UO126, diphenylene iodonium, as well as a combination of N-acetylcysteine with selenium all inhibited VEGF upregulation caused by erlotinib.	Acetylcysteine	110-126	vascular endothelial growth factor A	Homo sapiens	155-159
28560439-12	2017	Pretreatment with NAC abrogated the inhibitory effect of ISL on activation of STAT3 and blocked the cleavage of caspase-9, -7 and -3, and that of PARP in Caki cells.	Acetylcysteine	18-21	signal transducer and activator of transcription 3	Homo sapiens	78-83
28577939-6	2017	CONCLUSION: Cigarette smoke extract induces EGFR-TKI resistance via promoting EGFR signaling and ROS generation in NSCLC cell lines which could be suppressed by NAC.	Acetylcysteine	161-164	epidermal growth factor receptor	Homo sapiens	44-48
28577939-6	2017	CONCLUSION: Cigarette smoke extract induces EGFR-TKI resistance via promoting EGFR signaling and ROS generation in NSCLC cell lines which could be suppressed by NAC.	Acetylcysteine	161-164	epidermal growth factor receptor	Homo sapiens	78-82
28577939-7	2017	Alternatively, combined NAC with EGFR-TKIs to treat EGFR mutated NSCLC patients with smoking history may be a potential choice in clinical setting.	Acetylcysteine	24-27	epidermal growth factor receptor	Homo sapiens	52-56
28495448-7	2017	Furthermore, NAC reversed the effect of CM from Nrf2-depleted KC on UVB-induced apoptosis and inflammatory response in MC.	Acetylcysteine	13-16	NFE2 like bZIP transcription factor 2	Homo sapiens	48-52
28644070-6	2017	Both Y-27632 and NAC prevented PM-induced stress fiber formation and phospho-MLC accumulation in human lung ECs.	Acetylcysteine	17-20	modulator of VRAC current 1	Homo sapiens	77-80
28840690-5	2017	NAC could inhibit PPL-induced ROS excessive production and significantly reduce the release of IL-1beta.	Acetylcysteine	0-3	interleukin 1 beta	Mus musculus	95-103
28578026-5	2017	The apoptotic events (caspase-3 activation and DNA fragmentation) were abolished by pretreatment with antioxidants, N-acetyl-l-cysteine and polyethyleneglycol-conjugated catalase.	Acetylcysteine	116-135	caspase 3	Homo sapiens	22-31
28594401-7	2017	NAC also reversed the PDT-induced suppression of p-mTOR and p-Akt.	Acetylcysteine	0-3	mechanistic target of rapamycin kinase	Homo sapiens	51-55
28978056-8	2017	Remarkably, insulin-induced downstream signaling transduction and glucose transporter 4 expression were recovered with n-acetylcysteine co-treatment in 1alpha(OH)ase-silenced L02 hepatocytes.	Acetylcysteine	119-135	insulin	Homo sapiens	12-19
28978056-8	2017	Remarkably, insulin-induced downstream signaling transduction and glucose transporter 4 expression were recovered with n-acetylcysteine co-treatment in 1alpha(OH)ase-silenced L02 hepatocytes.	Acetylcysteine	119-135	cytochrome P450 family 27 subfamily B member 1	Homo sapiens	152-165
28380464-7	2017	N-Acetyl-L-Cysteine was shown to inhibit ROS generation, suppress permeabilization of lysosomal membranes, decrease levels of cathepsin B and cytochrome C in the cytosol, and inhibit Bax/Bcl2 ratio, caspase-9 and caspase-3 activity both in vitro and in vivo.	Acetylcysteine	0-19	cytochrome c, somatic	Homo sapiens	142-154
28380464-7	2017	N-Acetyl-L-Cysteine was shown to inhibit ROS generation, suppress permeabilization of lysosomal membranes, decrease levels of cathepsin B and cytochrome C in the cytosol, and inhibit Bax/Bcl2 ratio, caspase-9 and caspase-3 activity both in vitro and in vivo.	Acetylcysteine	0-19	BCL2 associated X, apoptosis regulator	Homo sapiens	183-186
28380464-7	2017	N-Acetyl-L-Cysteine was shown to inhibit ROS generation, suppress permeabilization of lysosomal membranes, decrease levels of cathepsin B and cytochrome C in the cytosol, and inhibit Bax/Bcl2 ratio, caspase-9 and caspase-3 activity both in vitro and in vivo.	Acetylcysteine	0-19	BCL2 apoptosis regulator	Homo sapiens	187-191
28380464-7	2017	N-Acetyl-L-Cysteine was shown to inhibit ROS generation, suppress permeabilization of lysosomal membranes, decrease levels of cathepsin B and cytochrome C in the cytosol, and inhibit Bax/Bcl2 ratio, caspase-9 and caspase-3 activity both in vitro and in vivo.	Acetylcysteine	0-19	caspase 3	Homo sapiens	213-222
28632169-6	2017	Pre-treatment with astaxanthin or with N-acetyl-cysteine (NAC) which is an antioxidant drug, significantly attenuated the palmitate-induced MCP-1 release through downregulation of phosphorylated c-Jun NH2-terminal protein kinase (JNK) pathways, and suppressed VEGF120 through the PI3K/Akt pathways relative to the cells stimulated with palmitate alone.	Acetylcysteine	39-56	thymoma viral proto-oncogene 1	Mus musculus	285-288
28632169-6	2017	Pre-treatment with astaxanthin or with N-acetyl-cysteine (NAC) which is an antioxidant drug, significantly attenuated the palmitate-induced MCP-1 release through downregulation of phosphorylated c-Jun NH2-terminal protein kinase (JNK) pathways, and suppressed VEGF120 through the PI3K/Akt pathways relative to the cells stimulated with palmitate alone.	Acetylcysteine	58-61	thymoma viral proto-oncogene 1	Mus musculus	285-288
28630426-3	2017	Our previous study revealed that ADR increased reactive oxygen species (ROS) generation and decreased glutathione (GSH) biosynthesis, while N-acetylcysteine, the ROS scavenger, reversed the over-expression of P-gp.	Acetylcysteine	140-156	ATP binding cassette subfamily B member 1	Homo sapiens	209-213
28630426-7	2017	In contrast, the over-expression of SLC7A11, or supplementation with sufficiently cystine, or treatment with N-acetylcysteine significantly decreased P-gp expression and activity.	Acetylcysteine	109-125	ATP binding cassette subfamily B member 1	Homo sapiens	150-154
28604588-8	2017	The antioxidants N-acetyl-l-cysteine and Trolox attenuated DHA-induced activation of PKCdelta, phosphorylation of Nrf2, and and its target protein expression.	Acetylcysteine	17-36	NFE2 like bZIP transcription factor 2	Homo sapiens	114-118
28499986-10	2017	The increase in AChE activity and decrease in pTrkB and MnSOD levels caused by STZ in the cerebral cortex and hippocampus, were prevented by the NAC and PHY treatments.	Acetylcysteine	145-148	superoxide dismutase 2, mitochondrial	Mus musculus	56-61
28499986-11	2017	The decrease in SYN, MAP2 and GFAP expressions were also prevented by NAC and PHY treatments.	Acetylcysteine	70-73	joined toes	Mus musculus	16-19
28499986-11	2017	The decrease in SYN, MAP2 and GFAP expressions were also prevented by NAC and PHY treatments.	Acetylcysteine	70-73	microtubule-associated protein 2	Mus musculus	21-25
28594401-7	2017	NAC also reversed the PDT-induced suppression of p-mTOR and p-Akt.	Acetylcysteine	0-3	AKT serine/threonine kinase 1	Homo sapiens	62-65
28588678-0	2017	Mechanism of N-acetyl-cysteine inhibition on the cytotoxicity induced by titanium dioxide nanoparticles in JB6 cells transfected with activator protein-1.	Acetylcysteine	13-30	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	134-153
28363167-3	2017	Specifically, A mitochondrial matrix protein (cyclophilin D, CyPD) is involved in emodin-induced apoptosis, and the inhibitor of CyPD (cyclosporin A) could almost completely suppressing the apoptosis; Moreover, as the expression of CyPD could be effectively inhibited by antioxidant N-acetyl-l-cysteine and epidermal growth factor (the activator of ERK), reactive oxygen species and ERK might be involved in the relevant role of CyPD.	Acetylcysteine	283-302	peptidylprolyl isomerase F	Homo sapiens	46-59
28363167-3	2017	Specifically, A mitochondrial matrix protein (cyclophilin D, CyPD) is involved in emodin-induced apoptosis, and the inhibitor of CyPD (cyclosporin A) could almost completely suppressing the apoptosis; Moreover, as the expression of CyPD could be effectively inhibited by antioxidant N-acetyl-l-cysteine and epidermal growth factor (the activator of ERK), reactive oxygen species and ERK might be involved in the relevant role of CyPD.	Acetylcysteine	283-302	peptidylprolyl isomerase F	Homo sapiens	129-133
28363167-3	2017	Specifically, A mitochondrial matrix protein (cyclophilin D, CyPD) is involved in emodin-induced apoptosis, and the inhibitor of CyPD (cyclosporin A) could almost completely suppressing the apoptosis; Moreover, as the expression of CyPD could be effectively inhibited by antioxidant N-acetyl-l-cysteine and epidermal growth factor (the activator of ERK), reactive oxygen species and ERK might be involved in the relevant role of CyPD.	Acetylcysteine	283-302	peptidylprolyl isomerase F	Homo sapiens	129-133
28363167-3	2017	Specifically, A mitochondrial matrix protein (cyclophilin D, CyPD) is involved in emodin-induced apoptosis, and the inhibitor of CyPD (cyclosporin A) could almost completely suppressing the apoptosis; Moreover, as the expression of CyPD could be effectively inhibited by antioxidant N-acetyl-l-cysteine and epidermal growth factor (the activator of ERK), reactive oxygen species and ERK might be involved in the relevant role of CyPD.	Acetylcysteine	283-302	peptidylprolyl isomerase F	Homo sapiens	129-133
28588678-7	2017	Furthermore, alternative studies have demonstrated that AP-1 luciferase activity induced by TiO2 NPs may be significantly inhibited by NAC.	Acetylcysteine	135-138	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	56-60
28712479-7	2017	Identically, N-acetylcysteine inhibited the increase of reactive oxygen species level induced by thrombin in platelets, and supported a link between cellular redox status and caspase activation in activated platelets.	Acetylcysteine	13-29	coagulation factor II, thrombin	Homo sapiens	97-105
28365254-5	2017	Moreover, arecoline-induced HIF-1alpha expression was downregulated by mitogen-activated protein kinase inhibitor U0126, phosphatidylinositol 3-kinase inhibitor LY294002, p38 inhibitor SB203580, cyclooxygenase-2 inhibitor NS-398, and glutathione precursor N-acetyl-L-cysteine (p&lt;0.05).	Acetylcysteine	256-275	hypoxia inducible factor 1 subunit alpha	Homo sapiens	28-38
28393248-7	2017	c-JUN N-terminal kinase (JNK)/insulin receptor substrate 1 (IRS1)/AKT/GSK signaling was explored using western blot analysis in HepG2 cells treated with high glucose and/or EGCG or N-acetyl-cysteine.	Acetylcysteine	181-198	mitogen-activated protein kinase 8	Homo sapiens	0-23
28393248-7	2017	c-JUN N-terminal kinase (JNK)/insulin receptor substrate 1 (IRS1)/AKT/GSK signaling was explored using western blot analysis in HepG2 cells treated with high glucose and/or EGCG or N-acetyl-cysteine.	Acetylcysteine	181-198	mitogen-activated protein kinase 8	Homo sapiens	25-28
28399781-6	2017	N-acetyl-l-cysteine (NAC), a ROS scavenger, partially reduced PCB 118-induced apoptosis and Bax/Bcl-2 ratios in HUVECs.	Acetylcysteine	0-19	BCL2 associated X, apoptosis regulator	Homo sapiens	92-95
28487945-3	2017	Nox4 and the Notch pathway were inhibited by N-acetylcysteine (NAC), diphenylene iodonium (DPI) or gamma-secretase inhibitor (DAPT).	Acetylcysteine	45-61	notch receptor 1	Homo sapiens	13-18
28487945-3	2017	Nox4 and the Notch pathway were inhibited by N-acetylcysteine (NAC), diphenylene iodonium (DPI) or gamma-secretase inhibitor (DAPT).	Acetylcysteine	63-66	notch receptor 1	Homo sapiens	13-18
28487945-10	2017	Inhibition of Nox4 by NAC and DPI inhibited the Notch signaling pathway and ROS generation, which prevented HKC cell apoptosis.	Acetylcysteine	22-25	notch receptor 1	Homo sapiens	48-53
28399781-6	2017	N-acetyl-l-cysteine (NAC), a ROS scavenger, partially reduced PCB 118-induced apoptosis and Bax/Bcl-2 ratios in HUVECs.	Acetylcysteine	0-19	pyruvate carboxylase	Homo sapiens	62-65
28399781-6	2017	N-acetyl-l-cysteine (NAC), a ROS scavenger, partially reduced PCB 118-induced apoptosis and Bax/Bcl-2 ratios in HUVECs.	Acetylcysteine	0-19	BCL2 apoptosis regulator	Homo sapiens	96-101
28341536-11	2017	Beyond that, the antioxidant N-acetyl cysteine (NAC) could reverse the changes of both cPLA2 and NF-kappaB caused by MGO.	Acetylcysteine	29-46	nuclear factor kappa B subunit 1	Homo sapiens	97-106
28653879-5	2017	In this study, doxorubicin-induced reactive oxygen species was shown to differentially affect cancer cells based on their TP53 genetic status; doxorubicin-induced apoptosis was attenuated by an antioxidant, N-acetylcysteine, in TP53 wild cells; however, N-acetylcysteine caused a synergistic increase in the apoptosis rate in TP53-altered cells.	Acetylcysteine	207-223	tumor protein p53	Homo sapiens	122-126
28653879-5	2017	In this study, doxorubicin-induced reactive oxygen species was shown to differentially affect cancer cells based on their TP53 genetic status; doxorubicin-induced apoptosis was attenuated by an antioxidant, N-acetylcysteine, in TP53 wild cells; however, N-acetylcysteine caused a synergistic increase in the apoptosis rate in TP53-altered cells.	Acetylcysteine	207-223	tumor protein p53	Homo sapiens	228-232
28653879-5	2017	In this study, doxorubicin-induced reactive oxygen species was shown to differentially affect cancer cells based on their TP53 genetic status; doxorubicin-induced apoptosis was attenuated by an antioxidant, N-acetylcysteine, in TP53 wild cells; however, N-acetylcysteine caused a synergistic increase in the apoptosis rate in TP53-altered cells.	Acetylcysteine	207-223	tumor protein p53	Homo sapiens	228-232
28653879-6	2017	N-acetylcysteine prevented phosphorylation of P53 protein that had been induced by doxorubicin.	Acetylcysteine	0-16	tumor protein p53	Homo sapiens	46-49
28653879-7	2017	However, N-acetylcysteine increased the cleavage of poly (ADP-ribose) polymerase in the presence of doxorubicin.	Acetylcysteine	9-25	poly(ADP-ribose) polymerase 1	Homo sapiens	52-80
28341536-11	2017	Beyond that, the antioxidant N-acetyl cysteine (NAC) could reverse the changes of both cPLA2 and NF-kappaB caused by MGO.	Acetylcysteine	48-51	nuclear factor kappa B subunit 1	Homo sapiens	97-106
28347754-6	2017	Moreover, Cd-induced oxidative stress intimately correlated with cytosolic Ca2+ mobilization, and N-acetylcysteine (NAC) markedly rescued Cd-blocked autophagosome-lysosome fusion and recruitment of Rab7 to autophagosomes in rPT cells, implying that Cd-induced autophagy inhibition was due to [Ca2+]c elevation-triggered oxidative stress.	Acetylcysteine	98-114	RAB7A, member RAS oncogene family	Rattus norvegicus	198-202
28347754-6	2017	Moreover, Cd-induced oxidative stress intimately correlated with cytosolic Ca2+ mobilization, and N-acetylcysteine (NAC) markedly rescued Cd-blocked autophagosome-lysosome fusion and recruitment of Rab7 to autophagosomes in rPT cells, implying that Cd-induced autophagy inhibition was due to [Ca2+]c elevation-triggered oxidative stress.	Acetylcysteine	116-119	RAB7A, member RAS oncogene family	Rattus norvegicus	198-202
27635524-4	2017	CIH rats treated with infliximab further increased TNF-alpha, IL-1beta, IL-6, and interferon-gamma diaphragm levels, whereas NAC induced a reduction only in TNF-alpha and IL-1beta levels in diaphragm and plasma.	Acetylcysteine	125-128	tumor necrosis factor	Rattus norvegicus	157-166
28507720-5	2017	Supplementary acetylcysteine can suppress this upregulation, revealing that the LAP increase may be connected with a deficiency in biothiols.	Acetylcysteine	14-28	leucine aminopeptidase 3	Mus musculus	80-83
28482716-6	2017	Moreover, N-acetyl-cysteine (NAC), an ROS scavenger, abrogated the effects of DHM on NF-kappaB-dependent autophagy.	Acetylcysteine	10-27	nuclear factor kappa B subunit 1	Homo sapiens	85-94
28482716-6	2017	Moreover, N-acetyl-cysteine (NAC), an ROS scavenger, abrogated the effects of DHM on NF-kappaB-dependent autophagy.	Acetylcysteine	29-32	nuclear factor kappa B subunit 1	Homo sapiens	85-94
27917510-9	2017	N-acetyl-l-cysteine suppressed MeHg-induced activation of IL-6 and IL-8 mRNA expression in U937 macrophages, indicating the effectiveness of N-acetyl-l-cysteine as a therapeutic drug in MeHg-induced inflammation.	Acetylcysteine	0-19	interleukin 6	Homo sapiens	58-62
27917510-9	2017	N-acetyl-l-cysteine suppressed MeHg-induced activation of IL-6 and IL-8 mRNA expression in U937 macrophages, indicating the effectiveness of N-acetyl-l-cysteine as a therapeutic drug in MeHg-induced inflammation.	Acetylcysteine	0-19	C-X-C motif chemokine ligand 8	Homo sapiens	67-71
27917510-9	2017	N-acetyl-l-cysteine suppressed MeHg-induced activation of IL-6 and IL-8 mRNA expression in U937 macrophages, indicating the effectiveness of N-acetyl-l-cysteine as a therapeutic drug in MeHg-induced inflammation.	Acetylcysteine	141-160	interleukin 6	Homo sapiens	58-62
27917510-9	2017	N-acetyl-l-cysteine suppressed MeHg-induced activation of IL-6 and IL-8 mRNA expression in U937 macrophages, indicating the effectiveness of N-acetyl-l-cysteine as a therapeutic drug in MeHg-induced inflammation.	Acetylcysteine	141-160	C-X-C motif chemokine ligand 8	Homo sapiens	67-71
28163174-8	2017	The areas positive for both C4bp and C3d were increased in the presence of N-acetylcysteine.	Acetylcysteine	75-91	complement component 4 binding protein alpha	Homo sapiens	28-32
27943387-5	2017	Results showed that ovariectomy resulted in bone loss with increased osteoclast surface, increased ROS levels, T cell activation, and increased TNF and RANKL levels in serum and in CD4 T cells; NAC supplementation largely prevented these alterations.	Acetylcysteine	194-197	tumor necrosis factor	Mus musculus	144-147
27635524-4	2017	CIH rats treated with infliximab further increased TNF-alpha, IL-1beta, IL-6, and interferon-gamma diaphragm levels, whereas NAC induced a reduction only in TNF-alpha and IL-1beta levels in diaphragm and plasma.	Acetylcysteine	125-128	interleukin 1 beta	Rattus norvegicus	171-179
27706903-7	2017	Importantly, the combination of N-acetylcysteine and tauroursodeoxycholic acid improved serum transaminase levels, reduced histopathological liver damage, UPR-activated CHOP, oxidative stress, caspase 1 expression, NLRP3 levels, IL-1beta levels and the expression of pro-inflammatory cytokines and this to a greater extend than N-acetylcysteine alone.	Acetylcysteine	32-48	interleukin 1 beta	Mus musculus	229-237
28314481-10	2017	The presence of N-acetyl-l-cysteine significantly prevented the inductive effect of GK, OC and ISO on MDR1 mRNA level.	Acetylcysteine	16-35	ATP binding cassette subfamily B member 1	Homo sapiens	102-106
28335600-9	2017	Compared with free NAC, the production of ROS, NO3-, NO2-, tumor necrosis factor-alpha (TNF-alpha), and interleukin (IL)-1beta from the LPS-stimulated microglia was considerably decreased when the cells were pretreated with NAC-NPs.	Acetylcysteine	224-227	tumor necrosis factor	Homo sapiens	47-86
28335600-9	2017	Compared with free NAC, the production of ROS, NO3-, NO2-, tumor necrosis factor-alpha (TNF-alpha), and interleukin (IL)-1beta from the LPS-stimulated microglia was considerably decreased when the cells were pretreated with NAC-NPs.	Acetylcysteine	224-227	interleukin 1 beta	Homo sapiens	104-126
28496415-10	2017	The activation of the MAPK/NF-kappaB signaling and induction of IL-8 to both CSE types were suppressed to similar levels by NAC, AMTB, or EGTA.	Acetylcysteine	124-127	C-X-C motif chemokine ligand 8	Homo sapiens	64-68
28422158-9	2017	When oxidative stress was blocked by exposing mice to N-acetylcysteine, induction of liver UGT1A1 and CYP2B10 by PEITC was prevented.	Acetylcysteine	54-70	cytochrome P450, family 2, subfamily b, polypeptide 10	Mus musculus	102-109
28503420-13	2017	In addition, antioxidant NAC attenuated H2O2-induced inhibition of ARPE-19 cell viability through alleviating reduction of EGFR, and phosphorylated and total AKT proteins.	Acetylcysteine	25-28	epidermal growth factor receptor	Homo sapiens	123-127
28503420-13	2017	In addition, antioxidant NAC attenuated H2O2-induced inhibition of ARPE-19 cell viability through alleviating reduction of EGFR, and phosphorylated and total AKT proteins.	Acetylcysteine	25-28	AKT serine/threonine kinase 1	Homo sapiens	158-161
28467758-9	2017	Intraperitoneal administration of NAC decreased IL-6 and TNF-alpha concentration to 294.6 and 17.1 pg/mL, respectively, and was more effective than SC or PO administration.	Acetylcysteine	34-37	interleukin 6	Rattus norvegicus	48-52
28467758-9	2017	Intraperitoneal administration of NAC decreased IL-6 and TNF-alpha concentration to 294.6 and 17.1 pg/mL, respectively, and was more effective than SC or PO administration.	Acetylcysteine	34-37	tumor necrosis factor	Rattus norvegicus	57-66
28427419-11	2017	TNF-alpha-mediated increased release of EVs can be blocked by either the glutaminase inhibitor, antioxidant N-acetyl-L-cysteine, or genetic knockout of glutaminase, suggesting that glutaminase plays an important role in astrocyte EV release during neuroinflammation.	Acetylcysteine	108-127	tumor necrosis factor	Mus musculus	0-9
28052869-5	2017	In vitro, exposure of podocytes to Aldo enhanced NLRP3, caspase-1, and IL-18 expressions in dose- and time-dependent manners, indicating an activation of NLRP3 inflammasome, which was significantly blocked by the mineralocorticoid receptor antagonist eplerenone or the antioxidant N-acetylcysteine.	Acetylcysteine	281-297	NLR family pyrin domain containing 3	Homo sapiens	154-159
28915583-0	2017	N-Acetylcysteine breaks resistance to trastuzumab caused by MUC4 overexpression in human HER2 positive BC-bearing nude mice monitored by 89Zr-Trastuzumab and 18F-FDG PET imaging.	Acetylcysteine	0-16	erb-b2 receptor tyrosine kinase 2	Homo sapiens	89-93
28915583-9	2017	These findings suggest that improving HER2-accessibility by reducing MUC4-masking with the mucolytic drug NAC, results in a higher anti-tumor effect of trastuzumab.	Acetylcysteine	106-109	erb-b2 receptor tyrosine kinase 2	Homo sapiens	38-42
28202418-6	2017	Our results showed that ROS inhibitor N-acetyl-l-cysteine (NAC) suppressed the upregulation of intracellular ROS and TXNIP expression.	Acetylcysteine	38-57	thioredoxin interacting protein	Mus musculus	117-122
28202418-6	2017	Our results showed that ROS inhibitor N-acetyl-l-cysteine (NAC) suppressed the upregulation of intracellular ROS and TXNIP expression.	Acetylcysteine	59-62	thioredoxin interacting protein	Mus musculus	117-122
28202418-7	2017	Furthermore, the cell apoptosis and expression of apoptotic protein were significantly attenuated after treatment of thrombin with NAC or NLRP3 antagonist (MCC950).	Acetylcysteine	131-134	coagulation factor II	Mus musculus	117-125
27539140-8	2017	Furthermore, treatment of cells with specific inhibitors of ERK and JNK or NAC significantly promoted the DHM-induced activation of caspase-9/-7/-3 and PARP cleavage and also sensitized the antitumorigenic effect of DHM on NSCLC cells.	Acetylcysteine	75-78	poly(ADP-ribose) polymerase 1	Homo sapiens	152-156
28108507-9	2017	Treatment of FLT3-ITD- and JAK2V617F-mutant cells with the antioxidant N-acetylcysteine diminished reactive oxygen species (ROS), restoring iHR and HR levels.	Acetylcysteine	71-87	fms related receptor tyrosine kinase 3	Homo sapiens	13-21
27531051-8	2017	OxS being drug-targetable, it represents an interesting therapeutic target for these incurable conditions, and following preclinical correction of the cell or animal model phenotype, the first clinical trials with the antioxidants N-acetylcysteine (SEPN1- and RYR1-related myopathies) or epigallocatechin-gallate (DMD) have been launched recently.	Acetylcysteine	231-247	ryanodine receptor 1	Homo sapiens	260-264
28485782-0	2017	NAC attenuates adriamycin-induced nephrotic syndrome in rats through regulating TLR4 signaling pathway.	Acetylcysteine	0-3	toll-like receptor 4	Rattus norvegicus	80-84
28485782-3	2017	The aim of this study was to evaluate the immunosuppressive effect of N-acetylcysteine (NAC) in the treatment of NS elucidate its interaction with TLR4 pathway in a rat model.	Acetylcysteine	70-86	toll-like receptor 4	Rattus norvegicus	147-151
28485782-3	2017	The aim of this study was to evaluate the immunosuppressive effect of N-acetylcysteine (NAC) in the treatment of NS elucidate its interaction with TLR4 pathway in a rat model.	Acetylcysteine	88-91	toll-like receptor 4	Rattus norvegicus	147-151
28485782-11	2017	After NAC treatment, TLR4 level was reduced.	Acetylcysteine	6-9	toll-like receptor 4	Rattus norvegicus	21-25
28485782-13	2017	Concomitantly, TNF-alpha, IL-6, and IL-1beta levels, which are indicators of immunological and informatory responses, were also decreased after NAC treatment.	Acetylcysteine	144-147	tumor necrosis factor	Rattus norvegicus	15-24
28485782-13	2017	Concomitantly, TNF-alpha, IL-6, and IL-1beta levels, which are indicators of immunological and informatory responses, were also decreased after NAC treatment.	Acetylcysteine	144-147	interleukin 6	Rattus norvegicus	26-30
28485782-13	2017	Concomitantly, TNF-alpha, IL-6, and IL-1beta levels, which are indicators of immunological and informatory responses, were also decreased after NAC treatment.	Acetylcysteine	144-147	interleukin 1 beta	Rattus norvegicus	36-44
28485782-14	2017	CONCLUSIONS: NAC treatment ameliorated nephrotic syndrome in NS rat models by suppressing TLR4 signaling, as well as immunological and inflammatory responses.	Acetylcysteine	13-16	toll-like receptor 4	Rattus norvegicus	90-94
28299863-3	2017	DKK3 knockdown by siRNA resulted in reactive oxygen species accumulation and subsequent apoptosis, which were abrogated by administration of the antioxidant N-acetyl-cysteine.	Acetylcysteine	157-174	dickkopf WNT signaling pathway inhibitor 3	Homo sapiens	0-4
27753160-6	2017	Short-term incubation either with an specific inhibitor of tumor necrosis factor receptor 1 signaling or an antioxidant N-acetyl-L-cysteine (NAC) prevents TNF-alpha-mediated ROS accumulation in HSCs.	Acetylcysteine	120-139	tumor necrosis factor	Homo sapiens	155-164
27753160-6	2017	Short-term incubation either with an specific inhibitor of tumor necrosis factor receptor 1 signaling or an antioxidant N-acetyl-L-cysteine (NAC) prevents TNF-alpha-mediated ROS accumulation in HSCs.	Acetylcysteine	141-144	tumor necrosis factor	Homo sapiens	155-164
28259956-6	2017	Furthermore, hydrogen peroxide (H2O2; an exogenous ROS) downregulated the expression and activity of CSE, and had similar effects as AngII, whereas the inhibitory effects of AngII were completely suppressed by N-acetyl-L-cysteine (a ROS scavenger).	Acetylcysteine	210-229	angiotensinogen	Homo sapiens	174-179
28401107-0	2017	Is N-acetylcysteine infusion an effective treatment option in L-asparaginase associated hepatotoxicity?	Acetylcysteine	3-19	asparaginase and isoaspartyl peptidase 1	Homo sapiens	62-76
28333148-8	2017	Diphenyleneiodonium (a NAD(P)H oxidase inhibitor) or N-acetylcysteine (an antioxidant) inhibited the salusin-beta-induced NFkappaB activation and inflammation.	Acetylcysteine	53-69	torsin family 2 member A	Homo sapiens	101-113
28199982-9	2017	NAC inhibited the cleavage of IL-1beta in DRGs, which is a critical substrate of MMP-9, and markedly suppressed glial activation and neuron excitability in spinal dorsal horn induced by remifentanil.	Acetylcysteine	0-3	interleukin 1 beta	Rattus norvegicus	30-38
28087840-9	2017	Reactive oxygen species (ROS) inhibitor, N-acetyl cysteine (NAC), suppressed TNF-alpha/Cholix-induced JNK and ERK phosphorylation, resulting in inhibition of PARP cleavage.	Acetylcysteine	41-58	tumor necrosis factor	Homo sapiens	77-86
28087840-9	2017	Reactive oxygen species (ROS) inhibitor, N-acetyl cysteine (NAC), suppressed TNF-alpha/Cholix-induced JNK and ERK phosphorylation, resulting in inhibition of PARP cleavage.	Acetylcysteine	41-58	mitogen-activated protein kinase 8	Homo sapiens	102-105
28087840-9	2017	Reactive oxygen species (ROS) inhibitor, N-acetyl cysteine (NAC), suppressed TNF-alpha/Cholix-induced JNK and ERK phosphorylation, resulting in inhibition of PARP cleavage.	Acetylcysteine	41-58	mitogen-activated protein kinase 1	Homo sapiens	110-113
28087840-9	2017	Reactive oxygen species (ROS) inhibitor, N-acetyl cysteine (NAC), suppressed TNF-alpha/Cholix-induced JNK and ERK phosphorylation, resulting in inhibition of PARP cleavage.	Acetylcysteine	41-58	poly(ADP-ribose) polymerase 1	Homo sapiens	158-162
28087840-9	2017	Reactive oxygen species (ROS) inhibitor, N-acetyl cysteine (NAC), suppressed TNF-alpha/Cholix-induced JNK and ERK phosphorylation, resulting in inhibition of PARP cleavage.	Acetylcysteine	60-63	tumor necrosis factor	Homo sapiens	77-86
28087840-9	2017	Reactive oxygen species (ROS) inhibitor, N-acetyl cysteine (NAC), suppressed TNF-alpha/Cholix-induced JNK and ERK phosphorylation, resulting in inhibition of PARP cleavage.	Acetylcysteine	60-63	mitogen-activated protein kinase 8	Homo sapiens	102-105
28087840-9	2017	Reactive oxygen species (ROS) inhibitor, N-acetyl cysteine (NAC), suppressed TNF-alpha/Cholix-induced JNK and ERK phosphorylation, resulting in inhibition of PARP cleavage.	Acetylcysteine	60-63	mitogen-activated protein kinase 1	Homo sapiens	110-113
28087840-9	2017	Reactive oxygen species (ROS) inhibitor, N-acetyl cysteine (NAC), suppressed TNF-alpha/Cholix-induced JNK and ERK phosphorylation, resulting in inhibition of PARP cleavage.	Acetylcysteine	60-63	poly(ADP-ribose) polymerase 1	Homo sapiens	158-162
28405169-5	2017	RESULTS: TGF-beta1-stimulated cells demonstrated a loss of H-ferritin, which was prevented by the antioxidant N-acetyl-L-cysteine (NAC) and inhibitors of lysosomal degradation.	Acetylcysteine	110-129	transforming growth factor beta 1	Homo sapiens	9-18
28405169-5	2017	RESULTS: TGF-beta1-stimulated cells demonstrated a loss of H-ferritin, which was prevented by the antioxidant N-acetyl-L-cysteine (NAC) and inhibitors of lysosomal degradation.	Acetylcysteine	131-134	transforming growth factor beta 1	Homo sapiens	9-18
28223539-10	2017	Furthermore, H2O2 treatment increased the phosphorylation of p65 and IkappaBalpha, which were decreased when treated with N-acetyl cysteine or thymol.	Acetylcysteine	122-139	nuclear factor of kappa light polypeptide gene enhancer in B cells inhibitor, alpha	Mus musculus	69-81
28303030-8	2017	Moreover, it was found that the activation of FPRs increased the generation of reactive oxygen species (ROS) and phosphorylation of AKT in the NSCs, while N-acetylcysteine and LY294002 inhibited the FPRs-stimulated increase in ROS generation and AKT phosphorylation, and blocked the FPRs-stimulated neural differentiation into neurons.	Acetylcysteine	155-171	thymoma viral proto-oncogene 1	Mus musculus	246-249
27038427-11	2017	In the NAC-LA subgroups, rates of apoptosis and necrosis, intracellular ROS production, and caspase-3/7 activity were significantly lower than in their paired LA subgroups (p &lt;= 0.023).	Acetylcysteine	7-10	caspase 3	Homo sapiens	92-101
28063998-9	2017	Furthermore, N-acetyl-cysteine (NAC), a ROS scavenger, abrogated the effects of brazilin on the NF-kappaB p65-dependent autophagy.	Acetylcysteine	13-30	nuclear factor kappa B subunit 1	Homo sapiens	96-105
28063998-9	2017	Furthermore, N-acetyl-cysteine (NAC), a ROS scavenger, abrogated the effects of brazilin on the NF-kappaB p65-dependent autophagy.	Acetylcysteine	32-35	nuclear factor kappa B subunit 1	Homo sapiens	96-105
28097492-12	2017	The CAP and H2O2-induced TRPM2 current densities were also decreased by the NADPH oxidase inhibitors apocynin and N-Acetylcysteine.	Acetylcysteine	114-130	transient receptor potential cation channel, subfamily M, member 2	Rattus norvegicus	25-30
27654302-7	2017	Meanwhile, fucoidan treatment increased the generation of intracellular ROS, whereas the over-elimination of ROS by N-acetylcysteine, an anti-oxidant, attenuated fucoidan-induced apoptosis, inhibition of hTERT, c-myc, and Sp1 expression, and reversed fucoidan-induced inactivation of the PI3K/Akt signaling pathway.	Acetylcysteine	116-132	AKT serine/threonine kinase 1	Homo sapiens	293-296
28178219-8	2017	However, pre-treatment with the antioxidant N-acetylcysteine (NAC) significantly inhibited the activation of Bax and prevented down-regulation of STAT3 target genes.	Acetylcysteine	44-60	BCL2 associated X, apoptosis regulator	Homo sapiens	109-112
28178219-8	2017	However, pre-treatment with the antioxidant N-acetylcysteine (NAC) significantly inhibited the activation of Bax and prevented down-regulation of STAT3 target genes.	Acetylcysteine	44-60	signal transducer and activator of transcription 3	Homo sapiens	146-151
28178219-8	2017	However, pre-treatment with the antioxidant N-acetylcysteine (NAC) significantly inhibited the activation of Bax and prevented down-regulation of STAT3 target genes.	Acetylcysteine	62-65	BCL2 associated X, apoptosis regulator	Homo sapiens	109-112
28178219-8	2017	However, pre-treatment with the antioxidant N-acetylcysteine (NAC) significantly inhibited the activation of Bax and prevented down-regulation of STAT3 target genes.	Acetylcysteine	62-65	signal transducer and activator of transcription 3	Homo sapiens	146-151
28178193-10	2017	Co-treatment with the antioxidant N-acetylcysteine completely abolished cearoin-mediated autophagy, ERK activation and apoptosis, suggesting the critical role of ROS in cearoin-induced anticancer effects.	Acetylcysteine	34-50	mitogen-activated protein kinase 1	Homo sapiens	100-103
28451559-13	2017	The NAC modulated the NaAsO2 associated alterations of CAT and SOD2 mRNA levels, therefore, the NaAsO2 might act through inducing reactive oxygen species.	Acetylcysteine	4-7	catalase	Homo sapiens	55-58
28118826-8	2017	Concentrations of NAC &gt;=300 muM inhibited the inflammatory response (release of IL-1beta, IL-8, and TNF-alpha) of human airways induced by the overnight stimulation with LPS, whereas lower concentrations of NAC (&gt;=1 muM) were sufficient to reduce the release of IL-6 elicited by LPS.	Acetylcysteine	18-21	interleukin 6	Homo sapiens	268-272
28118826-6	2017	Concentrations of NAC &gt;=1 muM reduced the pro-oxidant response (peroxidase activity, hydrogen peroxide, malondialdehyde, nitric oxide), and improved the anti-oxidant response (total anti-oxidant capacity, glutathione, superoxide dismutase) induced by LPS.	Acetylcysteine	18-21	latexin	Homo sapiens	29-32
28118826-9	2017	Both the anti-oxidant effect and the anti-inflammatory effect of NAC were inversely correlated with the release of NKA.	Acetylcysteine	65-68	tachykinin precursor 1	Homo sapiens	115-118
28118826-8	2017	Concentrations of NAC &gt;=300 muM inhibited the inflammatory response (release of IL-1beta, IL-8, and TNF-alpha) of human airways induced by the overnight stimulation with LPS, whereas lower concentrations of NAC (&gt;=1 muM) were sufficient to reduce the release of IL-6 elicited by LPS.	Acetylcysteine	18-21	latexin	Homo sapiens	31-34
28118826-8	2017	Concentrations of NAC &gt;=300 muM inhibited the inflammatory response (release of IL-1beta, IL-8, and TNF-alpha) of human airways induced by the overnight stimulation with LPS, whereas lower concentrations of NAC (&gt;=1 muM) were sufficient to reduce the release of IL-6 elicited by LPS.	Acetylcysteine	18-21	interleukin 1 beta	Homo sapiens	83-91
28054986-7	2017	Moreover, blockage of ROS production by using the ROS inhibitor N-acetyl-l-cysteine totally reversed SFN-mediated down-regulation of JAK2/Src-STAT3 signaling activation and the subsequent effects on apoptosis by blocking the induction of apoptosis-related genes in GBM cells.	Acetylcysteine	64-83	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	138-141
28118826-8	2017	Concentrations of NAC &gt;=300 muM inhibited the inflammatory response (release of IL-1beta, IL-8, and TNF-alpha) of human airways induced by the overnight stimulation with LPS, whereas lower concentrations of NAC (&gt;=1 muM) were sufficient to reduce the release of IL-6 elicited by LPS.	Acetylcysteine	18-21	C-X-C motif chemokine ligand 8	Homo sapiens	93-97
28118826-8	2017	Concentrations of NAC &gt;=300 muM inhibited the inflammatory response (release of IL-1beta, IL-8, and TNF-alpha) of human airways induced by the overnight stimulation with LPS, whereas lower concentrations of NAC (&gt;=1 muM) were sufficient to reduce the release of IL-6 elicited by LPS.	Acetylcysteine	18-21	tumor necrosis factor	Homo sapiens	103-112
28118826-8	2017	Concentrations of NAC &gt;=300 muM inhibited the inflammatory response (release of IL-1beta, IL-8, and TNF-alpha) of human airways induced by the overnight stimulation with LPS, whereas lower concentrations of NAC (&gt;=1 muM) were sufficient to reduce the release of IL-6 elicited by LPS.	Acetylcysteine	18-21	latexin	Homo sapiens	222-225
27926485-3	2017	Moreover, we found that p21(Waf1/Cip1) increased levels correlates with induction of ROS and senescence-associated cell death in U87 and T98 cell lines, which are reverted by N-acetyl cysteine pretreatment.	Acetylcysteine	175-192	cyclin dependent kinase inhibitor 1A	Homo sapiens	24-27
27926485-3	2017	Moreover, we found that p21(Waf1/Cip1) increased levels correlates with induction of ROS and senescence-associated cell death in U87 and T98 cell lines, which are reverted by N-acetyl cysteine pretreatment.	Acetylcysteine	175-192	cyclin dependent kinase inhibitor 1A	Homo sapiens	28-32
27926485-3	2017	Moreover, we found that p21(Waf1/Cip1) increased levels correlates with induction of ROS and senescence-associated cell death in U87 and T98 cell lines, which are reverted by N-acetyl cysteine pretreatment.	Acetylcysteine	175-192	cyclin dependent kinase inhibitor 1A	Homo sapiens	33-37
28045034-0	2017	Premature senescence of endothelial cells upon chronic exposure to TNFalpha can be prevented by N-acetyl cysteine and plumericin.	Acetylcysteine	96-113	tumor necrosis factor	Homo sapiens	67-75
28054986-7	2017	Moreover, blockage of ROS production by using the ROS inhibitor N-acetyl-l-cysteine totally reversed SFN-mediated down-regulation of JAK2/Src-STAT3 signaling activation and the subsequent effects on apoptosis by blocking the induction of apoptosis-related genes in GBM cells.	Acetylcysteine	64-83	signal transducer and activator of transcription 3	Homo sapiens	142-147
27717985-8	2017	TQ or NAC pretreatment significantly decreased elevated serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), and myeloperoxidase (MPO) activities, malondialdehyde (MDA) level, and NO production.	Acetylcysteine	6-9	glutamic-oxaloacetic transaminase 2	Rattus norvegicus	62-88
27600580-11	2017	Losartan and N-acetylcysteine could also reverse Ang II-induced changes.	Acetylcysteine	13-29	angiotensinogen	Rattus norvegicus	49-55
29061063-6	2017	RESULTS: Compared with Model group, The NAC and DXM groups were improved in H (et) E staining, the TGF-beta1 concentration of NAC and DXM groups were significantly reduced in BALF and lung tissue (p &lt; 0.05, respectively).	Acetylcysteine	126-129	transforming growth factor, beta 1	Rattus norvegicus	99-108
29061063-7	2017	TLR-4 and NF-kappab proteins of NAC and DXM groups were lower than that of Model group in IHC and WB assays (p &lt; 0.05, respectively).	Acetylcysteine	32-35	toll-like receptor 4	Rattus norvegicus	0-5
29061063-8	2017	CONCLUSION: NAC had effects to protect LPS induced lung injury via TLR-4/NF-kappab signaling pathway (Fig.	Acetylcysteine	12-15	toll-like receptor 4	Rattus norvegicus	67-72
28291959-8	2017	Diazoxide (DZ, a mitochondrial KATP channel opener) or pinacidil (Pin, a non-selective KATP channel opener) or N-acetyl-L-cysteine (NAC, a ROS scavenger) pre-treatment blocked the up-regulation of TLR4 and RIP3.	Acetylcysteine	111-130	toll-like receptor 4	Rattus norvegicus	197-201
27867098-7	2017	The induction of HO-1 expression by ammonia was dependent on ROS formation and prevented by N-acetylcysteine or rotenone.	Acetylcysteine	92-108	heme oxygenase 1	Mus musculus	17-21
27717985-8	2017	TQ or NAC pretreatment significantly decreased elevated serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), and myeloperoxidase (MPO) activities, malondialdehyde (MDA) level, and NO production.	Acetylcysteine	6-9	glutamic-oxaloacetic transaminase 2	Rattus norvegicus	90-93
28004071-8	2016	Administration of NAC could attenuate the alveolar wall structure damage induced by O3 exposure and reduce the amount of infiltrated inflammatory cells, total and differential leukocyte counts (P &lt; 0.05), as well as the IL-6, IL-8 (P &lt; 0.01) and MDA release (P &lt; 0.05).	Acetylcysteine	18-21	interleukin 6	Mus musculus	223-227
28157110-15	2017	Meanwhile, elevated Cx40 expression in cortex was also prevented by NAC treatment.	Acetylcysteine	68-71	gap junction protein, alpha 5	Rattus norvegicus	20-24
27777014-5	2016	The induction of HO-1 by 7-O-galloylquercetin was significantly suppressed by N-acetyl-l-cysteine and SB203580, indicating the involvement of reactive oxygen species and p38 mitogen-activated protein kinase activity, respectively.	Acetylcysteine	78-97	heme oxygenase 1	Mus musculus	17-21
29062463-7	2017	NAC exerts its protective effect likely by lowering oxidative stress, as supported by the reduction of 3-NT and SOD2 levels.	Acetylcysteine	0-3	superoxide dismutase 2, mitochondrial	Mus musculus	112-116
29456784-7	2017	In addition, acrolein-induced toxicity in idh2 shRNA-transfected LLC cells and in idh2 knockout mice was ameliorated by the antioxidant, N-acetylcysteine, through attenuation of oxidative stress resulting from idh2 deficiency.	Acetylcysteine	137-153	isocitrate dehydrogenase (NADP(+)) 2	Homo sapiens	42-46
28081748-8	2016	Inhibition of ROS generation by NAC resulted in a significant reduction of HVJ-E-induced Erk1/2, JNK, and p38 MAPK activation.	Acetylcysteine	32-35	mitogen-activated protein kinase 1	Mus musculus	110-114
27941930-8	2016	Furthermore, suppression of ASIC1-mediated generation of reactive oxygen species (ROS) by ROS scavengers, such as glutathione or N-acetyl-cysteine causes a decrease in ERK phosphorylation and degradation of IkappaBalpha.	Acetylcysteine	129-146	mitogen-activated protein kinase 1	Homo sapiens	168-171
27941930-8	2016	Furthermore, suppression of ASIC1-mediated generation of reactive oxygen species (ROS) by ROS scavengers, such as glutathione or N-acetyl-cysteine causes a decrease in ERK phosphorylation and degradation of IkappaBalpha.	Acetylcysteine	129-146	NFKB inhibitor alpha	Homo sapiens	207-219
27868128-5	2016	NAC significantly alleviated Cr(vi)-induced up-regulation of STIM1, phosphorylated-extracellular-signal-regulated kinases 1 and 2 (p-ERK1/2), ERK1/2 and nuclear factor kappaB (NF-kappaB).	Acetylcysteine	0-3	stromal interaction molecule 1	Homo sapiens	61-66
27868128-5	2016	NAC significantly alleviated Cr(vi)-induced up-regulation of STIM1, phosphorylated-extracellular-signal-regulated kinases 1 and 2 (p-ERK1/2), ERK1/2 and nuclear factor kappaB (NF-kappaB).	Acetylcysteine	0-3	mitogen-activated protein kinase 3	Homo sapiens	133-139
27868128-5	2016	NAC significantly alleviated Cr(vi)-induced up-regulation of STIM1, phosphorylated-extracellular-signal-regulated kinases 1 and 2 (p-ERK1/2), ERK1/2 and nuclear factor kappaB (NF-kappaB).	Acetylcysteine	0-3	mitogen-activated protein kinase 3	Homo sapiens	142-148
27639126-10	2016	ROS scavenger N-acetylcysteine (NAC) and NF-kappaB inhibitor PDTC showed similar effect on PA-induced secretion of TNF-alpha, IL-6, and expression of ICAM-1.	Acetylcysteine	14-30	tumor necrosis factor	Homo sapiens	115-124
27701797-6	2016	Moreover acute N-acetylcysteine also prevented the inhibition of LTP by TNFalpha, a putative mediator of Ass actions, and repeated systemic N-acetylcysteine treatment for 7 days reversed the delayed deleterious effect of Ass on LTP.	Acetylcysteine	15-31	tumor necrosis factor	Rattus norvegicus	72-80
27989750-6	2016	We further demonstrate that the radical scavenger N-acetyl-L-cysteine reverts hnRNPA2/B1 and PKM2 inhibition by genipin indicating a role for reactive oxygen species in the metabolic reprogramming of cancer cells mediated by UCP2.	Acetylcysteine	50-69	heterogeneous nuclear ribonucleoprotein A2/B1	Homo sapiens	78-85
27639126-10	2016	ROS scavenger N-acetylcysteine (NAC) and NF-kappaB inhibitor PDTC showed similar effect on PA-induced secretion of TNF-alpha, IL-6, and expression of ICAM-1.	Acetylcysteine	14-30	interleukin 6	Homo sapiens	126-130
27639126-10	2016	ROS scavenger N-acetylcysteine (NAC) and NF-kappaB inhibitor PDTC showed similar effect on PA-induced secretion of TNF-alpha, IL-6, and expression of ICAM-1.	Acetylcysteine	32-35	tumor necrosis factor	Homo sapiens	115-124
27639126-10	2016	ROS scavenger N-acetylcysteine (NAC) and NF-kappaB inhibitor PDTC showed similar effect on PA-induced secretion of TNF-alpha, IL-6, and expression of ICAM-1.	Acetylcysteine	32-35	interleukin 6	Homo sapiens	126-130
27639126-12	2016	In addition, insulin-triggered expression of p-IRS-1(Tyr), p-PI3K, p-AKT, p-eNOS and NO generation were inhibited by PA, which were also restored by both APN and NAC.	Acetylcysteine	162-165	insulin	Homo sapiens	13-20
26370073-9	2016	Blocking ROS production by N-acetyl cysteine (NAC) protected GC-1 cells from terbufos-induced cell death.	Acetylcysteine	27-44	guanylate cyclase 2e	Mus musculus	61-65
26370073-9	2016	Blocking ROS production by N-acetyl cysteine (NAC) protected GC-1 cells from terbufos-induced cell death.	Acetylcysteine	46-49	guanylate cyclase 2e	Mus musculus	61-65
27614430-3	2016	Moreover, the two vanadium compounds induced the activation of both PI3K/AKT and MAPK/ERK signaling pathways dose- and time-dependently, which could be counteracted with the antioxidant N-acetylcysteine.	Acetylcysteine	186-202	AKT serine/threonine kinase 1	Homo sapiens	73-76
27671340-11	2016	NAC supplementation dampened the accumulation of NGAL or L-FABP, hyaluronic acid, and nitric oxide in kidney tissue (p &lt; 0.01).	Acetylcysteine	0-3	fatty acid binding protein 1	Rattus norvegicus	57-63
27932980-8	2016	We found that pretreatment with NAC, DPI, or APO also attenuated the TNF-alpha-stimulated IKKalpha/beta and NF-kappaB p65 phosphorylation, NF-kappaB (p65) translocation, and NF-kappaB promoter activity in HPAEpiCs.	Acetylcysteine	32-35	tumor necrosis factor	Homo sapiens	69-78
26808296-7	2016	Pre-treatment of AGS cells with N-acetylcysteine, a well-known reactive oxygen species (ROS) scavenger, attenuated the H. pylori-induced activation of Erk, its binding to Snail promoter, inactivation of GSK-3beta, and accumulation of Snail.	Acetylcysteine	32-48	mitogen-activated protein kinase 1	Homo sapiens	151-154
26808296-7	2016	Pre-treatment of AGS cells with N-acetylcysteine, a well-known reactive oxygen species (ROS) scavenger, attenuated the H. pylori-induced activation of Erk, its binding to Snail promoter, inactivation of GSK-3beta, and accumulation of Snail.	Acetylcysteine	32-48	snail family transcriptional repressor 1	Homo sapiens	171-176
26808296-7	2016	Pre-treatment of AGS cells with N-acetylcysteine, a well-known reactive oxygen species (ROS) scavenger, attenuated the H. pylori-induced activation of Erk, its binding to Snail promoter, inactivation of GSK-3beta, and accumulation of Snail.	Acetylcysteine	32-48	snail family transcriptional repressor 1	Homo sapiens	234-239
27721085-7	2016	N-Acetyl-L-cysteine significantly inhibited the activation of MEK1/2, ERK1/2, p38 MAPK, and Nrf2.	Acetylcysteine	0-19	NFE2 like bZIP transcription factor 2	Rattus norvegicus	92-96
26756900-10	2016	Pre-treatment with a reactive oxygen species (ROS) scavenger, N-acetylcysteine, attenuated DOX-induced Jnk activation and subsequent p53 accumulation.	Acetylcysteine	62-78	mitogen-activated protein kinase 8	Homo sapiens	103-106
26756900-10	2016	Pre-treatment with a reactive oxygen species (ROS) scavenger, N-acetylcysteine, attenuated DOX-induced Jnk activation and subsequent p53 accumulation.	Acetylcysteine	62-78	tumor protein p53	Homo sapiens	133-136
27590200-5	2016	Apocynin, Akt inhibitor SH-5, Bay 11-7085 and N-acetylcysteine each attenuated the lipopolysaccharide-induced production of cytokines, PGE2, and chemokines, changes in the levels of Toll-like receptor-4, p-Akt, mTOR, and NF-kappaB, and production of reactive oxygen species in keratinocytes.	Acetylcysteine	46-62	AKT serine/threonine kinase 1	Homo sapiens	206-209
27590200-5	2016	Apocynin, Akt inhibitor SH-5, Bay 11-7085 and N-acetylcysteine each attenuated the lipopolysaccharide-induced production of cytokines, PGE2, and chemokines, changes in the levels of Toll-like receptor-4, p-Akt, mTOR, and NF-kappaB, and production of reactive oxygen species in keratinocytes.	Acetylcysteine	46-62	mechanistic target of rapamycin kinase	Homo sapiens	211-215
27932980-8	2016	We found that pretreatment with NAC, DPI, or APO also attenuated the TNF-alpha-stimulated IKKalpha/beta and NF-kappaB p65 phosphorylation, NF-kappaB (p65) translocation, and NF-kappaB promoter activity in HPAEpiCs.	Acetylcysteine	32-35	nuclear factor kappa B subunit 1	Homo sapiens	108-117
27932980-8	2016	We found that pretreatment with NAC, DPI, or APO also attenuated the TNF-alpha-stimulated IKKalpha/beta and NF-kappaB p65 phosphorylation, NF-kappaB (p65) translocation, and NF-kappaB promoter activity in HPAEpiCs.	Acetylcysteine	32-35	nuclear factor kappa B subunit 1	Homo sapiens	139-148
27932980-8	2016	We found that pretreatment with NAC, DPI, or APO also attenuated the TNF-alpha-stimulated IKKalpha/beta and NF-kappaB p65 phosphorylation, NF-kappaB (p65) translocation, and NF-kappaB promoter activity in HPAEpiCs.	Acetylcysteine	32-35	nuclear factor kappa B subunit 1	Homo sapiens	139-148
27669171-5	2016	This accumulation of ROS contributes toward the activation of the proapoptotic factor BAX upon BV6/TMZ cotreatment as several ROS scavengers (i.e. N-acetyl-L-cysteine, MnTBAP, or alpha-tocopherol) protect GBM cells against BV6/TMZ-mediated BAX activation.	Acetylcysteine	147-166	BCL2 associated X, apoptosis regulator	Homo sapiens	86-89
27484511-11	2016	Western blotting revealed that Z5 markedly stimulated the MAPK pathways, including ERK1/2, JNK and P38, however, the mechanisms were prevented by NAC.	Acetylcysteine	146-149	mitogen-activated protein kinase 3	Homo sapiens	58-62
27484511-11	2016	Western blotting revealed that Z5 markedly stimulated the MAPK pathways, including ERK1/2, JNK and P38, however, the mechanisms were prevented by NAC.	Acetylcysteine	146-149	mitogen-activated protein kinase 8	Homo sapiens	91-94
27484511-11	2016	Western blotting revealed that Z5 markedly stimulated the MAPK pathways, including ERK1/2, JNK and P38, however, the mechanisms were prevented by NAC.	Acetylcysteine	146-149	mitogen-activated protein kinase 1	Homo sapiens	99-102
27544755-8	2016	It inhibited nuclear factor erythroid 2-related factor 2 and glutathione S-transferase P in cisplatin-resistant HNC cells, resulting in increased ROS accumulation in HNC cells, an effect that could be blocked by the antioxidant N-acetyl-L-cysteine.	Acetylcysteine	228-247	NFE2 like bZIP transcription factor 2	Homo sapiens	13-56
27846303-6	2016	The antioxidant N-acetylcysteine (NAC) blocked the AF-induced increase of reactive oxygen species (ROS) production, the reduction of total EGFR, and the phosphorylation of multiple nodes in EGFR/MAPK signaling pathway.	Acetylcysteine	16-32	epidermal growth factor receptor	Homo sapiens	139-143
27846303-6	2016	The antioxidant N-acetylcysteine (NAC) blocked the AF-induced increase of reactive oxygen species (ROS) production, the reduction of total EGFR, and the phosphorylation of multiple nodes in EGFR/MAPK signaling pathway.	Acetylcysteine	16-32	epidermal growth factor receptor	Homo sapiens	190-194
27846303-6	2016	The antioxidant N-acetylcysteine (NAC) blocked the AF-induced increase of reactive oxygen species (ROS) production, the reduction of total EGFR, and the phosphorylation of multiple nodes in EGFR/MAPK signaling pathway.	Acetylcysteine	34-37	epidermal growth factor receptor	Homo sapiens	139-143
27846303-6	2016	The antioxidant N-acetylcysteine (NAC) blocked the AF-induced increase of reactive oxygen species (ROS) production, the reduction of total EGFR, and the phosphorylation of multiple nodes in EGFR/MAPK signaling pathway.	Acetylcysteine	34-37	epidermal growth factor receptor	Homo sapiens	190-194
26320741-5	2016	LPS and Pam3csk4 also induced IRAK1/4-, ERK- and ROS-dependent activation of activator protein-1 (AP-1), IL-1beta transcription, and IL-1beta processing because significant inhibition in AP-1 activity, IL-1beta transcription, Pro- and mature IL-beta expression, and caspase-1 activity was observed with PD98059, U0126, DPI, NAC, an IRAK1/4 inhibitor, tanshinone IIa, and IRAK1 siRNA treatment.	Acetylcysteine	324-327	mitogen-activated protein kinase 1	Homo sapiens	40-43
26320741-5	2016	LPS and Pam3csk4 also induced IRAK1/4-, ERK- and ROS-dependent activation of activator protein-1 (AP-1), IL-1beta transcription, and IL-1beta processing because significant inhibition in AP-1 activity, IL-1beta transcription, Pro- and mature IL-beta expression, and caspase-1 activity was observed with PD98059, U0126, DPI, NAC, an IRAK1/4 inhibitor, tanshinone IIa, and IRAK1 siRNA treatment.	Acetylcysteine	324-327	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	98-102
26659566-6	2016	Furthermore, IS increased IL-1beta-induced reactive oxygen species (ROS) production and this effect was inhibited by pretreatment with N-acetylcysteine (a ROS scavenger) or apocynin (a NADPH oxidase inhibitor).	Acetylcysteine	135-151	interleukin 1 beta	Homo sapiens	26-34
26320741-5	2016	LPS and Pam3csk4 also induced IRAK1/4-, ERK- and ROS-dependent activation of activator protein-1 (AP-1), IL-1beta transcription, and IL-1beta processing because significant inhibition in AP-1 activity, IL-1beta transcription, Pro- and mature IL-beta expression, and caspase-1 activity was observed with PD98059, U0126, DPI, NAC, an IRAK1/4 inhibitor, tanshinone IIa, and IRAK1 siRNA treatment.	Acetylcysteine	324-327	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	77-96
27733157-4	2016	We hypothesized that treatment with antioxidant N-acetylcysteine (NAC) could enhance cardiac Cav-3 expression and attenuate caveolae dysfunction and the accompanying eNOS/NO signaling abnormalities in diabetes.	Acetylcysteine	48-64	caveolin 3	Rattus norvegicus	93-98
26541884-5	2016	Simultaneously, NAC pre-incubation attenuated nuclear factor erythroid 2-like factor 2 (NRF2) activation by RA.	Acetylcysteine	16-19	NFE2 like bZIP transcription factor 2	Homo sapiens	46-86
26541884-5	2016	Simultaneously, NAC pre-incubation attenuated nuclear factor erythroid 2-like factor 2 (NRF2) activation by RA.	Acetylcysteine	16-19	NFE2 like bZIP transcription factor 2	Homo sapiens	88-92
27637085-5	2016	DUOX2 knockdown with short interfering RNA significantly decreased IFN-gamma-induced VEGF-A or HIF-1alpha up-regulation, as did treatment of pancreatic cancer cells with the NADPH oxidase inhibitor diphenylene iodonium, the multifunctional reduced thiol N-acetylcysteine, and the polyethylene glycol-modified form of the hydrogen peroxide detoxifying enzyme catalase.	Acetylcysteine	254-270	dual oxidase 2	Homo sapiens	0-5
27637085-5	2016	DUOX2 knockdown with short interfering RNA significantly decreased IFN-gamma-induced VEGF-A or HIF-1alpha up-regulation, as did treatment of pancreatic cancer cells with the NADPH oxidase inhibitor diphenylene iodonium, the multifunctional reduced thiol N-acetylcysteine, and the polyethylene glycol-modified form of the hydrogen peroxide detoxifying enzyme catalase.	Acetylcysteine	254-270	interferon gamma	Homo sapiens	67-76
27477353-9	2016	Furthermore, our results showed that antioxidant N-acetyl-L-cysteine (NAC) significantly inhibited CS-induced recruitment of TLR4 into lipid rafts as well as IL-8 production.	Acetylcysteine	49-68	toll-like receptor 4	Mus musculus	125-129
27474938-18	2016	In the presence of NAC, TCS enhanced mRNA expression of the cytochromes and AhR at 3 and 6h, respectively.	Acetylcysteine	19-22	aryl-hydrocarbon receptor	Mus musculus	76-79
27634458-6	2016	Treatments of SH-SY5Y cells with the chemical chaperone, 4-phenylbutyric acid and the ROS scavenger, N-acetyl-cysteine reduced the AA-induced expression of ATF4 protein and CHOP mRNA, and resulted in the suppression of apoptosis.	Acetylcysteine	101-118	DNA damage inducible transcript 3	Homo sapiens	173-177
27477353-9	2016	Furthermore, our results showed that antioxidant N-acetyl-L-cysteine (NAC) significantly inhibited CS-induced recruitment of TLR4 into lipid rafts as well as IL-8 production.	Acetylcysteine	70-73	toll-like receptor 4	Mus musculus	125-129
27733157-4	2016	We hypothesized that treatment with antioxidant N-acetylcysteine (NAC) could enhance cardiac Cav-3 expression and attenuate caveolae dysfunction and the accompanying eNOS/NO signaling abnormalities in diabetes.	Acetylcysteine	66-69	caveolin 3	Rattus norvegicus	93-98
27733157-9	2016	NAC attenuated the reductions of NO, Cav-3 and phosphorylated eNOS and mitigated the augmentation of O2-, nitrotyrosine and 15-F2t-isoprostane in diabetic myocardium.	Acetylcysteine	0-3	caveolin 3	Rattus norvegicus	37-42
27733157-11	2016	Immunoprecipitation analysis revealed that diabetic conditions decreased the association of Cav-3 and eNOS in isolated cardiomyocytes, which was enhanced by treatment with NAC.	Acetylcysteine	172-175	caveolin 3	Rattus norvegicus	92-97
27733157-13	2016	NAC treatment attenuated the reductions of Cav-3 expression and eNOS phosphorylation in HG-treated cardiomyocytes or H9C2 cells.	Acetylcysteine	0-3	caveolin 3	Rattus norvegicus	43-48
27733157-14	2016	NAC treatment attenuated HG and H/R induced cell injury, which was abolished during concomitant treatment with Cav-3 siRNA or eNOS siRNA.	Acetylcysteine	0-3	caveolin 3	Rattus norvegicus	111-116
27733157-16	2016	Antioxidant NAC attenuated myocardial dysfunction and myocardial I/R injury by improving Cav-3/eNOS signaling.	Acetylcysteine	12-15	caveolin 3	Rattus norvegicus	89-94
27572503-13	2016	In addition, the H2O2-induced elevation of p-ERK and p-NF-kappaB in BxPC-3 and Panc-1 cells were reduced by curcumin, NAC and PD 98059 (an ERK inhibitor).	Acetylcysteine	118-121	nuclear factor kappa B subunit 1	Homo sapiens	55-64
27785026-10	2016	The N-acetylcysteine supplement attenuated SiNPs-induced endothelial toxicity through inhibition of apoptosis and autophagy via MAPK/Bcl-2 and PI3K/Akt/mTOR signaling, as well as suppression of intracellular ROS property via activating antioxidant enzyme and Nrf2 signaling.	Acetylcysteine	4-20	BCL2 apoptosis regulator	Homo sapiens	133-138
27785026-10	2016	The N-acetylcysteine supplement attenuated SiNPs-induced endothelial toxicity through inhibition of apoptosis and autophagy via MAPK/Bcl-2 and PI3K/Akt/mTOR signaling, as well as suppression of intracellular ROS property via activating antioxidant enzyme and Nrf2 signaling.	Acetylcysteine	4-20	AKT serine/threonine kinase 1	Homo sapiens	148-151
27785026-10	2016	The N-acetylcysteine supplement attenuated SiNPs-induced endothelial toxicity through inhibition of apoptosis and autophagy via MAPK/Bcl-2 and PI3K/Akt/mTOR signaling, as well as suppression of intracellular ROS property via activating antioxidant enzyme and Nrf2 signaling.	Acetylcysteine	4-20	mechanistic target of rapamycin kinase	Homo sapiens	152-156
27785026-10	2016	The N-acetylcysteine supplement attenuated SiNPs-induced endothelial toxicity through inhibition of apoptosis and autophagy via MAPK/Bcl-2 and PI3K/Akt/mTOR signaling, as well as suppression of intracellular ROS property via activating antioxidant enzyme and Nrf2 signaling.	Acetylcysteine	4-20	NFE2 like bZIP transcription factor 2	Homo sapiens	259-263
27633119-6	2016	In addition, pretreatment with N-acetyl-cysteine (NAC) and SP600125, the inhibitor of ROS and JNK, induced MKN45 cell proliferation, prevented the cell apoptosis and released the cells from cycle arrest.	Acetylcysteine	31-48	mitogen-activated protein kinase 8	Homo sapiens	94-97
27633119-6	2016	In addition, pretreatment with N-acetyl-cysteine (NAC) and SP600125, the inhibitor of ROS and JNK, induced MKN45 cell proliferation, prevented the cell apoptosis and released the cells from cycle arrest.	Acetylcysteine	50-53	mitogen-activated protein kinase 8	Homo sapiens	94-97
27633119-7	2016	Finally, we found that pretreatment with NAC prevented the JNK, p53, caspase-9 and -3 protein phosphorylation induced by the polysaccharide, however, pretreatment with SP600125 did not affect the generation of ROS, suggesting that ROS is upstream of JNK.	Acetylcysteine	41-44	mitogen-activated protein kinase 8	Homo sapiens	59-62
27633119-7	2016	Finally, we found that pretreatment with NAC prevented the JNK, p53, caspase-9 and -3 protein phosphorylation induced by the polysaccharide, however, pretreatment with SP600125 did not affect the generation of ROS, suggesting that ROS is upstream of JNK.	Acetylcysteine	41-44	tumor protein p53	Homo sapiens	64-67
27633119-7	2016	Finally, we found that pretreatment with NAC prevented the JNK, p53, caspase-9 and -3 protein phosphorylation induced by the polysaccharide, however, pretreatment with SP600125 did not affect the generation of ROS, suggesting that ROS is upstream of JNK.	Acetylcysteine	41-44	mitogen-activated protein kinase 8	Homo sapiens	250-253
27698876-7	2016	Furthermore, the ROS inhibitor N-acetyl-L-cysteine was able to rescue the MAPK activation and PI3K/AKT inhibition induced by eupatilin.	Acetylcysteine	31-50	mitogen-activated protein kinase 3	Homo sapiens	74-78
27698876-7	2016	Furthermore, the ROS inhibitor N-acetyl-L-cysteine was able to rescue the MAPK activation and PI3K/AKT inhibition induced by eupatilin.	Acetylcysteine	31-50	AKT serine/threonine kinase 1	Homo sapiens	99-102
27620489-6	2016	The levels of p53 in YD8 and H460 cells decreased in a Cd concentration-dependent manner, which was inhibited by pretreatment with N-acetylcysteine.	Acetylcysteine	131-147	tumor protein p53	Homo sapiens	14-17
27457783-10	2016	NAC and selective inhibitors of CYP2B6 and CYP3A4 significantly reduced TMP covalent binding.	Acetylcysteine	0-3	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	43-49
27475664-5	2016	AOPPs stimulation induced ROS generation and NF-kappa B p65 phosphorylation, which could be inhibited by soluble receptor for advanced glycan end products (sRAGE), NADPH oxidase inhibitor (apocynin), ROS scavenger (N-acetyl-cysteine, NAC).	Acetylcysteine	215-232	nuclear factor kappa B subunit 1	Homo sapiens	45-55
27572503-13	2016	In addition, the H2O2-induced elevation of p-ERK and p-NF-kappaB in BxPC-3 and Panc-1 cells were reduced by curcumin, NAC and PD 98059 (an ERK inhibitor).	Acetylcysteine	118-121	mitogen-activated protein kinase 1	Homo sapiens	45-48
27440660-10	2016	Incubation of RPE cells with the antioxidant N-acetylcysteine under high glucose conditions restored normal migration and PEDF expression.	Acetylcysteine	45-61	serine (or cysteine) peptidase inhibitor, clade F, member 1	Mus musculus	122-126
27687768-7	2016	Furthermore, superoxide anion scavenger N-acetyl-L-cysteine (NAC) or NAD(P)H oxidase inhibitor apocynin inhibited Ang II-induced activation of Akt and ERK1/2 signaling.	Acetylcysteine	61-64	mitogen-activated protein kinase 3	Homo sapiens	151-157
27474168-9	2016	Moreover, NAC abrogated the effects of DHM on STAT3-dependent autophagy.	Acetylcysteine	10-13	signal transducer and activator of transcription 3	Homo sapiens	46-51
27620528-5	2016	Further studies demonstrated that the protective effect of NAC was associated with restoration of intracellular redox state by Nrf2-related regulation of expression of genes involved in intracellular glutathione (GSH) biosynthesis and inactivation of 4-HNE-induced phosphorylation of extracellular signal-regulated protein kinases (ERK1/2).	Acetylcysteine	59-62	NFE2 like bZIP transcription factor 2	Homo sapiens	127-131
27620528-5	2016	Further studies demonstrated that the protective effect of NAC was associated with restoration of intracellular redox state by Nrf2-related regulation of expression of genes involved in intracellular glutathione (GSH) biosynthesis and inactivation of 4-HNE-induced phosphorylation of extracellular signal-regulated protein kinases (ERK1/2).	Acetylcysteine	59-62	mitogen-activated protein kinase 3	Homo sapiens	332-338
27687768-7	2016	Furthermore, superoxide anion scavenger N-acetyl-L-cysteine (NAC) or NAD(P)H oxidase inhibitor apocynin inhibited Ang II-induced activation of Akt and ERK1/2 signaling.	Acetylcysteine	40-59	AKT serine/threonine kinase 1	Homo sapiens	143-146
27687768-7	2016	Furthermore, superoxide anion scavenger N-acetyl-L-cysteine (NAC) or NAD(P)H oxidase inhibitor apocynin inhibited Ang II-induced activation of Akt and ERK1/2 signaling.	Acetylcysteine	40-59	mitogen-activated protein kinase 3	Homo sapiens	151-157
27687768-7	2016	Furthermore, superoxide anion scavenger N-acetyl-L-cysteine (NAC) or NAD(P)H oxidase inhibitor apocynin inhibited Ang II-induced activation of Akt and ERK1/2 signaling.	Acetylcysteine	61-64	AKT serine/threonine kinase 1	Homo sapiens	143-146
27620528-7	2016	Importantly, either overexpression of MKP-1 or NAC treatment blocked 4-HNE-induced MKP-1 degradation, thereby protecting cell from apoptosis.	Acetylcysteine	47-50	dual specificity phosphatase 1	Homo sapiens	83-88
27557522-6	2016	In addition, Ca2+ levels and the expression of the Ca2+ channels, RyR1, SERCA, CACNA1S, TRPC1, and TRPC3 were recovered to normal levels by N-acetyl-L-cysteine (NAC) treatment compared with SelW knockdown cells.	Acetylcysteine	140-159	transient receptor potential cation channel subfamily C member 1	Gallus gallus	88-93
27658547-11	2016	N-acetylcysteine treatment suppressed Cd-induced activation of PKC-delta and Akt.	Acetylcysteine	0-16	AKT serine/threonine kinase 1	Rattus norvegicus	77-80
27171647-7	2016	Increased IL-8 secretion in HG was inhibited by pretreatment with an antioxidant, N-acetylcysteine, or a protein kinase C inhibitor, Ro31-8220.	Acetylcysteine	82-98	C-X-C motif chemokine ligand 8	Homo sapiens	10-14
27582555-8	2016	ROS scavengers (N-acetyl-L-cysteine, NAC, and glutathione, GSH) also blocked the IK-induced ROS production and HO-1 expression.	Acetylcysteine	16-35	heme oxygenase 1	Mus musculus	111-115
27577752-0	2016	N-acetylcysteine attenuates lipopolysaccharide-induced impairment in lamination of Ctip2-and Tbr1- expressing cortical neurons in the developing rat fetal brain.	Acetylcysteine	0-16	BAF chromatin remodeling complex subunit BCL11B	Rattus norvegicus	83-88
27854233-6	2016	In contrast, N-acetyl-cysteine had a beneficial effect on mitochondrial translation in TRMU and MTO1 deficient fibroblasts.	Acetylcysteine	13-30	tRNA mitochondrial 2-thiouridylase	Homo sapiens	87-91
27576730-9	2016	NOX4 knockdown and N-acetylcysteine (NAC) treatment illustrated that NOX4-derived ROS generation was critical for TGF-beta-induced SMAD phosphorylation and myofibroblast differentiation.	Acetylcysteine	19-35	transforming growth factor beta 1	Homo sapiens	114-122
27576730-9	2016	NOX4 knockdown and N-acetylcysteine (NAC) treatment illustrated that NOX4-derived ROS generation was critical for TGF-beta-induced SMAD phosphorylation and myofibroblast differentiation.	Acetylcysteine	37-40	transforming growth factor beta 1	Homo sapiens	114-122
27356894-6	2016	We further show that IL-2 signaling in memory CD4 T cells is improved by the antioxidant N-acetylcysteine.	Acetylcysteine	89-105	interleukin 2	Homo sapiens	21-25
27570977-6	2016	Moreover, the generation of reactive oxygen species (ROS) was detected in bladder cancer cells, upon treatment of vitamin K2 and the anti-oxidant N-acetyl cysteine (NAC) almost blocked the Vitamin K2-triggered apoptosis, loss of mitochondria membrane potential and activation of JNK and p38 MAPK.	Acetylcysteine	146-163	mitogen-activated protein kinase 8	Homo sapiens	279-282
27570977-6	2016	Moreover, the generation of reactive oxygen species (ROS) was detected in bladder cancer cells, upon treatment of vitamin K2 and the anti-oxidant N-acetyl cysteine (NAC) almost blocked the Vitamin K2-triggered apoptosis, loss of mitochondria membrane potential and activation of JNK and p38 MAPK.	Acetylcysteine	146-163	mitogen-activated protein kinase 14	Homo sapiens	287-290
27570977-6	2016	Moreover, the generation of reactive oxygen species (ROS) was detected in bladder cancer cells, upon treatment of vitamin K2 and the anti-oxidant N-acetyl cysteine (NAC) almost blocked the Vitamin K2-triggered apoptosis, loss of mitochondria membrane potential and activation of JNK and p38 MAPK.	Acetylcysteine	165-168	mitogen-activated protein kinase 8	Homo sapiens	279-282
27570977-6	2016	Moreover, the generation of reactive oxygen species (ROS) was detected in bladder cancer cells, upon treatment of vitamin K2 and the anti-oxidant N-acetyl cysteine (NAC) almost blocked the Vitamin K2-triggered apoptosis, loss of mitochondria membrane potential and activation of JNK and p38 MAPK.	Acetylcysteine	165-168	mitogen-activated protein kinase 14	Homo sapiens	287-290
27356894-6	2016	We further show that IL-2 signaling in memory CD4 T cells is improved by the antioxidant N-acetylcysteine.	Acetylcysteine	89-105	CD4 molecule	Homo sapiens	46-49
27208483-6	2016	In the meantime, however, the antioxidant N-acetylcysteine (NAC) was found to ameliorate Nrf2 expression and nuclear translocation as well as Gadd45b expression and MAPKs activation by repressing Sb2O3-induced ROS production.	Acetylcysteine	42-58	NFE2 like bZIP transcription factor 2	Homo sapiens	89-93
27208483-6	2016	In the meantime, however, the antioxidant N-acetylcysteine (NAC) was found to ameliorate Nrf2 expression and nuclear translocation as well as Gadd45b expression and MAPKs activation by repressing Sb2O3-induced ROS production.	Acetylcysteine	60-63	NFE2 like bZIP transcription factor 2	Homo sapiens	89-93
27061477-0	2016	The effect of N-acetylcysteine and calcium hydroxide on TNF-alpha and TGF-beta1 in lipopolysaccharide-activated macrophages.	Acetylcysteine	14-30	transforming growth factor beta 1	Homo sapiens	70-79
27288489-7	2016	Moreover, adiponectin-upregulated cPLA2 and COX-2 expression was significantly abrogated by ROS scavenger (N-acetylcysteine) or the inhibitors of NADPH oxidase (apocynin), mitochondrial complex I (rotenone), PKC (Ro31-8220, Go-6976, and rottlerin), and p300 (garcinol).	Acetylcysteine	107-123	adiponectin, C1Q and collagen domain containing	Homo sapiens	10-21
27288489-7	2016	Moreover, adiponectin-upregulated cPLA2 and COX-2 expression was significantly abrogated by ROS scavenger (N-acetylcysteine) or the inhibitors of NADPH oxidase (apocynin), mitochondrial complex I (rotenone), PKC (Ro31-8220, Go-6976, and rottlerin), and p300 (garcinol).	Acetylcysteine	107-123	prostaglandin-endoperoxide synthase 2	Homo sapiens	44-49
27221774-5	2016	Myricetin, Akt inhibitor, Bay 11-7085 (an inhibitor of NF-kappaB activation), rapamycin (mTOR inhibitor) and N-acetylcysteine attenuated TNF-alpha-induced activation of Akt, mTOR and NF-kappaB.	Acetylcysteine	109-125	tumor necrosis factor	Homo sapiens	137-146
27221774-5	2016	Myricetin, Akt inhibitor, Bay 11-7085 (an inhibitor of NF-kappaB activation), rapamycin (mTOR inhibitor) and N-acetylcysteine attenuated TNF-alpha-induced activation of Akt, mTOR and NF-kappaB.	Acetylcysteine	109-125	AKT serine/threonine kinase 1	Homo sapiens	169-172
27221774-5	2016	Myricetin, Akt inhibitor, Bay 11-7085 (an inhibitor of NF-kappaB activation), rapamycin (mTOR inhibitor) and N-acetylcysteine attenuated TNF-alpha-induced activation of Akt, mTOR and NF-kappaB.	Acetylcysteine	109-125	mechanistic target of rapamycin kinase	Homo sapiens	174-178
27221774-5	2016	Myricetin, Akt inhibitor, Bay 11-7085 (an inhibitor of NF-kappaB activation), rapamycin (mTOR inhibitor) and N-acetylcysteine attenuated TNF-alpha-induced activation of Akt, mTOR and NF-kappaB.	Acetylcysteine	109-125	nuclear factor kappa B subunit 1	Homo sapiens	183-192
27221774-6	2016	Myricetin and N-acetylcysteine attenuated the TNF-alpha-stimulated production of cytokines and chemokines, and production of reactive oxygen species in keratinocytes.	Acetylcysteine	14-30	tumor necrosis factor	Homo sapiens	46-55
27106722-13	2016	We also found that all changes induced by high glucose and insulin were attenuated by the anti-oxidant N-acetylcysteine (NAC) and, thus, depended on ROS production.	Acetylcysteine	103-119	insulin	Homo sapiens	59-66
26592462-10	2016	NAC also increased the expression of Zif268 in the nucleus accumbens and dorsolateral striatum of LgA rats.	Acetylcysteine	0-3	early growth response 1	Rattus norvegicus	37-43
27106722-13	2016	We also found that all changes induced by high glucose and insulin were attenuated by the anti-oxidant N-acetylcysteine (NAC) and, thus, depended on ROS production.	Acetylcysteine	121-124	insulin	Homo sapiens	59-66
27075430-7	2016	The administration of NAC blocked the maturation of interleukin-1beta, which is a critical substrate of MMPs, and markedly suppressed the neuronal activation induced by CCI, including inhibiting the phosphorylation of protein kinase Cgamma, NMDAR1, and mitogen-activated protein kinases.	Acetylcysteine	22-25	interleukin 1 beta	Rattus norvegicus	52-69
27208785-5	2016	Inhibition of ROS generation by N-acetyl cysteine, diphenyl iodonium and apocynin suppressed HDAC6-induced pro-inflammatory cytokines.	Acetylcysteine	32-49	histone deacetylase 6	Mus musculus	93-98
27445100-12	2016	In vitro, AngII induced hepatocyte EMT, which was inhibited by N-acetylcysteine (NAC), diphenylene iodonium (DPI), and NOX4 siRNA.	Acetylcysteine	63-79	angiotensinogen	Rattus norvegicus	10-15
27445100-12	2016	In vitro, AngII induced hepatocyte EMT, which was inhibited by N-acetylcysteine (NAC), diphenylene iodonium (DPI), and NOX4 siRNA.	Acetylcysteine	81-84	angiotensinogen	Rattus norvegicus	10-15
27043357-14	2016	Moreover, NAC abrogated the effects of capsaicin on Stat3-dependent autophagy.	Acetylcysteine	10-13	signal transducer and activator of transcription 3	Homo sapiens	52-57
27405449-7	2016	Lastly, the antioxidant N-acetylcysteine rescued the mitochondrial dysfunction and cell apoptosis that was induced by TRMU downregulation, suggesting that ROS accumulation contributed to the increased aminoglycosides sensitivity of HEI-OC-1 cells after TRMU downregulation.	Acetylcysteine	24-40	tRNA mitochondrial 2-thiouridylase	Homo sapiens	118-122
27405449-7	2016	Lastly, the antioxidant N-acetylcysteine rescued the mitochondrial dysfunction and cell apoptosis that was induced by TRMU downregulation, suggesting that ROS accumulation contributed to the increased aminoglycosides sensitivity of HEI-OC-1 cells after TRMU downregulation.	Acetylcysteine	24-40	tRNA mitochondrial 2-thiouridylase	Homo sapiens	253-257
27221553-9	2016	Furthermore, the blocking of ROS generation by antioxidant N-acetyl cysteine attenuated the HHS-induced release of cytochrome c, caspase activation and PI3K/Akt inactivation, thereby preventing HHS-induced apoptosis and reduction in cell viability.	Acetylcysteine	59-76	cytochrome c, somatic	Homo sapiens	115-127
27083477-14	2016	N-acetylcysteine (NAC) corrected MG-to-GSH ratio, and reduced diabetic brain infarct area, occludin glycation and permeability.	Acetylcysteine	18-21	occludin	Mus musculus	91-99
27005845-6	2016	Furthermore, we found that these inhibitory effects of SSBb were associated with reduced reactive oxygen species (ROS) because pretreating cells with N-acetyl-L-cysteine and NADPH oxidase inhibitor diphenyleneiodonium (DPI) inhibited LPS-induced TLR4 recruitment into lipid rafts and NF-kappaB activation.	Acetylcysteine	150-169	nuclear factor kappa B subunit 1	Homo sapiens	284-293
26851769-5	2016	NAC 50mg/kg/d administered 1h after initiation of hypothermia significantly decreased iNOS expression and caspase 3 activation in the injured hemisphere versus hypothermia alone.	Acetylcysteine	0-3	nitric oxide synthase 2	Rattus norvegicus	86-90
27221553-9	2016	Furthermore, the blocking of ROS generation by antioxidant N-acetyl cysteine attenuated the HHS-induced release of cytochrome c, caspase activation and PI3K/Akt inactivation, thereby preventing HHS-induced apoptosis and reduction in cell viability.	Acetylcysteine	59-76	AKT serine/threonine kinase 1	Homo sapiens	157-160
26134756-6	2016	RESULTS: RSV and NAC administration significantly improved liver index (RSV only), alanine transaminase (52, 52%), TNF-alpha (70, 70%), glucose (69, 80%), albumin (122, 114%), MDA (55, 63%), GSH (160, 152%), GST (84, 84%), TC (86, 86%), LDL-C (83, 81%), and leptin (59, 70%) levels compared with steatosis control values.	Acetylcysteine	17-20	tumor necrosis factor	Rattus norvegicus	115-124
27087133-12	2016	Brain cortex and hippocampus AChE and hippocampus BChE activities increase induced by STZ were also prevented by NAC treatment.	Acetylcysteine	113-116	butyrylcholinesterase	Mus musculus	50-54
27445853-10	2016	IH-induced increase in AMPK phosphorylation was totally abolished by NAC or compound C but not by ibuprofen.	Acetylcysteine	69-72	protein kinase AMP-activated catalytic subunit alpha 2	Rattus norvegicus	23-27
27106530-5	2016	NAC and Ac-DEVD-CHO partially reversed CuE-induced cleavage of caspase-3, caspase-7, and PARP.	Acetylcysteine	0-3	caspase 3	Homo sapiens	63-72
27106530-8	2016	CuE-triggered protein expression of p-AKT, p-mTOR, Beclin-1, and p-ULK1 was partially reversed by NAC pretreatment.	Acetylcysteine	98-101	AKT serine/threonine kinase 1	Homo sapiens	38-41
27106530-8	2016	CuE-triggered protein expression of p-AKT, p-mTOR, Beclin-1, and p-ULK1 was partially reversed by NAC pretreatment.	Acetylcysteine	98-101	mechanistic target of rapamycin kinase	Homo sapiens	45-49
27270209-11	2016	Pretreatment with N-acetylcysteine decreases phosphorylation of p53 in citral-treated ECC-1 and OVCAR-3.	Acetylcysteine	18-34	tumor protein p53	Homo sapiens	64-67
26958800-10	2016	Apoptosis, measured by caspase-3, was restored to sham group levels when NAC and DFO were administered.	Acetylcysteine	73-76	caspase 3	Sus scrofa	23-32
27253411-6	2016	Moreover, we found that erianin induced activation of c-Jun N-terminal kinase (JNK) signal pathway, which was also blocked by NAC.	Acetylcysteine	126-129	mitogen-activated protein kinase 8	Homo sapiens	54-77
27253411-6	2016	Moreover, we found that erianin induced activation of c-Jun N-terminal kinase (JNK) signal pathway, which was also blocked by NAC.	Acetylcysteine	126-129	mitogen-activated protein kinase 8	Homo sapiens	79-82
26906511-12	2016	NAC, DPI, and U0126 increased the protein expression of eNOS.	Acetylcysteine	0-3	nitric oxide synthase 3	Homo sapiens	56-60
26906511-13	2016	Furthermore, U0126 rather than DPI and NAC decreased the protein expression of p-ERK1/2.	Acetylcysteine	39-42	mitogen-activated protein kinase 3	Homo sapiens	81-87
27070098-8	2016	Bcl-2 antagonism also induced a mitochondrial proton leak that was prevented by the antioxidant N-acetyl-L-cysteine and, therefore, secondary to redox changes.	Acetylcysteine	96-115	B cell leukemia/lymphoma 2	Mus musculus	0-5
27081862-7	2016	The treatment of H9c2 cells with N-acetyl-L-cysteine (NAC), a scavenger of ROS, prior to DOX exposure, also markedly increased the phosphorylation of Akt and FoxO3a which was inhibited by DOX alone.	Acetylcysteine	33-52	AKT serine/threonine kinase 1	Rattus norvegicus	150-153
27081862-7	2016	The treatment of H9c2 cells with N-acetyl-L-cysteine (NAC), a scavenger of ROS, prior to DOX exposure, also markedly increased the phosphorylation of Akt and FoxO3a which was inhibited by DOX alone.	Acetylcysteine	54-57	AKT serine/threonine kinase 1	Rattus norvegicus	150-153
27006094-7	2016	Alternatively, an antioxidant N-acetyl-L-cysteine (NAC) significantly attenuated rosline"s effects on the mitochondrial membrane potential, caspases 3/7 and 9 activities, cell viabilities and the phosphorylation of Akt.	Acetylcysteine	30-49	caspase 3	Homo sapiens	140-158
27006094-7	2016	Alternatively, an antioxidant N-acetyl-L-cysteine (NAC) significantly attenuated rosline"s effects on the mitochondrial membrane potential, caspases 3/7 and 9 activities, cell viabilities and the phosphorylation of Akt.	Acetylcysteine	30-49	AKT serine/threonine kinase 1	Homo sapiens	215-218
27006094-7	2016	Alternatively, an antioxidant N-acetyl-L-cysteine (NAC) significantly attenuated rosline"s effects on the mitochondrial membrane potential, caspases 3/7 and 9 activities, cell viabilities and the phosphorylation of Akt.	Acetylcysteine	51-54	caspase 3	Homo sapiens	140-158
27006094-7	2016	Alternatively, an antioxidant N-acetyl-L-cysteine (NAC) significantly attenuated rosline"s effects on the mitochondrial membrane potential, caspases 3/7 and 9 activities, cell viabilities and the phosphorylation of Akt.	Acetylcysteine	51-54	AKT serine/threonine kinase 1	Homo sapiens	215-218
26152521-9	2016	Pretreatment of cells with ROS scavenger N-acetyl cysteine abrogated the inhibitory effect of CA on the JAK2-STAT3/Src-STAT3 signaling and rescued cells from CA-induced apoptosis by blocking the induction of p53 and the cleavage of caspase-3 and PARP in HCT116 cells.	Acetylcysteine	41-58	signal transducer and activator of transcription 3	Homo sapiens	109-114
26152521-9	2016	Pretreatment of cells with ROS scavenger N-acetyl cysteine abrogated the inhibitory effect of CA on the JAK2-STAT3/Src-STAT3 signaling and rescued cells from CA-induced apoptosis by blocking the induction of p53 and the cleavage of caspase-3 and PARP in HCT116 cells.	Acetylcysteine	41-58	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	115-118
26152521-9	2016	Pretreatment of cells with ROS scavenger N-acetyl cysteine abrogated the inhibitory effect of CA on the JAK2-STAT3/Src-STAT3 signaling and rescued cells from CA-induced apoptosis by blocking the induction of p53 and the cleavage of caspase-3 and PARP in HCT116 cells.	Acetylcysteine	41-58	signal transducer and activator of transcription 3	Homo sapiens	119-124
26152521-9	2016	Pretreatment of cells with ROS scavenger N-acetyl cysteine abrogated the inhibitory effect of CA on the JAK2-STAT3/Src-STAT3 signaling and rescued cells from CA-induced apoptosis by blocking the induction of p53 and the cleavage of caspase-3 and PARP in HCT116 cells.	Acetylcysteine	41-58	tumor protein p53	Homo sapiens	208-211
26152521-9	2016	Pretreatment of cells with ROS scavenger N-acetyl cysteine abrogated the inhibitory effect of CA on the JAK2-STAT3/Src-STAT3 signaling and rescued cells from CA-induced apoptosis by blocking the induction of p53 and the cleavage of caspase-3 and PARP in HCT116 cells.	Acetylcysteine	41-58	caspase 3	Homo sapiens	232-241
27097871-7	2016	Geraniin could generate intracellular reactive oxygen species (ROS), activate p38 MAPK then induce the apoptosis in MCF-7 cells, such phenomena was abrogated by pretreatment with N-acetyl-l-cysteine.	Acetylcysteine	179-198	mitogen-activated protein kinase 14	Homo sapiens	78-81
27035109-9	2016	Notably, the TRAIL tolerance in the SKOV3 and SKOV3/DDP cells could be abrogated by the oxidative stress scavenger N-acetyl-cysteine.	Acetylcysteine	115-132	TNF superfamily member 10	Homo sapiens	13-18
27035222-8	2016	ROS scavenger, N-acetyl-L-cysteine (NAC, 5 mM), was able to hinder the autophagy, apoptosis and phosphorylation of JNK, and JNK inhibitor (SP600125, 10 microM) significantly inhibited the autophagy and apoptosis, and attenuated the sensitivity of MG63 cells to AE-PDT.	Acetylcysteine	15-34	mitogen-activated protein kinase 8	Homo sapiens	115-118
27035222-8	2016	ROS scavenger, N-acetyl-L-cysteine (NAC, 5 mM), was able to hinder the autophagy, apoptosis and phosphorylation of JNK, and JNK inhibitor (SP600125, 10 microM) significantly inhibited the autophagy and apoptosis, and attenuated the sensitivity of MG63 cells to AE-PDT.	Acetylcysteine	15-34	mitogen-activated protein kinase 8	Homo sapiens	124-127
27035222-8	2016	ROS scavenger, N-acetyl-L-cysteine (NAC, 5 mM), was able to hinder the autophagy, apoptosis and phosphorylation of JNK, and JNK inhibitor (SP600125, 10 microM) significantly inhibited the autophagy and apoptosis, and attenuated the sensitivity of MG63 cells to AE-PDT.	Acetylcysteine	36-39	mitogen-activated protein kinase 8	Homo sapiens	115-118
27035222-8	2016	ROS scavenger, N-acetyl-L-cysteine (NAC, 5 mM), was able to hinder the autophagy, apoptosis and phosphorylation of JNK, and JNK inhibitor (SP600125, 10 microM) significantly inhibited the autophagy and apoptosis, and attenuated the sensitivity of MG63 cells to AE-PDT.	Acetylcysteine	36-39	mitogen-activated protein kinase 8	Homo sapiens	124-127
27206739-6	2016	Incubation of gLDL-exposed cells with the anti-oxidant N-acetyl-cysteine (NAC) reduced ERS, revealed by decreased eIF2alpha phosphorylation and CHOP gene expression and increased GRP78 expression, thus validating the interconnection between ERS and oxidative stress.	Acetylcysteine	55-72	DNA damage inducible transcript 3	Homo sapiens	144-148
27206739-6	2016	Incubation of gLDL-exposed cells with the anti-oxidant N-acetyl-cysteine (NAC) reduced ERS, revealed by decreased eIF2alpha phosphorylation and CHOP gene expression and increased GRP78 expression, thus validating the interconnection between ERS and oxidative stress.	Acetylcysteine	55-72	heat shock protein family A (Hsp70) member 5	Homo sapiens	179-184
27206739-6	2016	Incubation of gLDL-exposed cells with the anti-oxidant N-acetyl-cysteine (NAC) reduced ERS, revealed by decreased eIF2alpha phosphorylation and CHOP gene expression and increased GRP78 expression, thus validating the interconnection between ERS and oxidative stress.	Acetylcysteine	74-77	DNA damage inducible transcript 3	Homo sapiens	144-148
27206739-6	2016	Incubation of gLDL-exposed cells with the anti-oxidant N-acetyl-cysteine (NAC) reduced ERS, revealed by decreased eIF2alpha phosphorylation and CHOP gene expression and increased GRP78 expression, thus validating the interconnection between ERS and oxidative stress.	Acetylcysteine	74-77	heat shock protein family A (Hsp70) member 5	Homo sapiens	179-184
27206739-7	2016	Sal, PBA, NAC and inhibitors of p38 MAP kinase and NF-kB induced the decrease of VCAM-1 expression and of the ensuing monocyte adhesion induced by gLDL.	Acetylcysteine	10-13	vascular cell adhesion molecule 1	Homo sapiens	81-87
27035545-8	2016	However, N-acetylcysteine (NAC), a general ROS scavenger, completely blocked the DATS-induced ROS increase, inhibition of the PI3K/Akt pathway and cell apoptosis.	Acetylcysteine	9-25	AKT serine/threonine kinase 1	Homo sapiens	131-134
27035545-8	2016	However, N-acetylcysteine (NAC), a general ROS scavenger, completely blocked the DATS-induced ROS increase, inhibition of the PI3K/Akt pathway and cell apoptosis.	Acetylcysteine	27-30	AKT serine/threonine kinase 1	Homo sapiens	131-134
27102435-4	2016	HeLa cells treated with NAC exhibited a time- and concentration-dependent decrease in Notch3 levels and its downstream effectors Hes1 and HRT1 in a manner independent of f-secretase or glutathione.	Acetylcysteine	24-27	hes related family bHLH transcription factor with YRPW motif 1	Homo sapiens	138-142
27010086-11	2016	Furthermore, the expressions of NF-kappaB p65/RelA and phospho-NF-kappaB p65/RelA (Ser536) were suppressed after 2,5-HD exposure and restored by NAC pretreatment.	Acetylcysteine	145-148	synaptotagmin 1	Rattus norvegicus	42-45
27010086-11	2016	Furthermore, the expressions of NF-kappaB p65/RelA and phospho-NF-kappaB p65/RelA (Ser536) were suppressed after 2,5-HD exposure and restored by NAC pretreatment.	Acetylcysteine	145-148	synaptotagmin 1	Rattus norvegicus	73-76
27193329-5	2016	Most interestingly, treatment with N-Acetyl-cysteine (NAC) or beta-cyclodextrin (CD) can partially restore TDP-43 nuclear localization.	Acetylcysteine	35-52	TAR DNA binding protein	Homo sapiens	107-113
27193329-5	2016	Most interestingly, treatment with N-Acetyl-cysteine (NAC) or beta-cyclodextrin (CD) can partially restore TDP-43 nuclear localization.	Acetylcysteine	54-57	TAR DNA binding protein	Homo sapiens	107-113
27074555-6	2016	Interestingly, the ROS scavenger NAC attenuated carfilzomib/vorinostat-mediated activation of p38MAPK and JNK.	Acetylcysteine	33-36	mitogen-activated protein kinase 8	Homo sapiens	106-109
27041464-0	2016	N-acetylcysteine alleviates angiotensin II-mediated renal fibrosis in mouse obstructed kidneys.	Acetylcysteine	0-16	angiotensinogen (serpin peptidase inhibitor, clade A, member 8)	Mus musculus	28-42
27041464-1	2016	AIM: To investigate the effects of ROS scavenger N-acetylcysteine (NAC) on angiotensin II (Ang II)-mediated renal fibrosis in vivo and in vitro.	Acetylcysteine	49-65	angiotensinogen (serpin peptidase inhibitor, clade A, member 8)	Mus musculus	75-89
27041464-1	2016	AIM: To investigate the effects of ROS scavenger N-acetylcysteine (NAC) on angiotensin II (Ang II)-mediated renal fibrosis in vivo and in vitro.	Acetylcysteine	49-65	angiotensinogen (serpin peptidase inhibitor, clade A, member 8)	Mus musculus	91-97
27041464-1	2016	AIM: To investigate the effects of ROS scavenger N-acetylcysteine (NAC) on angiotensin II (Ang II)-mediated renal fibrosis in vivo and in vitro.	Acetylcysteine	67-70	angiotensinogen (serpin peptidase inhibitor, clade A, member 8)	Mus musculus	75-89
27041464-1	2016	AIM: To investigate the effects of ROS scavenger N-acetylcysteine (NAC) on angiotensin II (Ang II)-mediated renal fibrosis in vivo and in vitro.	Acetylcysteine	67-70	angiotensinogen (serpin peptidase inhibitor, clade A, member 8)	Mus musculus	91-97
27041464-12	2016	Pretreatment with NAC (5 mumol/L) blocked Ang II-induced oxidative stress and ECM production in the cells.	Acetylcysteine	18-21	angiotensinogen (serpin peptidase inhibitor, clade A, member 8)	Mus musculus	42-48
27041464-13	2016	CONCLUSION: In mouse obstructed kidneys, the fibrotic responses result from Ang II upregulation can be alleviated by the ROS scavenger N-acetylcysteine.	Acetylcysteine	135-151	angiotensinogen (serpin peptidase inhibitor, clade A, member 8)	Mus musculus	76-82
26452072-10	2016	In coordination with increased HDAC6 phosphorylation, CSE inhibited Akt and activated glycogen synthase kinase (GSK)-3beta; these effects were ameliorated by the antioxidant N-acetyl cysteine.	Acetylcysteine	174-191	histone deacetylase 6	Mus musculus	31-36
26846682-11	2016	N-acetylcysteine restored Brg1, Nrf2 and p-STAT3, and IsoPostC-induced protection in H9C2 cells exposed to HG and HR.	Acetylcysteine	0-16	NFE2 like bZIP transcription factor 2	Rattus norvegicus	32-36
26988587-15	2016	Reactive oxygen species inhibition with N-acetyl cysteine significantly inhibited both the phosphorylation of AKT and the migration of VSMCs.	Acetylcysteine	40-57	thymoma viral proto-oncogene 1	Mus musculus	110-113
26935987-8	2016	Cotreatment with N-acetyl-L-cysteine inhibited sulforaphane-inhibited invasion and upregulation of E-cadherin and almost completely abolished the sulforaphane-induced expression of Vimentin.	Acetylcysteine	17-36	cadherin 1	Homo sapiens	99-109
27162476-6	2016	Meanwhile, the observed increases in nuclear NF-kappaB, NOX4, p47(phox), and COX2 expression were attenuated by treatment with Bay 117082, N-acetyl-l-cysteine (NAC), or RSV.	Acetylcysteine	139-158	NSFL1 (p97) cofactor (p47)	Mus musculus	62-65
27162476-6	2016	Meanwhile, the observed increases in nuclear NF-kappaB, NOX4, p47(phox), and COX2 expression were attenuated by treatment with Bay 117082, N-acetyl-l-cysteine (NAC), or RSV.	Acetylcysteine	160-163	NSFL1 (p97) cofactor (p47)	Mus musculus	62-65
27084536-9	2016	Interestingly, pretreatment of MB cells with NAC or the pan-caspase inhibitor zVAD-fmk abrogated TQ-induced apoptosis, loss of cyclin B1 and NF-kappaB activity, suggesting that these TQ-mediated effects are oxidative stress- and caspase-dependent.	Acetylcysteine	45-48	nuclear factor kappa B subunit 1	Homo sapiens	141-150
26936454-7	2016	Furthermore, CA generated reactive oxygen species (ROS), and pretreatment with ROS scavenger N-acetyl cysteine (NAC) abrogated CA-induced cleavage of PARP and expression of p53.	Acetylcysteine	93-110	tumor protein p53	Homo sapiens	173-176
26936454-7	2016	Furthermore, CA generated reactive oxygen species (ROS), and pretreatment with ROS scavenger N-acetyl cysteine (NAC) abrogated CA-induced cleavage of PARP and expression of p53.	Acetylcysteine	112-115	tumor protein p53	Homo sapiens	173-176
26941030-13	2016	NAC ameliorates the carrageenan-induced prostatitis and prostate inflammation pain through miR-141 regulating Keap1/Nrf2 signaling.	Acetylcysteine	0-3	NFE2 like bZIP transcription factor 2	Homo sapiens	116-120
26655501-8	2016	Accordingly, NGR-peptide"s downregulation of 88 kDa progranulin protein was prevented by BAPTA and NAC.	Acetylcysteine	99-102	granulin precursor	Homo sapiens	52-63
27058530-7	2016	NAC blocked the field effects on cell proliferation and p38 activation, but not those on ERK1/2 activation.	Acetylcysteine	0-3	mitogen-activated protein kinase 1	Homo sapiens	56-59
26977590-0	2016	N-acetyl-cysteine prevents age-related hearing loss and the progressive loss of inner hair cells in gamma-glutamyl transferase 1 deficient mice.	Acetylcysteine	0-17	gamma-glutamyltransferase 1	Mus musculus	100-128
27008885-5	2016	Conversely, up-regulation of NLRP3 and caspase-1, expression of mature IL-1beta and IL-18 and improved cell survival with N-acetylcysteine treatment suggested that inflammasome activation and pyroptosis was the major cause of cone cell death.	Acetylcysteine	122-138	NLR family, pyrin domain containing 3	Rattus norvegicus	29-34
30123617-9	2016	In addition, we found that rasfonin increased the phosphorylation of c-Jun NH2-terminal kinase (JNK), which was inhibited by NAC.	Acetylcysteine	125-128	mitogen-activated protein kinase 8	Homo sapiens	69-94
30123617-9	2016	In addition, we found that rasfonin increased the phosphorylation of c-Jun NH2-terminal kinase (JNK), which was inhibited by NAC.	Acetylcysteine	125-128	mitogen-activated protein kinase 8	Homo sapiens	96-99
26941030-10	2016	Further, we found that NAC increased the expression of miR-141 and activated the Keap1/Nrf2 signaling.	Acetylcysteine	23-26	microRNA 141	Homo sapiens	55-62
26941030-10	2016	Further, we found that NAC increased the expression of miR-141 and activated the Keap1/Nrf2 signaling.	Acetylcysteine	23-26	kelch like ECH associated protein 1	Homo sapiens	81-86
27126918-11	2016	AVP-modulated expression of Hmgb1 protein was reduced by the addition of the antioxidant N-acetylcysteine (NAC).	Acetylcysteine	89-105	arginine vasopressin	Rattus norvegicus	0-3
26941030-10	2016	Further, we found that NAC increased the expression of miR-141 and activated the Keap1/Nrf2 signaling.	Acetylcysteine	23-26	NFE2 like bZIP transcription factor 2	Homo sapiens	87-91
26941030-12	2016	In addition, miR-141 inhibitor could reduce the effect of NAC on prostatitis.	Acetylcysteine	58-61	microRNA 141	Homo sapiens	13-20
26941030-13	2016	NAC ameliorates the carrageenan-induced prostatitis and prostate inflammation pain through miR-141 regulating Keap1/Nrf2 signaling.	Acetylcysteine	0-3	microRNA 141	Homo sapiens	91-98
26941030-13	2016	NAC ameliorates the carrageenan-induced prostatitis and prostate inflammation pain through miR-141 regulating Keap1/Nrf2 signaling.	Acetylcysteine	0-3	kelch like ECH associated protein 1	Homo sapiens	110-115
27126918-11	2016	AVP-modulated expression of Hmgb1 protein was reduced by the addition of the antioxidant N-acetylcysteine (NAC).	Acetylcysteine	107-110	arginine vasopressin	Rattus norvegicus	0-3
26586371-7	2016	By using Ca-074-Me, N-acetylcysteine and KN-62, we observed that the P2X7 receptor participated in the DBP-induced activation of NLRP3 inflammasome.	Acetylcysteine	20-36	purinergic receptor P2X 7	Homo sapiens	69-82
26586371-7	2016	By using Ca-074-Me, N-acetylcysteine and KN-62, we observed that the P2X7 receptor participated in the DBP-induced activation of NLRP3 inflammasome.	Acetylcysteine	20-36	NLR family pyrin domain containing 3	Homo sapiens	129-134
26612073-0	2016	Diabetes enhances oxidative stress-induced TRPM2 channel activity and its control by N-acetylcysteine in rat dorsal root ganglion and brain.	Acetylcysteine	85-101	transient receptor potential cation channel, subfamily M, member 2	Rattus norvegicus	43-48
26612073-3	2016	NAC may have a protective role on oxidative stress and calcium influx through regulation of the TRPM2 channel in diabetic neurons.	Acetylcysteine	0-3	transient receptor potential cation channel, subfamily M, member 2	Rattus norvegicus	96-101
26612073-11	2016	STZ + H2O2-induced TRPM2 gating was totally inhibited by NAC and partially inhibited by N-(p-amylcinnamoyl) anthranilic acid (ACA) and 2-aminoethyl diphenylborinate (2-APB).	Acetylcysteine	57-60	transient receptor potential cation channel, subfamily M, member 2	Rattus norvegicus	19-24
26612073-12	2016	GSH-Px activity and lipid peroxidation levels were also attenuated by NAC treatment.	Acetylcysteine	70-73	glutathione peroxidase 1	Rattus norvegicus	0-6
26612073-13	2016	In conclusion, we observed a modulatory role of NAC on oxidative stress and Ca(2+) entry through the TRPM2 channel in the diabetic DRG and brain.	Acetylcysteine	48-51	transient receptor potential cation channel, subfamily M, member 2	Rattus norvegicus	101-106
27028622-10	2016	Nicotine increased the Bax/Bcl-2 ratio, which was attenuated by N-acetyl-L-cysteine, the NF-kappaB inhibitor, Bay 11-7082, and hexamethonium, a non-specific nAChR blocker.	Acetylcysteine	64-83	BCL2 associated X, apoptosis regulator	Homo sapiens	23-26
26867644-10	2016	Consistently, up-regulation of GADD45 and GADD153 was significantly attenuated by NAC, suggesting that increased ROS and the resultant growth arrest of melanocytes may contribute to RD and RK-induced leukoderma.	Acetylcysteine	82-85	growth arrest and DNA-damage-inducible 45 alpha	Mus musculus	31-37
26548866-11	2016	Moreover, when N-acetylcysteine was present, increase of cell proliferation induced by downregulation of FoxO1, and upregulation of miR-155 was significantly inhibited.	Acetylcysteine	15-31	forkhead box O1	Homo sapiens	105-110
27028622-10	2016	Nicotine increased the Bax/Bcl-2 ratio, which was attenuated by N-acetyl-L-cysteine, the NF-kappaB inhibitor, Bay 11-7082, and hexamethonium, a non-specific nAChR blocker.	Acetylcysteine	64-83	BCL2 apoptosis regulator	Homo sapiens	27-32
26918336-9	2016	NAC inhibited nicotine-mediated increase in ROS production, recovered PKCepsilon gene expression and abrogated increased phosphorylation of GSK3beta.	Acetylcysteine	0-3	protein kinase C, epsilon	Rattus norvegicus	70-80
26923123-7	2016	Also, amelioration of oxidative stress, as shown by a decrease in malondialdehyde level and an increase in superoxide dismutase and catalase activities and glutathione level, was observed in the 30 mM-NAC-treated group in comparison to cells treated with H2O2 alone.	Acetylcysteine	201-204	catalase	Mus musculus	132-140
26898612-5	2016	N-acetylcysteine (NAC) was capable of decreasing Src phosphorylation, abrogating changes of epithelial to mesenchymal transition (EMT) markers instigated by CSE.	Acetylcysteine	0-16	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	49-52
26898612-5	2016	N-acetylcysteine (NAC) was capable of decreasing Src phosphorylation, abrogating changes of epithelial to mesenchymal transition (EMT) markers instigated by CSE.	Acetylcysteine	18-21	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	49-52
26898612-10	2016	NAC may alleviate smoking induced EGFR-TKI resistance through inhibiting Src activation and EMT reversal.	Acetylcysteine	0-3	epidermal growth factor receptor	Homo sapiens	34-38
26898612-10	2016	NAC may alleviate smoking induced EGFR-TKI resistance through inhibiting Src activation and EMT reversal.	Acetylcysteine	0-3	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	73-76
26898612-11	2016	NAC may be a promising adjuvant to reinforce the effect of EGFR-TKI.	Acetylcysteine	0-3	epidermal growth factor receptor	Homo sapiens	59-63
26908203-0	2016	Induction of IL-8(CXCL8) and MCP-1(CCL2) with oxidative stress and its inhibition with N-acetyl cysteine (NAC) in cell culture model using HK-2 cell.	Acetylcysteine	87-104	C-X-C motif chemokine ligand 8	Homo sapiens	13-17
26908203-0	2016	Induction of IL-8(CXCL8) and MCP-1(CCL2) with oxidative stress and its inhibition with N-acetyl cysteine (NAC) in cell culture model using HK-2 cell.	Acetylcysteine	106-109	C-X-C motif chemokine ligand 8	Homo sapiens	13-17
26908203-12	2016	Pre-incubation of the cells with the anti-oxidant N-acetyl cysteine (NAC) strongly suppressed the induction of both IL-8 and MCP-1 when stimulated with hydrogen peroxide and IL-1beta.	Acetylcysteine	50-67	C-X-C motif chemokine ligand 8	Homo sapiens	116-120
26908203-12	2016	Pre-incubation of the cells with the anti-oxidant N-acetyl cysteine (NAC) strongly suppressed the induction of both IL-8 and MCP-1 when stimulated with hydrogen peroxide and IL-1beta.	Acetylcysteine	50-67	interleukin 1 beta	Homo sapiens	174-182
26908203-12	2016	Pre-incubation of the cells with the anti-oxidant N-acetyl cysteine (NAC) strongly suppressed the induction of both IL-8 and MCP-1 when stimulated with hydrogen peroxide and IL-1beta.	Acetylcysteine	69-72	C-X-C motif chemokine ligand 8	Homo sapiens	116-120
26908203-12	2016	Pre-incubation of the cells with the anti-oxidant N-acetyl cysteine (NAC) strongly suppressed the induction of both IL-8 and MCP-1 when stimulated with hydrogen peroxide and IL-1beta.	Acetylcysteine	69-72	interleukin 1 beta	Homo sapiens	174-182
26934645-7	2016	Moreover, N-acetylcysteine (reactive oxygen species scavenger) blocked the SK inhibitor-induced increase in p21 and p53 expression but had no effect on the proteasomal degradation of SK1a.	Acetylcysteine	10-26	tumor protein p53	Homo sapiens	116-119
26969378-10	2016	N-acetyl-L-cysteine (NAC) administration, a scavenger agent of ROS, could down-regulate diosgenin-induced autophagy via reversion of mTOR pathway inhibition.	Acetylcysteine	0-19	mechanistic target of rapamycin kinase	Homo sapiens	133-137
26969378-10	2016	N-acetyl-L-cysteine (NAC) administration, a scavenger agent of ROS, could down-regulate diosgenin-induced autophagy via reversion of mTOR pathway inhibition.	Acetylcysteine	21-24	mechanistic target of rapamycin kinase	Homo sapiens	133-137
26809061-6	2016	p53 reporter gene assay and analyses of p53, Puma, Bax, and Bcl-2 protein levels indicated that NAC inhibited nickel(II)-induced activation of p53-mediated mitochondrial apoptotic pathway.	Acetylcysteine	96-99	BCL2 associated X, apoptosis regulator	Homo sapiens	51-54
26809061-6	2016	p53 reporter gene assay and analyses of p53, Puma, Bax, and Bcl-2 protein levels indicated that NAC inhibited nickel(II)-induced activation of p53-mediated mitochondrial apoptotic pathway.	Acetylcysteine	96-99	BCL2 apoptosis regulator	Homo sapiens	60-65
26291957-7	2016	Moreover, NAC or SB203580 (p38 MAPK inhibitor) blocked 7-MCPA-induced nuclear translocation of Nrf2, suggesting that 7-MCPA activated Nrf2 via a ROS-dependent p38 pathway.	Acetylcysteine	10-13	nuclear factor, erythroid derived 2, like 2	Mus musculus	95-99
26291957-7	2016	Moreover, NAC or SB203580 (p38 MAPK inhibitor) blocked 7-MCPA-induced nuclear translocation of Nrf2, suggesting that 7-MCPA activated Nrf2 via a ROS-dependent p38 pathway.	Acetylcysteine	10-13	nuclear factor, erythroid derived 2, like 2	Mus musculus	134-138
26831541-7	2016	In-vitro studies were also performed to assess the effect of NAC on lipopolysaccharide stimulated BAL cell production of TNF-alpha.	Acetylcysteine	61-64	tumor necrosis factor	Homo sapiens	121-130
26831541-10	2016	Our in vitro studies showed a significant decline in TNF-alpha production from LPS stimulated BAL cells treated with 5 and 10 mM of NAC.	Acetylcysteine	132-135	tumor necrosis factor	Homo sapiens	53-62
26433892-10	2016	At the signaling level, NAC augmented the protein abundance of total mTOR, phosphorylated mTOR, and phosphorylated 70S6 kinase as well as mRNA levels for mTOR and p70S6 kinase in IPEC-1 cells.	Acetylcysteine	24-27	mechanistic target of rapamycin kinase	Sus scrofa	69-73
26683377-8	2016	Also, the cell-permeable thiol N-acetyl l-cysteine, reverses DMF inhibition of the NFkappaB pathway, supporting the notion that the electrophile, DMF, acts via covalent modification.	Acetylcysteine	31-50	nuclear factor kappa B subunit 1	Homo sapiens	83-91
26836389-9	2016	HUA exposure directly increased the phospho-IRS1 (Ser307) response to insulin and inhibited that of phospho-Akt in H9C2 cardiomyocytes, which was blocked by NAC.	Acetylcysteine	157-160	thymoma viral proto-oncogene 1	Mus musculus	108-111
26859482-12	2016	DC cell culture supplemented with N-acetylcysteine, or alternatively grown in low oxygen, afforded significant proliferative benefits (proliferation: maximum 2-fold increase; NAC: 5-fold p53 decrease; low oxygen: maximum 3.5-fold p53 decrease).	Acetylcysteine	34-50	tumor protein p53	Homo sapiens	187-190
26859482-12	2016	DC cell culture supplemented with N-acetylcysteine, or alternatively grown in low oxygen, afforded significant proliferative benefits (proliferation: maximum 2-fold increase; NAC: 5-fold p53 decrease; low oxygen: maximum 3.5-fold p53 decrease).	Acetylcysteine	34-50	tumor protein p53	Homo sapiens	230-233
26859482-12	2016	DC cell culture supplemented with N-acetylcysteine, or alternatively grown in low oxygen, afforded significant proliferative benefits (proliferation: maximum 2-fold increase; NAC: 5-fold p53 decrease; low oxygen: maximum 3.5-fold p53 decrease).	Acetylcysteine	175-178	tumor protein p53	Homo sapiens	187-190
26433892-10	2016	At the signaling level, NAC augmented the protein abundance of total mTOR, phosphorylated mTOR, and phosphorylated 70S6 kinase as well as mRNA levels for mTOR and p70S6 kinase in IPEC-1 cells.	Acetylcysteine	24-27	mechanistic target of rapamycin kinase	Sus scrofa	90-94
26851027-4	2016	The specificity of ROS-mediated ATM-JNK activation was confirmed by treatment with N-acetylcysteine, a ROS scavenger.	Acetylcysteine	83-99	mitogen-activated protein kinase 8	Homo sapiens	36-39
26433892-10	2016	At the signaling level, NAC augmented the protein abundance of total mTOR, phosphorylated mTOR, and phosphorylated 70S6 kinase as well as mRNA levels for mTOR and p70S6 kinase in IPEC-1 cells.	Acetylcysteine	24-27	mechanistic target of rapamycin kinase	Sus scrofa	90-94
26433892-11	2016	Collectively, these results indicate that NAC upregulates expression of mTOR signaling proteins to stimulate protein synthesis in enterocytes independently of GSH generation.	Acetylcysteine	42-45	mechanistic target of rapamycin kinase	Sus scrofa	72-76
26548719-9	2016	CoQ0-induced Nrf2 activation appears to be regulated by ROS-JNK-signaling cascades, as evidenced by suppressed Nrf2 activation upon treatment with pharmacological inhibitors of ROS (N-acetylcysteine) and JNK (SP600125).	Acetylcysteine	182-198	nuclear factor, erythroid derived 2, like 2	Mus musculus	13-17
26919956-9	2016	CONCLUSIONS: N-Acetyl-l-cysteine can lower the incidence rate of infection-associated preterm labor by prohibiting the activation of the protein AP-1/MCP-1 and decreasing the expression of NF-kappaBp65 and TNF-alpha in the pregnant tissues of premature mice to reduce the inflammatory reactions.	Acetylcysteine	13-32	mast cell protease 1	Mus musculus	150-155
26919956-9	2016	CONCLUSIONS: N-Acetyl-l-cysteine can lower the incidence rate of infection-associated preterm labor by prohibiting the activation of the protein AP-1/MCP-1 and decreasing the expression of NF-kappaBp65 and TNF-alpha in the pregnant tissues of premature mice to reduce the inflammatory reactions.	Acetylcysteine	13-32	tumor necrosis factor	Mus musculus	206-215
26548719-9	2016	CoQ0-induced Nrf2 activation appears to be regulated by ROS-JNK-signaling cascades, as evidenced by suppressed Nrf2 activation upon treatment with pharmacological inhibitors of ROS (N-acetylcysteine) and JNK (SP600125).	Acetylcysteine	182-198	nuclear factor, erythroid derived 2, like 2	Mus musculus	111-115
26807660-9	2016	ROS scavenger N-acetyl-l-cysteine reversed inhibition of AKT pathway and expression of Foxp3 from 18.6% to 26.6% in T cells.	Acetylcysteine	14-33	thymoma viral proto-oncogene 1	Mus musculus	57-60
27003169-5	2016	Rap, an mTOR inhibitor and NAC, a ROS scavenger, blocked Cd-induced activation of Akt/mTOR signaling and apoptosis of neuronal cells.	Acetylcysteine	27-30	AKT serine/threonine kinase 1	Rattus norvegicus	82-85
27003169-6	2016	Furthermore, NAC blocked the decrease of B-cell lymphoma 2/Bcl-2 associated X protein (Bcl-2/Bax) ratio, release of cytochrome c, cleavage of caspase-3 and poly(ADP-ribose) polymerase (PARP), and nuclear translocation of apoptosis-inducing factor (AIF) and endonuclease G (Endo G).	Acetylcysteine	13-16	BCL2, apoptosis regulator	Rattus norvegicus	59-64
26707483-7	2016	Endothelial VCAM-1 induction by TNF-alpha was responsible for superoxide anion production being quenched by N-acetyl-cysteine and Tat-SOD.	Acetylcysteine	108-125	vascular cell adhesion molecule 1	Homo sapiens	12-18
27003169-6	2016	Furthermore, NAC blocked the decrease of B-cell lymphoma 2/Bcl-2 associated X protein (Bcl-2/Bax) ratio, release of cytochrome c, cleavage of caspase-3 and poly(ADP-ribose) polymerase (PARP), and nuclear translocation of apoptosis-inducing factor (AIF) and endonuclease G (Endo G).	Acetylcysteine	13-16	BCL2, apoptosis regulator	Rattus norvegicus	87-92
27003169-6	2016	Furthermore, NAC blocked the decrease of B-cell lymphoma 2/Bcl-2 associated X protein (Bcl-2/Bax) ratio, release of cytochrome c, cleavage of caspase-3 and poly(ADP-ribose) polymerase (PARP), and nuclear translocation of apoptosis-inducing factor (AIF) and endonuclease G (Endo G).	Acetylcysteine	13-16	endonuclease G	Rattus norvegicus	257-271
27003169-6	2016	Furthermore, NAC blocked the decrease of B-cell lymphoma 2/Bcl-2 associated X protein (Bcl-2/Bax) ratio, release of cytochrome c, cleavage of caspase-3 and poly(ADP-ribose) polymerase (PARP), and nuclear translocation of apoptosis-inducing factor (AIF) and endonuclease G (Endo G).	Acetylcysteine	13-16	endonuclease G	Rattus norvegicus	273-279
26707483-7	2016	Endothelial VCAM-1 induction by TNF-alpha was responsible for superoxide anion production being quenched by N-acetyl-cysteine and Tat-SOD.	Acetylcysteine	108-125	tumor necrosis factor	Homo sapiens	32-41
26177712-10	2016	However, in TNFalpha stimulated cells NAC treatment reduces only in part ICAM-1 expression and sICAM-1 release.	Acetylcysteine	38-41	tumor necrosis factor	Homo sapiens	12-20
26828938-11	2016	In addition, the translocation of BAX, release of Cytochrome C and the upregulated expression of apoptosis-related proteins after P-HY-SDT were observed, all of which were reversed by N-acetyl cysteine (NAC).	Acetylcysteine	184-201	BCL2 associated X, apoptosis regulator	Homo sapiens	34-37
25941092-9	2016	In gastric tissues NAC administration decreased the level of LPO and activity of CAT, which were increased by IND.	Acetylcysteine	19-22	catalase	Rattus norvegicus	81-84
26625208-7	2016	The generation of ROS in response to TMZ-POH seems to play a crucial role in the cell death process since the blockage of ROS production using the antioxidant N-acetyl-L-cysteine or catalase reversed the TMZ-POH-induced JNK activation, DNA damage, and cancer cell apoptosis.	Acetylcysteine	159-178	mitogen-activated protein kinase 8	Homo sapiens	220-223
27803454-9	2016	Consistently, overexpressed HIF-1alpha was decreased by isorhamnetin or N-acetyl-L-cysteine in HEK293 cells.	Acetylcysteine	72-91	hypoxia inducible factor 1 subunit alpha	Homo sapiens	28-38
26718128-5	2016	Furthermore, N-acetyl-cysteine, an antioxidant agent, markedly suppressed TPA-induced epithelial-to-mesenchymal transition, cell migration and activation of ERK.	Acetylcysteine	13-30	mitogen-activated protein kinase 1	Homo sapiens	157-160
26613808-10	2016	In accordance, hypoxia resulted in down-regulation of BKCa channel beta1 subunit, which was restored in the presence of N-acetylcysteine.	Acetylcysteine	120-136	Calcium-activated potassium channel subunit alpha-1	Ovis aries	54-58
26613808-11	2016	In addition, the N-acetylcysteine treatment significantly increased BKCa channel beta1 subunit abundance and BKCa channel current density in uterine arteries from pregnant sheep exposed to high-altitude hypoxia (3801 m, PaO2: 60 mmHg) for 110 days.	Acetylcysteine	17-33	Calcium-activated potassium channel subunit alpha-1	Ovis aries	68-72
26613808-11	2016	In addition, the N-acetylcysteine treatment significantly increased BKCa channel beta1 subunit abundance and BKCa channel current density in uterine arteries from pregnant sheep exposed to high-altitude hypoxia (3801 m, PaO2: 60 mmHg) for 110 days.	Acetylcysteine	17-33	Calcium-activated potassium channel subunit alpha-1	Ovis aries	109-113
26613808-12	2016	In uterine arteries of non-pregnant animals, hypoxia inhibited steroid hormone-induced up-regulation of BKCa channel current density and NS1619-mediated relaxations, which were reversed by N-acetylcysteine.	Acetylcysteine	189-205	Calcium-activated potassium channel subunit alpha-1	Ovis aries	104-108
26828938-11	2016	In addition, the translocation of BAX, release of Cytochrome C and the upregulated expression of apoptosis-related proteins after P-HY-SDT were observed, all of which were reversed by N-acetyl cysteine (NAC).	Acetylcysteine	184-201	cytochrome c, somatic	Homo sapiens	50-62
26828938-11	2016	In addition, the translocation of BAX, release of Cytochrome C and the upregulated expression of apoptosis-related proteins after P-HY-SDT were observed, all of which were reversed by N-acetyl cysteine (NAC).	Acetylcysteine	203-206	cytochrome c, somatic	Homo sapiens	50-62
25885549-9	2016	NAC also rescued the expression of 3-betaHSD, a major steroidogenic protein.	Acetylcysteine	0-3	hydroxy-delta-5-steroid dehydrogenase, 3 beta- and steroid delta-isomerase 1	Rattus norvegicus	35-44
27184952-9	2016	High-mobility group box 1 (HMGB1) was rapidly released and associated with TLR4 after TNF-alpha stimulation with a peak at 5 min, which was prevented by N-acetylcysteine, an antioxidant.	Acetylcysteine	153-169	tumor necrosis factor	Homo sapiens	86-95
26462568-8	2016	Compared with the control group, serum AST and ALT activities were higher in the APAP and APAP+NAC groups.	Acetylcysteine	95-98	glutamic-oxaloacetic transaminase 2	Rattus norvegicus	39-42
26462568-9	2016	APAP+NAC, APAP+MK, and APAP+NAC+MK groups had reduced serum ALT and AST activities than the group administered APAP alone.	Acetylcysteine	5-8	glutamic-oxaloacetic transaminase 2	Rattus norvegicus	68-71
26462568-9	2016	APAP+NAC, APAP+MK, and APAP+NAC+MK groups had reduced serum ALT and AST activities than the group administered APAP alone.	Acetylcysteine	28-31	glutamic-oxaloacetic transaminase 2	Rattus norvegicus	68-71
26111538-6	2016	Coincidently, both superoxide formation and ERK1/2 phosphorylation were observed in Met-5A cells exposed to MWCNTs and were diminished by pretreatment with the reactive oxidative species (ROS) scavenger, N-acetyl-l-(+)-cysteine (NAC).	Acetylcysteine	204-227	mitogen-activated protein kinase 3	Homo sapiens	44-50
26648023-12	2016	On the contrary, pretreatment with NAC partially inhibited GA plus TRAIL-induced apoptosis.	Acetylcysteine	35-38	TNF superfamily member 10	Homo sapiens	67-72
26635914-8	2016	However, the potent antioxidant, N-acetylcysteine (NAC) abrogated the effects of IH by inducing large CD66b(+)/LC3B(+) Gphi and increased both NADPH oxidase expression and phagocytosis.	Acetylcysteine	33-49	CEA cell adhesion molecule 8	Homo sapiens	102-107
26881256-4	2016	This study observed the expression of NLRP3 inflammasome signaling stimulated by high glucose, lipopolysaccharide, and reactive oxygen species (ROS) inhibitor N-acetyl-L-cysteine in glomerular mesangial cells, aiming to elucidate the mechanism by which the NLRP3 inflammasome signaling pathway may contribute to diabetic nephropathy.	Acetylcysteine	159-178	NLR family pyrin domain containing 3	Homo sapiens	38-43
26881256-4	2016	This study observed the expression of NLRP3 inflammasome signaling stimulated by high glucose, lipopolysaccharide, and reactive oxygen species (ROS) inhibitor N-acetyl-L-cysteine in glomerular mesangial cells, aiming to elucidate the mechanism by which the NLRP3 inflammasome signaling pathway may contribute to diabetic nephropathy.	Acetylcysteine	159-178	NLR family pyrin domain containing 3	Homo sapiens	257-262
25876056-6	2016	However, N-acetylcysteine (NAC), a scavenger of ROS, prevented the increase of ROS generation, attenuated the phosphorylation of the above kinases, and decreased the NF-kappaB activation as well as the expression of ICAM-1 and VCAM-1.	Acetylcysteine	9-25	nuclear factor kappa B subunit 1	Homo sapiens	166-175
25876056-6	2016	However, N-acetylcysteine (NAC), a scavenger of ROS, prevented the increase of ROS generation, attenuated the phosphorylation of the above kinases, and decreased the NF-kappaB activation as well as the expression of ICAM-1 and VCAM-1.	Acetylcysteine	9-25	vascular cell adhesion molecule 1	Homo sapiens	227-233
25876056-6	2016	However, N-acetylcysteine (NAC), a scavenger of ROS, prevented the increase of ROS generation, attenuated the phosphorylation of the above kinases, and decreased the NF-kappaB activation as well as the expression of ICAM-1 and VCAM-1.	Acetylcysteine	27-30	nuclear factor kappa B subunit 1	Homo sapiens	166-175
25876056-6	2016	However, N-acetylcysteine (NAC), a scavenger of ROS, prevented the increase of ROS generation, attenuated the phosphorylation of the above kinases, and decreased the NF-kappaB activation as well as the expression of ICAM-1 and VCAM-1.	Acetylcysteine	27-30	vascular cell adhesion molecule 1	Homo sapiens	227-233
27630715-0	2016	Corrigendum to "The Efficacy of Inositol and N-Acetyl Cysteine Administration (Ovaric HP) in Improving the Ovarian Function in Infertile Women with PCOS with or without Insulin Resistance".	Acetylcysteine	45-62	insulin	Homo sapiens	169-176
26682007-8	2016	Most importantly, the inactivation of Foxo3a induced by JC further led to an increase of intracellular ROS levels by suppressing ROS scavenging enzymes, and the antioxidant N-acetyl-L-cysteine and catalase successfully decreased JC-induced apoptosis.	Acetylcysteine	173-192	forkhead box O3	Homo sapiens	38-44
26635914-8	2016	However, the potent antioxidant, N-acetylcysteine (NAC) abrogated the effects of IH by inducing large CD66b(+)/LC3B(+) Gphi and increased both NADPH oxidase expression and phagocytosis.	Acetylcysteine	51-54	CEA cell adhesion molecule 8	Homo sapiens	102-107
27774335-4	2016	The aim of this study was to determine whether cotreatment of NAC and insulin-like growth factor-1 (IGF-1) efficiently protected against proteasome inhibitor-induced cytotoxicity in SH-SY5Y cells.	Acetylcysteine	62-65	insulin like growth factor 1	Homo sapiens	100-105
28105252-7	2016	Furthermore, we demonstrated that contrast exposure resulted in Trx1 downregulation and increased ASK1/p38 MAPK phosphorylation, which could be reversed by NACA and NAC.	Acetylcysteine	156-159	thioredoxin 1	Rattus norvegicus	64-68
28105252-7	2016	Furthermore, we demonstrated that contrast exposure resulted in Trx1 downregulation and increased ASK1/p38 MAPK phosphorylation, which could be reversed by NACA and NAC.	Acetylcysteine	156-159	mitogen-activated protein kinase kinase kinase 5	Rattus norvegicus	98-102
26895214-8	2016	PDTC and NAC markedly decreased the protein expression of IL-1beta (p &lt; 0.01) and increased the protein expression of DIO1 (p &lt; 0.01), respectively.	Acetylcysteine	9-12	interleukin 1 beta	Rattus norvegicus	58-66
26904167-6	2016	TGF-beta and hypoxia/reoxygenation increased the accumulation of reactive oxygen species (ROS), while treatment with N-acetyl-l-cysteine abolished the activation of Nrf2 and EGFR.	Acetylcysteine	117-136	NFE2 like bZIP transcription factor 2	Homo sapiens	165-169
26904167-6	2016	TGF-beta and hypoxia/reoxygenation increased the accumulation of reactive oxygen species (ROS), while treatment with N-acetyl-l-cysteine abolished the activation of Nrf2 and EGFR.	Acetylcysteine	117-136	epidermal growth factor receptor	Homo sapiens	174-178
26085342-7	2015	This increase is blocked by N-acetylcysteine, suggesting that production of reactive oxygen species immediately after wounding is involved in the LEI increase.	Acetylcysteine	28-44	serpin family B member 1	Bos taurus	146-149
27405163-12	2016	The expression levels of HIF-1alpha, Beclin-1 and Bnip3 (mitophagy marker molecular) increased remarkably after sodium nitrite treatment, which were reversed by NAC.	Acetylcysteine	161-164	hypoxia inducible factor 1 subunit alpha	Homo sapiens	25-35
27405163-12	2016	The expression levels of HIF-1alpha, Beclin-1 and Bnip3 (mitophagy marker molecular) increased remarkably after sodium nitrite treatment, which were reversed by NAC.	Acetylcysteine	161-164	BCL2 interacting protein 3	Homo sapiens	50-55
26667036-8	2015	In addition, C/EBPgamma-deficient newborns die from atelectasis and respiratory failure, which can be mitigated by in utero exposure to the antioxidant, N-acetyl-cysteine.	Acetylcysteine	153-170	CCAAT/enhancer binding protein (C/EBP), gamma	Mus musculus	13-23
25740810-8	2015	Accordingly, senescent rats chronically treated with the reducing agent N-acetyl-cysteine to prevent oxidative damage, show intact NMDAR activation linked to preserved D-serine levels and SR expression.	Acetylcysteine	72-89	serine racemase	Rattus norvegicus	188-190
26549478-6	2015	ROS scavenger (N-acetyl cysteine, NAC) could attenuate both the resveratrol induced caspase-3 activity and the formation of acidic vacuoles, but failed to attenuate resveratrol induced PEL cell death.	Acetylcysteine	15-32	caspase 3	Homo sapiens	84-93
26658309-9	2015	We also found that the antioxidant N-acetylcysteine (NAC) significantly attenuated Nrf2 activation after EPS, whereas the nitric oxide synthetase inhibitor Nomega-nitro-L-arginine methyl ester (L-NAME) did not.	Acetylcysteine	35-51	nuclear factor, erythroid derived 2, like 2	Mus musculus	83-87
26658309-9	2015	We also found that the antioxidant N-acetylcysteine (NAC) significantly attenuated Nrf2 activation after EPS, whereas the nitric oxide synthetase inhibitor Nomega-nitro-L-arginine methyl ester (L-NAME) did not.	Acetylcysteine	53-56	nuclear factor, erythroid derived 2, like 2	Mus musculus	83-87
26674585-12	2015	CONCLUSION: A 600 mg bid oral NAC treatment for 1-year on COPD patients without the L allele can improve the FEV1, FEV1% predicted, the SGRQ activity score, and the result of 6-minute walking distance test, and the exacerbation rate of the L allele carrier in COPD patients is much higher than in the COPD patients without the L allele.	Acetylcysteine	30-33	BH3 interacting domain death agonist	Homo sapiens	21-24
26523510-8	2015	Then, the effect of N-acetyl-L-cysteine (NAC) as a positive drug on ameliorating fibrogenesis in TGF-beta1-stimulated A549 cells was verified respectively by immunological and biophysical markers.	Acetylcysteine	20-39	transforming growth factor, beta 1	Rattus norvegicus	97-106
26523510-8	2015	Then, the effect of N-acetyl-L-cysteine (NAC) as a positive drug on ameliorating fibrogenesis in TGF-beta1-stimulated A549 cells was verified respectively by immunological and biophysical markers.	Acetylcysteine	41-44	transforming growth factor, beta 1	Rattus norvegicus	97-106
26852687-7	2015	Furthermore, pretreatment with N-acetyl-l-cysteine (NAC; a ROS scavenger) diminished the AOM-induced phosphorylation of ERK and JNK and AOM-induced HO-1 expression, suggesting that ERK and JNK are downstream mediators of ROS during the AOM-induced signalling of HO-1 expression.	Acetylcysteine	31-50	heme oxygenase 1	Mus musculus	148-152
26184564-4	2015	Previously, we demonstrated that N-acetyl cysteine (NAC) pretreatment up-regulates DUSP4 expression in endothelial cells, regulating p38 and ERK1/2 activities, and thus providing a protective effect against oxidative stress.	Acetylcysteine	33-50	dual specificity phosphatase 4	Mus musculus	83-88
26184564-4	2015	Previously, we demonstrated that N-acetyl cysteine (NAC) pretreatment up-regulates DUSP4 expression in endothelial cells, regulating p38 and ERK1/2 activities, and thus providing a protective effect against oxidative stress.	Acetylcysteine	52-55	dual specificity phosphatase 4	Mus musculus	83-88
26392121-7	2015	NAC effectively abrogates LPS-mediated TNF-alpha release from PBMC of both AIED patients and controls.	Acetylcysteine	0-3	tumor necrosis factor	Homo sapiens	39-48
26392121-9	2015	Given that NAC effectively abrogated LPS-mediated TNF-alpha release and exerted minimal effects on the downstream targets of this pathway, we feel NAC may be a rational adjunct therapy for this enigmatic disease, worthy of clinical exploration.	Acetylcysteine	11-14	tumor necrosis factor	Homo sapiens	50-59
26472194-8	2015	Antioxidants, such as glutathione and N-acetyl cysteine, significantly abrogated ROS production, ERK1/2 activation, and in turn, prevented SNG-induced autophagic cell death.	Acetylcysteine	38-55	mitogen-activated protein kinase 3	Homo sapiens	97-103
26431905-11	2015	NAC decreased SIRT1 phosphorylation and formation of the autophagy marker LC3II, which resulted in an increase in the apoptosis mediators gammaH2AX and cleaved/activated caspase-3.	Acetylcysteine	0-3	H2A.X variant histone	Mus musculus	138-147
26852687-7	2015	Furthermore, pretreatment with N-acetyl-l-cysteine (NAC; a ROS scavenger) diminished the AOM-induced phosphorylation of ERK and JNK and AOM-induced HO-1 expression, suggesting that ERK and JNK are downstream mediators of ROS during the AOM-induced signalling of HO-1 expression.	Acetylcysteine	31-50	heme oxygenase 1	Mus musculus	262-266
26852687-7	2015	Furthermore, pretreatment with N-acetyl-l-cysteine (NAC; a ROS scavenger) diminished the AOM-induced phosphorylation of ERK and JNK and AOM-induced HO-1 expression, suggesting that ERK and JNK are downstream mediators of ROS during the AOM-induced signalling of HO-1 expression.	Acetylcysteine	52-55	heme oxygenase 1	Mus musculus	148-152
26852687-7	2015	Furthermore, pretreatment with N-acetyl-l-cysteine (NAC; a ROS scavenger) diminished the AOM-induced phosphorylation of ERK and JNK and AOM-induced HO-1 expression, suggesting that ERK and JNK are downstream mediators of ROS during the AOM-induced signalling of HO-1 expression.	Acetylcysteine	52-55	heme oxygenase 1	Mus musculus	262-266
26343756-0	2015	N-acetyl cysteine protects human oral keratinocytes from Bis-GMA-induced apoptosis and cell cycle arrest by inhibiting reactive oxygen species-mediated mitochondrial dysfunction and the PI3K/Akt pathway.	Acetylcysteine	0-17	AKT serine/threonine kinase 1	Homo sapiens	191-194
26383538-6	2015	Desferoxamine and n-acetylcysteine ameliorated these deteriorations by inhibiting p38 MAPK and C/EBPalpha activity through iron chelation and ROS scavenging activity.	Acetylcysteine	18-34	CCAAT enhancer binding protein alpha	Homo sapiens	95-105
26364141-8	2015	Pretreatment with N-acetyl-l-cysteine (NAC) significantly inhibited intracellular ROS generation and increased cell viability, accompanied by a significant NF-kappaB inhibition and suppression of TLR4 and inflammatory cytokine MCP-1 expression.	Acetylcysteine	18-37	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	156-165
26364141-8	2015	Pretreatment with N-acetyl-l-cysteine (NAC) significantly inhibited intracellular ROS generation and increased cell viability, accompanied by a significant NF-kappaB inhibition and suppression of TLR4 and inflammatory cytokine MCP-1 expression.	Acetylcysteine	18-37	toll-like receptor 4	Mus musculus	196-200
26364141-8	2015	Pretreatment with N-acetyl-l-cysteine (NAC) significantly inhibited intracellular ROS generation and increased cell viability, accompanied by a significant NF-kappaB inhibition and suppression of TLR4 and inflammatory cytokine MCP-1 expression.	Acetylcysteine	39-42	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	156-165
26364141-8	2015	Pretreatment with N-acetyl-l-cysteine (NAC) significantly inhibited intracellular ROS generation and increased cell viability, accompanied by a significant NF-kappaB inhibition and suppression of TLR4 and inflammatory cytokine MCP-1 expression.	Acetylcysteine	39-42	toll-like receptor 4	Mus musculus	196-200
26265456-7	2015	In addition, the antioxidant agent N-acetylcysteine (NAC) reduces NF-kappaB activation, ERK phosphorylation, and IL-1beta production in Hcy-exposed macrophages, indicating the importance of ROS in this pro-inflammatory process.	Acetylcysteine	35-51	mitogen-activated protein kinase 1	Mus musculus	88-91
26265456-7	2015	In addition, the antioxidant agent N-acetylcysteine (NAC) reduces NF-kappaB activation, ERK phosphorylation, and IL-1beta production in Hcy-exposed macrophages, indicating the importance of ROS in this pro-inflammatory process.	Acetylcysteine	35-51	interleukin 1 beta	Mus musculus	113-121
26265456-7	2015	In addition, the antioxidant agent N-acetylcysteine (NAC) reduces NF-kappaB activation, ERK phosphorylation, and IL-1beta production in Hcy-exposed macrophages, indicating the importance of ROS in this pro-inflammatory process.	Acetylcysteine	53-56	mitogen-activated protein kinase 1	Mus musculus	88-91
26265456-7	2015	In addition, the antioxidant agent N-acetylcysteine (NAC) reduces NF-kappaB activation, ERK phosphorylation, and IL-1beta production in Hcy-exposed macrophages, indicating the importance of ROS in this pro-inflammatory process.	Acetylcysteine	53-56	interleukin 1 beta	Mus musculus	113-121
26625143-7	2015	SIM, NAC and APO were found to attenuate the HFD induced elevation of serum TNF-alpha, soluble TNFR1 (sTNFR1), 3-nitro-tyrosine.	Acetylcysteine	5-8	tumor necrosis factor	Mus musculus	76-85
26625143-13	2015	SIM, APO, and NAC either partially inhibit or completely block the TNF-alpha induced H2O2 or superoxide production.	Acetylcysteine	14-17	tumor necrosis factor	Mus musculus	67-76
26343756-8	2015	We found that Bis-GMA inhibited the phosphorylation of Akt, whereas the amount of phosphorylated Akt was reverted to the control level in the presence of NAC.	Acetylcysteine	154-157	AKT serine/threonine kinase 1	Homo sapiens	97-100
26344001-5	2015	This IL-1beta expression in OASFs is attenuated by N-acetylcysteine (NAC), inhibitors of ASK1, p38, or JNK, or treatment with berberine.	Acetylcysteine	51-67	interleukin 1 beta	Rattus norvegicus	5-13
26436146-4	2015	As the glucose oxidase cascade leads to the generation of H2O2 and catalase catalyzes the decomposition of H2O2, these two biocatalytic procedures can be probed by the Fenton reaction-mediated quenching of NAC-AuNCs.	Acetylcysteine	206-209	catalase	Homo sapiens	58-75
25867066-4	2015	We show that BV6/TNFalpha-induced cell death depends on ROS production, as several ROS scavengers such as butylated hydroxyanisole, N-acetylcysteine, alpha-tocopherol and ethyl pyruvate significantly rescue cell death.	Acetylcysteine	132-148	tumor necrosis factor	Homo sapiens	17-25
26436146-0	2015	Fenton reaction-mediated fluorescence quenching of N-acetyl-L-cysteine-protected gold nanoclusters: analytical applications of hydrogen peroxide, glucose, and catalase detection.	Acetylcysteine	51-70	catalase	Homo sapiens	159-167
26344001-5	2015	This IL-1beta expression in OASFs is attenuated by N-acetylcysteine (NAC), inhibitors of ASK1, p38, or JNK, or treatment with berberine.	Acetylcysteine	69-72	interleukin 1 beta	Rattus norvegicus	5-13
26335060-3	2015	The LPS-inducible IL-1beta was significantly suppressed by pretreatment with the NO scavenger 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl 3-oxide, but not by pretreatment with the O2(-) scavenger N-acetyl cysteine, suggesting the close association of NO with IL-1beta induction.	Acetylcysteine	210-227	interleukin 1 beta	Homo sapiens	18-26
26542776-12	2015	Treatment with the antioxidant N-acetyl cysteine (NAC) abrogated the catabolic effect of excessive ROS and TNF-alpha in vitro.	Acetylcysteine	31-48	tumor necrosis factor	Rattus norvegicus	107-116
26542776-12	2015	Treatment with the antioxidant N-acetyl cysteine (NAC) abrogated the catabolic effect of excessive ROS and TNF-alpha in vitro.	Acetylcysteine	50-53	tumor necrosis factor	Rattus norvegicus	107-116
26303969-2	2015	We investigated how Nrf2/HO-1 pathway affects osteoblast differentiation of MC3T3-E1 cells in response to hydrogen peroxide (H2O2), N-acetyl cysteine (NAC), or both.	Acetylcysteine	132-149	nuclear factor, erythroid derived 2, like 2	Mus musculus	20-24
25199686-8	2015	Endosulfan-induced Akt/MAPK pathways and COX-2 expression were attenuated by DPI, a specific NOX inhibitor, and the ROS scavenger N-acetylcysteine.	Acetylcysteine	130-146	thymoma viral proto-oncogene 1	Mus musculus	19-22
26139573-0	2015	Spectroscopic and molecular docking studies on the interaction between N-acetyl cysteine and bovine serum albumin.	Acetylcysteine	71-88	albumin	Homo sapiens	100-113
26139573-1	2015	The interaction between N-acetyl cysteine (NAC) and bovine serum albumin (BSA) was investigated by UV-vis, fluorescence spectroscopy, and molecular docking methods.	Acetylcysteine	24-41	albumin	Homo sapiens	59-72
26139573-1	2015	The interaction between N-acetyl cysteine (NAC) and bovine serum albumin (BSA) was investigated by UV-vis, fluorescence spectroscopy, and molecular docking methods.	Acetylcysteine	43-46	albumin	Homo sapiens	59-72
26303969-0	2015	N-acetyl cysteine inhibits H2O2-mediated reduction in the mineralization of MC3T3-E1 cells by down-regulating Nrf2/HO-1 pathway.	Acetylcysteine	0-17	nuclear factor, erythroid derived 2, like 2	Mus musculus	110-114
26303969-0	2015	N-acetyl cysteine inhibits H2O2-mediated reduction in the mineralization of MC3T3-E1 cells by down-regulating Nrf2/HO-1 pathway.	Acetylcysteine	0-17	heme oxygenase 1	Mus musculus	115-119
26303969-2	2015	We investigated how Nrf2/HO-1 pathway affects osteoblast differentiation of MC3T3-E1 cells in response to hydrogen peroxide (H2O2), N-acetyl cysteine (NAC), or both.	Acetylcysteine	132-149	heme oxygenase 1	Mus musculus	25-29
26303969-7	2015	Collectively, our findings suggest that H2O2-mediated activation of Nrf2/HO-1 pathway negatively regulates the osteoblast differentiation, which is inhibited by NAC.	Acetylcysteine	161-164	nuclear factor, erythroid derived 2, like 2	Mus musculus	68-72
26303969-7	2015	Collectively, our findings suggest that H2O2-mediated activation of Nrf2/HO-1 pathway negatively regulates the osteoblast differentiation, which is inhibited by NAC.	Acetylcysteine	161-164	heme oxygenase 1	Mus musculus	73-77
26294195-9	2015	Using an aminotransferase falling to below 50% of peak as the basis for discontinuing acetylcysteine would have resulted in antidotal treatment being stopped 24 (IQR: 9.6, 40) hours earlier (and in no cases later) using AST rather than ALT.	Acetylcysteine	86-100	solute carrier family 17 member 5	Homo sapiens	220-223
25920891-0	2015	A review on the possible molecular mechanism of action of N-acetylcysteine against insulin resistance and type-2 diabetes development.	Acetylcysteine	58-74	insulin	Homo sapiens	83-90
25920891-4	2015	In this review we aimed to focus on the protective effects of NAC against insulin resistance.	Acetylcysteine	62-65	insulin	Homo sapiens	74-81
25920891-7	2015	Further, NAC has anti-inflammatory and anti-apoptotic properties which can have positive effects during the inflammatory process in insulin resistance.	Acetylcysteine	9-12	insulin	Homo sapiens	132-139
25920891-8	2015	Moreover, NAC can modulate certain signaling pathways in both insulin target cells and beta cells.	Acetylcysteine	10-13	insulin	Homo sapiens	62-69
26210583-2	2015	In this work, the effect of N-acetyl-L-cysteine-capped CdTe quantum dots with fluorescence emission peak at 612 nm (QDs-612) on copper-zinc superoxide dismutase (Cu/ZnSOD) at molecular and cellular level was investigated using isothermal titration calorimetry, spectroscopic techniques, cell counting kit-8, and total SOD assay.	Acetylcysteine	28-47	superoxide dismutase 1, soluble	Mus musculus	162-170
26210583-2	2015	In this work, the effect of N-acetyl-L-cysteine-capped CdTe quantum dots with fluorescence emission peak at 612 nm (QDs-612) on copper-zinc superoxide dismutase (Cu/ZnSOD) at molecular and cellular level was investigated using isothermal titration calorimetry, spectroscopic techniques, cell counting kit-8, and total SOD assay.	Acetylcysteine	28-47	superoxide dismutase 1, soluble	Mus musculus	167-170
25843654-6	2015	HNE induced the nuclear accumulation of Nrf2 and enhanced UCP3 expression, effects prevented by the antioxidant N-acetylcysteine.	Acetylcysteine	112-128	nuclear factor, erythroid derived 2, like 2	Mus musculus	40-44
26299281-5	2015	Exposure of H9c2 cardiac myocytes to DOX upregulated the expression levels of phosphorylated ERK1/2, which had been reduced by pretreatment with NaHS or N-acetyl-L-cysteine, a ROS scavenger.	Acetylcysteine	153-172	mitogen-activated protein kinase 3	Homo sapiens	93-99
26215453-8	2015	Interestingly, ANG II-dependent repression of Npr1 gene expression and guanylyl cyclase (GC) activity was completely restored on treatment with losartan, while only a partial reversal was observed in NAC- and PDTC-co-treated cells.	Acetylcysteine	200-203	angiotensinogen	Rattus norvegicus	15-21
26316066-5	2015	In addition, we demonstrate the synergistic effect of CO and NAC both for the inhibition of nitric oxide (formation) and in the expression of tumour-necrosis factor (TNF)-alpha.	Acetylcysteine	61-64	tumor necrosis factor	Homo sapiens	142-176
26516435-12	2015	Twelve hours after hospitalization, the aspartate aminotransferase (AST) level in the group treated with NAC was significantly higher than in the group treated with the combination of NAC and cimetidine (IU/L30.1 +- 110.0 versus IU/L26.38 +- 94.93, p = 0.044).	Acetylcysteine	105-108	solute carrier family 17 member 5	Homo sapiens	40-66
26516435-12	2015	Twelve hours after hospitalization, the aspartate aminotransferase (AST) level in the group treated with NAC was significantly higher than in the group treated with the combination of NAC and cimetidine (IU/L30.1 +- 110.0 versus IU/L26.38 +- 94.93, p = 0.044).	Acetylcysteine	105-108	solute carrier family 17 member 5	Homo sapiens	68-71
26356671-6	2015	RESULTS: a) without copper supplementation, exogenous SOD potentiated sub-toxic DSF toxicity antagonized by sub-toxic TTM or by the anti-oxidant N-acetylcysteine; b) exogenous glucose oxidase, another H2O2 generator resembled exogenous SOD in potentiating sub-toxic DSF.	Acetylcysteine	145-161	superoxide dismutase 1	Homo sapiens	54-57
26264138-7	2015	The growth inhibitory effect of P53 was partially reversed by the antioxidant N-acetylcysteine.	Acetylcysteine	78-94	tumor protein p53	Homo sapiens	32-35
26291278-6	2015	Conversely, arsenite-induced H3S10 phosphorylation and HO-1 expression were blocked by N-acetylcysteine (NAC), the c-Jun N-terminal kinase (JNK) inhibitor SP600125, and JNK knockdown (siJNK).	Acetylcysteine	105-108	mitogen-activated protein kinase 8	Homo sapiens	169-172
26408691-4	2015	Treatment of tumor cells with the antioxidant N-acetylcysteine was able to prevent Zn(2+)-induced apoptosis, as well as the increase of p53 and FAS ligand protein induced by zinc.	Acetylcysteine	46-62	tumor protein p53	Homo sapiens	136-139
26194066-6	2015	The antioxidant N-acetyl-cysteine (NAC) inhibited phosphorylation of ERK, but not p38, suggesting that secretion of IL-8 in KU812 cells treated with Der f 1 is dependent on ROS, ERK MAPK and p38 MAPK.	Acetylcysteine	16-33	C-X-C motif chemokine ligand 8	Homo sapiens	116-120
26194066-6	2015	The antioxidant N-acetyl-cysteine (NAC) inhibited phosphorylation of ERK, but not p38, suggesting that secretion of IL-8 in KU812 cells treated with Der f 1 is dependent on ROS, ERK MAPK and p38 MAPK.	Acetylcysteine	16-33	mitogen-activated protein kinase 14	Homo sapiens	191-194
26194066-6	2015	The antioxidant N-acetyl-cysteine (NAC) inhibited phosphorylation of ERK, but not p38, suggesting that secretion of IL-8 in KU812 cells treated with Der f 1 is dependent on ROS, ERK MAPK and p38 MAPK.	Acetylcysteine	35-38	C-X-C motif chemokine ligand 8	Homo sapiens	116-120
26194066-6	2015	The antioxidant N-acetyl-cysteine (NAC) inhibited phosphorylation of ERK, but not p38, suggesting that secretion of IL-8 in KU812 cells treated with Der f 1 is dependent on ROS, ERK MAPK and p38 MAPK.	Acetylcysteine	35-38	mitogen-activated protein kinase 14	Homo sapiens	191-194
26043815-5	2015	LA and NAC prevented these effects by the modulation of ERK and HO1 pathways.	Acetylcysteine	7-10	mitogen-activated protein kinase 1	Homo sapiens	56-59
26297045-5	2015	We found that hypoxic stress increased ROS production as well as Stat3 activation and that ROS inhibitors (diphenyleneiodonium, rotenone and myxothiazol) and an antioxidant (N-acetyl-L-cysteine) blocked Stat3 activation under hypoxic conditions.	Acetylcysteine	174-193	signal transducer and activator of transcription 3	Homo sapiens	203-208
26305941-7	2015	Treatment with N-acetyl-l-cysteine, a potent antioxidant, abolished lipid peroxidation activity and ameliorated EAE in IFN-gamma-signaling-deficient mice.	Acetylcysteine	15-34	interferon gamma	Mus musculus	119-128
26149761-5	2015	Indeed, both cytotoxicity and ERK1/2 activation are prevented by exposing the cells to the anti-oxidant N-acetylcysteine.	Acetylcysteine	104-120	mitogen-activated protein kinase 3	Homo sapiens	30-36
26445536-8	2015	Although N-acetylcysteine inhibited the AuNP-induced Nrf2 nuclear translocation, the AuNPs did not promote intracellular reactive oxygen species production or endoplasmic reticulum stress in the ECs.	Acetylcysteine	9-25	NFE2 like bZIP transcription factor 2	Homo sapiens	53-57
26132720-5	2015	NAC treatment of CASQ1-null muscles/mice normalized caffeine sensitivity during in vitro contracture tests, Ca transients in single fibers, and significantly reduced the percentage of fibers undergoing rhabdomyolysis (37.6 +- 2.5%, 38/101 fibers in 3 mice; 11.6 +- 1.1%, 21/186 fibers in 5 mice).	Acetylcysteine	0-3	calsequestrin 1	Mus musculus	17-22
26132720-3	2015	RESULTS: NAC and Trolox significantly protected CASQ1-null mice from lethal episodes, with mortality being 79% (n = 14), 25% (n = 16), and 20% (n = 5) during halothane exposure and 86% (n = 21), 29% (n = 21), and 33% (n = 6) during heat stress in untreated, NAC-treated, and Trolox-treated mice, respectively.	Acetylcysteine	9-12	calsequestrin 1	Mus musculus	48-53
32262475-7	2015	Moreover, the autophagy activated by TEGDMA occurred via the AMPK/mTOR pathway, which could be abrogated by NAC pretreatment.	Acetylcysteine	108-111	mechanistic target of rapamycin kinase	Homo sapiens	66-70
26235743-10	2015	Pretreatment with the antioxidants N-acetyl cysteine or glutathione attenuated 8m-induced apoptosis and JNK activation in HCT116 cells.	Acetylcysteine	35-52	mitogen-activated protein kinase 8	Homo sapiens	104-107
26116711-9	2015	Similarly, exercise-induced changes in whole blood expression of VEGF, endothelial nitric oxide synthase and phosphatidylinositol 3-kinase R2 were blunted after NAC.	Acetylcysteine	161-164	vascular endothelial growth factor A	Homo sapiens	65-69
26116711-9	2015	Similarly, exercise-induced changes in whole blood expression of VEGF, endothelial nitric oxide synthase and phosphatidylinositol 3-kinase R2 were blunted after NAC.	Acetylcysteine	161-164	nitric oxide synthase 3	Homo sapiens	71-104
26132720-4	2015	During heat challenge, an increase in core temperature in CASQ1-null mice (42.3  +- 0.1 C, n=10) was significantly reduced by both NAC and Trolox (40.6  +- 0.3 C, n = 6 and 40.5  +- 0.2 C, n = 6).	Acetylcysteine	131-134	calsequestrin 1	Mus musculus	58-63
26224008-7	2015	Angiotensin II (Ang II)-induced BP responses were significantly higher in nicotine-treated group than in saline-treated control group, and NAC treatment blocked the nicotine-induced increase in BP response.	Acetylcysteine	139-142	angiotensinogen	Rattus norvegicus	16-22
24677730-3	2015	Pretreatment with reactive oxygen species (ROS) scavenger, N-acetylcysteine (NAC), attenuated NP-induced ROS production, COX-2 expression, and IL-6 and PGE2 release in TM4 cells.	Acetylcysteine	59-75	interleukin 6	Mus musculus	143-147
24677730-5	2015	Furthermore, NAC blocked NP-induced activation of NF-kappaB.	Acetylcysteine	13-16	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	50-59
24677730-3	2015	Pretreatment with reactive oxygen species (ROS) scavenger, N-acetylcysteine (NAC), attenuated NP-induced ROS production, COX-2 expression, and IL-6 and PGE2 release in TM4 cells.	Acetylcysteine	77-80	interleukin 6	Mus musculus	143-147
26021820-11	2015	This phenomenon was confirmed with suppressed nuclear Nrf2 activation, and consequently diminished antioxidant genes in cells treated with respective pharmacological inhibitors (LY294002, GF109203X, and N-acetylcysteine).	Acetylcysteine	203-219	NFE2 like bZIP transcription factor 2	Homo sapiens	54-58
25998424-6	2015	Both resveratrol and NAC partially restored DeltaPsim and ROS levels and prevented GAG release and cell loss and normalized SOD1 and SOD2 protein expression.	Acetylcysteine	21-24	superoxide dismutase [Mn], mitochondrial	Equus caballus	133-137
25766794-6	2015	Addition of N-acetylcysteine (NAC) or glutathione (GSH) partially suppressed induction of DNA fragmentation, apoptosis and caspase-3 activation by MMFDS and BMFDS.	Acetylcysteine	12-28	caspase 3	Homo sapiens	123-132
26118633-9	2015	Finally, we demonstrated that SSD decreased the level of reactive oxygen species (ROS) accumulation and that the specific ROS scavenger N-acetylcysteine (NAC) markedly inhibited the DDP-induced activation of MAPK and phosphorylation of the downstream signal NF-kappaB, which in turn reduced the levels of pro-inflammatory cytokine release and iNOS gene expression.	Acetylcysteine	136-152	nuclear factor kappa B subunit 1	Homo sapiens	258-267
26118633-9	2015	Finally, we demonstrated that SSD decreased the level of reactive oxygen species (ROS) accumulation and that the specific ROS scavenger N-acetylcysteine (NAC) markedly inhibited the DDP-induced activation of MAPK and phosphorylation of the downstream signal NF-kappaB, which in turn reduced the levels of pro-inflammatory cytokine release and iNOS gene expression.	Acetylcysteine	136-152	nitric oxide synthase 2	Homo sapiens	343-347
26118633-9	2015	Finally, we demonstrated that SSD decreased the level of reactive oxygen species (ROS) accumulation and that the specific ROS scavenger N-acetylcysteine (NAC) markedly inhibited the DDP-induced activation of MAPK and phosphorylation of the downstream signal NF-kappaB, which in turn reduced the levels of pro-inflammatory cytokine release and iNOS gene expression.	Acetylcysteine	154-157	nuclear factor kappa B subunit 1	Homo sapiens	258-267
26118633-9	2015	Finally, we demonstrated that SSD decreased the level of reactive oxygen species (ROS) accumulation and that the specific ROS scavenger N-acetylcysteine (NAC) markedly inhibited the DDP-induced activation of MAPK and phosphorylation of the downstream signal NF-kappaB, which in turn reduced the levels of pro-inflammatory cytokine release and iNOS gene expression.	Acetylcysteine	154-157	nitric oxide synthase 2	Homo sapiens	343-347
26296767-3	2015	In this study, we showed that the HCV-induced activation and mitochondrial accumulation of Bax were significantly attenuated by treatment with a general antioxidant, N-acetyl cysteine (NAC), or a specific c-Jun N-terminal kinase (JNK) inhibitor, SP600125, with the result suggesting that the reactive oxygen species (ROS)/JNK signalling pathway is upstream of Bax activation in HCV-induced apoptosis.	Acetylcysteine	166-183	BCL2 associated X, apoptosis regulator	Homo sapiens	91-94
26296767-3	2015	In this study, we showed that the HCV-induced activation and mitochondrial accumulation of Bax were significantly attenuated by treatment with a general antioxidant, N-acetyl cysteine (NAC), or a specific c-Jun N-terminal kinase (JNK) inhibitor, SP600125, with the result suggesting that the reactive oxygen species (ROS)/JNK signalling pathway is upstream of Bax activation in HCV-induced apoptosis.	Acetylcysteine	166-183	mitogen-activated protein kinase 8	Homo sapiens	322-325
26296767-3	2015	In this study, we showed that the HCV-induced activation and mitochondrial accumulation of Bax were significantly attenuated by treatment with a general antioxidant, N-acetyl cysteine (NAC), or a specific c-Jun N-terminal kinase (JNK) inhibitor, SP600125, with the result suggesting that the reactive oxygen species (ROS)/JNK signalling pathway is upstream of Bax activation in HCV-induced apoptosis.	Acetylcysteine	166-183	BCL2 associated X, apoptosis regulator	Homo sapiens	360-363
26296767-3	2015	In this study, we showed that the HCV-induced activation and mitochondrial accumulation of Bax were significantly attenuated by treatment with a general antioxidant, N-acetyl cysteine (NAC), or a specific c-Jun N-terminal kinase (JNK) inhibitor, SP600125, with the result suggesting that the reactive oxygen species (ROS)/JNK signalling pathway is upstream of Bax activation in HCV-induced apoptosis.	Acetylcysteine	185-188	BCL2 associated X, apoptosis regulator	Homo sapiens	91-94
26296767-5	2015	The HCV-induced increase in the Bim mRNA and protein levels was significantly counteracted by treatment with NAC or SP600125, suggesting that the ROS/JNK signalling pathway is involved in Bim upregulation.	Acetylcysteine	109-112	mitogen-activated protein kinase 8	Homo sapiens	150-153
26133502-6	2015	The persistence of residual DNA damage even in the presence of free radical scavenger N-acetyl cysteine, suggested that the influence of Nrf2 on DNA repair was not linked to its antioxidant functions.	Acetylcysteine	86-103	NFE2 like bZIP transcription factor 2	Homo sapiens	137-141
26116162-10	2015	The inhibitory effects of celastrol on LPS binding to MD2 were reversed by thiol donors (N-acetyl-L-cysteine and dithiothreitol), suggesting that the thiol reactivity of celastrol contributes to its inhibitory effects on TLR4 activation in macrophages.	Acetylcysteine	89-108	toll-like receptor 4	Mus musculus	221-225
26093296-3	2015	In this study, we found that angiotensin II dose-dependently increased the expression of Col1a1, Col3a1 and alpha-smooth muscle actin, which were blocked by ROS (reactive oxygen species) scavenger N-acetyl cysteine (NAC).	Acetylcysteine	197-214	angiotensinogen	Homo sapiens	29-43
26093296-3	2015	In this study, we found that angiotensin II dose-dependently increased the expression of Col1a1, Col3a1 and alpha-smooth muscle actin, which were blocked by ROS (reactive oxygen species) scavenger N-acetyl cysteine (NAC).	Acetylcysteine	216-219	angiotensinogen	Homo sapiens	29-43
27103891-5	2015	However, NAC pre-treatment significantly inhibited the activation of caspase-3 and PARP cleavage and reduced Bcl-xL levels.	Acetylcysteine	9-12	caspase 3	Homo sapiens	69-78
27103891-5	2015	However, NAC pre-treatment significantly inhibited the activation of caspase-3 and PARP cleavage and reduced Bcl-xL levels.	Acetylcysteine	9-12	poly(ADP-ribose) polymerase 1	Homo sapiens	83-87
27103891-5	2015	However, NAC pre-treatment significantly inhibited the activation of caspase-3 and PARP cleavage and reduced Bcl-xL levels.	Acetylcysteine	9-12	BCL2 like 1	Homo sapiens	109-115
25953698-9	2015	GSH or NAC treatment inhibited DMF-induced JNK, p38, and ERK activation in CT26 cells.	Acetylcysteine	7-10	mitogen-activated protein kinase 1	Mus musculus	57-60
25971793-5	2015	Parthenolide, Akt inhibitor, Bay 11-7085, and N-acetylcysteine each attenuated the lipopolysaccharide-induced production of IL-1beta and PGE2, increase in the levels of cyclooxygenase, formation of reactive oxygen species, increase in the levels of Toll-like receptor-4, and activation of the Akt/mTOR and NF-kappaB in keratinocytes.	Acetylcysteine	46-62	interleukin 1 beta	Homo sapiens	124-132
25971793-5	2015	Parthenolide, Akt inhibitor, Bay 11-7085, and N-acetylcysteine each attenuated the lipopolysaccharide-induced production of IL-1beta and PGE2, increase in the levels of cyclooxygenase, formation of reactive oxygen species, increase in the levels of Toll-like receptor-4, and activation of the Akt/mTOR and NF-kappaB in keratinocytes.	Acetylcysteine	46-62	AKT serine/threonine kinase 1	Homo sapiens	293-296
25971793-5	2015	Parthenolide, Akt inhibitor, Bay 11-7085, and N-acetylcysteine each attenuated the lipopolysaccharide-induced production of IL-1beta and PGE2, increase in the levels of cyclooxygenase, formation of reactive oxygen species, increase in the levels of Toll-like receptor-4, and activation of the Akt/mTOR and NF-kappaB in keratinocytes.	Acetylcysteine	46-62	mechanistic target of rapamycin kinase	Homo sapiens	297-301
25971793-5	2015	Parthenolide, Akt inhibitor, Bay 11-7085, and N-acetylcysteine each attenuated the lipopolysaccharide-induced production of IL-1beta and PGE2, increase in the levels of cyclooxygenase, formation of reactive oxygen species, increase in the levels of Toll-like receptor-4, and activation of the Akt/mTOR and NF-kappaB in keratinocytes.	Acetylcysteine	46-62	nuclear factor kappa B subunit 1	Homo sapiens	306-315
26088922-10	2015	Antioxidant NAC decreased HIF-1alpha/VEGF expression and inhibited BE(2)-C cell growth.	Acetylcysteine	12-15	hypoxia inducible factor 1 subunit alpha	Homo sapiens	26-36
26088922-10	2015	Antioxidant NAC decreased HIF-1alpha/VEGF expression and inhibited BE(2)-C cell growth.	Acetylcysteine	12-15	vascular endothelial growth factor A	Homo sapiens	37-41
26274909-11	2015	NAC rescued hDPCs from DMAE-CB-induced apoptosis, accompanied by lower level of MMP loss and caspase-3 activity.	Acetylcysteine	0-3	caspase 3	Homo sapiens	93-102
25766794-6	2015	Addition of N-acetylcysteine (NAC) or glutathione (GSH) partially suppressed induction of DNA fragmentation, apoptosis and caspase-3 activation by MMFDS and BMFDS.	Acetylcysteine	30-33	caspase 3	Homo sapiens	123-132
25503516-5	2015	N-acetyl-cysteine (ROS scavenger) or hexamethonium [nicotinic acetylcholine receptor (nAChR) antagonist] attenuated the CSE-induced increase in intracellular ROS, activation of AMPK and NF-kappaB, as well as IL-8 induction, which suggests that nAChRs and ROS are important.	Acetylcysteine	0-17	cholinergic receptor nicotinic alpha 4 subunit	Homo sapiens	86-91
25713411-9	2015	Antioxidant (N-acetylcysteine) suppressed albumin-induced ER stress and decrements in precursor and mature forms of integrin-beta1.	Acetylcysteine	13-29	integrin subunit beta 1	Rattus norvegicus	116-130
25575547-0	2015	The anti-inflammatory effects of acetaminophen and N-acetylcysteine through suppression of the NLRP3 inflammasome pathway in LPS-challenged piglet mononuclear phagocytes.	Acetylcysteine	51-67	NLR family pyrin domain containing 3	Homo sapiens	95-100
25575547-6	2015	AAP (0.5-1.0 mM) and NAC (0.5-1.0 mM) used individually or in combination could down-regulate protein expression of cleaved caspase-1 and mRNA expression of IL-1beta, IL-18 and NLRP3.	Acetylcysteine	21-24	caspase 1	Homo sapiens	124-133
25575547-6	2015	AAP (0.5-1.0 mM) and NAC (0.5-1.0 mM) used individually or in combination could down-regulate protein expression of cleaved caspase-1 and mRNA expression of IL-1beta, IL-18 and NLRP3.	Acetylcysteine	21-24	interleukin 1 beta	Homo sapiens	157-165
25575547-6	2015	AAP (0.5-1.0 mM) and NAC (0.5-1.0 mM) used individually or in combination could down-regulate protein expression of cleaved caspase-1 and mRNA expression of IL-1beta, IL-18 and NLRP3.	Acetylcysteine	21-24	NLR family pyrin domain containing 3	Homo sapiens	177-182
25575547-8	2015	The combined use of AAP plus NAC had better inhibition action on the NLRP3 inflammasome pathway.	Acetylcysteine	29-32	NLR family pyrin domain containing 3	Homo sapiens	69-74
25575547-9	2015	These results indicate that the anti-inflammatory effects of AAP and NAC occur via the regulation on mRNA expression of NLRP3 and activation of caspase-1.	Acetylcysteine	69-72	NLR family pyrin domain containing 3	Homo sapiens	120-125
25575547-9	2015	These results indicate that the anti-inflammatory effects of AAP and NAC occur via the regulation on mRNA expression of NLRP3 and activation of caspase-1.	Acetylcysteine	69-72	caspase 1	Homo sapiens	144-153
25575547-10	2015	The anti-inflammatory activity of AAP and NAC could be related to the suppression of NLRP3 inflammasome pathway under LPS stimulation.	Acetylcysteine	42-45	NLR family pyrin domain containing 3	Homo sapiens	85-90
26305534-7	2015	The addition of NAC markedly reduced the high glucose-induced ROS activation, Annexin-PI-positive cells, and levels of cleaved caspase-3, BAX, IL-6, and TNF-alpha.	Acetylcysteine	16-19	BCL2 associated X, apoptosis regulator	Homo sapiens	138-141
26305534-7	2015	The addition of NAC markedly reduced the high glucose-induced ROS activation, Annexin-PI-positive cells, and levels of cleaved caspase-3, BAX, IL-6, and TNF-alpha.	Acetylcysteine	16-19	interleukin 6	Homo sapiens	143-147
26305534-7	2015	The addition of NAC markedly reduced the high glucose-induced ROS activation, Annexin-PI-positive cells, and levels of cleaved caspase-3, BAX, IL-6, and TNF-alpha.	Acetylcysteine	16-19	tumor necrosis factor	Homo sapiens	153-162
25204891-8	2015	Profiling of MAPKs revealed activation of JNK upon hesperetin treatment which was abrogated upon NAC pre-treatment.	Acetylcysteine	97-100	mitogen-activated protein kinase 8	Homo sapiens	42-45
25557231-8	2015	Silencing Nrf2 also inhibited the protective effects of baicalein, sulforaphane, and N-acetylcysteine and resulted in high ROS levels, suggesting ROS elimination was mediated by Nrf2.	Acetylcysteine	85-101	nuclear factor, erythroid derived 2, like 2	Mus musculus	10-14
25557231-7	2015	Co-treatment of cells with hydrogen peroxide and N-acetylcysteine or the Nrf2 inducer sulforaphane reduced hydrogen peroxide-induced damage in a similar fashion to baicalein, while the Nrf2 inhibitor retinoic acid blocked the protective effect of baicalein.	Acetylcysteine	49-65	nuclear factor, erythroid derived 2, like 2	Mus musculus	185-189
25503516-5	2015	N-acetyl-cysteine (ROS scavenger) or hexamethonium [nicotinic acetylcholine receptor (nAChR) antagonist] attenuated the CSE-induced increase in intracellular ROS, activation of AMPK and NF-kappaB, as well as IL-8 induction, which suggests that nAChRs and ROS are important.	Acetylcysteine	0-17	nuclear factor kappa B subunit 1	Homo sapiens	186-195
25503516-5	2015	N-acetyl-cysteine (ROS scavenger) or hexamethonium [nicotinic acetylcholine receptor (nAChR) antagonist] attenuated the CSE-induced increase in intracellular ROS, activation of AMPK and NF-kappaB, as well as IL-8 induction, which suggests that nAChRs and ROS are important.	Acetylcysteine	0-17	C-X-C motif chemokine ligand 8	Homo sapiens	208-212
26006043-0	2015	Suppression of methylmercury-induced IL-6 and MCP-1 expressions by N-acetylcysteine in U-87MG human astrocytoma cells.	Acetylcysteine	67-83	interleukin 6	Homo sapiens	37-41
23871548-10	2015	With acetylcysteine filters, the pressure drop over 4 cmH2O occurred earlier and had a good relationship between the degree of pressure drop and doses.	Acetylcysteine	5-19	troponin T2, cardiac type	Homo sapiens	54-58
26006043-7	2015	MeHg-induced expression of MCP-1 and IL-6 mRNA was reduced by 10-20% in the presence of 5mM NAC (co-treatment experiment) compared to cells treated with MeHg only.	Acetylcysteine	92-95	interleukin 6	Homo sapiens	37-41
26006043-8	2015	Pre-treatment of cells with 0.5 or 5mM NAC at 0.5 or 1h and its subsequent washout before MeHg addition suppressed MCP-1 and IL-6 cytokine expressions.	Acetylcysteine	39-42	interleukin 6	Homo sapiens	125-129
26081590-7	2015	Furthermore, TUDCA decreased SAN-induced ROS production, and NAC attenuated SAN-induced GRP78 and CHOP expression.	Acetylcysteine	61-64	heat shock protein family A (Hsp70) member 5	Homo sapiens	88-93
25863775-12	2015	ATP potently promoted ROS generation in HDPFs; N-acetyl cysteine inhibited ROS production, caspase-1 activation and IL-1beta secretion induced by ATP.	Acetylcysteine	47-64	caspase 1	Homo sapiens	91-100
25863775-12	2015	ATP potently promoted ROS generation in HDPFs; N-acetyl cysteine inhibited ROS production, caspase-1 activation and IL-1beta secretion induced by ATP.	Acetylcysteine	47-64	interleukin 1 beta	Homo sapiens	116-124
26081590-7	2015	Furthermore, TUDCA decreased SAN-induced ROS production, and NAC attenuated SAN-induced GRP78 and CHOP expression.	Acetylcysteine	61-64	DNA damage inducible transcript 3	Homo sapiens	98-102
25138434-7	2015	Moreover, both N-acetylcysteine and the superoxide dismutase mimetic, MnTBAP, reversed quercetin-induced intracellular reactive oxygen species production, ERK activation, and subsequent cell death.	Acetylcysteine	15-31	mitogen-activated protein kinase 1	Homo sapiens	155-158
26133975-11	2015	Addition of NAC reduced epithelial cell ROS, but not MAC ROS, for up to 4 h. TT1 and MAC cells internalised all NP formats, whereas only a small fraction of AT2 cells internalized ANP (not UNP or CNP).	Acetylcysteine	12-15	2',3'-cyclic nucleotide 3' phosphodiesterase	Homo sapiens	196-199
26002468-6	2015	The antioxidant N-Acety-l-Cysteine (NAC) was found to attenuate the JNK and p38 MAPK activation with a concomitant reduction of PA-induced autophagy and apoptosis.	Acetylcysteine	16-34	mitogen-activated protein kinase 8	Homo sapiens	68-71
26002468-6	2015	The antioxidant N-Acety-l-Cysteine (NAC) was found to attenuate the JNK and p38 MAPK activation with a concomitant reduction of PA-induced autophagy and apoptosis.	Acetylcysteine	16-34	mitogen-activated protein kinase 14	Homo sapiens	76-79
25284589-11	2015	Gln starvation markedly increases ROS levels in Hace1(-/-) but not in wt MEFs, and treatment with the antioxidant N-acetyl cysteine or the TCA cycle intermediate oxaloacetate efficiently rescues Gln starvation-induced ROS elevation and cell death in Hace1(-/-) MEFs.	Acetylcysteine	114-131	HECT domain and ankyrin repeat containing, E3 ubiquitin protein ligase 1	Mus musculus	48-53
25284589-11	2015	Gln starvation markedly increases ROS levels in Hace1(-/-) but not in wt MEFs, and treatment with the antioxidant N-acetyl cysteine or the TCA cycle intermediate oxaloacetate efficiently rescues Gln starvation-induced ROS elevation and cell death in Hace1(-/-) MEFs.	Acetylcysteine	114-131	HECT domain and ankyrin repeat containing, E3 ubiquitin protein ligase 1	Mus musculus	250-255
26198099-8	2015	Furthermore, LPS-induced apoptosis was blocked by antioxidant N-acetylcysteine or NF-kappaB inhibitor via down-regulating Fas expression.	Acetylcysteine	62-78	toll-like receptor 4	Mus musculus	13-16
26184135-11	2015	Inhibition of ROS by N-acetyl-cysteine reversed the m-NO-ASA-mediated translocation of p50 in to the nucleus.	Acetylcysteine	21-38	nuclear factor kappa B subunit 1	Homo sapiens	87-90
25931014-10	2015	Although cells expressing hyperactivated AKT1 displayed higher levels of reactive oxygen species both in vitro and in vivo, the addition of the antioxidant N-acetyl-L-cysteine significantly reduced apoptosis.	Acetylcysteine	156-175	thymoma viral proto-oncogene 1	Mus musculus	41-45
26199914-0	2015	N-Acetyl Cysteine Inhibits Endothelin-1-Induced ROS Dependent Cardiac Hypertrophy through Superoxide Dismutase Regulation.	Acetylcysteine	0-17	endothelin 1	Rattus norvegicus	27-39
26199914-2	2015	N-Acetyl cysteine (NAC) can enhance the SOD activity, so the aim of this study is to highlight the inhibitory role of NAC against endothelin-1 (ET-1)-induced cardiac hypertrophy.	Acetylcysteine	0-17	endothelin 1	Rattus norvegicus	130-142
26199914-2	2015	N-Acetyl cysteine (NAC) can enhance the SOD activity, so the aim of this study is to highlight the inhibitory role of NAC against endothelin-1 (ET-1)-induced cardiac hypertrophy.	Acetylcysteine	19-22	endothelin 1	Rattus norvegicus	130-142
26199914-2	2015	N-Acetyl cysteine (NAC) can enhance the SOD activity, so the aim of this study is to highlight the inhibitory role of NAC against endothelin-1 (ET-1)-induced cardiac hypertrophy.	Acetylcysteine	118-121	endothelin 1	Rattus norvegicus	130-142
25976560-6	2015	Prolonged exposure to palmitate increased reactive oxygen species (ROS) production, and the antioxidant, N-acetylcysteine (NAC), partially prevented the detrimental effects induced by palmitate on beta cells, resulting in decreased GLP-1 levels.	Acetylcysteine	105-121	glucagon	Homo sapiens	232-237
26339453-0	2015	N-acetylcysteine protects against liver injure induced by carbon tetrachloride via activation of the Nrf2/HO-1 pathway.	Acetylcysteine	0-16	NFE2 like bZIP transcription factor 2	Rattus norvegicus	101-105
26339453-6	2015	Thus, Aim of the present study was to investigate potential hepatic protective role of NAC and to delineate its mechanism of action against carbon tetrachloride (CCl4)-induced liver injury in models of rat.	Acetylcysteine	87-90	C-C motif chemokine ligand 4	Rattus norvegicus	162-166
26339453-7	2015	Our results showed that the alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities as well as malondialdehyde (MDA) contents decreased significantly in CCl4-induced rats with NAC treatment.	Acetylcysteine	199-202	glutamic-oxaloacetic transaminase 2	Rattus norvegicus	63-89
26339453-7	2015	Our results showed that the alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities as well as malondialdehyde (MDA) contents decreased significantly in CCl4-induced rats with NAC treatment.	Acetylcysteine	199-202	glutamic-oxaloacetic transaminase 2	Rattus norvegicus	91-94
26339453-7	2015	Our results showed that the alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities as well as malondialdehyde (MDA) contents decreased significantly in CCl4-induced rats with NAC treatment.	Acetylcysteine	199-202	C-C motif chemokine ligand 4	Rattus norvegicus	176-180
26339453-9	2015	Treatment with NAC had been shown to an increase in nuclear factor erythroid 2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1) mRNA levels.	Acetylcysteine	15-18	NFE2 like bZIP transcription factor 2	Rattus norvegicus	52-95
26339453-9	2015	Treatment with NAC had been shown to an increase in nuclear factor erythroid 2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1) mRNA levels.	Acetylcysteine	15-18	NFE2 like bZIP transcription factor 2	Rattus norvegicus	97-101
25976560-6	2015	Prolonged exposure to palmitate increased reactive oxygen species (ROS) production, and the antioxidant, N-acetylcysteine (NAC), partially prevented the detrimental effects induced by palmitate on beta cells, resulting in decreased GLP-1 levels.	Acetylcysteine	123-126	glucagon	Homo sapiens	232-237
26339453-10	2015	In conclusion, these results suggested that NAC upregulated HO-1 through the activation of Nrf2 pathway and protected rat against CCl4-induced liver injure.	Acetylcysteine	44-47	NFE2 like bZIP transcription factor 2	Rattus norvegicus	91-95
26339453-10	2015	In conclusion, these results suggested that NAC upregulated HO-1 through the activation of Nrf2 pathway and protected rat against CCl4-induced liver injure.	Acetylcysteine	44-47	C-C motif chemokine ligand 4	Rattus norvegicus	130-134
25815442-12	2015	The western blot analysis demonstrated that treatment of the SKOV3/TR cells with NAC reduced the protein expression of Tyro3, and the inhibitory effect of NAC on the phosphorylation of Akt was increased, which may have had a positive effect on the proliferation of the SKOV3/TR cells.	Acetylcysteine	155-158	AKT serine/threonine kinase 1	Homo sapiens	185-188
25869503-7	2015	Furthermore, when the radiation-induced increase in reactive oxygen species (ROS) generation was prevented by the anti-oxidant N-acetyl-L-cysteine, eNOS Ser-1177 phosphorylation and Thr-495 dephosphorylation in irradiated HUVECs were significantly reduced.	Acetylcysteine	127-146	nitric oxide synthase 3	Homo sapiens	148-152
26100173-10	2015	In addition, treatment with N-acetylcysteine, an antioxidant, inhibited the CSE-augmented phosphorylation of ERK and MUC5AC.	Acetylcysteine	28-44	mitogen-activated protein kinase 1	Homo sapiens	109-112
25815442-12	2015	The western blot analysis demonstrated that treatment of the SKOV3/TR cells with NAC reduced the protein expression of Tyro3, and the inhibitory effect of NAC on the phosphorylation of Akt was increased, which may have had a positive effect on the proliferation of the SKOV3/TR cells.	Acetylcysteine	81-84	TYRO3 protein tyrosine kinase	Homo sapiens	119-124
25817893-13	2015	In contrast to ascorbic acid, trolox, and deferoxamine, N-acetylcysteine suppressed the EA-induced upregulation of GADD153, although not of HO-1.	Acetylcysteine	56-72	DNA damage inducible transcript 3	Homo sapiens	115-122
26653649-12	2015	After TD and NAC monotherapy, the IL-6 content decreased to 79.22 +- 9.65 pg/ml and 81.63 +- 5.72 pg/ml, and it decreased more significantly after combined medication (74.37 +- 3.17 pg/ml).	Acetylcysteine	13-16	interleukin 6	Rattus norvegicus	34-38
26653649-14	2015	After TD and NAC monotherapy, the TNF-alpha content decreased to 50.48 +- 2.76 pg/ml and 54.28 +- 4.30 pg/ml, and it decreased more significantly after combined medication (49.10 +- 4.98 pg/ml).	Acetylcysteine	13-16	tumor necrosis factor	Rattus norvegicus	34-43
26653649-15	2015	CONCLUSION: NAC and TD could reduce MDA, TNF-alpha and IL-6 levels in lung tissue, and alleviate SiO2-induced pulmonary fibrosis in rats.	Acetylcysteine	12-15	tumor necrosis factor	Rattus norvegicus	41-50
26653649-15	2015	CONCLUSION: NAC and TD could reduce MDA, TNF-alpha and IL-6 levels in lung tissue, and alleviate SiO2-induced pulmonary fibrosis in rats.	Acetylcysteine	12-15	interleukin 6	Rattus norvegicus	55-59
25687825-8	2015	Supplementation of thiols in Nrf2(-/-) cocultures via addition of glutathione ester, N-acetylcysteine, beta-mercaptoethanol, or cysteine itself restored T cell proliferation as well as cytotoxicity by increasing intracellular GSH.	Acetylcysteine	85-101	NFE2 like bZIP transcription factor 2	Homo sapiens	29-33
26122524-9	2015	Expression levels of mature brain-derived neurotrophic factor (BDNF) and phosphorylated cAMP response element binding protein (CREB) were significantly enhanced by treatment with either PMC-12 or NAC.	Acetylcysteine	196-199	cAMP responsive element binding protein 1	Mus musculus	88-125
26122524-9	2015	Expression levels of mature brain-derived neurotrophic factor (BDNF) and phosphorylated cAMP response element binding protein (CREB) were significantly enhanced by treatment with either PMC-12 or NAC.	Acetylcysteine	196-199	cAMP responsive element binding protein 1	Mus musculus	127-131
26104799-14	2015	N-acetyl-cysteine, a scavenger of reactive oxygen species (ROS), inhibited Cu(II)-Abeta-elicited microglial release of TNF-alpha and nitric oxide as well as the microglia-mediated neurotoxic effect.	Acetylcysteine	0-17	tumor necrosis factor	Homo sapiens	119-128
25697727-10	2015	Finally, addition of the antioxidant N-acetylcysteine inhibited activation of Erk1/2 by cigarette smoke and precluded the cigarette smoke-induced decrease of CFTR.	Acetylcysteine	37-53	mitogen-activated protein kinase 3	Homo sapiens	78-84
25697727-10	2015	Finally, addition of the antioxidant N-acetylcysteine inhibited activation of Erk1/2 by cigarette smoke and precluded the cigarette smoke-induced decrease of CFTR.	Acetylcysteine	37-53	CF transmembrane conductance regulator	Homo sapiens	158-162
25058850-6	2015	MDP (an NLRC2 agonist), NAC and AZM, but not Tri-DAP (an NLRC1 agonist), increased IL-6 production in CF cells, indicating that in CF cells IL-6 upregulation is independent of NLRC1, but involves the activation of NLRC2.	Acetylcysteine	24-27	interleukin 6	Homo sapiens	83-87
25058850-6	2015	MDP (an NLRC2 agonist), NAC and AZM, but not Tri-DAP (an NLRC1 agonist), increased IL-6 production in CF cells, indicating that in CF cells IL-6 upregulation is independent of NLRC1, but involves the activation of NLRC2.	Acetylcysteine	24-27	interleukin 6	Homo sapiens	140-144
26058063-10	2015	NAC treatment or AON overexpression with reduced ROS formation effectively prevented PM-induced reduction of BMSCs population and proliferation with partial recovery of P-Akt level.	Acetylcysteine	0-3	thymoma viral proto-oncogene 1	Mus musculus	171-174
26131370-10	2015	The effect of reactive oxygen species on sclerostin expression was examined by treating cells with 1 mM H2O2 or 20 mM N-acetylcysteine.	Acetylcysteine	118-134	sclerostin	Homo sapiens	41-51
26131370-15	2015	In addition, N-acetylcysteine treatment or knockdown of TNFalpha attenuated high glucose-induced sclerostin expression.	Acetylcysteine	13-29	sclerostin	Homo sapiens	97-107
26484027-11	2015	N-acetyl cysteine and apocynin alleviated activation of ERK and p38 MAPK.	Acetylcysteine	0-17	mitogen-activated protein kinase 3	Homo sapiens	56-59
25972196-6	2015	Furthermore, the attenuation of ATO-induced ROS and the resulting oxidative DNA damage by N-acetyl-L-cysteine (NAC), a potent antioxidant, significantly reduced the activation of PARP-1 and NF-kappaB in ATO-treated cells.	Acetylcysteine	90-109	nuclear factor kappa B subunit 1	Homo sapiens	190-199
25972196-6	2015	Furthermore, the attenuation of ATO-induced ROS and the resulting oxidative DNA damage by N-acetyl-L-cysteine (NAC), a potent antioxidant, significantly reduced the activation of PARP-1 and NF-kappaB in ATO-treated cells.	Acetylcysteine	90-109	poly(ADP-ribose) polymerase 1	Homo sapiens	179-185
25834143-9	2015	Furthermore, NAC treatment could inhibit NLRP3 inflammasome formation and caspase-1 activation and suppress the release of IL-1beta and IL-18 from H. pylori-infected THP-1 cells.	Acetylcysteine	13-16	NLR family pyrin domain containing 3	Homo sapiens	41-46
25834143-9	2015	Furthermore, NAC treatment could inhibit NLRP3 inflammasome formation and caspase-1 activation and suppress the release of IL-1beta and IL-18 from H. pylori-infected THP-1 cells.	Acetylcysteine	13-16	caspase 1	Homo sapiens	74-83
25834143-9	2015	Furthermore, NAC treatment could inhibit NLRP3 inflammasome formation and caspase-1 activation and suppress the release of IL-1beta and IL-18 from H. pylori-infected THP-1 cells.	Acetylcysteine	13-16	interleukin 1 beta	Homo sapiens	123-131
25834143-9	2015	Furthermore, NAC treatment could inhibit NLRP3 inflammasome formation and caspase-1 activation and suppress the release of IL-1beta and IL-18 from H. pylori-infected THP-1 cells.	Acetylcysteine	13-16	GLI family zinc finger 2	Homo sapiens	166-171
25935150-6	2015	Furthermore, Abeta stimulated the production of reactive oxygen species in endothelial cells and concomitant treatments of the cells with the antioxidant N-acetyl-cysteine (NAC) prevented Abeta effects in promoting HSP90/eNOS interaction and rescued agonist-mediated Akt and eNOS phosphorylation.	Acetylcysteine	154-171	amyloid beta precursor protein	Homo sapiens	13-18
25732260-7	2015	This finding was reversed in response to the NFkappaB inhibitor N-acetyl cysteine (NAC).	Acetylcysteine	64-81	nuclear factor kappa B subunit 1	Homo sapiens	45-53
25732260-7	2015	This finding was reversed in response to the NFkappaB inhibitor N-acetyl cysteine (NAC).	Acetylcysteine	83-86	nuclear factor kappa B subunit 1	Homo sapiens	45-53
25817791-8	2015	We assume that the NAC- and DHLA-induced stimulation of the E-cadherin-catenin pathway contributes to the increased internalization of the grimelysin producing bacteria within transformed cells.	Acetylcysteine	19-22	cadherin 1	Homo sapiens	60-70
25961745-8	2015	3-MA, NAC and DPI inhibited HG-induced interleukin-6 production in BMSCs.	Acetylcysteine	6-9	interleukin 6	Homo sapiens	39-52
26023321-7	2015	An anti-oxidant, N-acetylcysteine completely blocked insulin-induced up-regulation of SGLT2 as well as increase in glucose absorption by tubular cells.	Acetylcysteine	17-33	insulin	Homo sapiens	53-60
25940438-8	2015	Moreover, silencing of S100A11 stimulated mitochondrial superoxide production, which was decreased by AACOCF(3), as well as N-acetyl-L-cysteine, which also mimicked the effect of PLA(2) inhibitor on NSCLC chemosensitization upon S100A11 silencing.	Acetylcysteine	124-143	S100 calcium binding protein A11	Homo sapiens	23-30
25781201-8	2015	AhR antagonists (alpha-naphthoflavone, CH223191) or antioxidants (N-acetyl-l-cysteine, EUK-134) attenuated 5F 203-mediated JNK and p38 activation, depending on the cell type.	Acetylcysteine	66-85	mitogen-activated protein kinase 8	Homo sapiens	123-126
25781201-8	2015	AhR antagonists (alpha-naphthoflavone, CH223191) or antioxidants (N-acetyl-l-cysteine, EUK-134) attenuated 5F 203-mediated JNK and p38 activation, depending on the cell type.	Acetylcysteine	66-85	mitogen-activated protein kinase 14	Homo sapiens	131-134
25935150-6	2015	Furthermore, Abeta stimulated the production of reactive oxygen species in endothelial cells and concomitant treatments of the cells with the antioxidant N-acetyl-cysteine (NAC) prevented Abeta effects in promoting HSP90/eNOS interaction and rescued agonist-mediated Akt and eNOS phosphorylation.	Acetylcysteine	154-171	amyloid beta precursor protein	Homo sapiens	188-193
25935150-6	2015	Furthermore, Abeta stimulated the production of reactive oxygen species in endothelial cells and concomitant treatments of the cells with the antioxidant N-acetyl-cysteine (NAC) prevented Abeta effects in promoting HSP90/eNOS interaction and rescued agonist-mediated Akt and eNOS phosphorylation.	Acetylcysteine	154-171	AKT serine/threonine kinase 1	Homo sapiens	267-270
25935150-6	2015	Furthermore, Abeta stimulated the production of reactive oxygen species in endothelial cells and concomitant treatments of the cells with the antioxidant N-acetyl-cysteine (NAC) prevented Abeta effects in promoting HSP90/eNOS interaction and rescued agonist-mediated Akt and eNOS phosphorylation.	Acetylcysteine	173-176	amyloid beta precursor protein	Homo sapiens	13-18
25935150-6	2015	Furthermore, Abeta stimulated the production of reactive oxygen species in endothelial cells and concomitant treatments of the cells with the antioxidant N-acetyl-cysteine (NAC) prevented Abeta effects in promoting HSP90/eNOS interaction and rescued agonist-mediated Akt and eNOS phosphorylation.	Acetylcysteine	173-176	amyloid beta precursor protein	Homo sapiens	188-193
25935150-6	2015	Furthermore, Abeta stimulated the production of reactive oxygen species in endothelial cells and concomitant treatments of the cells with the antioxidant N-acetyl-cysteine (NAC) prevented Abeta effects in promoting HSP90/eNOS interaction and rescued agonist-mediated Akt and eNOS phosphorylation.	Acetylcysteine	173-176	AKT serine/threonine kinase 1	Homo sapiens	267-270
25619687-10	2015	ANT inhibition or anti-oxidant strategy (N-acetylcysteine) prevented SR Ca(2+) leak, FKBP12.6 depletion and RyR2 oxidation/S-nitrosylation induced by PC.	Acetylcysteine	41-57	FK506 binding protein 1b	Mus musculus	85-93
25862169-5	2015	Culture of MDA-MB-231 and HeLa cells on the antioxidant N-acetyl cysteine (NAC) blunted NF-kappaB transcriptional activity, and long-term culture on low doses of NAC resulted in coordinate reductions in steady-state ROS levels, acquisition of an epithelial morphology, as well as upregulation of epithelial and downregulation of mesenchymal marker gene expression.	Acetylcysteine	56-73	nuclear factor kappa B subunit 1	Homo sapiens	88-97
25862169-5	2015	Culture of MDA-MB-231 and HeLa cells on the antioxidant N-acetyl cysteine (NAC) blunted NF-kappaB transcriptional activity, and long-term culture on low doses of NAC resulted in coordinate reductions in steady-state ROS levels, acquisition of an epithelial morphology, as well as upregulation of epithelial and downregulation of mesenchymal marker gene expression.	Acetylcysteine	75-78	nuclear factor kappa B subunit 1	Homo sapiens	88-97
25862169-5	2015	Culture of MDA-MB-231 and HeLa cells on the antioxidant N-acetyl cysteine (NAC) blunted NF-kappaB transcriptional activity, and long-term culture on low doses of NAC resulted in coordinate reductions in steady-state ROS levels, acquisition of an epithelial morphology, as well as upregulation of epithelial and downregulation of mesenchymal marker gene expression.	Acetylcysteine	162-165	nuclear factor kappa B subunit 1	Homo sapiens	88-97
25607112-12	2015	In addition, the inhibition of ROS by N-acetyl-L-cysteine had similar effects as AZM on the expression of VEGF and epithelial cell structural proteins and also enhanced cell proliferation.	Acetylcysteine	38-57	vascular endothelial growth factor A	Homo sapiens	106-110
25701684-11	2015	NAC suppressed hyperosmolarity-induced rises in ROS levels, NLRP3 inflammasome formation and activation, caspase-1 activity and IL-1beta release.	Acetylcysteine	0-3	NLR family pyrin domain containing 3	Homo sapiens	60-65
25701684-11	2015	NAC suppressed hyperosmolarity-induced rises in ROS levels, NLRP3 inflammasome formation and activation, caspase-1 activity and IL-1beta release.	Acetylcysteine	0-3	caspase 1	Homo sapiens	105-114
25701684-11	2015	NAC suppressed hyperosmolarity-induced rises in ROS levels, NLRP3 inflammasome formation and activation, caspase-1 activity and IL-1beta release.	Acetylcysteine	0-3	interleukin 1 beta	Homo sapiens	128-136
25373316-8	2015	ROS inhibition by N-acetyl-L-cysteine prevented the inhibition of PTP1B phosphatase activity induced by PAR1-AP and the PAR4-AP, but had no effect on PAR1/4-mediated activation of Met and PDGFR in Hep3B cells.	Acetylcysteine	18-37	coagulation factor II thrombin receptor	Homo sapiens	104-108
25738249-5	2015	Pemetrexed-induced apoptosis, which was prevented by pretreatment with N-acetyl-cysteine (NAC), was mediated by effects on the mitochondria, including mitochondrial membrane potential transition (MPT) and cytosolic release of cytochrome c, and also involved regulation of SIRT1 expression.	Acetylcysteine	71-88	cytochrome c, somatic	Homo sapiens	226-238
25580997-9	2015	Furthermore, a ROS scavenger, N-acetylcysteine (NAC), clearly suppressed the decrease in mitochondrial membrane potential, increase of caspase-3/7 activity, and apoptosis after PL treatment.	Acetylcysteine	30-46	caspase 3	Homo sapiens	135-144
25580997-9	2015	Furthermore, a ROS scavenger, N-acetylcysteine (NAC), clearly suppressed the decrease in mitochondrial membrane potential, increase of caspase-3/7 activity, and apoptosis after PL treatment.	Acetylcysteine	48-51	caspase 3	Homo sapiens	135-144
25738249-5	2015	Pemetrexed-induced apoptosis, which was prevented by pretreatment with N-acetyl-cysteine (NAC), was mediated by effects on the mitochondria, including mitochondrial membrane potential transition (MPT) and cytosolic release of cytochrome c, and also involved regulation of SIRT1 expression.	Acetylcysteine	90-93	cytochrome c, somatic	Homo sapiens	226-238
25361473-6	2015	Treatment with NAC, DFX, or NAC plus DFX significantly decreased H2O2 production (24, 58, and 72%, respectively), and levels of 4-HNE-protein adducts (62, 33, and 71%, respectively), TNF-alpha (32, 29, and 31%, respectively), and NF-kappaB (34, 38, and 52%, respectively) on dystrophic muscle cells.	Acetylcysteine	15-18	tumor necrosis factor	Mus musculus	183-192
25361473-6	2015	Treatment with NAC, DFX, or NAC plus DFX significantly decreased H2O2 production (24, 58, and 72%, respectively), and levels of 4-HNE-protein adducts (62, 33, and 71%, respectively), TNF-alpha (32, 29, and 31%, respectively), and NF-kappaB (34, 38, and 52%, respectively) on dystrophic muscle cells.	Acetylcysteine	28-31	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	230-239
25361473-6	2015	Treatment with NAC, DFX, or NAC plus DFX significantly decreased H2O2 production (24, 58, and 72%, respectively), and levels of 4-HNE-protein adducts (62, 33, and 71%, respectively), TNF-alpha (32, 29, and 31%, respectively), and NF-kappaB (34, 38, and 52%, respectively) on dystrophic muscle cells.	Acetylcysteine	15-18	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	230-239
25361473-7	2015	DISCUSSION: This study demonstrates that mdx muscle cells are able to produce key oxidative stress and inflammatory markers, without the interference of inflammatory cells, and shows that NAC plus DFX reduced the inflammatory and oxidative stress indicators, mainly H2O2 production and NF-kappaB levels by dystrophic fibers.	Acetylcysteine	188-191	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	286-295
25361473-6	2015	Treatment with NAC, DFX, or NAC plus DFX significantly decreased H2O2 production (24, 58, and 72%, respectively), and levels of 4-HNE-protein adducts (62, 33, and 71%, respectively), TNF-alpha (32, 29, and 31%, respectively), and NF-kappaB (34, 38, and 52%, respectively) on dystrophic muscle cells.	Acetylcysteine	28-31	tumor necrosis factor	Mus musculus	183-192
25832424-8	2015	Pretreatment of the cells with the ROS scavenger N-acetyl-L-cysteine, ERK inhibitor PD98059 or NF-kappaB inhibitor PDTC blocked CRP-stimulated RAGE expression, but pretreatment with the NADPH oxidase inhibitor DPI, JNK inhibitor SP600125 or p38 MAPK inhibitor SB203580 did not significantly alter CRP-stimulated RAGE expression.	Acetylcysteine	49-68	C-reactive protein	Homo sapiens	128-131
25724285-7	2015	Pre-treatment of EUK-134 or NAC alone altered the level of total free radical generation, LPO, GSH content and catalytic activity of MPO, SOD, GR and GPx and the expression of metallothionein I and II towards normalcy.	Acetylcysteine	28-31	metallothionein 1	Rattus norvegicus	176-193
25681565-7	2015	GA-induced alpha-SMA, FN, TGF-beta and caspase 3 expressions were completely suppressed by the NADPH oxidase inhibitor apocynin (Apo), the reactive oxygen species (ROS) scavenger N-acetylcysteine (NAC) and the latent antioxidant Astragaloside IV (AS-IV).	Acetylcysteine	179-195	caspase 3	Homo sapiens	39-48
25915766-7	2015	Similar to cell proliferation, GSH, NAC and L-cysteine but not D-cysteine, completely restored the processing of caspase-8 and caspase-3 to their respective subunits in z-FA-FMK-treated activated T cells.	Acetylcysteine	36-39	caspase 3	Homo sapiens	127-136
25909282-7	2015	NAC/AAP prevents apoptotic cell death via decreasing the activation of BAX, increasing the expression of BCL2, and reducing cytochrome c release from mitochondria that might lead to the activation of caspase cascade.	Acetylcysteine	0-3	BCL2 associated X, apoptosis regulator	Homo sapiens	71-74
25909282-7	2015	NAC/AAP prevents apoptotic cell death via decreasing the activation of BAX, increasing the expression of BCL2, and reducing cytochrome c release from mitochondria that might lead to the activation of caspase cascade.	Acetylcysteine	0-3	BCL2 apoptosis regulator	Homo sapiens	105-109
25909282-7	2015	NAC/AAP prevents apoptotic cell death via decreasing the activation of BAX, increasing the expression of BCL2, and reducing cytochrome c release from mitochondria that might lead to the activation of caspase cascade.	Acetylcysteine	0-3	cytochrome c, somatic	Homo sapiens	124-136
26075051-7	2015	Providing ad libitum access to N-acetylcysteine in the drinking water for 2 months normalized GSH/GSSG ratio, reduced mitochondrial damage (down to 8.9%), and improved grip strength (from 46 +- 3 to 59 +- 2 mN/gr) in CASQ1-null mice.	Acetylcysteine	31-47	calsequestrin 1	Mus musculus	217-222
24962643-8	2015	Additionally, the NF-kappaB inhibitor N-acetylcysteine (NAC) exerted similar inhibitory effects as ALA on COX-2 and iNOS expression.	Acetylcysteine	38-54	nitric oxide synthase 2	Rattus norvegicus	116-120
24962643-8	2015	Additionally, the NF-kappaB inhibitor N-acetylcysteine (NAC) exerted similar inhibitory effects as ALA on COX-2 and iNOS expression.	Acetylcysteine	56-59	nitric oxide synthase 2	Rattus norvegicus	116-120
25872712-7	2015	Treatment with NAC caused remarkable recovery from these NaF-induced responses.	Acetylcysteine	15-18	C-X-C motif chemokine ligand 8	Homo sapiens	57-60
25872712-9	2015	NAC effectively blocked the activation of ER stress, suggesting that NaF-induced ROS is an early event that triggers ER stress.	Acetylcysteine	0-3	C-X-C motif chemokine ligand 8	Homo sapiens	69-72
25680460-8	2015	Abeta oligomer-induced IL-1beta production was inhibited not only by the cathepsin B inhibitor CA-074-Me but also by the reactive oxygen species (ROS) inhibitor N-acetylcysteine.	Acetylcysteine	161-177	interleukin 1 beta	Mus musculus	23-31
25406100-11	2015	The in vitro experiments showed that Nano-TiO2 significantly and dose-dependently increased the ROS production and the expressions of HIF-1alpha and TGFbeta in human renal proximal tubular cells, which could be reversed by N-acetylcysteine treatment.	Acetylcysteine	223-239	hypoxia inducible factor 1 subunit alpha	Homo sapiens	134-144
25406100-11	2015	The in vitro experiments showed that Nano-TiO2 significantly and dose-dependently increased the ROS production and the expressions of HIF-1alpha and TGFbeta in human renal proximal tubular cells, which could be reversed by N-acetylcysteine treatment.	Acetylcysteine	223-239	transforming growth factor beta 1	Homo sapiens	149-156
25620135-12	2015	N-acetyl-l-cysteine (NAC) (5mM), an antioxidant, significantly inhibited the endostatin-induced Akt phosphorylation.	Acetylcysteine	0-19	AKT serine/threonine kinase 1	Rattus norvegicus	96-99
25620135-12	2015	N-acetyl-l-cysteine (NAC) (5mM), an antioxidant, significantly inhibited the endostatin-induced Akt phosphorylation.	Acetylcysteine	21-24	AKT serine/threonine kinase 1	Rattus norvegicus	96-99
25527773-6	2015	ANG II induced cerebral endothelial dysfunction only in WT mice (P &lt; 0.05), which was reversed (P &lt; 0.05) by either N-acetyl-l-cysteine, apocynin, gp91ds-tat, or indomethacin, suggesting the contribution of reactive oxygen species from Nox2 and Cox-derived contractile factors.	Acetylcysteine	122-141	angiotensinogen (serpin peptidase inhibitor, clade A, member 8)	Mus musculus	0-6
24612076-0	2015	Glutamate transporter GLT-1 mediates N-acetylcysteine inhibition of cocaine reinstatement.	Acetylcysteine	37-53	solute carrier family 1 member 2	Rattus norvegicus	22-27
24612076-9	2015	In contrast, suppressing NAC-induced restoration of GLT-1 not only prevented NAC from inhibiting reinstatement, but augmented the capacity of cues to reinstate cocaine seeking.	Acetylcysteine	25-28	solute carrier family 1 member 2	Rattus norvegicus	52-57
24612076-9	2015	In contrast, suppressing NAC-induced restoration of GLT-1 not only prevented NAC from inhibiting reinstatement, but augmented the capacity of cues to reinstate cocaine seeking.	Acetylcysteine	77-80	solute carrier family 1 member 2	Rattus norvegicus	52-57
24612076-10	2015	We hypothesized that the increased reinstatement after inhibiting NAC induction of GLT-1 resulted from increased extracellular glutamate, and show that augmented reinstatement is prevented by blocking mGluR5.	Acetylcysteine	66-69	solute carrier family 1 member 2	Rattus norvegicus	83-88
24612076-11	2015	Restoring GLT-1, not cystine-glutamate exchange, is a key mechanism whereby daily NAC reduces cue-induced cocaine reinstatement.	Acetylcysteine	82-85	solute carrier family 1 member 2	Rattus norvegicus	10-15
25619390-12	2015	Incubation in a high-glucose medium induced oxidative stress and activation of TLR-4/MyD-88 signaling in cultured myocytes in vitro, which were significantly attenuated by pretreatment with N-acetylcysteine.	Acetylcysteine	190-206	toll-like receptor 4	Rattus norvegicus	79-84
25178491-8	2015	Moreover, PYDDT-induced apoptosis as well as activation of JNK was abrogated by the pretreatment with antioxidant N-acetylcysteine.	Acetylcysteine	114-130	mitogen-activated protein kinase 8	Homo sapiens	59-62
25481834-6	2015	The cells treated with low dose of TNF-alpha for prolonged period induce cell death which was rescued in the presence of zVAD.fmk, a caspase inhibitor and N-acetyl-cysteine (NAC), an antioxidant.	Acetylcysteine	155-172	tumor necrosis factor	Homo sapiens	35-44
25481834-6	2015	The cells treated with low dose of TNF-alpha for prolonged period induce cell death which was rescued in the presence of zVAD.fmk, a caspase inhibitor and N-acetyl-cysteine (NAC), an antioxidant.	Acetylcysteine	174-177	tumor necrosis factor	Homo sapiens	35-44
25666878-8	2015	Neutrophil lipid peroxidation, apoptosis, caspase-3, caspase-9, cytosolic reactive oxygen species production, and mitochondrial membrane depolarization values were decreased by NAC treatment although neutrophil glutathione peroxidase and reduced glutathione levels were increased by the NAC treatment.	Acetylcysteine	177-180	caspase 3	Homo sapiens	42-51
25666878-9	2015	Serum lipid peroxidation, luteinizing hormone, testosterone, insulin, interleukin-1 beta, and homocysteine levels were decreased by NAC treatment although serum vitamin A, beta-carotene, vitamin E, and total antioxidant status were increased by the NAC treatment.	Acetylcysteine	132-135	insulin	Homo sapiens	61-68
25666878-9	2015	Serum lipid peroxidation, luteinizing hormone, testosterone, insulin, interleukin-1 beta, and homocysteine levels were decreased by NAC treatment although serum vitamin A, beta-carotene, vitamin E, and total antioxidant status were increased by the NAC treatment.	Acetylcysteine	132-135	interleukin 1 beta	Homo sapiens	70-88
25581570-12	2015	Furthermore, AGE- or MGO-induced increased expression of VEGF and MCP-1 was significantly reduced in the presence of NAC or SB203580.	Acetylcysteine	117-120	vascular endothelial growth factor A	Homo sapiens	57-61
24756473-5	2015	Further, pretreatment of 50 mM glucose-treated VL-17A cells with NAC or UDCA decreased oxidative stress (levels of reactive oxygen species and protein carbonylation), apoptosis (caspase 3 activity and annexin V-propidium iodide positive cells) and glutathionylated protein formation, a measure of oxidative stress.	Acetylcysteine	65-68	caspase 3	Homo sapiens	178-187
25607831-8	2015	Pretreatment with N-acetyl-cysteine (NAC), the inhibitor of ROS, or with SP600125, the inhibitor of JNK, prevented the apoptosis and the high expression of p-JNK, p53, caspase-9 and caspase-3 in CDK5RAP1-deficient MCF-7 cells.	Acetylcysteine	18-35	mitogen-activated protein kinase 8	Homo sapiens	158-161
25607831-8	2015	Pretreatment with N-acetyl-cysteine (NAC), the inhibitor of ROS, or with SP600125, the inhibitor of JNK, prevented the apoptosis and the high expression of p-JNK, p53, caspase-9 and caspase-3 in CDK5RAP1-deficient MCF-7 cells.	Acetylcysteine	18-35	tumor protein p53	Homo sapiens	163-166
25607831-8	2015	Pretreatment with N-acetyl-cysteine (NAC), the inhibitor of ROS, or with SP600125, the inhibitor of JNK, prevented the apoptosis and the high expression of p-JNK, p53, caspase-9 and caspase-3 in CDK5RAP1-deficient MCF-7 cells.	Acetylcysteine	18-35	caspase 3	Homo sapiens	182-191
25607831-8	2015	Pretreatment with N-acetyl-cysteine (NAC), the inhibitor of ROS, or with SP600125, the inhibitor of JNK, prevented the apoptosis and the high expression of p-JNK, p53, caspase-9 and caspase-3 in CDK5RAP1-deficient MCF-7 cells.	Acetylcysteine	37-40	mitogen-activated protein kinase 8	Homo sapiens	158-161
25607831-8	2015	Pretreatment with N-acetyl-cysteine (NAC), the inhibitor of ROS, or with SP600125, the inhibitor of JNK, prevented the apoptosis and the high expression of p-JNK, p53, caspase-9 and caspase-3 in CDK5RAP1-deficient MCF-7 cells.	Acetylcysteine	37-40	tumor protein p53	Homo sapiens	163-166
25607831-8	2015	Pretreatment with N-acetyl-cysteine (NAC), the inhibitor of ROS, or with SP600125, the inhibitor of JNK, prevented the apoptosis and the high expression of p-JNK, p53, caspase-9 and caspase-3 in CDK5RAP1-deficient MCF-7 cells.	Acetylcysteine	37-40	caspase 3	Homo sapiens	182-191
25226206-8	2015	Treatment of mESCs with AA and NAC led to a dose-dependent decrease in Sox17 and Foxa2 expression.	Acetylcysteine	31-34	forkhead box A2	Mus musculus	81-86
25581570-11	2015	Western blot showed that MGO and AGE increased the phosphorylation levels of p38 MAPK, which was significantly attenuated after treatment of NAC or p38 MAPK inhibitor SB203580.	Acetylcysteine	141-144	mitogen-activated protein kinase 14	Homo sapiens	77-80
23836369-9	2015	N-acetylcysteine, an ROS scavenger, inhibited 2-ABP-induced activation of ERK and JNK, the cell death and caspase-3 activity, which suggested that oxidative stress plays a crucial role in apoptosis through activation of caspase-3 in a ROS/JNK-dependent signaling cascade.	Acetylcysteine	0-16	mitogen-activated protein kinase 1	Homo sapiens	74-77
24849033-6	2015	Accordantly, pre-incubation with the GSH precursor N-acetylcysteine attenuated TGFbeta1-stimulated EMT gene changes.	Acetylcysteine	51-67	transforming growth factor, beta 1	Rattus norvegicus	79-87
25444914-5	2015	Pretreatment of cells with the ROS scavenger N-acetylcysteine completely blocked the apoptosis induced by combination treatment, and recovered expression of AKT inactivation, which revealed the important role of ROS in apoptosis and AKT regulation.	Acetylcysteine	45-61	AKT serine/threonine kinase 1	Homo sapiens	157-160
25444914-5	2015	Pretreatment of cells with the ROS scavenger N-acetylcysteine completely blocked the apoptosis induced by combination treatment, and recovered expression of AKT inactivation, which revealed the important role of ROS in apoptosis and AKT regulation.	Acetylcysteine	45-61	AKT serine/threonine kinase 1	Homo sapiens	233-236
23836369-9	2015	N-acetylcysteine, an ROS scavenger, inhibited 2-ABP-induced activation of ERK and JNK, the cell death and caspase-3 activity, which suggested that oxidative stress plays a crucial role in apoptosis through activation of caspase-3 in a ROS/JNK-dependent signaling cascade.	Acetylcysteine	0-16	mitogen-activated protein kinase 8	Homo sapiens	82-85
23836369-9	2015	N-acetylcysteine, an ROS scavenger, inhibited 2-ABP-induced activation of ERK and JNK, the cell death and caspase-3 activity, which suggested that oxidative stress plays a crucial role in apoptosis through activation of caspase-3 in a ROS/JNK-dependent signaling cascade.	Acetylcysteine	0-16	caspase 3	Homo sapiens	106-115
23836369-9	2015	N-acetylcysteine, an ROS scavenger, inhibited 2-ABP-induced activation of ERK and JNK, the cell death and caspase-3 activity, which suggested that oxidative stress plays a crucial role in apoptosis through activation of caspase-3 in a ROS/JNK-dependent signaling cascade.	Acetylcysteine	0-16	caspase 3	Homo sapiens	220-229
23836369-9	2015	N-acetylcysteine, an ROS scavenger, inhibited 2-ABP-induced activation of ERK and JNK, the cell death and caspase-3 activity, which suggested that oxidative stress plays a crucial role in apoptosis through activation of caspase-3 in a ROS/JNK-dependent signaling cascade.	Acetylcysteine	0-16	mitogen-activated protein kinase 8	Homo sapiens	239-242
26394653-10	2015	NAC also reversed TDT-induced depolarization of Deltapsi, MDC staining, up-regulation of Bax, cleaved-PARP, Beclin-1, LC3-II, and cell viability.	Acetylcysteine	0-3	BCL2 associated X, apoptosis regulator	Homo sapiens	89-92
25611380-9	2015	Furthermore, the antioxidant N-acetylcysteine rescued Bmi1(-/-) hair cells from neomycin injury both in vitro and in vivo, suggesting that ROS accumulation was mainly responsible for the increased aminoglycosides sensitivity in Bmi1(-/-) hair cells.	Acetylcysteine	29-45	Bmi1 polycomb ring finger oncogene	Mus musculus	54-58
25611380-9	2015	Furthermore, the antioxidant N-acetylcysteine rescued Bmi1(-/-) hair cells from neomycin injury both in vitro and in vivo, suggesting that ROS accumulation was mainly responsible for the increased aminoglycosides sensitivity in Bmi1(-/-) hair cells.	Acetylcysteine	29-45	Bmi1 polycomb ring finger oncogene	Mus musculus	228-232
25514170-5	2015	Pretreatment of these cells with the deoxidant N-acetylcysteine blocked the inhibitory effect of adiponectin.	Acetylcysteine	47-63	adiponectin, C1Q and collagen domain containing	Homo sapiens	97-108
26119951-4	2015	Treatment with glutamate alone led to suppressed protein level of mature brain-derived neurotrophic factor (BDNF) and phosphorylated cAMP response element binding protein (CREB); however, pretreatment with either WEPM or anti-oxidant N-acetyl-L-cysteine (NAC) resulted in the significant enhancement of levels of these proteins.	Acetylcysteine	234-253	cAMP responsive element binding protein 1	Mus musculus	172-176
26119951-4	2015	Treatment with glutamate alone led to suppressed protein level of mature brain-derived neurotrophic factor (BDNF) and phosphorylated cAMP response element binding protein (CREB); however, pretreatment with either WEPM or anti-oxidant N-acetyl-L-cysteine (NAC) resulted in the significant enhancement of levels of these proteins.	Acetylcysteine	255-258	cAMP responsive element binding protein 1	Mus musculus	172-176
26119951-5	2015	In addition, levels of mature BDNF expression and CREB phosphorylation were increased by combined treatment with WEPM, NAC, and intracellular Ca (2+) inhibitor BAPTA compared to other treatment groups.	Acetylcysteine	119-122	cAMP responsive element binding protein 1	Mus musculus	50-54
25096201-9	2015	NAC significantly protected against MDMA-induced apoptosis and the up- and down-regulation of Bax and Bcl-2, respectively.	Acetylcysteine	0-3	BCL2, apoptosis regulator	Rattus norvegicus	102-107
25653524-14	2015	Western blot analyses revealed translocation of BAX and cytochrome C, downregulated expression of Bcl-2, and upregulated expression of cleaved caspase-9, cleaved caspase-3, and cleaved poly(ADP-ribose) polymerase in the SDT group, which were reversed by NAC.	Acetylcysteine	254-257	BCL2 associated X, apoptosis regulator	Homo sapiens	48-51
25047070-13	2015	Effects of QD232 on Src/FAK and STAT3 phosphorylation were blocked by N-acetylcysteine or glutathione.	Acetylcysteine	70-86	signal transducer and activator of transcription 3	Mus musculus	32-37
25591776-9	2015	RESULTS: PM treatment significantly decreased circulating EPC population, promoted apoptosis of EPCs in association with increased ROS production and serum TNF-alpha and IL-1beta levels, which could be effectively reversed by either NAC treatment or overexpression of AON.	Acetylcysteine	233-236	tumor necrosis factor	Mus musculus	156-165
25591776-9	2015	RESULTS: PM treatment significantly decreased circulating EPC population, promoted apoptosis of EPCs in association with increased ROS production and serum TNF-alpha and IL-1beta levels, which could be effectively reversed by either NAC treatment or overexpression of AON.	Acetylcysteine	233-236	interleukin 1 beta	Mus musculus	170-178
25998312-9	2015	N-acetylcysteine (NAC) significantly reduced ROS levels and reversed the effects of CdCl2 on MAPK signaling.	Acetylcysteine	0-16	mitogen-activated protein kinase 3	Homo sapiens	93-97
25998312-9	2015	N-acetylcysteine (NAC) significantly reduced ROS levels and reversed the effects of CdCl2 on MAPK signaling.	Acetylcysteine	18-21	mitogen-activated protein kinase 3	Homo sapiens	93-97
26477273-8	2015	Both NAC and apocynin abolished the enhancing effects of urate on Kv1.5 expression.	Acetylcysteine	5-8	potassium voltage-gated channel, shaker-related subfamily, member 5	Mus musculus	66-71
25283714-10	2015	Pretreatment with N-acetyl-L-cysteine (aROS scavenger) reversed the increased active caspase-3 expression induced by 6d-UVA, indicating the involvement of ROS in 6d-UVA-induced apoptosis.	Acetylcysteine	18-37	caspase 3	Homo sapiens	85-94
26477273-10	2015	NAC abolished phosphorylation of ERK by urate.	Acetylcysteine	0-3	mitogen-activated protein kinase 1	Mus musculus	33-36
26022265-5	2015	Cocaine, opioids, ethanol, nicotine, amphetamines, and cannabinoids each affect GLT-1 expression and glutamate uptake, and restoring GLT-1 expression with N-acetylcysteine or ceftriaxone shows promise in correcting pre-clinical and clinical manifestations of drug addiction.	Acetylcysteine	155-171	solute carrier family 1 member 2	Homo sapiens	133-138
25327779-7	2015	Treatment with the antioxidant N-acetylcysteine significantly attenuated protein conversion of interleukin 1beta after hepatic I/R.	Acetylcysteine	31-47	interleukin 1 beta	Homo sapiens	95-112
25445966-8	2015	Both NAC and GSH, thus attenuated the expression of iNOS and COX-2 by suppressing NF-kappaB activation, indicating that 5-DRL suppresses LPS-induced iNOS and COX-2 expression through downregulation of the ROS-dependent NF-kappaB signaling pathway.	Acetylcysteine	5-8	nitric oxide synthase 2, inducible	Mus musculus	52-56
25463279-11	2015	Moreover, TNF-alpha-enhanced IKK-beta activity was also inhibited by (polyethylene glycol) PEG-catalase, N-acetylcysteine (NAC), and vitamin E. In conclusion, these results suggest that AR reduces VCAM-1 and ICAM-1 expression through NADPH oxidase-dependent IKK/NF-kappaB pathways in TNF-alpha-induced HUVECs, which finally suppress monocyte-HUVECs adhesion.	Acetylcysteine	105-121	tumor necrosis factor	Homo sapiens	10-19
25463279-11	2015	Moreover, TNF-alpha-enhanced IKK-beta activity was also inhibited by (polyethylene glycol) PEG-catalase, N-acetylcysteine (NAC), and vitamin E. In conclusion, these results suggest that AR reduces VCAM-1 and ICAM-1 expression through NADPH oxidase-dependent IKK/NF-kappaB pathways in TNF-alpha-induced HUVECs, which finally suppress monocyte-HUVECs adhesion.	Acetylcysteine	123-126	tumor necrosis factor	Homo sapiens	10-19
26572172-9	2015	Administration of NAC attenuated those CS-induced adverse effects in the mice and increased anti-inflammatory factor IL-10 levels in BAL fluids significantly (all p &lt; 0.05).	Acetylcysteine	18-21	interleukin 10	Mus musculus	117-122
25553484-8	2015	The effects of NAC are associated with some intestinal cell signaling pathways, such as EGFR, TLR4, apoptosis and tight junction signaling.	Acetylcysteine	15-18	epidermal growth factor receptor	Homo sapiens	88-92
25445966-8	2015	Both NAC and GSH, thus attenuated the expression of iNOS and COX-2 by suppressing NF-kappaB activation, indicating that 5-DRL suppresses LPS-induced iNOS and COX-2 expression through downregulation of the ROS-dependent NF-kappaB signaling pathway.	Acetylcysteine	5-8	nitric oxide synthase 2, inducible	Mus musculus	149-153
25738016-11	2015	We found that patients who had received NAC had lower mortality, lower peak values of AST/ALT, and shorter hospital stay.	Acetylcysteine	40-43	solute carrier family 17 member 5	Homo sapiens	86-89
25821351-3	2015	The expression of IL-2, IL-6, TNF-alpha, and IFN-gamma was significantly reduced in the NAC-treated groups.	Acetylcysteine	88-91	interleukin 6	Mus musculus	24-28
25821351-3	2015	The expression of IL-2, IL-6, TNF-alpha, and IFN-gamma was significantly reduced in the NAC-treated groups.	Acetylcysteine	88-91	tumor necrosis factor	Mus musculus	30-39
25821351-3	2015	The expression of IL-2, IL-6, TNF-alpha, and IFN-gamma was significantly reduced in the NAC-treated groups.	Acetylcysteine	88-91	interferon gamma	Mus musculus	45-54
25821351-4	2015	NAC activated PI3K/Akt pathway and inhibited the activation of NF-kappaB.	Acetylcysteine	0-3	thymoma viral proto-oncogene 1	Mus musculus	19-22
25821351-6	2015	Our results demonstrate that NAC can alleviate ConA-induced hepatitis by regulating the PI3K/Akt pathway and reducing the late stages of autophagy.	Acetylcysteine	29-32	thymoma viral proto-oncogene 1	Mus musculus	93-96
25527729-5	2015	Furthermore, JNK and ERK activation could be inhibited by both DPI and a free radicals scavenger N-acetyl cysteine.	Acetylcysteine	97-114	mitogen-activated protein kinase 1	Homo sapiens	21-24
26366134-0	2015	Comprehensive metabolome analyses reveal N-acetylcysteine-responsive accumulation of kynurenine in systemic lupus erythematosus: implications for activation of the mechanistic target of rapamycin.	Acetylcysteine	41-57	mechanistic target of rapamycin kinase	Homo sapiens	164-195
26366134-12	2015	The PPP-connected and NAC-responsive accumulation of kynurenine and its stimulation of mTOR are identified as novel metabolic checkpoints in lupus pathogenesis.	Acetylcysteine	22-25	mechanistic target of rapamycin kinase	Homo sapiens	87-91
25338626-8	2015	The ROS scavenger N-acetyl-L-cysteine inhibits bortezomib-induced ROS production and abrogates the phosphorylation of Src, epidermal growth factor receptor and Akt.	Acetylcysteine	18-37	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	118-121
25338626-8	2015	The ROS scavenger N-acetyl-L-cysteine inhibits bortezomib-induced ROS production and abrogates the phosphorylation of Src, epidermal growth factor receptor and Akt.	Acetylcysteine	18-37	epidermal growth factor receptor	Homo sapiens	123-155
25338626-8	2015	The ROS scavenger N-acetyl-L-cysteine inhibits bortezomib-induced ROS production and abrogates the phosphorylation of Src, epidermal growth factor receptor and Akt.	Acetylcysteine	18-37	AKT serine/threonine kinase 1	Homo sapiens	160-163
25527729-5	2015	Furthermore, JNK and ERK activation could be inhibited by both DPI and a free radicals scavenger N-acetyl cysteine.	Acetylcysteine	97-114	mitogen-activated protein kinase 8	Homo sapiens	13-16
25997958-7	2015	In addition, NAC completely blocked phosphorylation of JNK and p38 MAPK induced by capsaicin.	Acetylcysteine	13-16	mitogen-activated protein kinase 8	Homo sapiens	55-58
25997958-7	2015	In addition, NAC completely blocked phosphorylation of JNK and p38 MAPK induced by capsaicin.	Acetylcysteine	13-16	mitogen-activated protein kinase 14	Homo sapiens	63-66
25308201-9	2015	Both azithromycin and n-acetyl cysteine suppressed CD4 T-cell granzyme B production, but only azithromycin was effective at reducing CD8+ T-cell granzyme B production in vitro.	Acetylcysteine	22-39	CD4 molecule	Homo sapiens	51-54
26576075-7	2015	The use of ROS scavenger N-acetylcysteine (NAC) partially reversed NLRP3 inflammasome activity in cells exposed to burn serum.	Acetylcysteine	25-41	NLR family, pyrin domain containing 3	Rattus norvegicus	67-72
26576075-7	2015	The use of ROS scavenger N-acetylcysteine (NAC) partially reversed NLRP3 inflammasome activity in cells exposed to burn serum.	Acetylcysteine	43-46	NLR family, pyrin domain containing 3	Rattus norvegicus	67-72
25473894-5	2015	Significantly, JNK inhibition promoted 5-FU- and GEM-induced increase in intracellular reactive oxygen species (ROS), and scavenging intracellular ROS by use of N-acetylcysteine impaired JNK inhibition-mediated promotion of the cytotoxicity of 5-FU and GEM.	Acetylcysteine	161-177	mitogen-activated protein kinase 8	Homo sapiens	187-190
25516653-5	2014	RESULTS: T3 upregulates AMPK signaling, including the upstream kinases Ca(2+)-calmodulin-dependent protein kinase kinase-beta and transforming growth factor-beta-activated kinase-1, with T3-induced reactive oxygen species having a causal role due to its suppression by pretreatment with the antioxidant NAC.	Acetylcysteine	303-306	protein kinase AMP-activated catalytic subunit alpha 2	Rattus norvegicus	24-28
25148872-4	2014	Our results show that the pretreatment with well known antioxidants such as trolox and N-acetyl cysteine (NAC) partially reduced the apoptotic effects due to the administration of TNFalpha plus cycloheximide.	Acetylcysteine	87-104	tumor necrosis factor	Homo sapiens	180-188
25023940-8	2014	Pretreatment with the ROS scavenger N-acetyl-cysteine abolishes the PL-induced up-regulation of CHOP and its target genes, suggesting an essential role for ROS in PL-induced CHOP activation.	Acetylcysteine	36-53	DNA damage inducible transcript 3	Homo sapiens	96-100
25023940-8	2014	Pretreatment with the ROS scavenger N-acetyl-cysteine abolishes the PL-induced up-regulation of CHOP and its target genes, suggesting an essential role for ROS in PL-induced CHOP activation.	Acetylcysteine	36-53	DNA damage inducible transcript 3	Homo sapiens	174-178
23765509-5	2014	Moreover, cell death was found to be associated with cytochrome c release and cleavage of caspases and of poly(ADP-ribose) polymerase, and completely abrogated by the free-radical scavenger N-acetyl-L-cysteine.	Acetylcysteine	190-209	cytochrome c, somatic	Homo sapiens	53-65
23765509-5	2014	Moreover, cell death was found to be associated with cytochrome c release and cleavage of caspases and of poly(ADP-ribose) polymerase, and completely abrogated by the free-radical scavenger N-acetyl-L-cysteine.	Acetylcysteine	190-209	poly(ADP-ribose) polymerase 1	Homo sapiens	106-133
29805908-14	2014	Pretreatment with NAC attenuated Abeta42 induced P-selectin localization, while NAC alone did not significantly affect P selectin localization.	Acetylcysteine	18-21	selectin, platelet	Mus musculus	49-59
25581647-8	2014	Chronic EtOH increased the expression of mitochondrial biogenesis genes including peroxisome proliferator-activated receptor gamma-coactivator-1 alpha and mitochondrial transcription factor A, and mitochondrial DNA; co-administration of EtOH and NAC prevented these effects.	Acetylcysteine	246-249	PPARG coactivator 1 alpha	Rattus norvegicus	82-150
25308836-8	2014	Scavenging of ROS by antioxidant N-acetyl-cysteine (NAC) inhibited caspase-3 activity and rescued the cells from apoptosis.	Acetylcysteine	33-50	caspase 3	Homo sapiens	67-76
25308836-8	2014	Scavenging of ROS by antioxidant N-acetyl-cysteine (NAC) inhibited caspase-3 activity and rescued the cells from apoptosis.	Acetylcysteine	52-55	caspase 3	Homo sapiens	67-76
25148872-4	2014	Our results show that the pretreatment with well known antioxidants such as trolox and N-acetyl cysteine (NAC) partially reduced the apoptotic effects due to the administration of TNFalpha plus cycloheximide.	Acetylcysteine	106-109	tumor necrosis factor	Homo sapiens	180-188
25350954-6	2014	The activation of NFkappaB in KB/TP cells was suppressed by the antioxidants N-acetylcysteine and EUK-8.	Acetylcysteine	77-93	nuclear factor kappa B subunit 1	Homo sapiens	18-26
25193743-9	2014	Interestingly, inhibition of ROS with N-acetylcysteine abrogated Akt/Gsk-3beta activation and the LA-induced cytoprotection following SNP stimulation.	Acetylcysteine	38-54	AKT serine/threonine kinase 1	Rattus norvegicus	65-68
25134437-5	2014	N-acetylcysteine (a general antioxidant) attenuated the CSE-induced ASK-1 and p38 MAPK activation and cell apoptosis, suggesting a triggering role of ROS in ASK-1/p38 MAPK activation during apoptotic progression.	Acetylcysteine	0-16	mitogen-activated protein kinase 14	Homo sapiens	78-81
25134437-5	2014	N-acetylcysteine (a general antioxidant) attenuated the CSE-induced ASK-1 and p38 MAPK activation and cell apoptosis, suggesting a triggering role of ROS in ASK-1/p38 MAPK activation during apoptotic progression.	Acetylcysteine	0-16	mitogen-activated protein kinase 14	Homo sapiens	163-166
25910366-8	2014	RESULTS: The ALT and AST values were significantly lower in I/R+NAC group.	Acetylcysteine	64-67	glutamic-oxaloacetic transaminase 2	Rattus norvegicus	21-24
24910977-0	2014	Spectroscopic investigations on the effect of N-acetyl-L-cysteine-capped CdTe Quantum Dots on catalase.	Acetylcysteine	46-65	catalase	Homo sapiens	94-102
24910977-5	2014	In this work, the effect of N-Acetyl-L-cysteine-Capped CdTe Quantum Dots with fluorescence emission peak at 612 nm (QDs-612) on CAT was investigated by fluorescence, synchronous fluorescence, fluorescence lifetime, ultraviolet-visible (UV-vis) absorption and circular dichroism (CD) techniques.	Acetylcysteine	28-47	catalase	Homo sapiens	128-131
25461556-7	2014	The involvement of ROS in DR5 upregulation confirmed that pretreatment with antioxidants, including N-acetyl-L-cysteine and glutathione, significantly inhibits CPT-TRAIL-induced cell death by suppressing DR5 expression.	Acetylcysteine	100-119	TNF superfamily member 10	Homo sapiens	160-169
25489418-5	2014	Treatment with arsenite also induced reactive oxygen species (ROS) production, and pretreatment with a ROS scavenger N-acetyl-L-cysteine (NAC) completely reversed the observed effect of arsenite on eNOS-Thr(497) phosphorylation.	Acetylcysteine	117-136	nitric oxide synthase 3	Bos taurus	198-202
25489418-5	2014	Treatment with arsenite also induced reactive oxygen species (ROS) production, and pretreatment with a ROS scavenger N-acetyl-L-cysteine (NAC) completely reversed the observed effect of arsenite on eNOS-Thr(497) phosphorylation.	Acetylcysteine	138-141	nitric oxide synthase 3	Bos taurus	198-202
26273528-8	2014	This defect could be rescued through treatment with the radical scavenger N-acetyl cysteine (NAC), suggesting that increased reactive species stress might impair early osteoblastogenesis in BMSCs and lead to the failure of bone acquisition observed in Nrf2(-/-) animals.	Acetylcysteine	74-91	nuclear factor, erythroid derived 2, like 2	Mus musculus	252-256
26273528-8	2014	This defect could be rescued through treatment with the radical scavenger N-acetyl cysteine (NAC), suggesting that increased reactive species stress might impair early osteoblastogenesis in BMSCs and lead to the failure of bone acquisition observed in Nrf2(-/-) animals.	Acetylcysteine	93-96	nuclear factor, erythroid derived 2, like 2	Mus musculus	252-256
25386077-7	2014	In addition, NAC treatment significantly reduced caspase-3 activity and apoptosis after reperfusion, which correlated with the protein expression of Bcl-2 and Bcl-xl.	Acetylcysteine	13-16	B cell leukemia/lymphoma 2	Mus musculus	149-154
25369051-9	2014	Crucially, administration of N-acetylcysteine, a ROS scavenger, abrogated the effect of PA-2 on p53 acetylation and mitochondria translocation, thus identifying RONS as proximal molecules mediating the anticancer effect of PA-2.	Acetylcysteine	29-45	tumor protein p53	Homo sapiens	96-99
24819310-5	2014	N-acetyl cysteine application (intraperitoneal, 50 mg/kg/day) was started 3 days prior to CCl4 injection and continued during the experimental period.	Acetylcysteine	0-17	C-C motif chemokine ligand 4	Rattus norvegicus	90-94
24819310-12	2014	The results of the present study indicate that N-acetyl cysteine has a protective effect on CCl4-induced DNA damage.	Acetylcysteine	47-64	C-C motif chemokine ligand 4	Rattus norvegicus	92-96
25289048-4	2014	Pretreatment with N-acetylcysteine, an antioxidant chemical compound, inhibited the activation of ASK1, JNK and Bim, as well as the apoptosis induced by casticin.	Acetylcysteine	18-34	mitogen-activated protein kinase 8	Homo sapiens	104-107
25079371-2	2014	The amide form of N-acetylcysteine (NACA) overcomes these limitations while maintaining a high antioxidant potential, and shows promise for combating secondary pathogenesis attributed to oxidative stress.	Acetylcysteine	18-34	nascent polypeptide associated complex subunit alpha	Homo sapiens	36-40
24963595-6	2014	However, pre-treatment with n-acetyl cysteine, an ROS scavenger, and SB202190, a p38MAPK inhibitor, significantly inhibited VA-induced ROS generation, EGFR inhibition, p38MAPK activation and apoptosis.	Acetylcysteine	28-45	epidermal growth factor receptor	Homo sapiens	151-155
25096910-6	2014	We found that treatment with CAY10598 generated reactive oxygen species (ROS) and pretreatment of cells with N-acetyl cysteine rescued cells from apoptosis by abrogating the inhibitory effect of CAY10598 on the activation of JAK2/STAT3 signaling.	Acetylcysteine	109-126	signal transducer and activator of transcription 3	Homo sapiens	230-235
25016575-5	2014	However, when N-acetyl cysteine (NAC), an antioxidant, is added, STAT3 phosphorylation is decreased.	Acetylcysteine	14-31	signal transducer and activator of transcription 3	Homo sapiens	65-70
25016575-11	2014	The decrease in the phosphorylation of JAK2 and JAK3, earlier in the process, could explain the downregulation of STAT3 and offer a hypothesis on the mechanism of action of NAC antioxidant properties which were confirmed by a decrease in the level of S-glutathionylation of proteins.	Acetylcysteine	173-176	signal transducer and activator of transcription 3	Homo sapiens	114-119
25016575-13	2014	In summary, NAC appears as a potential regulator of the STAT3 pathway.	Acetylcysteine	12-15	signal transducer and activator of transcription 3	Homo sapiens	56-61
25016575-5	2014	However, when N-acetyl cysteine (NAC), an antioxidant, is added, STAT3 phosphorylation is decreased.	Acetylcysteine	33-36	signal transducer and activator of transcription 3	Homo sapiens	65-70
25016575-6	2014	In this study, we show that in activated human memory B cells, NAC inhibited STAT3 phosphorylation on tyrosine 705 but not on Serine 727.	Acetylcysteine	63-66	signal transducer and activator of transcription 3	Homo sapiens	77-82
25016575-7	2014	Moreover, higher concentrations of NAC decreased STAT3 synthesis.	Acetylcysteine	35-38	signal transducer and activator of transcription 3	Homo sapiens	49-54
25016575-9	2014	Furthermore, two kinases involved in STAT3 activation, known as JAK2 and JAK3, appeared down-regulated in presence of NAC.	Acetylcysteine	118-121	signal transducer and activator of transcription 3	Homo sapiens	37-42
25218171-6	2014	DSCR1 transfection-induced changes were increased by treatment with IL-1beta, which was suppressed by NAC and BAPTA.	Acetylcysteine	102-105	interleukin 1 beta	Homo sapiens	68-76
25128739-11	2014	Increased HO-1 by HIS was detected at both protein and mRNA levels along with an increase in intracellular peroxide, and this was inhibited by the translational inhibitor, cycloheximide (CHX), the transcriptional inhibitor, actinomycin D (Act D), and the reactive oxygen species scavenger, N-acetylcysteine (NAC).	Acetylcysteine	290-306	heme oxygenase 1	Mus musculus	10-14
25128739-11	2014	Increased HO-1 by HIS was detected at both protein and mRNA levels along with an increase in intracellular peroxide, and this was inhibited by the translational inhibitor, cycloheximide (CHX), the transcriptional inhibitor, actinomycin D (Act D), and the reactive oxygen species scavenger, N-acetylcysteine (NAC).	Acetylcysteine	308-311	heme oxygenase 1	Mus musculus	10-14
24952277-9	2014	NAC treated L450W endothelium showed significant upregulation of iNos, whereas Grp78 and Chop were downregulated compared to untreated L450W endothelium by real time PCR and Western blotting.	Acetylcysteine	0-3	nitric oxide synthase 2, inducible	Mus musculus	65-69
25368550-9	2014	BK transiently decreased human RPE (ARPE-19) cell monolayer resistance, and this effect was blocked by vasoinhibins, L-NAME, and NAC.	Acetylcysteine	129-132	kininogen 1	Homo sapiens	0-2
25048970-10	2014	27OH-C and total lipids from LDL and oxLDL independently increased Abeta production by SH-SY5Y cells, and Abeta accumulation could be inhibited by desipramine and by N-acetylcysteine.	Acetylcysteine	166-182	amyloid beta precursor protein	Homo sapiens	67-72
25048970-10	2014	27OH-C and total lipids from LDL and oxLDL independently increased Abeta production by SH-SY5Y cells, and Abeta accumulation could be inhibited by desipramine and by N-acetylcysteine.	Acetylcysteine	166-182	amyloid beta precursor protein	Homo sapiens	106-111
24111577-7	2014	Pretreatment with Nrf2 small interfering RNA, GSH depletion by buthionine sulfoximine and diethyl maleate, and with antioxidants by N-acetylcysteine and vitamin E, blocked DFO-stimulated osteoblastic differentiation.	Acetylcysteine	132-148	NFE2 like bZIP transcription factor 2	Homo sapiens	18-22
24299490-0	2014	N-acetyl-L-cysteine protects against cadmium-induced neuronal apoptosis by inhibiting ROS-dependent activation of Akt/mTOR pathway in mouse brain.	Acetylcysteine	0-19	thymoma viral proto-oncogene 1	Mus musculus	114-117
24734887-0	2014	Protective effect of N-acetylcysteine (NAC) on renal ischemia/reperfusion injury through Nrf2 signaling pathway.	Acetylcysteine	21-37	NFE2 like bZIP transcription factor 2	Homo sapiens	89-93
24734887-0	2014	Protective effect of N-acetylcysteine (NAC) on renal ischemia/reperfusion injury through Nrf2 signaling pathway.	Acetylcysteine	39-42	NFE2 like bZIP transcription factor 2	Homo sapiens	89-93
24734887-1	2014	The aim of this study was to investigate whether N-acetylcysteine (NAC), a known antioxidant, can protect kidney against ischemic injury through regulating Nrf2 signaling pathway.	Acetylcysteine	49-65	NFE2 like bZIP transcription factor 2	Homo sapiens	156-160
24734887-1	2014	The aim of this study was to investigate whether N-acetylcysteine (NAC), a known antioxidant, can protect kidney against ischemic injury through regulating Nrf2 signaling pathway.	Acetylcysteine	67-70	NFE2 like bZIP transcription factor 2	Homo sapiens	156-160
24734887-6	2014	We found that NAC significantly increased Nrf2 and downstream HO-1 expression.	Acetylcysteine	14-17	NFE2 like bZIP transcription factor 2	Homo sapiens	42-46
24734887-7	2014	Furthermore, NAC significantly decreased cleaved caspase 3, p53 and renal epithelial tubular cell apoptosis.	Acetylcysteine	13-16	tumor protein p53	Homo sapiens	60-63
24734887-9	2014	These findings suggest that the protective action of NAC on ischemia renal injury is associated closely with Nrf2 signaling pathway.	Acetylcysteine	53-56	NFE2 like bZIP transcription factor 2	Homo sapiens	109-113
24299490-8	2014	The protective effect of NAC was mediated, at least partially, by elevating the activities of Cu/Zn-superoxide dismutase, catalase and glutathione peroxidase, as well as the level of glutathione in the brain.	Acetylcysteine	25-28	catalase	Mus musculus	122-130
24299490-9	2014	Furthermore, Cd-induced activation of Akt/mTOR pathway in the brain was also inhibited by NAC.	Acetylcysteine	90-93	thymoma viral proto-oncogene 1	Mus musculus	38-41
24299490-11	2014	CONCLUSIONS: NAC protects against Cd-induced neuronal apoptosis in mouse brain partially by inhibiting ROS-dependent activation of Akt/mTOR pathway.	Acetylcysteine	13-16	thymoma viral proto-oncogene 1	Mus musculus	131-134
25181540-8	2014	In addition, mouse tracheal venular endothelial cells studied in vitro after exposure to cyclic stretch (18% elongation) or thrombin both demonstrated increased p-selectin expression that was significantly attenuated by NG-nitro-L-arginine methyl ester, N-acetylcysteine amide (NACA) and excess BH4.	Acetylcysteine	254-270	coagulation factor II	Mus musculus	124-132
25272228-5	2014	TCDD-induced HIF-1alpha stabilization and Akt phosphorylation was inhibited by pretreatment with wortmannin (a phosphatidylinositol 3-kinase (PI3K) inhibitor) or N-acetylcysteine (a ROS scavenger).	Acetylcysteine	162-178	hypoxia inducible factor 1 subunit alpha	Homo sapiens	13-23
25264893-0	2014	N-acetylcysteine attenuates ischemia-reperfusion-induced apoptosis and autophagy in mouse liver via regulation of the ROS/JNK/Bcl-2 pathway.	Acetylcysteine	0-16	B cell leukemia/lymphoma 2	Mus musculus	126-131
25264893-8	2014	We hypothesized that the mechanism of NAC may involve the ROS/JNK/Bcl-2 pathway.	Acetylcysteine	38-41	B cell leukemia/lymphoma 2	Mus musculus	66-71
25264893-13	2014	In addition, JNK, p-JNK, Bax, TNF-alpha, NF-kappaB, IL2, IL6 and levels were also decreased in NAC-treated mice.	Acetylcysteine	95-98	tumor necrosis factor	Mus musculus	30-39
25264893-13	2014	In addition, JNK, p-JNK, Bax, TNF-alpha, NF-kappaB, IL2, IL6 and levels were also decreased in NAC-treated mice.	Acetylcysteine	95-98	interleukin 6	Mus musculus	57-60
24905542-10	2014	The clinical antidote N-acetylcysteine offered almost complete protection even if administered 6h after APAP and a partial protection when given at 15 h. CONCLUSION: These data highlight important mechanistic events in APAP toxicity in PHH and indicate a critical role of JNK in the progression of injury after APAP in humans.	Acetylcysteine	22-38	mitogen-activated protein kinase 8	Homo sapiens	272-275
25002534-5	2014	However, pretreatment with N-acetylcysteine or diphenylene iodonium significantly reduced the OC differentiation, as well as the ROS accumulation and NF-kappaB activation, that were enhanced by TRP14 depletion.	Acetylcysteine	27-43	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	150-159
24952131-0	2014	Suppression of prolactin signaling by pyrrolidine dithiocarbamate is alleviated by N-acetylcysteine in mammary epithelial cells.	Acetylcysteine	83-99	prolactin	Homo sapiens	15-24
24952131-6	2014	Instead, the pro-oxidant activity of PDTC is involved as inclusion of the antioxidant N-acetylcysteine restores prolactin signaling.	Acetylcysteine	86-102	prolactin	Homo sapiens	112-121
25181540-8	2014	In addition, mouse tracheal venular endothelial cells studied in vitro after exposure to cyclic stretch (18% elongation) or thrombin both demonstrated increased p-selectin expression that was significantly attenuated by NG-nitro-L-arginine methyl ester, N-acetylcysteine amide (NACA) and excess BH4.	Acetylcysteine	254-270	selectin, platelet	Mus musculus	161-171
24946181-4	2014	The systematic administration of an antioxidant (N-acetyl-cysteine, NAC) to R6/2 mice suppressed the activation of AMPK-alpha1, reduced neuronal toxicity, which was assessed by the activation of caspases, increased neuronal density, ameliorated ventricle enlargement, and improved motor dysfunction.	Acetylcysteine	49-66	protein kinase, AMP-activated, alpha 1 catalytic subunit	Mus musculus	115-126
25202081-8	2014	Pre-treatment with N-acetylcysteine blocked loss of MMP, caused increase of Bcl-2-associated X protein (Bax)/B-cell lymphoma 2 (Bcl-2) ratio, caspase-8 activation, and apoptosis induced by equol.	Acetylcysteine	19-35	BCL2 associated X, apoptosis regulator	Homo sapiens	76-102
25202081-8	2014	Pre-treatment with N-acetylcysteine blocked loss of MMP, caused increase of Bcl-2-associated X protein (Bax)/B-cell lymphoma 2 (Bcl-2) ratio, caspase-8 activation, and apoptosis induced by equol.	Acetylcysteine	19-35	BCL2 associated X, apoptosis regulator	Homo sapiens	104-107
25202081-8	2014	Pre-treatment with N-acetylcysteine blocked loss of MMP, caused increase of Bcl-2-associated X protein (Bax)/B-cell lymphoma 2 (Bcl-2) ratio, caspase-8 activation, and apoptosis induced by equol.	Acetylcysteine	19-35	BCL2 apoptosis regulator	Homo sapiens	76-81
25257100-0	2014	N-acetyl-L-cysteine sensitizes pancreatic cancers to gemcitabine by targeting the NFkappaB pathway.	Acetylcysteine	0-19	nuclear factor kappa B subunit 1	Homo sapiens	82-90
25257100-3	2014	Previously, we demonstrated in human MIA PaCa-2 pancreatic cancer cells that N-acetyl-l-cysteine (NAC), a glutathione (GSH) precursor, prevents NFkappaB activation via S-glutathionylation of p65-NFkappaB, thereby blunting expression of survival genes.	Acetylcysteine	77-96	nuclear factor kappa B subunit 1	Homo sapiens	144-152
25257100-3	2014	Previously, we demonstrated in human MIA PaCa-2 pancreatic cancer cells that N-acetyl-l-cysteine (NAC), a glutathione (GSH) precursor, prevents NFkappaB activation via S-glutathionylation of p65-NFkappaB, thereby blunting expression of survival genes.	Acetylcysteine	77-96	nuclear factor kappa B subunit 1	Homo sapiens	195-203
25257100-3	2014	Previously, we demonstrated in human MIA PaCa-2 pancreatic cancer cells that N-acetyl-l-cysteine (NAC), a glutathione (GSH) precursor, prevents NFkappaB activation via S-glutathionylation of p65-NFkappaB, thereby blunting expression of survival genes.	Acetylcysteine	98-101	nuclear factor kappa B subunit 1	Homo sapiens	144-152
25257100-3	2014	Previously, we demonstrated in human MIA PaCa-2 pancreatic cancer cells that N-acetyl-l-cysteine (NAC), a glutathione (GSH) precursor, prevents NFkappaB activation via S-glutathionylation of p65-NFkappaB, thereby blunting expression of survival genes.	Acetylcysteine	98-101	nuclear factor kappa B subunit 1	Homo sapiens	195-203
25257100-4	2014	In this study, we documented the molecular sites of S-glutathionylation of p65, and we investigated whether NAC can suppress NFkappaB signaling and augment a therapeutic response to gemcitabine in vivo.	Acetylcysteine	108-111	nuclear factor kappa B subunit 1	Homo sapiens	125-133
25257100-13	2014	Together, these results indicate that adjunct therapy with NAC prevents NFkappaB activation and improves gemcitabine chemotherapeutic efficacy.	Acetylcysteine	59-62	nuclear factor kappa B subunit 1	Homo sapiens	72-80
24933620-5	2014	Cadmium-induced decrease in phosphorylated Akt1 correlated with increased association of wild-type (WT) Akt1 with PP2A, which was absent in the C296-310S Akt1 mutant and was also abolished by N-acetylcysteine treatment.	Acetylcysteine	192-208	thymoma viral proto-oncogene 1	Mus musculus	43-47
24833327-2	2014	The objective of this study was to compare the effect of high-dose NAC (600 mg bid) between high-risk and low-risk Chinese patients with COPD.	Acetylcysteine	67-70	BH3 interacting domain death agonist	Homo sapiens	79-82
24833327-9	2014	CONCLUSIONS: High-dose NAC (600 mg bid) for 1 year reduces exacerbations and prolongs time to first exacerbation in high-risk but not in low-risk Chinese patients with COPD.	Acetylcysteine	23-26	BH3 interacting domain death agonist	Homo sapiens	35-38
24933620-5	2014	Cadmium-induced decrease in phosphorylated Akt1 correlated with increased association of wild-type (WT) Akt1 with PP2A, which was absent in the C296-310S Akt1 mutant and was also abolished by N-acetylcysteine treatment.	Acetylcysteine	192-208	thymoma viral proto-oncogene 1	Mus musculus	104-108
24973647-13	2014	Pretreatment with NAC prevents p38 overactivation and thus protects the endothelium from this oxidative stress.	Acetylcysteine	18-21	mitogen-activated protein kinase 1	Homo sapiens	31-34
24933620-5	2014	Cadmium-induced decrease in phosphorylated Akt1 correlated with increased association of wild-type (WT) Akt1 with PP2A, which was absent in the C296-310S Akt1 mutant and was also abolished by N-acetylcysteine treatment.	Acetylcysteine	192-208	thymoma viral proto-oncogene 1	Mus musculus	104-108
24970110-8	2014	Furthermore, catalase and glutathione S-transferase, whose activities were reduced due to aspartame treatment, remained decreased even after N-acetylcysteine exposure.	Acetylcysteine	141-157	catalase	Rattus norvegicus	13-21
25177911-8	2014	Furthermore, compared with the IH group, antioxidant (NAC) pretreatment significantly decreased IH-mediated beta-cell apoptosis and reversed the ratio of Bcl-2/Bax expression (P&lt;0.05).	Acetylcysteine	54-57	BCL2, apoptosis regulator	Rattus norvegicus	154-159
24928737-5	2014	Resistance to OGD was conferred by inhibiting caspase-3 with DEVD-CHO and oxidative stress by the antioxidant N-acetylcysteine (NAC).	Acetylcysteine	110-126	caspase 3	Homo sapiens	46-55
24928737-5	2014	Resistance to OGD was conferred by inhibiting caspase-3 with DEVD-CHO and oxidative stress by the antioxidant N-acetylcysteine (NAC).	Acetylcysteine	128-131	caspase 3	Homo sapiens	46-55
24976129-6	2014	In addition, the N-acetylcysteine inhibited ROS/RNS generation, elevation of antioxidants level, expression of ERK1/2, Akt, tuberin phosphorylation, resulted in deceased 8-OHdG accumulation and upregulation of OGG1 protein expression suggesting no involvement of Akt and ERK1/2MAPK pathways after CEES and LPS challenge.	Acetylcysteine	17-33	thymoma viral proto-oncogene 1	Mus musculus	119-122
24976129-6	2014	In addition, the N-acetylcysteine inhibited ROS/RNS generation, elevation of antioxidants level, expression of ERK1/2, Akt, tuberin phosphorylation, resulted in deceased 8-OHdG accumulation and upregulation of OGG1 protein expression suggesting no involvement of Akt and ERK1/2MAPK pathways after CEES and LPS challenge.	Acetylcysteine	17-33	thymoma viral proto-oncogene 1	Mus musculus	263-266
24976129-6	2014	In addition, the N-acetylcysteine inhibited ROS/RNS generation, elevation of antioxidants level, expression of ERK1/2, Akt, tuberin phosphorylation, resulted in deceased 8-OHdG accumulation and upregulation of OGG1 protein expression suggesting no involvement of Akt and ERK1/2MAPK pathways after CEES and LPS challenge.	Acetylcysteine	17-33	mitogen-activated protein kinase 1	Mus musculus	277-281
24799199-5	2014	However, NAC pretreatment alleviated OTA-induced ROS overproduction, the loss of mitochondrial membrane potential (DeltaPsim), and the decrease in superoxide dismutase (SOD) activity.	Acetylcysteine	9-12	superoxide dismutase 1	Homo sapiens	147-167
24799199-5	2014	However, NAC pretreatment alleviated OTA-induced ROS overproduction, the loss of mitochondrial membrane potential (DeltaPsim), and the decrease in superoxide dismutase (SOD) activity.	Acetylcysteine	9-12	superoxide dismutase 1	Homo sapiens	169-172
24836981-14	2014	NAC also down-regulated both increases in NLRP3, ASC, caspase-1 and IL-1beta mRNA levels, along with their immunostaining.	Acetylcysteine	0-3	interleukin 1 beta	Mus musculus	68-76
24799199-7	2014	In addition, NAC pretreatment partly ameliorated OTA-induced S-phase arrest by preventing the down-regulation of cyclin A2, cyclin E1 and CDK2 expression in HEK-293 cells.	Acetylcysteine	13-16	cyclin A2	Homo sapiens	113-122
25202950-3	2014	The THP-1 macrophages were pretreated with N-acetyl-cysteine at different doses for 24 h before the palmitic acid cultivation.	Acetylcysteine	43-60	GLI family zinc finger 2	Homo sapiens	4-9
24938881-9	2014	Abrin also shown to increase in stress factor associated proteins SAPK/JNK, c-fos and c-jun levels which were effectively suppressed by NAC and trolox.	Acetylcysteine	136-139	mitogen-activated protein kinase 8	Homo sapiens	71-74
24870979-7	2014	Conversely, cellular apoptosis, generation of ROS, activation of caspase-3, -9 as well as PARP cleavage were significantly attenuated by pretreatment with an antioxidant, N-acetylcysteine (NAC).	Acetylcysteine	171-187	caspase 3	Homo sapiens	65-78
24870979-7	2014	Conversely, cellular apoptosis, generation of ROS, activation of caspase-3, -9 as well as PARP cleavage were significantly attenuated by pretreatment with an antioxidant, N-acetylcysteine (NAC).	Acetylcysteine	171-187	poly(ADP-ribose) polymerase 1	Homo sapiens	90-94
24870979-7	2014	Conversely, cellular apoptosis, generation of ROS, activation of caspase-3, -9 as well as PARP cleavage were significantly attenuated by pretreatment with an antioxidant, N-acetylcysteine (NAC).	Acetylcysteine	189-192	caspase 3	Homo sapiens	65-78
24870979-7	2014	Conversely, cellular apoptosis, generation of ROS, activation of caspase-3, -9 as well as PARP cleavage were significantly attenuated by pretreatment with an antioxidant, N-acetylcysteine (NAC).	Acetylcysteine	189-192	poly(ADP-ribose) polymerase 1	Homo sapiens	90-94
24907397-9	2014	Moreover, N-acetyl-L-cysteine significantly inhibited reactive oxygen/nitrogen species generation, elevated antioxidants levels, inhibited Akt, ERK1/2, tuberin phosphorylation, decreased 8-hydroxydeoxyguanosine accumulation and upregulated 8-oxoG-DNA glycosylase expression.	Acetylcysteine	10-29	AKT serine/threonine kinase 1	Homo sapiens	139-142
24907397-9	2014	Moreover, N-acetyl-L-cysteine significantly inhibited reactive oxygen/nitrogen species generation, elevated antioxidants levels, inhibited Akt, ERK1/2, tuberin phosphorylation, decreased 8-hydroxydeoxyguanosine accumulation and upregulated 8-oxoG-DNA glycosylase expression.	Acetylcysteine	10-29	mitogen-activated protein kinase 3	Homo sapiens	144-150
23070635-6	2014	Levels of AST, ALT and TOS, PT and INR were decreased in groups treated with NAC and erdosteine after acetaminophen administration, but the levels of TAC and GSH were increased.	Acetylcysteine	77-80	glutamic-oxaloacetic transaminase 2	Rattus norvegicus	10-13
24824652-6	2014	An antioxidant, N-acetyl-L-cysteine (NAC), prevented IH-induced hepatic insulin resistance in parallel with prevention of decreased IkappaBalpha content, increased JNK phosphorylation (markers of IKKbeta and JNK activation, respectively), increased serine phosphorylation of IRS-1 and IRS-2, and impaired insulin signaling in the liver without affecting IH-induced hepatic PKCdelta activation.	Acetylcysteine	16-35	inhibitor of nuclear factor kappa B kinase subunit beta	Rattus norvegicus	196-203
24946211-9	2014	The anti-oxidant N-acetylcysteine (NAC), the P53 inhibitor pifithrin-alpha (PFTalpha) as well as P53 siRNA knockdown suppressed berberine-induced P53 mitochondrial translocation and Cyp-D association, thus inhibiting mitochondrial membrane potential (MMP) decrease and prostate cancer cell necrosis.	Acetylcysteine	17-33	peptidylprolyl isomerase F	Homo sapiens	182-187
24946211-9	2014	The anti-oxidant N-acetylcysteine (NAC), the P53 inhibitor pifithrin-alpha (PFTalpha) as well as P53 siRNA knockdown suppressed berberine-induced P53 mitochondrial translocation and Cyp-D association, thus inhibiting mitochondrial membrane potential (MMP) decrease and prostate cancer cell necrosis.	Acetylcysteine	35-38	peptidylprolyl isomerase F	Homo sapiens	182-187
24769509-6	2014	Suppression of reactive oxygen species with N-acetylcysteine reduced levels of Bip protein and ubiquitination levels of cellular proteins during ASK treatment, leading to protection of cells from apoptosis.	Acetylcysteine	44-60	growth differentiation factor 10	Homo sapiens	79-82
24845567-4	2014	Pretreatment of lung cancer cells with the antioxidant N-acetyl-cysteine markedly suppressed the cell death induced by combined treatment with TWIST1 siRNA and ATO or IR.	Acetylcysteine	55-72	twist family bHLH transcription factor 1	Homo sapiens	143-149
24824652-6	2014	An antioxidant, N-acetyl-L-cysteine (NAC), prevented IH-induced hepatic insulin resistance in parallel with prevention of decreased IkappaBalpha content, increased JNK phosphorylation (markers of IKKbeta and JNK activation, respectively), increased serine phosphorylation of IRS-1 and IRS-2, and impaired insulin signaling in the liver without affecting IH-induced hepatic PKCdelta activation.	Acetylcysteine	16-35	insulin receptor substrate 1	Rattus norvegicus	275-280
24824652-6	2014	An antioxidant, N-acetyl-L-cysteine (NAC), prevented IH-induced hepatic insulin resistance in parallel with prevention of decreased IkappaBalpha content, increased JNK phosphorylation (markers of IKKbeta and JNK activation, respectively), increased serine phosphorylation of IRS-1 and IRS-2, and impaired insulin signaling in the liver without affecting IH-induced hepatic PKCdelta activation.	Acetylcysteine	16-35	insulin receptor substrate 2	Rattus norvegicus	285-290
24824652-6	2014	An antioxidant, N-acetyl-L-cysteine (NAC), prevented IH-induced hepatic insulin resistance in parallel with prevention of decreased IkappaBalpha content, increased JNK phosphorylation (markers of IKKbeta and JNK activation, respectively), increased serine phosphorylation of IRS-1 and IRS-2, and impaired insulin signaling in the liver without affecting IH-induced hepatic PKCdelta activation.	Acetylcysteine	37-40	inhibitor of nuclear factor kappa B kinase subunit beta	Rattus norvegicus	196-203
24824652-6	2014	An antioxidant, N-acetyl-L-cysteine (NAC), prevented IH-induced hepatic insulin resistance in parallel with prevention of decreased IkappaBalpha content, increased JNK phosphorylation (markers of IKKbeta and JNK activation, respectively), increased serine phosphorylation of IRS-1 and IRS-2, and impaired insulin signaling in the liver without affecting IH-induced hepatic PKCdelta activation.	Acetylcysteine	37-40	insulin receptor substrate 1	Rattus norvegicus	275-280
24824652-6	2014	An antioxidant, N-acetyl-L-cysteine (NAC), prevented IH-induced hepatic insulin resistance in parallel with prevention of decreased IkappaBalpha content, increased JNK phosphorylation (markers of IKKbeta and JNK activation, respectively), increased serine phosphorylation of IRS-1 and IRS-2, and impaired insulin signaling in the liver without affecting IH-induced hepatic PKCdelta activation.	Acetylcysteine	37-40	insulin receptor substrate 2	Rattus norvegicus	285-290
24726884-8	2014	N-acetylcysteine (NAC), an antioxidant, suppressed the phosphorylation of ATM and p53 and, to a less extent, Chk2, but NAC increased the phosphorylation and nuclear foci formation of H2AX.	Acetylcysteine	0-16	H2A.X variant histone	Mus musculus	183-187
24722831-4	2014	It appears that reactive oxygen species (ROS) function as signaling molecules for all the three pathways because pretreatment with N-acetylcysteine, a scavenger of ROS, almost completely abolished TNF-alpha secretion and significantly reduced the number of apoptotic and autophagic cells.	Acetylcysteine	131-147	tumor necrosis factor	Homo sapiens	197-206
24085626-6	2014	CoCl2-induced increase of Bax/Bcl-2 ratio and Caspase-3 expression was attenuated by RA, NAC and SB203580 (p38MAPK inhibitor).	Acetylcysteine	89-92	BCL2, apoptosis regulator	Rattus norvegicus	30-35
24726884-8	2014	N-acetylcysteine (NAC), an antioxidant, suppressed the phosphorylation of ATM and p53 and, to a less extent, Chk2, but NAC increased the phosphorylation and nuclear foci formation of H2AX.	Acetylcysteine	18-21	H2A.X variant histone	Mus musculus	183-187
24726884-8	2014	N-acetylcysteine (NAC), an antioxidant, suppressed the phosphorylation of ATM and p53 and, to a less extent, Chk2, but NAC increased the phosphorylation and nuclear foci formation of H2AX.	Acetylcysteine	119-122	H2A.X variant histone	Mus musculus	183-187
24726884-9	2014	Interestingly, NAC increased apoptosis, which may account for the observed H2AX activation.	Acetylcysteine	15-18	H2A.X variant histone	Mus musculus	75-79
24794623-12	2014	Decreased expression of IL1-beta was observed only in animals treated with NAC.	Acetylcysteine	75-78	interleukin-1 beta	Cavia porcellus	24-32
24795232-7	2014	The induction of HO-1 by R-scy was inhibited by pretreatment with an antioxidant, N-acetyl-cysteine (NAC), as well as SB203580 and LY294002, inhibitors for p38 MAPK and PI3K/Akt, respectively.	Acetylcysteine	101-104	thymoma viral proto-oncogene 1	Mus musculus	174-177
24795232-7	2014	The induction of HO-1 by R-scy was inhibited by pretreatment with an antioxidant, N-acetyl-cysteine (NAC), as well as SB203580 and LY294002, inhibitors for p38 MAPK and PI3K/Akt, respectively.	Acetylcysteine	82-99	heme oxygenase 1	Mus musculus	17-21
24795232-7	2014	The induction of HO-1 by R-scy was inhibited by pretreatment with an antioxidant, N-acetyl-cysteine (NAC), as well as SB203580 and LY294002, inhibitors for p38 MAPK and PI3K/Akt, respectively.	Acetylcysteine	101-104	heme oxygenase 1	Mus musculus	17-21
25083175-10	2014	RESULTS: Serum levels of luteinizing hormone (LH), total testosterone, cholester- ol and triglyceride, insulin and leptin significantly reduced in the MTF and NAC groups compared to the placebo (p&lt;0.01).	Acetylcysteine	159-162	insulin	Homo sapiens	103-110
25083175-12	2014	The serum levels of malonyldialdehyde (MDA), insulin and leptin reduced significantly after treatment in the MTF+NAC group compared to the placebo (p&lt;0.05).	Acetylcysteine	113-116	insulin	Homo sapiens	45-52
24609059-9	2014	The inflammatory effects of mitochondrial damage appeared to be dependent on ROS production and NF-kappaB activation since the inflammatory response was counteracted by both N-acetylcysteine and mitoTEMPO and it was also reduced by BAY-117085.	Acetylcysteine	174-190	nuclear factor kappa B subunit 1	Homo sapiens	96-105
23475579-5	2014	Overexpression of anti-oxidant enzymes superoxide dismutase 1 (SOD1), SOD2, and catalase, or pretreatment with the pharmacological inhibitor N-acetylcysteine (NAC) significantly attenuated both pso-mediated ROS generation and pso-mediated growth inhibition in CaP cells.	Acetylcysteine	141-157	superoxide dismutase 1	Homo sapiens	63-67
23475579-5	2014	Overexpression of anti-oxidant enzymes superoxide dismutase 1 (SOD1), SOD2, and catalase, or pretreatment with the pharmacological inhibitor N-acetylcysteine (NAC) significantly attenuated both pso-mediated ROS generation and pso-mediated growth inhibition in CaP cells.	Acetylcysteine	159-162	superoxide dismutase 1	Homo sapiens	39-61
25176089-6	2014	NAC treatment obviously alleviated intestinal damages induced by CPB, decreased the levels of intestinal MDA, TNF-alpha, IL-6 and serum DAO and increased activity of SOD, GSH, and GSH-Px in the intestines.	Acetylcysteine	0-3	tumor necrosis factor	Rattus norvegicus	110-119
25176089-6	2014	NAC treatment obviously alleviated intestinal damages induced by CPB, decreased the levels of intestinal MDA, TNF-alpha, IL-6 and serum DAO and increased activity of SOD, GSH, and GSH-Px in the intestines.	Acetylcysteine	0-3	interleukin 6	Rattus norvegicus	121-125
24735948-10	2014	In addition, N-acetylcysteine, an antioxidant, attenuated chrysotile asbestos-induced dephosphorylation of P-AKT and completely abolished phosphorylation/activation of JNK.	Acetylcysteine	13-29	mitogen-activated protein kinase 8	Homo sapiens	168-171
24810974-8	2014	When malathion-treated rats were compared to NAC supplemented rats, leukocytosis, T cell count and IL-1beta, IL-6, INF-gamma expression were reduced.	Acetylcysteine	45-48	interleukin 1 beta	Rattus norvegicus	99-107
24964211-13	2014	The protection conferred by the free radical scavenger N-acetyl-cysteine indicates that the FASN inhibitors induced apoptosis through an oxidative stress-associated mechanism.	Acetylcysteine	55-72	fatty acid synthase	Mus musculus	92-96
24726524-10	2014	NAC attenuated BLM induced oxidative damage, changes in E-cadherin and vimentin expressions and collagen deposition in the sclerotic skin of mice.	Acetylcysteine	0-3	cadherin 1	Mus musculus	56-66
24064905-6	2014	Importantly, the effect of above DNA damage response was prevented by N-acetyl-l-cysteine (a reactive oxygen species scavenger), and NU7026 (a DNA-PK inhibitor) could attenuate DNA-PK catalytic subunit and phosphorylation of H2A.X on Ser139 expression in comparison with HMJ-38 alone treated HUVECs.	Acetylcysteine	70-89	protein kinase, DNA-activated, catalytic subunit	Homo sapiens	177-201
24919544-10	2014	N-acetyl-L-cysteine (NAC), a free radical scavenger, also reduced ROS production and AKT phosphorylation, resulting in apoptotic cell death.	Acetylcysteine	0-19	AKT serine/threonine kinase 1	Homo sapiens	85-88
24633404-5	2014	The in-line reaction of polyamines with o-phthalaldehyde and N-acetyl-L-cysteine yields fluorescent derivatives which are separated on a reversed-phase C18 column and detected by a fluorometer at an excitation wavelength of 340 nm and an emission wavelength of 450 nm.	Acetylcysteine	61-80	Bardet-Biedl syndrome 9	Homo sapiens	152-155
24500986-7	2014	In PRA, CYP2E1-induced suppression of GLUT4 expression was blocked by chlormethiazole (CYP2E1-specific inhibitor) and the antioxidants vitamin E and N-acetyl-l-cysteine.	Acetylcysteine	149-168	cytochrome P450, family 2, subfamily e, polypeptide 1	Rattus norvegicus	8-14
24915933-14	2014	N-acetyl-L-cysteine (NAC), an antioxidant, can partially attenuate DS/Cu complex-induced apoptosis and block JNK activation in vitro.	Acetylcysteine	0-19	mitogen-activated protein kinase 8	Homo sapiens	109-112
24612036-5	2014	The reported findings link an impaired cholesterol oxidative metabolism to an excessive beta-amyloidogenesis and point to NAC as an efficient inhibitor of oxysterols-induced Abeta toxic peptide accumulation in the brain.	Acetylcysteine	122-125	amyloid beta precursor protein	Homo sapiens	174-179
24531650-8	2014	RESULTS: In vivo, N-acetylcysteine ameliorated the D-GalN/LPS-induced hepatotoxicity and reduced GSK3beta activity; GSK3beta inhibition increased hepatic superoxide dismutase activity and the glutathione content, decreased malondialdehyde production in the liver tissues; while GSK3beta inhibition suppressed the JNK activation in the liver and decreased cytochrome c release from mitochondria.	Acetylcysteine	18-34	galanin and GMAP prepropeptide	Mus musculus	53-57
24531650-8	2014	RESULTS: In vivo, N-acetylcysteine ameliorated the D-GalN/LPS-induced hepatotoxicity and reduced GSK3beta activity; GSK3beta inhibition increased hepatic superoxide dismutase activity and the glutathione content, decreased malondialdehyde production in the liver tissues; while GSK3beta inhibition suppressed the JNK activation in the liver and decreased cytochrome c release from mitochondria.	Acetylcysteine	18-34	mitogen-activated protein kinase 8	Homo sapiens	313-316
24531650-8	2014	RESULTS: In vivo, N-acetylcysteine ameliorated the D-GalN/LPS-induced hepatotoxicity and reduced GSK3beta activity; GSK3beta inhibition increased hepatic superoxide dismutase activity and the glutathione content, decreased malondialdehyde production in the liver tissues; while GSK3beta inhibition suppressed the JNK activation in the liver and decreased cytochrome c release from mitochondria.	Acetylcysteine	18-34	cytochrome c, somatic	Homo sapiens	355-367
24792472-3	2014	Pretreatment with N-acetylcysteine (NAC) reduced COX-2 expression and PGE2 release induced by PDT.	Acetylcysteine	18-34	prostaglandin-endoperoxide synthase 2	Homo sapiens	49-54
24631677-8	2014	In fact, pre-treatment with the antioxidant N-acetyl cysteine blocked PIMT dopamine-associated down-regulation.	Acetylcysteine	44-61	protein-L-isoaspartate (D-aspartate) O-methyltransferase	Homo sapiens	70-74
24930874-5	2014	These stimuli-induced sheddings of HB-EGF were inhibited by N-acetyl-L-cysteine (NAC), suggesting the involvement of ROS.	Acetylcysteine	60-79	proheparin-binding EGF-like growth factor	Chlorocebus sabaeus	35-41
24930874-5	2014	These stimuli-induced sheddings of HB-EGF were inhibited by N-acetyl-L-cysteine (NAC), suggesting the involvement of ROS.	Acetylcysteine	81-84	proheparin-binding EGF-like growth factor	Chlorocebus sabaeus	35-41
24700345-9	2014	Pretreatment of T24 cells with the antioxidant N-acetylcysteine (NAC) significantly inhibited activation of caspase-3 and MAPK-p38 and prevented inactivation of Akt and Bcl-2.	Acetylcysteine	47-63	caspase 3	Homo sapiens	108-117
24700345-9	2014	Pretreatment of T24 cells with the antioxidant N-acetylcysteine (NAC) significantly inhibited activation of caspase-3 and MAPK-p38 and prevented inactivation of Akt and Bcl-2.	Acetylcysteine	47-63	AKT serine/threonine kinase 1	Homo sapiens	161-164
24700345-9	2014	Pretreatment of T24 cells with the antioxidant N-acetylcysteine (NAC) significantly inhibited activation of caspase-3 and MAPK-p38 and prevented inactivation of Akt and Bcl-2.	Acetylcysteine	47-63	BCL2 apoptosis regulator	Homo sapiens	169-174
24700345-9	2014	Pretreatment of T24 cells with the antioxidant N-acetylcysteine (NAC) significantly inhibited activation of caspase-3 and MAPK-p38 and prevented inactivation of Akt and Bcl-2.	Acetylcysteine	65-68	caspase 3	Homo sapiens	108-117
24700345-9	2014	Pretreatment of T24 cells with the antioxidant N-acetylcysteine (NAC) significantly inhibited activation of caspase-3 and MAPK-p38 and prevented inactivation of Akt and Bcl-2.	Acetylcysteine	65-68	AKT serine/threonine kinase 1	Homo sapiens	161-164
24700345-9	2014	Pretreatment of T24 cells with the antioxidant N-acetylcysteine (NAC) significantly inhibited activation of caspase-3 and MAPK-p38 and prevented inactivation of Akt and Bcl-2.	Acetylcysteine	65-68	BCL2 apoptosis regulator	Homo sapiens	169-174
24769205-8	2014	HUA induced oxidative stress, and the antioxidant NAC blocked HUA-induced IRS1 activation and Akt inhibition in HepG2 cells.	Acetylcysteine	50-53	AKT serine/threonine kinase 1	Homo sapiens	94-97
24792472-3	2014	Pretreatment with N-acetylcysteine (NAC) reduced COX-2 expression and PGE2 release induced by PDT.	Acetylcysteine	36-39	prostaglandin-endoperoxide synthase 2	Homo sapiens	49-54
24525097-6	2014	The cellular expression of 5-lipoxygenase, however, was up-regulated by 200 muM genistein and the addition of 5-lipoxygenase inhibitor (Zileuton) decreased genistein-induced intracellular ROS level, close to that from the addition of the ROS scavenger, N-acetylcysteine.	Acetylcysteine	253-269	arachidonate 5-lipoxygenase	Homo sapiens	27-41
24798751-0	2014	Topical N-acetylcysteine accelerates wound healing in vitro and in vivo via the PKC/Stat3 pathway.	Acetylcysteine	8-24	signal transducer and activator of transcription 3	Homo sapiens	84-89
24798751-7	2014	In addition, Nac induced collagenous expression of MMP-1 via the PKC/Stat3 signaling pathway.	Acetylcysteine	13-16	signal transducer and activator of transcription 3	Homo sapiens	69-74
24819505-4	2014	Overexpression of Nrf2 or HO-1 resulted in upregulation of TP in NCI-H292 cells, an effect mimicked by treatment with an antioxidant N-acetylcysteine and partially reversed by HO-1 knockdown.	Acetylcysteine	133-149	NFE2 like bZIP transcription factor 2	Homo sapiens	18-22
24578384-15	2014	Both N-acetyl-l-cysteine and U0126 significantly inhibited CTRP3-induced upregulation of Runx2 and calcified nodule formation.	Acetylcysteine	5-24	RUNX family transcription factor 2	Rattus norvegicus	89-94
24525097-6	2014	The cellular expression of 5-lipoxygenase, however, was up-regulated by 200 muM genistein and the addition of 5-lipoxygenase inhibitor (Zileuton) decreased genistein-induced intracellular ROS level, close to that from the addition of the ROS scavenger, N-acetylcysteine.	Acetylcysteine	253-269	arachidonate 5-lipoxygenase	Homo sapiens	110-124
24556569-4	2014	MSG (20 mM)-induced reactive oxygen species (ROS) generation and apoptotic cell death were significantly attenuated by NAC (500 muM) pretreatment.	Acetylcysteine	119-122	latexin	Homo sapiens	128-131
24488173-4	2014	The present results also show that the pretreatment with well-known antioxidants such as trolox and N-acetyl cysteine partially reduced the caspase activation caused by the administration of TNFalpha.	Acetylcysteine	100-117	tumor necrosis factor	Homo sapiens	191-199
24556569-6	2014	In addition, NAC significantly attenuated MSG-induced endoplasmic reticulum (ER) stress markers, such as XBP1 splicing and CHOP, PERK, and GRP78 up-regulation.	Acetylcysteine	13-16	DNA damage inducible transcript 3	Homo sapiens	123-127
24556569-6	2014	In addition, NAC significantly attenuated MSG-induced endoplasmic reticulum (ER) stress markers, such as XBP1 splicing and CHOP, PERK, and GRP78 up-regulation.	Acetylcysteine	13-16	heat shock protein family A (Hsp70) member 5	Homo sapiens	139-144
24556569-7	2014	Furthermore, NAC prevented the changes of MSG-induced Bcl-2 expression level.	Acetylcysteine	13-16	BCL2 apoptosis regulator	Homo sapiens	54-59
24686235-5	2014	With 1.0mM NAC, ~30% of the injected Cd-HSA complex eluted as such, while the mobilized Cd was lost on the column.	Acetylcysteine	11-14	albumin	Homo sapiens	40-43
24284420-8	2014	When antioxidants such as vitamin C, N-acetylcysteine, and Trolox were applied to MNT1 cells, melanin levels decreased in parallel with FoxO3a nuclear translocation, and this effect disappeared with FoxO3a-directed small interfering RNA treatment.	Acetylcysteine	37-53	forkhead box O3	Homo sapiens	136-142
24284420-8	2014	When antioxidants such as vitamin C, N-acetylcysteine, and Trolox were applied to MNT1 cells, melanin levels decreased in parallel with FoxO3a nuclear translocation, and this effect disappeared with FoxO3a-directed small interfering RNA treatment.	Acetylcysteine	37-53	forkhead box O3	Homo sapiens	199-205
24583398-11	2014	NAC treatment decreased MMP-3 production in CD-ISMEFs and removed the enhancement due to TNFalpha.	Acetylcysteine	0-3	matrix metallopeptidase 3	Homo sapiens	24-29
24435707-12	2014	Further, pretreatment of the cells with NAC attenuated EGF-induced STAT3 phosphorylation.	Acetylcysteine	40-43	signal transducer and activator of transcription 3	Homo sapiens	67-72
24117464-4	2014	Experimental studies demonstrating that N-acetylcysteine (NAC) inhibits PLT binding to endothelial cell-secreted and anchored UL VWF multimers suggest that NAC may be useful in the treatment of TTP.	Acetylcysteine	40-56	von Willebrand factor	Homo sapiens	129-132
24117464-4	2014	Experimental studies demonstrating that N-acetylcysteine (NAC) inhibits PLT binding to endothelial cell-secreted and anchored UL VWF multimers suggest that NAC may be useful in the treatment of TTP.	Acetylcysteine	58-61	von Willebrand factor	Homo sapiens	129-132
24117464-4	2014	Experimental studies demonstrating that N-acetylcysteine (NAC) inhibits PLT binding to endothelial cell-secreted and anchored UL VWF multimers suggest that NAC may be useful in the treatment of TTP.	Acetylcysteine	156-159	von Willebrand factor	Homo sapiens	129-132
24690178-7	2014	Treatment with N-Acetyl Cysteine decreased ROS production and JNK/p38 phosphorylation but had minimal affect on ATF2 suggesting a direct interaction of GTPpi with this transcription factor.	Acetylcysteine	15-32	mitogen-activated protein kinase 14	Homo sapiens	66-69
24686172-5	2014	Notably, SASP sensitized breast cancer cells to inhibitors of the type I IGF receptor (IGF-IR) in a manner reversed by the reactive oxygen species (ROS) scavenger N-acetyl-L-cysteine.	Acetylcysteine	163-182	aspartic peptidase retroviral like 1	Homo sapiens	9-13
24583398-11	2014	NAC treatment decreased MMP-3 production in CD-ISMEFs and removed the enhancement due to TNFalpha.	Acetylcysteine	0-3	tumor necrosis factor	Homo sapiens	89-97
24583398-15	2014	NAC and curcumin normalize MMP-3 levels mainly in TNFalpha stimulated cells.	Acetylcysteine	0-3	matrix metallopeptidase 3	Homo sapiens	27-32
24583398-15	2014	NAC and curcumin normalize MMP-3 levels mainly in TNFalpha stimulated cells.	Acetylcysteine	0-3	tumor necrosis factor	Homo sapiens	50-58
24583398-16	2014	A modulation of MMP-3 production by NAC and curcumin due to their direct action on transcriptional factors has been also suggested.	Acetylcysteine	36-39	matrix metallopeptidase 3	Homo sapiens	16-21
24164541-4	2014	HN2-induced EGFR phosphorylation and IL-6 secretion in NHBECs were inhibited by the antioxidant N-acetyl-L-cysteine (NAC) and by the flavoprotein inhibitor diphenyleneiodonium chloride (DPI).	Acetylcysteine	96-115	epidermal growth factor receptor	Homo sapiens	12-16
24530511-11	2014	N-acetyl-cysteine, a scavenger of reactive oxygen species (ROS), abrogated copper(II)-elicited microglial release of TNF-alpha and nitric oxide and subsequent neurotoxicity.	Acetylcysteine	0-17	tumor necrosis factor	Mus musculus	117-126
24164541-4	2014	HN2-induced EGFR phosphorylation and IL-6 secretion in NHBECs were inhibited by the antioxidant N-acetyl-L-cysteine (NAC) and by the flavoprotein inhibitor diphenyleneiodonium chloride (DPI).	Acetylcysteine	96-115	interleukin 6	Homo sapiens	37-41
24588654-6	2014	Moreover, treatment of NHEKs with Z-Ligustilide increased reactive oxygen species (ROS) and L-N-acetylcysteine (L-NAC, an antioxidant) attenuated Z-ligustilide-induced Nrf2 nuclear translocation and HO-1 expression.	Acetylcysteine	92-110	NFE2 like bZIP transcription factor 2	Homo sapiens	168-172
24492200-7	2014	The reducing agent N-acetylcysteine eliminated the effects of selenium on ERK activation, proliferation, and mobility.	Acetylcysteine	19-35	mitogen-activated protein kinase 1	Mus musculus	74-77
24337903-5	2014	LicA also induced reactive oxygen species (ROS) accumulation and the anti-oxidant N-acetylcysteine reduced LicA-induced cell death and CHOP expression.	Acetylcysteine	82-98	DNA damage inducible transcript 3	Homo sapiens	135-139
24588654-6	2014	Moreover, treatment of NHEKs with Z-Ligustilide increased reactive oxygen species (ROS) and L-N-acetylcysteine (L-NAC, an antioxidant) attenuated Z-ligustilide-induced Nrf2 nuclear translocation and HO-1 expression.	Acetylcysteine	112-117	NFE2 like bZIP transcription factor 2	Homo sapiens	168-172
24681574-13	2014	IFN-gamma treatment increased the accumulation of intracellular ROS in melanocytes, while ROS scavenger N-acetyl cysteine (NAC) effectively inhibited IFN-gamma induced p21 expression and melanocyte senescence.	Acetylcysteine	104-121	interferon gamma	Homo sapiens	150-159
24481553-7	2014	Moreover, carnosol generated reactive oxygen species (ROS), and pretreatment with N-acetyl cysteine abrogated carnosol-induced cleavage of caspase-3 and PARP.	Acetylcysteine	82-99	caspase 3	Homo sapiens	139-148
24481553-7	2014	Moreover, carnosol generated reactive oxygen species (ROS), and pretreatment with N-acetyl cysteine abrogated carnosol-induced cleavage of caspase-3 and PARP.	Acetylcysteine	82-99	poly(ADP-ribose) polymerase 1	Homo sapiens	153-157
24519543-2	2014	N-acetylcysteine (NAC) and selenium (Se) display neuroprotective activities mediated at least in part by their antioxidant and anti-inflammatory properties although there is no report on oxidative stress, antioxidant vitamin, interleukin-1 beta (IL)-1beta and IL-4 levels in brain and blood of TBI-induced rats.	Acetylcysteine	18-21	interleukin 1 beta	Rattus norvegicus	226-255
24519543-9	2014	The lipid peroxidation and IL-1beta values were decreased by NAC and Se treatments.	Acetylcysteine	61-64	interleukin 1 beta	Rattus norvegicus	27-35
24691097-3	2014	Treatment with TGFbeta1 enhanced the levels of reactive oxygen species (ROS) and TGFbeta1-stimulated EMT gene changes, including an increase in profibrotic fibronectin-1 and collagen 1A1, were diminished by the antioxidant N-acetylcysteine.	Acetylcysteine	223-239	transforming growth factor beta 1	Homo sapiens	15-23
24691097-3	2014	Treatment with TGFbeta1 enhanced the levels of reactive oxygen species (ROS) and TGFbeta1-stimulated EMT gene changes, including an increase in profibrotic fibronectin-1 and collagen 1A1, were diminished by the antioxidant N-acetylcysteine.	Acetylcysteine	223-239	transforming growth factor beta 1	Homo sapiens	81-89
24691097-3	2014	Treatment with TGFbeta1 enhanced the levels of reactive oxygen species (ROS) and TGFbeta1-stimulated EMT gene changes, including an increase in profibrotic fibronectin-1 and collagen 1A1, were diminished by the antioxidant N-acetylcysteine.	Acetylcysteine	223-239	fibronectin 1	Homo sapiens	156-169
24613855-5	2014	ALA acid and NAC supplementation post sodium tungstate exposure increased GSH and also, was beneficial in the recovery of altered superoxide dismutase and catalase activity, besides, significantly reducing blood and tissue reactive oxygen species and TBARS levels.	Acetylcysteine	13-16	catalase	Rattus norvegicus	155-163
24449419-9	2014	N-acetylcysteine, a glutathione (GSH) precursor, blocked Cd2+-evoked PTEN degradation as well as Akt phosphorylation.	Acetylcysteine	0-16	phosphatase and tensin homolog	Mus musculus	69-73
24449419-9	2014	N-acetylcysteine, a glutathione (GSH) precursor, blocked Cd2+-evoked PTEN degradation as well as Akt phosphorylation.	Acetylcysteine	0-16	thymoma viral proto-oncogene 1	Mus musculus	97-100
24681574-13	2014	IFN-gamma treatment increased the accumulation of intracellular ROS in melanocytes, while ROS scavenger N-acetyl cysteine (NAC) effectively inhibited IFN-gamma induced p21 expression and melanocyte senescence.	Acetylcysteine	104-121	cyclin dependent kinase inhibitor 1A	Homo sapiens	168-171
24681574-13	2014	IFN-gamma treatment increased the accumulation of intracellular ROS in melanocytes, while ROS scavenger N-acetyl cysteine (NAC) effectively inhibited IFN-gamma induced p21 expression and melanocyte senescence.	Acetylcysteine	123-126	interferon gamma	Homo sapiens	150-159
24681574-13	2014	IFN-gamma treatment increased the accumulation of intracellular ROS in melanocytes, while ROS scavenger N-acetyl cysteine (NAC) effectively inhibited IFN-gamma induced p21 expression and melanocyte senescence.	Acetylcysteine	123-126	cyclin dependent kinase inhibitor 1A	Homo sapiens	168-171
24681574-14	2014	IL-6 and HSP-70 release was significantly induced by IFN-gamma treatment, which was largely inhibited by NAC.	Acetylcysteine	105-108	interleukin 6	Homo sapiens	0-4
24681574-14	2014	IL-6 and HSP-70 release was significantly induced by IFN-gamma treatment, which was largely inhibited by NAC.	Acetylcysteine	105-108	interferon gamma	Homo sapiens	53-62
24293519-9	2014	ROS inhibitors, Tiron, and N-acetylcysteine inhibited Ang II-induced intracellular CyPA acetylation and also AcK-CyPA secretion.	Acetylcysteine	27-43	Activated Cdc42 kinase	Drosophila melanogaster	109-112
24651440-10	2014	Moreover, the antioxidant N-acetylcysteine prevented phosphorylation of both JNK and c-Jun.	Acetylcysteine	26-42	mitogen-activated protein kinase 8	Homo sapiens	77-80
24653672-5	2014	Here, we describe that 24 h incubation of primary hippocampal neurons with iron enhanced agonist-induced RyR-mediated Ca(2) (+) release and promoted mitochondrial network fragmentation in 43% of neurons, a response significantly prevented by RyR inhibition and by the antioxidant agent N-acetyl-L-cysteine.	Acetylcysteine	286-305	ryanodine receptor 1	Homo sapiens	242-245
24431405-8	2014	We also demonstrate that curcumin-mediated caspase-1 activation is oxidant dependent by using N-acetyl-L-cysteine (NAC) to inhibit pyroptosis.	Acetylcysteine	94-113	caspase 1	Homo sapiens	43-52
24577230-1	2014	We investigated whether treatment with N-acetylcysteine (NAC) reduces oxidative stress intensity and restores the expression and activities of superoxide dismutase (Sod1, SOD), catalase (Cat, CAT) and glutathione peroxidase (Gpx1, GPx) in lead-exposed workers.	Acetylcysteine	39-55	superoxide dismutase 1	Homo sapiens	165-169
24424051-9	2014	Furthermore, the ROS scavengers N-acetyl cysteine and 2-phenyl-1,2-benzisoselenazol-3-(2H)-one blocked the effect of I(-) on Akt phosphorylation.	Acetylcysteine	32-49	AKT serine/threonine kinase 1	Rattus norvegicus	125-128
24577230-1	2014	We investigated whether treatment with N-acetylcysteine (NAC) reduces oxidative stress intensity and restores the expression and activities of superoxide dismutase (Sod1, SOD), catalase (Cat, CAT) and glutathione peroxidase (Gpx1, GPx) in lead-exposed workers.	Acetylcysteine	39-55	superoxide dismutase 1	Homo sapiens	171-174
24577230-1	2014	We investigated whether treatment with N-acetylcysteine (NAC) reduces oxidative stress intensity and restores the expression and activities of superoxide dismutase (Sod1, SOD), catalase (Cat, CAT) and glutathione peroxidase (Gpx1, GPx) in lead-exposed workers.	Acetylcysteine	39-55	catalase	Homo sapiens	177-185
24577230-1	2014	We investigated whether treatment with N-acetylcysteine (NAC) reduces oxidative stress intensity and restores the expression and activities of superoxide dismutase (Sod1, SOD), catalase (Cat, CAT) and glutathione peroxidase (Gpx1, GPx) in lead-exposed workers.	Acetylcysteine	39-55	catalase	Homo sapiens	187-190
24577230-1	2014	We investigated whether treatment with N-acetylcysteine (NAC) reduces oxidative stress intensity and restores the expression and activities of superoxide dismutase (Sod1, SOD), catalase (Cat, CAT) and glutathione peroxidase (Gpx1, GPx) in lead-exposed workers.	Acetylcysteine	39-55	catalase	Homo sapiens	192-195
24577230-1	2014	We investigated whether treatment with N-acetylcysteine (NAC) reduces oxidative stress intensity and restores the expression and activities of superoxide dismutase (Sod1, SOD), catalase (Cat, CAT) and glutathione peroxidase (Gpx1, GPx) in lead-exposed workers.	Acetylcysteine	57-60	superoxide dismutase 1	Homo sapiens	165-169
24577230-1	2014	We investigated whether treatment with N-acetylcysteine (NAC) reduces oxidative stress intensity and restores the expression and activities of superoxide dismutase (Sod1, SOD), catalase (Cat, CAT) and glutathione peroxidase (Gpx1, GPx) in lead-exposed workers.	Acetylcysteine	57-60	superoxide dismutase 1	Homo sapiens	171-174
24577230-1	2014	We investigated whether treatment with N-acetylcysteine (NAC) reduces oxidative stress intensity and restores the expression and activities of superoxide dismutase (Sod1, SOD), catalase (Cat, CAT) and glutathione peroxidase (Gpx1, GPx) in lead-exposed workers.	Acetylcysteine	57-60	catalase	Homo sapiens	177-185
24577230-1	2014	We investigated whether treatment with N-acetylcysteine (NAC) reduces oxidative stress intensity and restores the expression and activities of superoxide dismutase (Sod1, SOD), catalase (Cat, CAT) and glutathione peroxidase (Gpx1, GPx) in lead-exposed workers.	Acetylcysteine	57-60	catalase	Homo sapiens	187-190
24577230-1	2014	We investigated whether treatment with N-acetylcysteine (NAC) reduces oxidative stress intensity and restores the expression and activities of superoxide dismutase (Sod1, SOD), catalase (Cat, CAT) and glutathione peroxidase (Gpx1, GPx) in lead-exposed workers.	Acetylcysteine	57-60	catalase	Homo sapiens	192-195
23640957-7	2014	Furthermore, ROS scavenger N-acetyl L-cysteine attenuated beta-sitosterol-mediated sub-G1 accumulation, PARP cleavage, JNK and AMPK activation in U266 cells.	Acetylcysteine	27-46	poly(ADP-ribose) polymerase 1	Homo sapiens	104-108
24380754-7	2014	N-acetyl cysteine (NAC) inhibitedIK-induced Bcl-2 family-mediated apoptosis.	Acetylcysteine	0-17	B cell leukemia/lymphoma 2	Mus musculus	44-49
24380754-7	2014	N-acetyl cysteine (NAC) inhibitedIK-induced Bcl-2 family-mediated apoptosis.	Acetylcysteine	19-22	B cell leukemia/lymphoma 2	Mus musculus	44-49
24296245-4	2014	Our results demonstrated that pretreatment with NAC increased protein levels of hypoxia-inducible factor-1alpha (HIF-1alpha), the regulatable subunit of HIF-1, and its target proteins erythropoietin (EPO) and glucose transporter (GLUT)-3, in the ipsilateral hemispheres of rodents subjected to 90min middle cerebral artery occlusion (MCAO) and 24h reperfusion.	Acetylcysteine	48-51	hypoxia inducible factor 1 subunit alpha	Homo sapiens	80-111
24296245-4	2014	Our results demonstrated that pretreatment with NAC increased protein levels of hypoxia-inducible factor-1alpha (HIF-1alpha), the regulatable subunit of HIF-1, and its target proteins erythropoietin (EPO) and glucose transporter (GLUT)-3, in the ipsilateral hemispheres of rodents subjected to 90min middle cerebral artery occlusion (MCAO) and 24h reperfusion.	Acetylcysteine	48-51	hypoxia inducible factor 1 subunit alpha	Homo sapiens	113-123
24296245-4	2014	Our results demonstrated that pretreatment with NAC increased protein levels of hypoxia-inducible factor-1alpha (HIF-1alpha), the regulatable subunit of HIF-1, and its target proteins erythropoietin (EPO) and glucose transporter (GLUT)-3, in the ipsilateral hemispheres of rodents subjected to 90min middle cerebral artery occlusion (MCAO) and 24h reperfusion.	Acetylcysteine	48-51	hypoxia inducible factor 1 subunit alpha	Homo sapiens	113-118
24296245-4	2014	Our results demonstrated that pretreatment with NAC increased protein levels of hypoxia-inducible factor-1alpha (HIF-1alpha), the regulatable subunit of HIF-1, and its target proteins erythropoietin (EPO) and glucose transporter (GLUT)-3, in the ipsilateral hemispheres of rodents subjected to 90min middle cerebral artery occlusion (MCAO) and 24h reperfusion.	Acetylcysteine	48-51	erythropoietin	Homo sapiens	184-198
24296245-4	2014	Our results demonstrated that pretreatment with NAC increased protein levels of hypoxia-inducible factor-1alpha (HIF-1alpha), the regulatable subunit of HIF-1, and its target proteins erythropoietin (EPO) and glucose transporter (GLUT)-3, in the ipsilateral hemispheres of rodents subjected to 90min middle cerebral artery occlusion (MCAO) and 24h reperfusion.	Acetylcysteine	48-51	erythropoietin	Homo sapiens	200-203
24296245-6	2014	Suppressing HIF-1 activity with two widely used pharmacological inhibitors, YC-1 and 2ME2, and specific knockout of neuronal HIF-1alpha abolished NAC"s neuroprotective effects.	Acetylcysteine	146-149	hypoxia inducible factor 1 subunit alpha	Homo sapiens	12-17
24296245-6	2014	Suppressing HIF-1 activity with two widely used pharmacological inhibitors, YC-1 and 2ME2, and specific knockout of neuronal HIF-1alpha abolished NAC"s neuroprotective effects.	Acetylcysteine	146-149	hypoxia inducible factor 1 subunit alpha	Homo sapiens	125-135
24296245-8	2014	Furthermore, we determined the mechanism of NAC-mediated HIF-1alpha induction.	Acetylcysteine	44-47	hypoxia inducible factor 1 subunit alpha	Homo sapiens	57-67
24296245-9	2014	We observed that NAC pretreatment upregulated heat-shock protein 90 (Hsp90) expression and increased the interaction of Hsp90 with HIF-1alpha in ischemic brains.	Acetylcysteine	17-20	hypoxia inducible factor 1 subunit alpha	Homo sapiens	131-141
24296245-12	2014	These results strongly indicate that HIF-1 plays an important role in NAC-mediated neuroprotection and provide a new molecular mechanism involved in the antioxidant"s neuroprotection in ischemic stroke.	Acetylcysteine	70-73	hypoxia inducible factor 1 subunit alpha	Homo sapiens	37-42
24355171-9	2014	TQ also generated reactive oxygen species (ROS) and pretreatment with N-acetyl cysteine (NAC) abrogated TQ-induced ROS accumulation, Akt and AMPKalpha activation, Nrf2 nuclear localization, the ARE-luciferase activity, and HO-1 expression in HaCaT cells.	Acetylcysteine	70-87	AKT serine/threonine kinase 1	Homo sapiens	133-136
24355171-9	2014	TQ also generated reactive oxygen species (ROS) and pretreatment with N-acetyl cysteine (NAC) abrogated TQ-induced ROS accumulation, Akt and AMPKalpha activation, Nrf2 nuclear localization, the ARE-luciferase activity, and HO-1 expression in HaCaT cells.	Acetylcysteine	70-87	NFE2 like bZIP transcription factor 2	Homo sapiens	163-167
24355171-9	2014	TQ also generated reactive oxygen species (ROS) and pretreatment with N-acetyl cysteine (NAC) abrogated TQ-induced ROS accumulation, Akt and AMPKalpha activation, Nrf2 nuclear localization, the ARE-luciferase activity, and HO-1 expression in HaCaT cells.	Acetylcysteine	89-92	AKT serine/threonine kinase 1	Homo sapiens	133-136
24355171-9	2014	TQ also generated reactive oxygen species (ROS) and pretreatment with N-acetyl cysteine (NAC) abrogated TQ-induced ROS accumulation, Akt and AMPKalpha activation, Nrf2 nuclear localization, the ARE-luciferase activity, and HO-1 expression in HaCaT cells.	Acetylcysteine	89-92	NFE2 like bZIP transcription factor 2	Homo sapiens	163-167
23640957-7	2014	Furthermore, ROS scavenger N-acetyl L-cysteine attenuated beta-sitosterol-mediated sub-G1 accumulation, PARP cleavage, JNK and AMPK activation in U266 cells.	Acetylcysteine	27-46	mitogen-activated protein kinase 8	Homo sapiens	119-122
24586814-7	2014	Inhibition of ROS production by N-acetyl-cysteine (NAC) partially restored the mitochondrial membrane potential, inhibited ERK activity, elevated caspase-3 activity and PARP cleavage, and, eventually, switched the TCHQ-induced necrosis to apoptosis.	Acetylcysteine	32-49	mitogen-activated protein kinase 1	Homo sapiens	123-126
24586814-7	2014	Inhibition of ROS production by N-acetyl-cysteine (NAC) partially restored the mitochondrial membrane potential, inhibited ERK activity, elevated caspase-3 activity and PARP cleavage, and, eventually, switched the TCHQ-induced necrosis to apoptosis.	Acetylcysteine	32-49	caspase 3	Homo sapiens	146-155
24586814-7	2014	Inhibition of ROS production by N-acetyl-cysteine (NAC) partially restored the mitochondrial membrane potential, inhibited ERK activity, elevated caspase-3 activity and PARP cleavage, and, eventually, switched the TCHQ-induced necrosis to apoptosis.	Acetylcysteine	32-49	poly(ADP-ribose) polymerase 1	Homo sapiens	169-173
24586814-7	2014	Inhibition of ROS production by N-acetyl-cysteine (NAC) partially restored the mitochondrial membrane potential, inhibited ERK activity, elevated caspase-3 activity and PARP cleavage, and, eventually, switched the TCHQ-induced necrosis to apoptosis.	Acetylcysteine	51-54	mitogen-activated protein kinase 1	Homo sapiens	123-126
24586814-7	2014	Inhibition of ROS production by N-acetyl-cysteine (NAC) partially restored the mitochondrial membrane potential, inhibited ERK activity, elevated caspase-3 activity and PARP cleavage, and, eventually, switched the TCHQ-induced necrosis to apoptosis.	Acetylcysteine	51-54	caspase 3	Homo sapiens	146-155
24586814-7	2014	Inhibition of ROS production by N-acetyl-cysteine (NAC) partially restored the mitochondrial membrane potential, inhibited ERK activity, elevated caspase-3 activity and PARP cleavage, and, eventually, switched the TCHQ-induced necrosis to apoptosis.	Acetylcysteine	51-54	poly(ADP-ribose) polymerase 1	Homo sapiens	169-173
24499192-9	2014	Moreover, it was shown that PCN induced oxidative stress in U937 cells and N-acetyl cysteine, an antioxidant, was able to inhibit PCN-induced IL-8 protein expression.	Acetylcysteine	75-92	C-X-C motif chemokine ligand 8	Homo sapiens	142-146
24533448-10	2014	Furthermore, pregestational diabetes increased ROS, impaired cell proliferation, and altered Gata4, Gata5 and Vegf-a expression in the fetal heart of diabetic offspring, which were all prevented by NAC treatment.	Acetylcysteine	198-201	GATA binding protein 4	Mus musculus	93-98
24507776-7	2014	Treatment with the ROS scavenger N-acetyl cysteine attenuated the Irofulven-induced cytotoxicity in ERCC6L2-knockdown cells and abolished ERCCGL2 traffic to the mitochondria and nucleus in response to this DNA-damaging agent.	Acetylcysteine	33-50	ERCC excision repair 6 like 2	Homo sapiens	100-107
24556678-9	2014	Furthermore, thioridazine increased the production of reactive oxygen species (ROS) in Caki cells, and ROS scavengers (N-acetylcysteine, glutathione ethyl ester, and trolox) inhibited thioridazine plus TRAIL-induced apoptosis, as well as Akt inhibition and the downregulation of c-FLIP(L) and Mcl-1.	Acetylcysteine	119-135	TNF superfamily member 10	Homo sapiens	202-207
24239319-7	2014	RESULTS: Although the ALT and AST values in the group administered CCl4 were significantly higher than in all the other groups (P&lt;0.05), there was no significant difference between the control group and the groups administered CCl4 combined with L-carnitine, N-acetylcysteine and genistein (P&gt;0.05).	Acetylcysteine	262-278	C-C motif chemokine ligand 4	Rattus norvegicus	67-71
24370495-4	2014	DOX-induced increases in reactive oxygen species levels and the expression of MDR1 mRNA were inhibited by N-acetylcysteine, an antioxidant, and the DOX-induced increase in reactive oxygen species levels and DOX-induced overexpression of MDR1 mRNA and P-gp were inhibited by UDCA.	Acetylcysteine	106-122	ATP binding cassette subfamily B member 1	Homo sapiens	78-82
24370495-4	2014	DOX-induced increases in reactive oxygen species levels and the expression of MDR1 mRNA were inhibited by N-acetylcysteine, an antioxidant, and the DOX-induced increase in reactive oxygen species levels and DOX-induced overexpression of MDR1 mRNA and P-gp were inhibited by UDCA.	Acetylcysteine	106-122	ATP binding cassette subfamily B member 1	Homo sapiens	237-241
24370495-4	2014	DOX-induced increases in reactive oxygen species levels and the expression of MDR1 mRNA were inhibited by N-acetylcysteine, an antioxidant, and the DOX-induced increase in reactive oxygen species levels and DOX-induced overexpression of MDR1 mRNA and P-gp were inhibited by UDCA.	Acetylcysteine	106-122	ATP binding cassette subfamily B member 1	Homo sapiens	251-255
24504121-3	2014	Here, we have found that long-time N-acetyl-L-cysteine treatment at low-concentration increases phosphorylation of extracellular signal-regulated kinase 1/2 and AKT, which are essential for the induction of proinflammatory cytokines including interleukin 1beta and interleukin 6 in lipopolysaccharide-stimulated RAW264.7 cells.	Acetylcysteine	35-54	thymoma viral proto-oncogene 1	Mus musculus	115-164
24504121-3	2014	Here, we have found that long-time N-acetyl-L-cysteine treatment at low-concentration increases phosphorylation of extracellular signal-regulated kinase 1/2 and AKT, which are essential for the induction of proinflammatory cytokines including interleukin 1beta and interleukin 6 in lipopolysaccharide-stimulated RAW264.7 cells.	Acetylcysteine	35-54	interleukin 1 beta	Mus musculus	243-260
24504121-3	2014	Here, we have found that long-time N-acetyl-L-cysteine treatment at low-concentration increases phosphorylation of extracellular signal-regulated kinase 1/2 and AKT, which are essential for the induction of proinflammatory cytokines including interleukin 1beta and interleukin 6 in lipopolysaccharide-stimulated RAW264.7 cells.	Acetylcysteine	35-54	interleukin 6	Mus musculus	265-278
24239319-10	2014	CONCLUSIONS: In our study, L-carnitine, N-acetylcysteine and genistein showed significant protective effects in liver fibrosis induced by CCl4.	Acetylcysteine	40-56	C-C motif chemokine ligand 4	Rattus norvegicus	138-142
24378401-5	2014	Rotundarpene, Akt inhibitor, Bay 11-7085 and N-acetylcysteine each attenuated the lipoteichoic acid- or peptidoglycan-induced production of cytokines and chemokines, expression of TLR-2, activation of NF-kappaB and Akt, and formation of reactive oxygen species in keratinocytes.	Acetylcysteine	45-61	toll like receptor 2	Homo sapiens	180-185
24378401-5	2014	Rotundarpene, Akt inhibitor, Bay 11-7085 and N-acetylcysteine each attenuated the lipoteichoic acid- or peptidoglycan-induced production of cytokines and chemokines, expression of TLR-2, activation of NF-kappaB and Akt, and formation of reactive oxygen species in keratinocytes.	Acetylcysteine	45-61	AKT serine/threonine kinase 1	Homo sapiens	215-218
24477002-9	2014	Because somatic mutations in p53 occur late in tumor progression, antioxidants may accelerate the growth of early tumors or precancerous lesions in high-risk populations such as smokers and patients with chronic obstructive pulmonary disease who receive NAC to relieve mucus production.	Acetylcysteine	254-257	tumor protein p53	Homo sapiens	29-32
24486459-5	2014	Notably, NAC and GSH abolished the LPS-induced expression of iNOS and Cox-2 in BV2 microglial cells by inhibiting NF-kappaB activity.	Acetylcysteine	9-12	nitric oxide synthase 2, inducible	Mus musculus	61-65
24486459-5	2014	Notably, NAC and GSH abolished the LPS-induced expression of iNOS and Cox-2 in BV2 microglial cells by inhibiting NF-kappaB activity.	Acetylcysteine	9-12	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	114-123
24481965-7	2014	Both hypoxia and exogenously added AngII or Dp44mT under normoxia stimulated UII expression, whereas AngII receptor blockers, JNK inhibitors (SP600125), JNK siRNA, or N-acetyl-l-cysteine (NAC) suppressed UII expression.	Acetylcysteine	188-191	angiotensinogen	Rattus norvegicus	35-40
24239896-6	2014	In addition, the CM-mediated induction of HO-1 and activation of Nrf2 was abolished by acetylcysteine.	Acetylcysteine	87-101	NFE2 like bZIP transcription factor 2	Homo sapiens	65-69
24489685-7	2014	Pretreatment of AGS cells with N-acetylcysteine or dithiothreitol attenuated DATS-induced nuclear localization of Nrf2 and the expression of HO-1 and NQO1.	Acetylcysteine	31-47	nuclear factor, erythroid derived 2, like 2	Mus musculus	114-118
24489685-7	2014	Pretreatment of AGS cells with N-acetylcysteine or dithiothreitol attenuated DATS-induced nuclear localization of Nrf2 and the expression of HO-1 and NQO1.	Acetylcysteine	31-47	heme oxygenase 1	Mus musculus	141-145
24239970-9	2014	Pretreatment with the antioxidant NAC (2mM) prevented DEX-induced decrease in Cbfa1 mRNA.	Acetylcysteine	34-37	RUNX family transcription factor 2	Homo sapiens	78-83
24157283-9	2014	Additionally, exposure of Neuro-2a cells to iAs triggered endoplasmic reticulum (ER) stress identified through several key molecules (GRP 78, CHOP, XBP-1, and caspase-12), which was prevented by NAC.	Acetylcysteine	195-198	heat shock protein 5	Mus musculus	134-140
24161787-7	2014	Moreover, the andrographolide-induced Hsp90 cleavage, Src degradation, inhibition of transformation, and induction of apoptosis were abolished by a ROS inhibitor, N-acetyl-cysteine.	Acetylcysteine	163-180	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	54-57
24157283-9	2014	Additionally, exposure of Neuro-2a cells to iAs triggered endoplasmic reticulum (ER) stress identified through several key molecules (GRP 78, CHOP, XBP-1, and caspase-12), which was prevented by NAC.	Acetylcysteine	195-198	X-box binding protein 1	Mus musculus	148-153
23880890-12	2014	RESULTS: Leuprolide acetate, amifostine and NAC caused significant decreases in the mean implant areas and significant decreases in serum and peritoneal TNF-alpha levels.	Acetylcysteine	44-47	tumor necrosis factor	Rattus norvegicus	153-162
24476312-7	2014	CeKD-induced cell apoptosis and ROS generation, as well as JNK activation, were inhibited by the antioxidant N-acetyl-L-cysteine.	Acetylcysteine	109-128	mitogen-activated protein kinase 8	Homo sapiens	59-62
24449779-9	2014	Treatment with either SIL or N-acetylcysteine reduced both proliferation of fibroblast cell lines and basal/IL-13-induced production of collagen I, indicating that besides inhibiting IL-13 production during infection, SIL antioxidant properties most likely contribute to inhibition of collagen production downstream of IL-13.	Acetylcysteine	29-45	interleukin 13	Mus musculus	108-113
24449779-9	2014	Treatment with either SIL or N-acetylcysteine reduced both proliferation of fibroblast cell lines and basal/IL-13-induced production of collagen I, indicating that besides inhibiting IL-13 production during infection, SIL antioxidant properties most likely contribute to inhibition of collagen production downstream of IL-13.	Acetylcysteine	29-45	interleukin 13	Mus musculus	183-188
24449779-9	2014	Treatment with either SIL or N-acetylcysteine reduced both proliferation of fibroblast cell lines and basal/IL-13-induced production of collagen I, indicating that besides inhibiting IL-13 production during infection, SIL antioxidant properties most likely contribute to inhibition of collagen production downstream of IL-13.	Acetylcysteine	29-45	interleukin 13	Mus musculus	183-188
23985782-2	2014	In particular, compounds that increase expression of the astroglial glutamate transporter GLT-1 (N-acetylcysteine and ceftriaxone) can decrease measures of drug seeking.	Acetylcysteine	97-113	solute carrier family 1 member 2	Rattus norvegicus	90-95
24307203-8	2014	In addition, NAC suppressed NiNP-induced caspase-3 activity.	Acetylcysteine	13-16	caspase 3	Homo sapiens	41-50
24738081-6	2014	LQ-mediated cell viability reduction, mitochondrial dysfunction, apoptosis related protein abnormal expressions, and JNK and P38 activation were partially abolished by N-Acetyl-L-cysteine (a ROS inhibitor) pretreatment.	Acetylcysteine	168-187	mitogen-activated protein kinase 8	Homo sapiens	117-120
24738081-6	2014	LQ-mediated cell viability reduction, mitochondrial dysfunction, apoptosis related protein abnormal expressions, and JNK and P38 activation were partially abolished by N-Acetyl-L-cysteine (a ROS inhibitor) pretreatment.	Acetylcysteine	168-187	mitogen-activated protein kinase 14	Homo sapiens	125-128
24114663-7	2014	ROS inhibitor (N-acetyl cysteine, NAC) significantly inhibited pro-inflammatory cytokines release and NF-kappaB and MAPKs activation, indicating that ISO attenuated neuroinflammation by inhibiting the ROS-related MAPK/NF-kappaB signaling pathway.	Acetylcysteine	15-32	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	102-111
24114663-7	2014	ROS inhibitor (N-acetyl cysteine, NAC) significantly inhibited pro-inflammatory cytokines release and NF-kappaB and MAPKs activation, indicating that ISO attenuated neuroinflammation by inhibiting the ROS-related MAPK/NF-kappaB signaling pathway.	Acetylcysteine	15-32	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	218-227
24211992-5	2014	The LCA-induced ROS production is inhibited by the co-treatment of LCA and free radical scavenger N-acetyl-cysteine (NAC), on the contrary, the proliferation rate and ROS production increase when treated by the combination of LCA and L-buthionine-(S,R)-sulfoximine (BSO).	Acetylcysteine	98-115	clathrin light chain A	Homo sapiens	4-7
24211992-5	2014	The LCA-induced ROS production is inhibited by the co-treatment of LCA and free radical scavenger N-acetyl-cysteine (NAC), on the contrary, the proliferation rate and ROS production increase when treated by the combination of LCA and L-buthionine-(S,R)-sulfoximine (BSO).	Acetylcysteine	117-120	clathrin light chain A	Homo sapiens	4-7
24211992-5	2014	The LCA-induced ROS production is inhibited by the co-treatment of LCA and free radical scavenger N-acetyl-cysteine (NAC), on the contrary, the proliferation rate and ROS production increase when treated by the combination of LCA and L-buthionine-(S,R)-sulfoximine (BSO).	Acetylcysteine	117-120	clathrin light chain A	Homo sapiens	67-70
24211992-5	2014	The LCA-induced ROS production is inhibited by the co-treatment of LCA and free radical scavenger N-acetyl-cysteine (NAC), on the contrary, the proliferation rate and ROS production increase when treated by the combination of LCA and L-buthionine-(S,R)-sulfoximine (BSO).	Acetylcysteine	117-120	clathrin light chain A	Homo sapiens	67-70
24552822-6	2014	Intriguingly, copper-dependent inhibition of NFkappaB can be reversed by the addition of the reducing agent, N-acetylcysteine (NAC).	Acetylcysteine	109-125	nuclear factor kappa B subunit 1	Homo sapiens	45-53
24552822-6	2014	Intriguingly, copper-dependent inhibition of NFkappaB can be reversed by the addition of the reducing agent, N-acetylcysteine (NAC).	Acetylcysteine	127-130	nuclear factor kappa B subunit 1	Homo sapiens	45-53
24211866-6	2014	In addition, OLO-2 provokes the generation of reactive oxygen species (ROS) in HepG2 cells, while the antioxidant N-acetyl cysteine (NAC) almost completely blocks OLO-2-induced apoptosis and the activation of p38 and JNK.	Acetylcysteine	114-131	mitogen-activated protein kinase 14	Homo sapiens	209-212
24211866-6	2014	In addition, OLO-2 provokes the generation of reactive oxygen species (ROS) in HepG2 cells, while the antioxidant N-acetyl cysteine (NAC) almost completely blocks OLO-2-induced apoptosis and the activation of p38 and JNK.	Acetylcysteine	114-131	mitogen-activated protein kinase 8	Homo sapiens	217-220
24211866-6	2014	In addition, OLO-2 provokes the generation of reactive oxygen species (ROS) in HepG2 cells, while the antioxidant N-acetyl cysteine (NAC) almost completely blocks OLO-2-induced apoptosis and the activation of p38 and JNK.	Acetylcysteine	133-136	mitogen-activated protein kinase 14	Homo sapiens	209-212
24211866-6	2014	In addition, OLO-2 provokes the generation of reactive oxygen species (ROS) in HepG2 cells, while the antioxidant N-acetyl cysteine (NAC) almost completely blocks OLO-2-induced apoptosis and the activation of p38 and JNK.	Acetylcysteine	133-136	mitogen-activated protein kinase 8	Homo sapiens	217-220
24872935-7	2014	Hepatic superoxide dismutase (SOD), catalase, and glutathione levels were significantly decreased as a result of I/R injury, but they were increased in groups treated with NAC.	Acetylcysteine	172-175	catalase	Rattus norvegicus	36-44
24876842-5	2014	Among the 91 PCOS patients treated with NAC + Inositol + folic, insulin resistance was present in 44 subjects (A) and absent in 47 (B).	Acetylcysteine	40-43	insulin	Homo sapiens	64-71
24693334-3	2014	Biochemical analysis demonstrated that the NAC treatment also antagonized hyperphosphorylation of cardiac ryanodine receptors (RyR2) and significantly restored depleted protein levels of both RyR2 and calstabin2.	Acetylcysteine	43-46	FKBP prolyl isomerase 1B	Rattus norvegicus	201-211
25402962-8	2014	To examine the role of oxidative stress in regulating GRP78 and CHOP expression, RPE cells were pretreated with the antioxidant N-acetylcysteine (NAC) for 2 h. RNA interference of GRP78 performed by short hairpin RNA was used to evaluate the effect of GRP78 in blue light-mediated damage of RPE cells.	Acetylcysteine	128-144	heat shock protein family A (Hsp70) member 5	Homo sapiens	180-185
25402962-8	2014	To examine the role of oxidative stress in regulating GRP78 and CHOP expression, RPE cells were pretreated with the antioxidant N-acetylcysteine (NAC) for 2 h. RNA interference of GRP78 performed by short hairpin RNA was used to evaluate the effect of GRP78 in blue light-mediated damage of RPE cells.	Acetylcysteine	128-144	heat shock protein family A (Hsp70) member 5	Homo sapiens	180-185
25402962-11	2014	Pretreatment with NAC attenuated the expression of 2 ER stress markers, especially CHOP in A2E and blue light-treated RPE cells.	Acetylcysteine	18-21	DNA damage inducible transcript 3	Homo sapiens	83-87
23718729-4	2013	TXNIP-knockout mice (TKO) or wild-type (WT) treated with the reduced glutathione (GSH)-precursor, N-acetyl cysteine (WT-NAC, 500 mg/kg) were compared to WT using hypoxia-induced neovascularization model.	Acetylcysteine	98-115	thioredoxin interacting protein	Mus musculus	0-5
25669694-8	2014	Moreover, NAC suppressed IL-8 and IL-beta formation and thus seems to be favorable agent for improving surfactant therapy in MAS.	Acetylcysteine	10-13	interleukin-8	Oryctolagus cuniculus	25-29
24434384-0	2014	The effect of treatment with N-acetylcysteine on the serum levels of C-reactive protein and interleukin-6 in patients on hemodialysis.	Acetylcysteine	29-45	C-reactive protein	Homo sapiens	69-87
24434384-0	2014	The effect of treatment with N-acetylcysteine on the serum levels of C-reactive protein and interleukin-6 in patients on hemodialysis.	Acetylcysteine	29-45	interleukin 6	Homo sapiens	92-105
24434384-3	2014	We aimed to assess the effect of three months treatment with oral NAC on the plasma levels of inflammatory mediators like interleukin-6 (IL-6) and C-reactive protein (hs-CRP) in patients on hemodialysis (HD).	Acetylcysteine	66-69	interleukin 6	Homo sapiens	122-135
24434384-3	2014	We aimed to assess the effect of three months treatment with oral NAC on the plasma levels of inflammatory mediators like interleukin-6 (IL-6) and C-reactive protein (hs-CRP) in patients on hemodialysis (HD).	Acetylcysteine	66-69	interleukin 6	Homo sapiens	137-141
24434384-3	2014	We aimed to assess the effect of three months treatment with oral NAC on the plasma levels of inflammatory mediators like interleukin-6 (IL-6) and C-reactive protein (hs-CRP) in patients on hemodialysis (HD).	Acetylcysteine	66-69	C-reactive protein	Homo sapiens	147-165
24434384-10	2014	In three subjects who were less than 40 years old, the hs-CRP and IL-6 levels showed an increase following NAC treatment.	Acetylcysteine	107-110	interleukin 6	Homo sapiens	66-70
24434384-11	2014	Our study found that short-term oral NAC treatment might result in the reduction of IL-6 and hs-CRP in patients who are on regular HD.	Acetylcysteine	37-40	interleukin 6	Homo sapiens	84-88
24988605-8	2014	Inhibitors of CXCL8 (such as N-acetyl-L-cysteine) cause a decrease of exacerbation frequency and clinical symptoms.	Acetylcysteine	29-48	C-X-C motif chemokine ligand 8	Homo sapiens	14-19
23726389-8	2013	It also inhibited Fas, caspase-3, caspase-8 and integrin alphavbeta6 (alphavbeta6) gene expressions in the NAC-treated piglets.	Acetylcysteine	107-110	caspase 3	Homo sapiens	23-32
24211779-8	2013	Disruption of EAJ and phosphorylation of VE-cadherin induced by interaction of MDA-MB-231 cells with HUVECs were attenuated when HUVECs were pretreated with an antioxidant, N-acetylcysteine (NAC) or AHCC.	Acetylcysteine	173-189	cadherin 5	Homo sapiens	41-52
24211779-8	2013	Disruption of EAJ and phosphorylation of VE-cadherin induced by interaction of MDA-MB-231 cells with HUVECs were attenuated when HUVECs were pretreated with an antioxidant, N-acetylcysteine (NAC) or AHCC.	Acetylcysteine	191-194	cadherin 5	Homo sapiens	41-52
24099794-1	2013	The successful clinical management of lung cancer is limited by frequent loss-of-function mutations in p53 which cooperates with chronic oxidant-stress induced adaptations in mercapturic acid pathway (MAP) which in turn regulates critical intracellular signaling cascades that determine therapeutic refractoriness.	Acetylcysteine	175-191	tumor protein p53	Homo sapiens	103-106
24126683-4	2013	The present study shows that PN promoted the phosphorylation of EGF receptor (phospho-EGFR) at Tyr1173, an event which was observed already at 1 h of incubation with 25 microM PN and reached a peak at 8-16 h. This effect seemed to be a consequence of ROS production, because N-acetylcysteine (NAC), a powerful ROS scavenger, prevented the increment of phospho-EGFR levels.	Acetylcysteine	275-291	epidermal growth factor receptor	Homo sapiens	86-90
24128853-9	2013	NAC treatment prevented the activation of p38 MAP kinase and rescued the survivin protein levels.	Acetylcysteine	0-3	mitogen-activated protein kinase 14	Homo sapiens	42-45
24126683-4	2013	The present study shows that PN promoted the phosphorylation of EGF receptor (phospho-EGFR) at Tyr1173, an event which was observed already at 1 h of incubation with 25 microM PN and reached a peak at 8-16 h. This effect seemed to be a consequence of ROS production, because N-acetylcysteine (NAC), a powerful ROS scavenger, prevented the increment of phospho-EGFR levels.	Acetylcysteine	293-296	epidermal growth factor receptor	Homo sapiens	86-90
24001789-10	2013	Antioxidative N-acetyl-cysteine (NAC) strongly inhibited the level of Egr-1 and phosphorylated ERK expression in ZnO-NPs treated cells.	Acetylcysteine	14-31	mitogen-activated protein kinase 1	Homo sapiens	95-98
23792775-4	2013	Here, we examined mechanisms of chemoprotection by NAC against Cd(II), Co(II), and Cr(VI) in human cells.	Acetylcysteine	51-54	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	71-76
23792775-5	2013	We found that NAC displayed a broad-spectrum chemoprotective activity against all three metals, including suppression of cytotoxicity, apoptosis, p53 activation, and HSP72 and HIF-1alpha upregulation.	Acetylcysteine	14-17	tumor protein p53	Homo sapiens	146-149
23792775-5	2013	We found that NAC displayed a broad-spectrum chemoprotective activity against all three metals, including suppression of cytotoxicity, apoptosis, p53 activation, and HSP72 and HIF-1alpha upregulation.	Acetylcysteine	14-17	heat shock protein family A (Hsp70) member 1A	Homo sapiens	166-171
23792775-5	2013	We found that NAC displayed a broad-spectrum chemoprotective activity against all three metals, including suppression of cytotoxicity, apoptosis, p53 activation, and HSP72 and HIF-1alpha upregulation.	Acetylcysteine	14-17	hypoxia inducible factor 1 subunit alpha	Homo sapiens	176-186
23792775-9	2013	Suppression of Co(II) uptake resulted from a rapid formation of Co(II)-NAC conjugates that were unable to enter cells.	Acetylcysteine	71-74	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	15-21
23792775-9	2013	Suppression of Co(II) uptake resulted from a rapid formation of Co(II)-NAC conjugates that were unable to enter cells.	Acetylcysteine	71-74	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	64-70
24001789-10	2013	Antioxidative N-acetyl-cysteine (NAC) strongly inhibited the level of Egr-1 and phosphorylated ERK expression in ZnO-NPs treated cells.	Acetylcysteine	33-36	mitogen-activated protein kinase 1	Homo sapiens	95-98
23792775-11	2013	Good clinical safety and effectiveness in Co(II) sequestration suggest that NAC could be useful in the prevention of tissue accumulation and toxic effects of Co ions released by cobalt-chromium hip prostheses.	Acetylcysteine	76-79	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	42-48
24025361-10	2013	BBMD3 increased the production of reactive oxygen species (ROS) and ROS scavenger, N-acetylcysteine (NAC), could block the phosphorylation of JNK and c-Jun induced by BBMD3.	Acetylcysteine	83-99	mitogen-activated protein kinase 8	Homo sapiens	142-145
24121502-3	2013	Pretreatment with the antioxidant N-acetyl-L-cysteine prevented ouabain-stimulated Na/K-ATPase c-Src signaling, protein carbonylation, redistribution of Na/K-ATPase and sodium/proton exchanger isoform 3, and inhibition of active transepithelial (22)Na(+) transport.	Acetylcysteine	34-53	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	95-100
24041743-5	2013	Interestingly, pretreatment of AML cell lines and primary AML cells with N-acetylcysteine or glutathione rescues them from apoptosis (and concomitant PARP cleavage) and Akt hypophosphorylation, implicating a key role of reactive oxygen species (ROS) in OSU-A9-related cytotoxicity.	Acetylcysteine	73-89	poly(ADP-ribose) polymerase 1	Homo sapiens	150-154
24041743-5	2013	Interestingly, pretreatment of AML cell lines and primary AML cells with N-acetylcysteine or glutathione rescues them from apoptosis (and concomitant PARP cleavage) and Akt hypophosphorylation, implicating a key role of reactive oxygen species (ROS) in OSU-A9-related cytotoxicity.	Acetylcysteine	73-89	AKT serine/threonine kinase 1	Homo sapiens	169-172
24877026-7	2013	ROS plays a role in down-regulation of Bcl-2, since treatment with PM in the presence of various ROS modulators, e.g., n-acetylcysteine (NAC), a general purpose antioxidant; diphenylene iodonium (DPI), a NADPH inhibitor; rotenone (ROT), a mitochondrial electron transport chain interrupter rotenone or MnTBAP, a O2 scavenger, attenuated the down-regulation of Bcl-2.	Acetylcysteine	119-135	BCL2 apoptosis regulator	Homo sapiens	39-44
24877026-7	2013	ROS plays a role in down-regulation of Bcl-2, since treatment with PM in the presence of various ROS modulators, e.g., n-acetylcysteine (NAC), a general purpose antioxidant; diphenylene iodonium (DPI), a NADPH inhibitor; rotenone (ROT), a mitochondrial electron transport chain interrupter rotenone or MnTBAP, a O2 scavenger, attenuated the down-regulation of Bcl-2.	Acetylcysteine	137-140	BCL2 apoptosis regulator	Homo sapiens	39-44
24877026-7	2013	ROS plays a role in down-regulation of Bcl-2, since treatment with PM in the presence of various ROS modulators, e.g., n-acetylcysteine (NAC), a general purpose antioxidant; diphenylene iodonium (DPI), a NADPH inhibitor; rotenone (ROT), a mitochondrial electron transport chain interrupter rotenone or MnTBAP, a O2 scavenger, attenuated the down-regulation of Bcl-2.	Acetylcysteine	137-140	BCL2 apoptosis regulator	Homo sapiens	360-365
23992566-8	2013	Following the ERalpha degradation, reactive oxygen species (ROS) was produced in the SNIPER(ER)-treated MCF-7 cells, and an anti-oxidant N-acetylcysteine inhibited the necrotic cell death.	Acetylcysteine	137-153	estrogen receptor 1	Homo sapiens	14-21
23975535-10	2013	NAC protected against MDMA-induced cell death and the up -regulation of Bax and Caspase-3, in addition to the down-regulation of Bcl-2.	Acetylcysteine	0-3	BCL2, apoptosis regulator	Rattus norvegicus	129-134
24142350-6	2013	Similarly to ZNS effects, the treatment with N-acetyl-cysteine (100 muM) displayed significant protective effects against rotenone-induced ROS production and Deltapsim at 4 and 12 h respectively, reaching the maximal extent at 24 h. Additionally, ZNS displayed antiapoptotic effects, as demonstrated by flow cytometric analysis of annexin V/propidium iodide double staining, and significant attenuated rotenone-increased caspase 3 activity.	Acetylcysteine	45-62	latexin	Homo sapiens	68-71
24142350-6	2013	Similarly to ZNS effects, the treatment with N-acetyl-cysteine (100 muM) displayed significant protective effects against rotenone-induced ROS production and Deltapsim at 4 and 12 h respectively, reaching the maximal extent at 24 h. Additionally, ZNS displayed antiapoptotic effects, as demonstrated by flow cytometric analysis of annexin V/propidium iodide double staining, and significant attenuated rotenone-increased caspase 3 activity.	Acetylcysteine	45-62	caspase 3	Homo sapiens	421-430
24244749-7	2013	Acetaldehyde, a metabolic product of alcohol dehydrogenase, induced significant cell death, depolarization of MMP, and caspase-3 activation as ethanol and this damage was also averted by NAC.	Acetylcysteine	187-190	caspase 3	Homo sapiens	119-128
24134840-5	2013	c-Jun N-terminal protein kinase (JNK) activation by curcumin was dependent on MST1, since MST1 inhibition by RNAi or NAC largely inhibited curcumin-induced JNK activation.	Acetylcysteine	117-120	mitogen-activated protein kinase 8	Homo sapiens	0-31
24134840-5	2013	c-Jun N-terminal protein kinase (JNK) activation by curcumin was dependent on MST1, since MST1 inhibition by RNAi or NAC largely inhibited curcumin-induced JNK activation.	Acetylcysteine	117-120	mitogen-activated protein kinase 8	Homo sapiens	33-36
24134840-5	2013	c-Jun N-terminal protein kinase (JNK) activation by curcumin was dependent on MST1, since MST1 inhibition by RNAi or NAC largely inhibited curcumin-induced JNK activation.	Acetylcysteine	117-120	mitogen-activated protein kinase 8	Homo sapiens	156-159
24025361-10	2013	BBMD3 increased the production of reactive oxygen species (ROS) and ROS scavenger, N-acetylcysteine (NAC), could block the phosphorylation of JNK and c-Jun induced by BBMD3.	Acetylcysteine	101-104	mitogen-activated protein kinase 8	Homo sapiens	142-145
23609920-9	2013	N-acetyl- L-cysteine (NAC), NG-nitro-L-arginine methyl ester (L-NAME) and pyrrolidine dithiocarbamate (PDTC), partially rescued apoptotic beta-cells, suggesting involvement of NF-kappaB-iNOS-nitrite in this process.	Acetylcysteine	0-20	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	176-185
24184570-7	2013	The addition of N-acetyl cysteine (NAC, a well-known antioxidant) could effectively attenuate the GS-2-induced ROS enhancement and subsequent apoptosis.	Acetylcysteine	16-33	patatin like phospholipase domain containing 4	Homo sapiens	98-102
24184570-7	2013	The addition of N-acetyl cysteine (NAC, a well-known antioxidant) could effectively attenuate the GS-2-induced ROS enhancement and subsequent apoptosis.	Acetylcysteine	35-38	patatin like phospholipase domain containing 4	Homo sapiens	98-102
24184570-8	2013	NAC attenuated the induced inhibition on expression of topos, indicating that topos might be the target of GS-2-induced ROS.	Acetylcysteine	0-3	patatin like phospholipase domain containing 4	Homo sapiens	107-111
24008345-7	2013	NAC, but not SPL, suppressed oxidative stress in MIN6 cells, as revealed by the decrease in inducible NOS levels and expression of the proteins p22-phox and p67-phox.	Acetylcysteine	0-3	dynein cytoplasmic 1 heavy chain 1	Mus musculus	144-147
23786532-7	2013	The intracellular reactive oxygen species (ROS) was significantly enhanced by SDT, and pre-treatment with ROS scavenger N-acetylcysteine (NAC) partially alleviated SDT-induced cell viability loss, DNA fragmentation, mitochondria membrane potential (MMP) dissipation, caspase-3 activation, but interestingly MAPK activation was not affected much by NAC.	Acetylcysteine	120-136	caspase 3	Homo sapiens	267-276
23786532-7	2013	The intracellular reactive oxygen species (ROS) was significantly enhanced by SDT, and pre-treatment with ROS scavenger N-acetylcysteine (NAC) partially alleviated SDT-induced cell viability loss, DNA fragmentation, mitochondria membrane potential (MMP) dissipation, caspase-3 activation, but interestingly MAPK activation was not affected much by NAC.	Acetylcysteine	138-141	caspase 3	Homo sapiens	267-276
23757055-6	2013	In contrast, NAC and a PI3K inhibitor, LY-294002, reversed the down-regulation of osteogenic markers and the up-regulation of adipogenic markers as well as the activation of Akt under high glucose.	Acetylcysteine	13-16	AKT serine/threonine kinase 1	Rattus norvegicus	174-177
23609920-9	2013	N-acetyl- L-cysteine (NAC), NG-nitro-L-arginine methyl ester (L-NAME) and pyrrolidine dithiocarbamate (PDTC), partially rescued apoptotic beta-cells, suggesting involvement of NF-kappaB-iNOS-nitrite in this process.	Acetylcysteine	0-20	nitric oxide synthase 2, inducible	Mus musculus	186-190
25610275-10	2013	Erdosteine and NAC significantly reduced the local induction of bax and caspase 3 and significantly increased the reduced local production of bcl-2.	Acetylcysteine	15-18	BCL2, apoptosis regulator	Rattus norvegicus	142-147
23948373-4	2013	We compared the insulin activation of PI3K-Akt (glucose uptake) and ERK-MAPK (pro-inflammation) signaling pathways, intracellular and mitochondrial oxidative stress (DCF and MitoSOX Red), and their responses to the antioxidant N-acetylcysteine (NAC).	Acetylcysteine	227-243	insulin	Homo sapiens	16-23
23948373-4	2013	We compared the insulin activation of PI3K-Akt (glucose uptake) and ERK-MAPK (pro-inflammation) signaling pathways, intracellular and mitochondrial oxidative stress (DCF and MitoSOX Red), and their responses to the antioxidant N-acetylcysteine (NAC).	Acetylcysteine	245-248	insulin	Homo sapiens	16-23
23948373-8	2013	Following treatment with the antioxidant NAC, cybrid B4 cells showed significantly reduced insulin-induced phosphorylation of P38 and increased GLUT1/GLUT4 translocation to the cell membrane, suggesting that NAC may divert insulin signaling from pro-inflammation to glucose uptake.	Acetylcysteine	41-44	insulin	Homo sapiens	91-98
23948373-8	2013	Following treatment with the antioxidant NAC, cybrid B4 cells showed significantly reduced insulin-induced phosphorylation of P38 and increased GLUT1/GLUT4 translocation to the cell membrane, suggesting that NAC may divert insulin signaling from pro-inflammation to glucose uptake.	Acetylcysteine	41-44	insulin	Homo sapiens	223-230
23948373-8	2013	Following treatment with the antioxidant NAC, cybrid B4 cells showed significantly reduced insulin-induced phosphorylation of P38 and increased GLUT1/GLUT4 translocation to the cell membrane, suggesting that NAC may divert insulin signaling from pro-inflammation to glucose uptake.	Acetylcysteine	208-211	insulin	Homo sapiens	91-98
23948373-8	2013	Following treatment with the antioxidant NAC, cybrid B4 cells showed significantly reduced insulin-induced phosphorylation of P38 and increased GLUT1/GLUT4 translocation to the cell membrane, suggesting that NAC may divert insulin signaling from pro-inflammation to glucose uptake.	Acetylcysteine	208-211	insulin	Homo sapiens	223-230
24020587-8	2013	In addition, SAL induced cell proliferation in estrogen receptor (ER)-negative MCF-10A cells, and the proliferation was inhibited by an antioxidant N-acetylcysteine and an epidermal growth factor receptor (EGFR) inhibitor AG1478, suggesting that reactive oxygen species may participate in the proliferation of MCF-10A cells via EGFR activation.	Acetylcysteine	148-164	epidermal growth factor receptor	Homo sapiens	328-332
23297002-6	2013	Moreover, treatment of RASMCs with EuTL increased reactive oxygen species (ROS) accumulation and nuclear translocation of nuclear factor-E2-related factor 2 (Nrf2); however, this translocation was also inhibited by NAC.	Acetylcysteine	215-218	NFE2 like bZIP transcription factor 2	Rattus norvegicus	158-162
23747931-0	2013	N-Acetylcysteine and allopurinol up-regulated the Jak/STAT3 and PI3K/Akt pathways via adiponectin and attenuated myocardial postischemic injury in diabetes.	Acetylcysteine	0-16	AKT serine/threonine kinase 1	Rattus norvegicus	69-72
23747931-3	2013	We postulated that NAC and ALP attenuated diabetic MI/R injury by up-regulating phosphatidylinositol 3-kinase/Akt (PI3K/Akt) and Janus kinase 2/signal transducer and activator of transcription-3 (JAK2/STAT3) pathways subsequent to adiponectin (APN) activation.	Acetylcysteine	19-22	AKT serine/threonine kinase 1	Rattus norvegicus	110-113
23747931-6	2013	NAC and ALP decreased MI/R injury in D rats, enhanced phosphorylation of Akt and STAT3, and increased NO and APN.	Acetylcysteine	0-3	AKT serine/threonine kinase 1	Rattus norvegicus	73-76
23747931-7	2013	High glucose and hypoxia/reoxygenation exposure induced cell death and Akt and STAT3 inactivation in cultured cardiomyocytes, which were prevented by NAC and ALP.	Acetylcysteine	150-153	AKT serine/threonine kinase 1	Rattus norvegicus	71-74
23747931-11	2013	In conclusion, NAC and ALP prevented diabetic MI/R injury through PI3K/Akt and Jak2/STAT3 and cardiac APN may serve as a mediator via AdipoR2 in this process.	Acetylcysteine	15-18	AKT serine/threonine kinase 1	Rattus norvegicus	71-74
22989604-9	2013	Reduced superoxide levels and DCF in the exer+NAC group were associated with decreased Akt, AMPK and eNOS phosphorylation.	Acetylcysteine	46-49	AKT serine/threonine kinase 1	Rattus norvegicus	87-90
23925941-11	2013	NAC and NAC + HBOT groups had significant decreases in hepatic neopterin, TNF-alpha, and IL-6 levels compared with the APAP group.	Acetylcysteine	0-3	tumor necrosis factor	Rattus norvegicus	74-83
23925941-11	2013	NAC and NAC + HBOT groups had significant decreases in hepatic neopterin, TNF-alpha, and IL-6 levels compared with the APAP group.	Acetylcysteine	0-3	interleukin 6	Rattus norvegicus	89-93
23925941-11	2013	NAC and NAC + HBOT groups had significant decreases in hepatic neopterin, TNF-alpha, and IL-6 levels compared with the APAP group.	Acetylcysteine	8-11	tumor necrosis factor	Rattus norvegicus	74-83
23925941-11	2013	NAC and NAC + HBOT groups had significant decreases in hepatic neopterin, TNF-alpha, and IL-6 levels compared with the APAP group.	Acetylcysteine	8-11	interleukin 6	Rattus norvegicus	89-93
24273890-9	2013	Prior treatment with the antioxidant, N-acetylcysteine, partly blocked the apoptosis and expression of caspase-3 induced by the drug combination; apoptosis and expression of caspase-3 were also reversed by inhibitors of JNK or p38.	Acetylcysteine	38-54	caspase 3	Homo sapiens	103-112
24273890-9	2013	Prior treatment with the antioxidant, N-acetylcysteine, partly blocked the apoptosis and expression of caspase-3 induced by the drug combination; apoptosis and expression of caspase-3 were also reversed by inhibitors of JNK or p38.	Acetylcysteine	38-54	caspase 3	Homo sapiens	174-183
24273890-9	2013	Prior treatment with the antioxidant, N-acetylcysteine, partly blocked the apoptosis and expression of caspase-3 induced by the drug combination; apoptosis and expression of caspase-3 were also reversed by inhibitors of JNK or p38.	Acetylcysteine	38-54	mitogen-activated protein kinase 1	Homo sapiens	227-230
24397138-14	2013	CONCLUSION: NAC can relieve ischemia reperfusion injury in rats" heart transplantation by improving myocardial SOD content, and reducing active Caspase-3 activity and AI, which has a protective effect on myocardial cell of donor heart.	Acetylcysteine	12-15	superoxide dismutase 1	Homo sapiens	111-114
23433299-5	2013	Indeed, pretreatment with N-acetyl cysteine, a ROS scavenger, reversed GSE-induced apoptosis, and promoted ERK phosphorylation.	Acetylcysteine	26-43	mitogen-activated protein kinase 1	Homo sapiens	107-110
22989604-9	2013	Reduced superoxide levels and DCF in the exer+NAC group were associated with decreased Akt, AMPK and eNOS phosphorylation.	Acetylcysteine	46-49	protein kinase AMP-activated catalytic subunit alpha 2	Rattus norvegicus	92-96
22532030-10	2013	NAC supplementation enhanced plasma EGF concentration and intestinal EGFR mRNA levels.	Acetylcysteine	0-3	epidermal growth factor receptor	Homo sapiens	69-73
23766377-8	2013	Furthermore, AGEs decreased messenger RNA (mRNA) level of dimethylarginine dimethylaminohydrolase (DDAH)-II, an enzyme for ADMA degradation, reduced its total enzymatic activity and resultantly increased ADMA, all of which were completely blocked by an antioxidant, N-acetylcysteine.	Acetylcysteine	266-282	dimethylarginine dimethylaminohydrolase 2	Homo sapiens	58-107
24064061-4	2013	We confirmed that TGF-beta1 secretion is increased by androgen treatment in DP-6, whereas androgen-inducible TGF-beta1 was significantly suppressed by the ROS-scavenger, N-acetyl cysteine.	Acetylcysteine	170-187	transforming growth factor, beta 1	Rattus norvegicus	109-118
23640046-14	2013	Our results indicate that NAC blocked CAPE-mediated AKT/XIAP inhibition and protected the cells from apoptosis.	Acetylcysteine	26-29	AKT serine/threonine kinase 1	Homo sapiens	52-55
24048773-0	2013	N-Acetylcysteine effects on transforming growth factor-beta and tumor necrosis factor-alpha serum levels as pro-fibrotic and inflammatory biomarkers in patients following ST-segment elevation myocardial infarction.	Acetylcysteine	0-16	tumor necrosis factor	Homo sapiens	64-91
24048773-3	2013	To the best of our knowledge, this is the first study that has evaluated the effect of NAC on TNF-alpha and TGF-beta levels in patients with AMI.	Acetylcysteine	87-90	tumor necrosis factor	Homo sapiens	94-103
24048773-3	2013	To the best of our knowledge, this is the first study that has evaluated the effect of NAC on TNF-alpha and TGF-beta levels in patients with AMI.	Acetylcysteine	87-90	transforming growth factor beta 1	Homo sapiens	108-116
24048773-8	2013	CONCLUSIONS: Receiving NAC could prevent TGF-beta levels from increasing after 72 h as compared with not receiving NAC.	Acetylcysteine	23-26	transforming growth factor beta 1	Homo sapiens	41-49
24001404-14	2013	In addition, NAC prevented the AA-induced increase in caspase-3 protein, while stimulating claudin-1 protein expression in the colonic mucosa.	Acetylcysteine	13-16	caspase 3	Homo sapiens	54-63
23475548-2	2013	This study evaluated the protective effect of NAC on under carbon tetrachloride (CCl4)-induced acute liver injury in the rat.	Acetylcysteine	46-49	C-C motif chemokine ligand 4	Rattus norvegicus	81-85
23590859-0	2013	N-acetyl-cysteine prevents toxic oxidative effects induced by IFN-alpha in human neurons.	Acetylcysteine	0-17	interferon alpha 1	Homo sapiens	62-71
23590859-9	2013	A co-treatment with N-acetyl-cysteine (NAC; 5 mm), a potent antioxidant and mitochondrial modulator, was able to counteract all of these IFN-alpha-induced effects.	Acetylcysteine	20-37	interferon alpha 1	Homo sapiens	137-146
23590859-9	2013	A co-treatment with N-acetyl-cysteine (NAC; 5 mm), a potent antioxidant and mitochondrial modulator, was able to counteract all of these IFN-alpha-induced effects.	Acetylcysteine	39-42	interferon alpha 1	Homo sapiens	137-146
23590859-11	2013	We suggest that NAC, already tested for the treatment of psychiatric disorders, may be useful to prevent IFN-alpha-induced central side-effects in a safe and effective way.	Acetylcysteine	16-19	interferon alpha 1	Homo sapiens	105-114
23804706-9	2013	N-acetylcysteine blocked reduction in the levels of Mcl-1, c-FLIP, and intracellular GSH as well as apoptosis in HL-60 cells treated by either compound.	Acetylcysteine	0-16	CASP8 and FADD like apoptosis regulator	Homo sapiens	59-65
24325097-5	2013	The effects of N-acetyl cysteine (NAC) on UA-induced levels of ROS, mRNA and protein of CRP in HUVECs were also observed.	Acetylcysteine	15-32	C-reactive protein	Homo sapiens	88-91
24325097-5	2013	The effects of N-acetyl cysteine (NAC) on UA-induced levels of ROS, mRNA and protein of CRP in HUVECs were also observed.	Acetylcysteine	34-37	C-reactive protein	Homo sapiens	88-91
24325097-9	2013	NAC reduced UA-induced levels of ROS, mRNA and protein of CRP in HUVECs compared with those of 12 mg/dL UA induced group(P&lt;0.	Acetylcysteine	0-3	C-reactive protein	Homo sapiens	58-61
23666527-4	2013	NAC was able to partially suppress phenotypes in both antisense-induced (NPC1ASO) and germline (Npc1-/-) knockout genetic mouse models, confirming the presence of an oxidative stress-related mechanism in progression of NPC1 phenotypes and suggesting NAC as a potential molecule for treatment.	Acetylcysteine	0-3	NPC intracellular cholesterol transporter 1	Mus musculus	96-100
23950953-12	2013	Both L5-induced ROS and CRP production were attenuated by ROS inhibitor N-acetyl cysteine.	Acetylcysteine	72-89	C-reactive protein	Homo sapiens	24-27
24015194-0	2013	Both PKA and Epac pathways mediate N-acetylcysteine-induced Connexin43 preservation in rats with myocardial infarction.	Acetylcysteine	35-51	gap junction protein, alpha 1	Rattus norvegicus	60-70
24015194-8	2013	Attenuated connexin43 expression and function were blunted after administering N-acetylcysteine, assessed by immunofluorescent analysis, dye coupling, Western blotting, and real-time quantitative RT-PCR of connexin43.	Acetylcysteine	79-95	gap junction protein, alpha 1	Rattus norvegicus	11-21
24015194-8	2013	Attenuated connexin43 expression and function were blunted after administering N-acetylcysteine, assessed by immunofluorescent analysis, dye coupling, Western blotting, and real-time quantitative RT-PCR of connexin43.	Acetylcysteine	79-95	gap junction protein, alpha 1	Rattus norvegicus	206-216
24015194-10	2013	In an ex vivo study, enhanced connexin43 levels afforded by N-acetylcysteine were partially blocked by either H-89 (a PKA inhibitor) or brefeldin A (an Epac-signaling inhibitor) and completely blocked when H-89 and brefeldin A were given in combination.	Acetylcysteine	60-76	gap junction protein, alpha 1	Rattus norvegicus	30-40
24015194-12	2013	These findings suggest that N-acetylcysteine protects ventricular arrhythmias by attenuating reduced connexin43 expression and function via both PKA- and Epac-dependent pathways, which converge through the inactivation of glycogen synthase kinase-3beta.	Acetylcysteine	28-44	gap junction protein, alpha 1	Rattus norvegicus	101-111
23583729-13	2013	Treatment with NAC reduces AD-1-induced p38 phosphorylation, which indicates that ROS generation is involved in the AD-1-induced p38 activation.	Acetylcysteine	15-18	mitogen-activated protein kinase 14	Homo sapiens	40-43
23583729-13	2013	Treatment with NAC reduces AD-1-induced p38 phosphorylation, which indicates that ROS generation is involved in the AD-1-induced p38 activation.	Acetylcysteine	15-18	mitogen-activated protein kinase 14	Homo sapiens	129-132
23623839-6	2013	NAC treatment caused a reduction of extracellular medium pH to acidic and an increase in Akt phosphorylation, after which the replacement with NAC-free medium returned them to control levels within 24h.	Acetylcysteine	0-3	AKT serine/threonine kinase 1	Homo sapiens	89-92
23771710-8	2013	NAC attenuated silica-induced increases in TNF-alpha, IL-8 and hsCRP in BALF and serum.	Acetylcysteine	0-3	tumor necrosis factor	Rattus norvegicus	43-52
23519142-4	2013	The rhNRG-1 inhibited DOX-induced autophagy, reduced reactive oxygen species production and increased protein expression of Bcl-2, effects that were recapitulated when the cells were treated with the antioxidant N-acetylcysteine.	Acetylcysteine	212-228	BCL2, apoptosis regulator	Rattus norvegicus	124-129
23186260-11	2013	At 72 h after treatment, the intensity of staining for COX2 was significantly higher after saline than after NAC treatment (p &lt; 0.05).	Acetylcysteine	109-112	prostaglandin-endoperoxide synthase 2	Equus caballus	55-59
23718696-8	2013	Pretreatment with l-buthionine-(S,R)-sulfoximine and N-acetylcysteine prior to TBQ exposure of HepG2 cells suggested that the Keap1-TBQ adduct appears to undergo GSH-mediated S-transarylation because the resulting alterations in the intracellular GSH concentration affected Nrf2 activation caused by TBQ.	Acetylcysteine	53-69	kelch like ECH associated protein 1	Homo sapiens	126-131
23765110-6	2013	RESULTS: Concomitant administration of CsA and NAC significantly improved renal function and attenuated tubulointerstitial fibrosis, and these changes were accompanied by decreased urinary 8-OHdG level and increased MnSOD expression.	Acetylcysteine	47-50	superoxide dismutase 2, mitochondrial	Mus musculus	216-221
23765110-7	2013	NAC treatment preserved Klotho gene expression compared with CsA treatment alone (P &lt; 0.05), and this correlated with urinary 8-OHdG excretion (r = -0.934) and MnSOD expression (r = 0.873, P &lt; 0.001 for both).	Acetylcysteine	0-3	superoxide dismutase 2, mitochondrial	Mus musculus	163-168
23867003-8	2013	NAC induced p53 and reduced p65 protein expression through activation of PPARalpha.	Acetylcysteine	0-3	tumor protein p53	Homo sapiens	12-15
23867003-9	2013	Silencing of p53 and overexpression of p65 blocked the effect of NAC on PDK1 promoter activity and protein expression.	Acetylcysteine	65-68	tumor protein p53	Homo sapiens	13-16
23867003-10	2013	CONCLUSION: Our results show that NAC inhibits PDK1 expression through PPARalpha-mediated induction of p53 and inhibition of p65 protein expression.	Acetylcysteine	34-37	tumor protein p53	Homo sapiens	103-106
23578993-1	2013	Aim of present study was to investigate the effect of NAC on experimental chronic hepatotoxicity models induced by carbon tetrachloride (CCl4) and thioacetamide (TAA).	Acetylcysteine	54-57	C-C motif chemokine ligand 4	Rattus norvegicus	137-141
23761083-10	2013	The levels of MCP-1, CCL11, and IL-6 increased after light exposure were suppressed by NAC.	Acetylcysteine	87-90	mast cell protease 1	Mus musculus	14-19
23578993-11	2013	Serum markers of liver damage (AST, ALT, ALP and Bilirubin) were increased by CCl4 and TAA intoxication (p&lt;0.001), whereas co-treatment with NAC reversed such changes (p&lt;0.001).	Acetylcysteine	144-147	glutamic-oxaloacetic transaminase 2	Rattus norvegicus	31-34
23578993-11	2013	Serum markers of liver damage (AST, ALT, ALP and Bilirubin) were increased by CCl4 and TAA intoxication (p&lt;0.001), whereas co-treatment with NAC reversed such changes (p&lt;0.001).	Acetylcysteine	144-147	C-C motif chemokine ligand 4	Rattus norvegicus	78-82
23545271-4	2013	NAC may also have a regulator role on TRPV1 channel activity in the dorsal root ganglion (DRG) neuron.	Acetylcysteine	0-3	transient receptor potential cation channel, subfamily V, member 1	Mus musculus	38-43
23545271-12	2013	When NAC and GSH were included in the patch pipette as well as extracellularly in the chamber, TRPV1 channels were not activated by CAP and H2O2.	Acetylcysteine	5-8	transient receptor potential cation channel, subfamily V, member 1	Mus musculus	95-100
23874481-11	2013	Treatment with NAC, curcumin, and EGCG markedly inhibited arecoline induced Snail expression (p&lt;0.05).	Acetylcysteine	15-18	snail family transcriptional repressor 1	Homo sapiens	76-81
23761083-10	2013	The levels of MCP-1, CCL11, and IL-6 increased after light exposure were suppressed by NAC.	Acetylcysteine	87-90	chemokine (C-C motif) ligand 11	Mus musculus	21-26
23874481-14	2013	In addition, arecoline induced Snail expression was downregulated by NAC, curcumin, and EGCG.	Acetylcysteine	69-72	snail family transcriptional repressor 1	Homo sapiens	31-36
23545271-15	2013	In conclusion, in our experimental model, TRPV1 channels are involved in the oxidative stress-induced neuronal death, and negative modulation of this channel activity by GSH and NAC pretreatment may account for their neuroprotective activity against oxidative stress.	Acetylcysteine	178-181	transient receptor potential cation channel, subfamily V, member 1	Mus musculus	42-47
23761083-10	2013	The levels of MCP-1, CCL11, and IL-6 increased after light exposure were suppressed by NAC.	Acetylcysteine	87-90	interleukin 6	Mus musculus	32-36
23719546-8	2013	NAC also blunted the increase in phosphorylation of protein kinase B, mammalian target of rapamycin, p70 ribosomal S6 kinase, ribosomal protein S6, and mitogen activated protein kinase p38 at 2 and 8 d after exercise.	Acetylcysteine	0-3	mechanistic target of rapamycin kinase	Homo sapiens	70-99
23874646-8	2013	The response by 1,000 nm LxB relied on a robust production of reactive oxygen species (ROS), since IL-1beta production was remarkably reduced by ROS inhibitors such as diphenylene iodonium (DPI) and N-acetylcysteine (NAC).	Acetylcysteine	199-215	interleukin 1 beta	Homo sapiens	99-107
23874646-8	2013	The response by 1,000 nm LxB relied on a robust production of reactive oxygen species (ROS), since IL-1beta production was remarkably reduced by ROS inhibitors such as diphenylene iodonium (DPI) and N-acetylcysteine (NAC).	Acetylcysteine	217-220	interleukin 1 beta	Homo sapiens	99-107
23874646-9	2013	In contrast, IL-1beta production by 20 nm LxB was augmented by NAC and in BMDM deficient in thioredoxin-binding protein-2 (TBP-2), a negative regulator of the ROS scavenger thioredoxin.	Acetylcysteine	63-66	interleukin 1 beta	Homo sapiens	13-21
23719546-8	2013	NAC also blunted the increase in phosphorylation of protein kinase B, mammalian target of rapamycin, p70 ribosomal S6 kinase, ribosomal protein S6, and mitogen activated protein kinase p38 at 2 and 8 d after exercise.	Acetylcysteine	0-3	mitogen-activated protein kinase 14	Homo sapiens	185-188
23546866-7	2013	Antioxidant N-acetyl cysteine attenuated ASK1 dephosphorylation and p38 MAPK activation, indicating that shikonin-induced ROS is involved in the activation of Akt/ASK1/p38 pathway.	Acetylcysteine	12-29	mitogen-activated protein kinase 14	Homo sapiens	68-71
23546866-7	2013	Antioxidant N-acetyl cysteine attenuated ASK1 dephosphorylation and p38 MAPK activation, indicating that shikonin-induced ROS is involved in the activation of Akt/ASK1/p38 pathway.	Acetylcysteine	12-29	AKT serine/threonine kinase 1	Homo sapiens	159-162
23546866-7	2013	Antioxidant N-acetyl cysteine attenuated ASK1 dephosphorylation and p38 MAPK activation, indicating that shikonin-induced ROS is involved in the activation of Akt/ASK1/p38 pathway.	Acetylcysteine	12-29	mitogen-activated protein kinase 14	Homo sapiens	168-171
23567873-9	2013	Stimulation of endothelial cells with EGCG produced intracellular ROS, whereas treatment with N-acetylcysteine (NAC) blocked EGCG-induced expression of eNOS and CaMKKII.	Acetylcysteine	94-110	nitric oxide synthase 3	Homo sapiens	152-156
23386420-7	2013	The concurrent incubation of NT2 cells with bleomycin/H2O2 and NAC (5 mM) for 24 h abolished bleomycin/H2O2-dependent increases in Caspase-3, -8, -9 activities, Bax and Cyt-c levels and bleomycin/H2O2-dependent decrease in Bcl-2 level.	Acetylcysteine	63-66	caspase 3	Homo sapiens	131-148
23386420-7	2013	The concurrent incubation of NT2 cells with bleomycin/H2O2 and NAC (5 mM) for 24 h abolished bleomycin/H2O2-dependent increases in Caspase-3, -8, -9 activities, Bax and Cyt-c levels and bleomycin/H2O2-dependent decrease in Bcl-2 level.	Acetylcysteine	63-66	BCL2 associated X, apoptosis regulator	Homo sapiens	161-164
23386420-7	2013	The concurrent incubation of NT2 cells with bleomycin/H2O2 and NAC (5 mM) for 24 h abolished bleomycin/H2O2-dependent increases in Caspase-3, -8, -9 activities, Bax and Cyt-c levels and bleomycin/H2O2-dependent decrease in Bcl-2 level.	Acetylcysteine	63-66	BCL2 apoptosis regulator	Homo sapiens	223-228
23307410-7	2013	NAC significantly inhibited accumulation of inflammatory cells and downregulated iNOS expression and TNF-alpha serum levels.	Acetylcysteine	0-3	nitric oxide synthase 2	Rattus norvegicus	81-85
23307410-7	2013	NAC significantly inhibited accumulation of inflammatory cells and downregulated iNOS expression and TNF-alpha serum levels.	Acetylcysteine	0-3	tumor necrosis factor	Rattus norvegicus	101-110
23065916-8	2013	After one month of NAC both p50-p50/p50-p65 dimers were significantly reduced (P&lt;.004 and .006).	Acetylcysteine	19-22	nuclear factor kappa B subunit 1	Homo sapiens	28-31
23065916-8	2013	After one month of NAC both p50-p50/p50-p65 dimers were significantly reduced (P&lt;.004 and .006).	Acetylcysteine	19-22	nuclear factor kappa B subunit 1	Homo sapiens	32-35
23065916-8	2013	After one month of NAC both p50-p50/p50-p65 dimers were significantly reduced (P&lt;.004 and .006).	Acetylcysteine	19-22	nuclear factor kappa B subunit 1	Homo sapiens	32-35
23567873-9	2013	Stimulation of endothelial cells with EGCG produced intracellular ROS, whereas treatment with N-acetylcysteine (NAC) blocked EGCG-induced expression of eNOS and CaMKKII.	Acetylcysteine	112-115	nitric oxide synthase 3	Homo sapiens	152-156
23395854-4	2013	The antioxidant N-acetylcysteine completely inhibited the increase in HSPA1A and DNAJB1 mRNA levels upon methionine starvation, indicating that this increase is a response to oxidative stress resulting from a lack of methionine.	Acetylcysteine	16-32	heat shock protein family A (Hsp70) member 1A	Homo sapiens	70-76
23619020-10	2013	An increase in intracellular reactive oxygen species (ROS) was observed in AC-treated cells, whereas the antioxidant N-acetylcysteine (NAC) prevented AC-induced cell death, HER-2/neu depletion, PI3K/Akt inactivation, and Bcl-2/Bax dysregulation, indicating that AC-induced cell death was mediated by ROS generation.	Acetylcysteine	117-133	erb-b2 receptor tyrosine kinase 2	Homo sapiens	173-178
23619020-10	2013	An increase in intracellular reactive oxygen species (ROS) was observed in AC-treated cells, whereas the antioxidant N-acetylcysteine (NAC) prevented AC-induced cell death, HER-2/neu depletion, PI3K/Akt inactivation, and Bcl-2/Bax dysregulation, indicating that AC-induced cell death was mediated by ROS generation.	Acetylcysteine	135-138	erb-b2 receptor tyrosine kinase 2	Homo sapiens	173-178
23604711-7	2013	In addition, the strain-mediated induction of HO-1 and activation of Nrf2 was abolished by the antioxidant N-acetyl-l-cysteine.	Acetylcysteine	107-126	NFE2 like bZIP transcription factor 2	Homo sapiens	69-73
23776698-10	2013	In addition, NAC completely blocked phosphorylation of JNK and p38 MAPK induced by AGE-BSA.	Acetylcysteine	13-16	mitogen-activated protein kinase 8	Homo sapiens	55-58
23776698-10	2013	In addition, NAC completely blocked phosphorylation of JNK and p38 MAPK induced by AGE-BSA.	Acetylcysteine	13-16	mitogen-activated protein kinase 14	Homo sapiens	63-66
22727548-0	2013	N-acetylcysteine treatment reduces TNF-alpha levels and myonecrosis in diaphragm muscle of mdx mice.	Acetylcysteine	0-16	tumor necrosis factor	Mus musculus	35-44
22727548-4	2013	In this study we investigated whether the antioxidant N-acetylcysteine (NAC) decreases TNF-alpha levels and protects the diaphragm muscle of mdx mice against necrosis.	Acetylcysteine	54-70	tumor necrosis factor	Mus musculus	87-96
22727548-4	2013	In this study we investigated whether the antioxidant N-acetylcysteine (NAC) decreases TNF-alpha levels and protects the diaphragm muscle of mdx mice against necrosis.	Acetylcysteine	72-75	tumor necrosis factor	Mus musculus	87-96
22727548-7	2013	RESULTS: NAC reduced TNF-alpha and 4-HNE-protein adducts levels, inflammation, creatine kinase levels, and myonecrosis in diaphragm muscle.	Acetylcysteine	9-12	tumor necrosis factor	Mus musculus	21-30
23817939-5	2013	NAC infusion (100 mg/kg) was administered as soon as ALF was diagnosed, based on low GCS scores, raised transaminases and prolonged prothrombin/INR.	Acetylcysteine	0-3	coagulation factor II, thrombin	Homo sapiens	132-143
22959059-12	2013	The apoptotic effect of EGCG and the p38 activation were blocked by pretreatment of cells with the ROS scavenger N-acetylcysteine.	Acetylcysteine	113-129	mitogen-activated protein kinase 14	Homo sapiens	37-40
23717422-6	2013	In addition, sanguinarine effectively increased the activation of the c-Jun N-terminal kinase (JNK) and the expression of the early growth response gene-1 (Egr-1), which was recovered by pretreatment with NAC.	Acetylcysteine	205-208	mitogen-activated protein kinase 8	Homo sapiens	70-93
23717422-6	2013	In addition, sanguinarine effectively increased the activation of the c-Jun N-terminal kinase (JNK) and the expression of the early growth response gene-1 (Egr-1), which was recovered by pretreatment with NAC.	Acetylcysteine	205-208	mitogen-activated protein kinase 8	Homo sapiens	95-98
23114871-6	2013	The ROS scavenger N-acetyl cysteine reduced both the amount of cleaved poly(ADP-ribose) polymerase (PARP) and the extent of cancer cell loss.	Acetylcysteine	18-35	poly(ADP-ribose) polymerase 1	Homo sapiens	71-98
23114871-6	2013	The ROS scavenger N-acetyl cysteine reduced both the amount of cleaved poly(ADP-ribose) polymerase (PARP) and the extent of cancer cell loss.	Acetylcysteine	18-35	poly(ADP-ribose) polymerase 1	Homo sapiens	100-104
23492188-0	2013	N-acetylcysteine protects murine alveolar type II cells from cigarette smoke injury in a nuclear erythroid 2-related factor-2-independent manner.	Acetylcysteine	0-16	nuclear factor, erythroid derived 2, like 2	Mus musculus	89-125
23492188-8	2013	Moreover, NAC decreased the injury of ATII cells obtained from Nrf2(-/-) mice.	Acetylcysteine	10-13	nuclear factor, erythroid derived 2, like 2	Mus musculus	63-67
23492188-9	2013	Our results suggest that Nrf2-GSH signaling is important for the protective activity of NAC.	Acetylcysteine	88-91	nuclear factor, erythroid derived 2, like 2	Mus musculus	25-29
23687429-9	2013	Pretreatment with N-acetylcysteine or vitamin C reversed the enhanced proliferation capacity and the induction of transforming growth factor, beta 1, interleukin-1beta and superoxide anion of GO fibroblasts in response to 6.25 muM H2O2.	Acetylcysteine	18-34	transforming growth factor beta 1	Homo sapiens	114-148
23325162-8	2013	CONCLUSION: The decreased risk of transplantation or death or of transplantation alone with intravenous NAC in early coma grade patients with non-acetaminophen induced ALF was reflected in improvement in parameters related to hepatocyte necrosis and bile excretion including ALT and bilirubin, but not in INR, creatinine, or AST.	Acetylcysteine	104-107	solute carrier family 17 member 5	Homo sapiens	325-328
22841545-4	2013	Selenium treatment induced phosphorylation of DNA-PKcs on Thr-2647 and Ser-2056, the extent of which was decreased in the presence of ATM kinase inhibitor KU 55933 or the antioxidants N-acetylcysteine or 2,2,6,6-tetramethylpiperidine-1-oxyl.	Acetylcysteine	184-200	protein kinase, DNA-activated, catalytic subunit	Homo sapiens	46-54
23518073-7	2013	Pretreatment with the anti-oxidant N-acetylcysteine (NAC) inhibited B4-mediated effects, including cytotoxicity, ROS production, mitochondrial membrane depolarization increase in intracellular Ca2+, cytochrome c release, PARP cleavage, and AIF translocation.	Acetylcysteine	35-51	cytochrome c, somatic	Homo sapiens	199-211
23518073-7	2013	Pretreatment with the anti-oxidant N-acetylcysteine (NAC) inhibited B4-mediated effects, including cytotoxicity, ROS production, mitochondrial membrane depolarization increase in intracellular Ca2+, cytochrome c release, PARP cleavage, and AIF translocation.	Acetylcysteine	35-51	poly(ADP-ribose) polymerase 1	Homo sapiens	221-225
23518073-7	2013	Pretreatment with the anti-oxidant N-acetylcysteine (NAC) inhibited B4-mediated effects, including cytotoxicity, ROS production, mitochondrial membrane depolarization increase in intracellular Ca2+, cytochrome c release, PARP cleavage, and AIF translocation.	Acetylcysteine	53-56	cytochrome c, somatic	Homo sapiens	199-211
23518073-7	2013	Pretreatment with the anti-oxidant N-acetylcysteine (NAC) inhibited B4-mediated effects, including cytotoxicity, ROS production, mitochondrial membrane depolarization increase in intracellular Ca2+, cytochrome c release, PARP cleavage, and AIF translocation.	Acetylcysteine	53-56	poly(ADP-ribose) polymerase 1	Homo sapiens	221-225
23687429-9	2013	Pretreatment with N-acetylcysteine or vitamin C reversed the enhanced proliferation capacity and the induction of transforming growth factor, beta 1, interleukin-1beta and superoxide anion of GO fibroblasts in response to 6.25 muM H2O2.	Acetylcysteine	18-34	interleukin 1 beta	Homo sapiens	150-167
23818365-11	2013	Pretreatment with N-acetylcysteine (NAC) blocked ROS generation and resulted in loss of mitochondrial membrane potential, release of cytochrome C and apoptosis induced by pristimerin.	Acetylcysteine	18-34	cytochrome c, somatic	Homo sapiens	133-145
23434081-8	2013	The levels of inflammatory cytokines (TNF-alpha, IL-1beta, IL-6, and IL-10) in piglet plasma of the NAC group (mixed feeding concentration of 1200 mg/kg) were significantly lower at 3h after LPS stimulation (P&lt;0.05).	Acetylcysteine	100-103	tumor necrosis factor	Homo sapiens	38-47
23434081-8	2013	The levels of inflammatory cytokines (TNF-alpha, IL-1beta, IL-6, and IL-10) in piglet plasma of the NAC group (mixed feeding concentration of 1200 mg/kg) were significantly lower at 3h after LPS stimulation (P&lt;0.05).	Acetylcysteine	100-103	interleukin 1 beta	Homo sapiens	49-57
23434081-8	2013	The levels of inflammatory cytokines (TNF-alpha, IL-1beta, IL-6, and IL-10) in piglet plasma of the NAC group (mixed feeding concentration of 1200 mg/kg) were significantly lower at 3h after LPS stimulation (P&lt;0.05).	Acetylcysteine	100-103	interleukin 6	Homo sapiens	59-63
23407882-7	2013	Both NAC and DPI suppressed indoxyl sulfate-induced expression of NF-kappaB p65 and CREB.	Acetylcysteine	5-8	nuclear factor kappa B subunit 1	Homo sapiens	66-75
23333652-7	2013	Finally, we showed that CHOP induction by t10,c12 CLA was dependent on ROS production and that the anti-oxidant N-acetyl-cysteine reduced CHOP induction-dependent cell death.	Acetylcysteine	112-129	DNA damage inducible transcript 3	Homo sapiens	138-142
23818365-11	2013	Pretreatment with N-acetylcysteine (NAC) blocked ROS generation and resulted in loss of mitochondrial membrane potential, release of cytochrome C and apoptosis induced by pristimerin.	Acetylcysteine	36-39	cytochrome c, somatic	Homo sapiens	133-145
22996809-13	2013	Plumbagin-induced cell death was mediated, at least in part, by activation of ERK and was due to generation of reactive oxygen species, because it was abolished by the anti-oxidant N-acetyl-L-cysteine.	Acetylcysteine	181-200	mitogen-activated protein kinase 1	Mus musculus	78-81
23522537-8	2013	However, pachymic acid and N-acetyl-L-cysteine (control antioxidant) restored cell viability and ALP activity damaged by AH plus.	Acetylcysteine	27-46	alopecia, recessive	Mus musculus	97-100
23416263-6	2013	Pretreatment with the antioxidant N-acetyl-cysteine (NAC): reduced the induction of ROS and MDA by CeO2 nanoparticles; recovered the activity of SOD, GSH-px and CAT; reduced the phosphorylation levels of ERK1/2, JNK and p38; and attenuated CeO2 nanoparticles-induced damage and apoptosis in SMMC-7721 cells.	Acetylcysteine	34-51	catalase	Homo sapiens	161-164
23490067-6	2013	Suppression of TPA+AA-induced ERK protein phosphorylation by PD98059 and NAC was detected, and AA enhanced ERK protein phosphorylation by TPA was in HL-60 cells.	Acetylcysteine	73-76	mitogen-activated protein kinase 1	Homo sapiens	30-33
23416263-6	2013	Pretreatment with the antioxidant N-acetyl-cysteine (NAC): reduced the induction of ROS and MDA by CeO2 nanoparticles; recovered the activity of SOD, GSH-px and CAT; reduced the phosphorylation levels of ERK1/2, JNK and p38; and attenuated CeO2 nanoparticles-induced damage and apoptosis in SMMC-7721 cells.	Acetylcysteine	34-51	mitogen-activated protein kinase 3	Homo sapiens	204-210
23416263-6	2013	Pretreatment with the antioxidant N-acetyl-cysteine (NAC): reduced the induction of ROS and MDA by CeO2 nanoparticles; recovered the activity of SOD, GSH-px and CAT; reduced the phosphorylation levels of ERK1/2, JNK and p38; and attenuated CeO2 nanoparticles-induced damage and apoptosis in SMMC-7721 cells.	Acetylcysteine	34-51	mitogen-activated protein kinase 8	Homo sapiens	212-215
23416263-6	2013	Pretreatment with the antioxidant N-acetyl-cysteine (NAC): reduced the induction of ROS and MDA by CeO2 nanoparticles; recovered the activity of SOD, GSH-px and CAT; reduced the phosphorylation levels of ERK1/2, JNK and p38; and attenuated CeO2 nanoparticles-induced damage and apoptosis in SMMC-7721 cells.	Acetylcysteine	34-51	mitogen-activated protein kinase 1	Homo sapiens	220-223
23416263-6	2013	Pretreatment with the antioxidant N-acetyl-cysteine (NAC): reduced the induction of ROS and MDA by CeO2 nanoparticles; recovered the activity of SOD, GSH-px and CAT; reduced the phosphorylation levels of ERK1/2, JNK and p38; and attenuated CeO2 nanoparticles-induced damage and apoptosis in SMMC-7721 cells.	Acetylcysteine	53-56	catalase	Homo sapiens	161-164
23416263-6	2013	Pretreatment with the antioxidant N-acetyl-cysteine (NAC): reduced the induction of ROS and MDA by CeO2 nanoparticles; recovered the activity of SOD, GSH-px and CAT; reduced the phosphorylation levels of ERK1/2, JNK and p38; and attenuated CeO2 nanoparticles-induced damage and apoptosis in SMMC-7721 cells.	Acetylcysteine	53-56	mitogen-activated protein kinase 3	Homo sapiens	204-210
23416263-6	2013	Pretreatment with the antioxidant N-acetyl-cysteine (NAC): reduced the induction of ROS and MDA by CeO2 nanoparticles; recovered the activity of SOD, GSH-px and CAT; reduced the phosphorylation levels of ERK1/2, JNK and p38; and attenuated CeO2 nanoparticles-induced damage and apoptosis in SMMC-7721 cells.	Acetylcysteine	53-56	mitogen-activated protein kinase 8	Homo sapiens	212-215
23416263-6	2013	Pretreatment with the antioxidant N-acetyl-cysteine (NAC): reduced the induction of ROS and MDA by CeO2 nanoparticles; recovered the activity of SOD, GSH-px and CAT; reduced the phosphorylation levels of ERK1/2, JNK and p38; and attenuated CeO2 nanoparticles-induced damage and apoptosis in SMMC-7721 cells.	Acetylcysteine	53-56	mitogen-activated protein kinase 1	Homo sapiens	220-223
26417226-6	2013	NAC significantly decreased neutrophil and eosinophil count in BALF as well as inflammatory cytokines (IL-13 and IL-5).We concluded that addition of NAC to asthma therapy has beneficial preventive effects in an animal model of steroid resistant acute exacerbation of asthma.	Acetylcysteine	149-152	interleukin 13	Mus musculus	103-108
23140664-0	2013	Early-life insults impair parvalbumin interneurons via oxidative stress: reversal by N-acetylcysteine.	Acetylcysteine	85-101	parvalbumin	Mus musculus	26-37
23364789-5	2013	Menadione-induced apoptosis and the PRC stress program were blocked by the antioxidant N-acetylcysteine.	Acetylcysteine	87-103	PPARG related coactivator 1	Homo sapiens	36-39
23292300-8	2013	However, the quenching of ROS generation with antioxidant N-acetyl-L-cysteine conferred significant protection against cordycepin-elicited ROS generation, disruption of the MMP, modulation of Bcl-2 and IAP family proteins, caspase-3 and -9 activation and apoptosis.	Acetylcysteine	58-77	BCL2 apoptosis regulator	Homo sapiens	192-197
23187459-4	2013	Pretreatment with N-acetylcysteine (NAC) significantly inhibited nutlin-3-induced DR5 upregulation and cell death induced by the combined treatment with nutlin-3 and TRAIL, suggesting that reactive oxygen species (ROS) mediate nutlin-3-induced DR5 upregulation, which contributes toward TRAIL-mediated apoptosis.	Acetylcysteine	18-34	TNF superfamily member 10	Homo sapiens	166-171
23187459-4	2013	Pretreatment with N-acetylcysteine (NAC) significantly inhibited nutlin-3-induced DR5 upregulation and cell death induced by the combined treatment with nutlin-3 and TRAIL, suggesting that reactive oxygen species (ROS) mediate nutlin-3-induced DR5 upregulation, which contributes toward TRAIL-mediated apoptosis.	Acetylcysteine	18-34	TNF superfamily member 10	Homo sapiens	287-292
23187459-4	2013	Pretreatment with N-acetylcysteine (NAC) significantly inhibited nutlin-3-induced DR5 upregulation and cell death induced by the combined treatment with nutlin-3 and TRAIL, suggesting that reactive oxygen species (ROS) mediate nutlin-3-induced DR5 upregulation, which contributes toward TRAIL-mediated apoptosis.	Acetylcysteine	36-39	TNF superfamily member 10	Homo sapiens	166-171
23187459-4	2013	Pretreatment with N-acetylcysteine (NAC) significantly inhibited nutlin-3-induced DR5 upregulation and cell death induced by the combined treatment with nutlin-3 and TRAIL, suggesting that reactive oxygen species (ROS) mediate nutlin-3-induced DR5 upregulation, which contributes toward TRAIL-mediated apoptosis.	Acetylcysteine	36-39	TNF superfamily member 10	Homo sapiens	287-292
23187459-6	2013	Interestingly, a combined treatment with NAC and PUMA small interfering RNAs significantly blocks nutlin-3-induced and TRAIL-induced apoptosis.	Acetylcysteine	41-44	TNF superfamily member 10	Homo sapiens	119-124
23353715-7	2013	Further analysis showed that NAC attenuated the Cd-induced upregulation of testicular glucose-regulated protein 78 (GRP78), an important ER molecular chaperone.	Acetylcysteine	29-32	heat shock protein 5	Mus musculus	86-114
23353715-7	2013	Further analysis showed that NAC attenuated the Cd-induced upregulation of testicular glucose-regulated protein 78 (GRP78), an important ER molecular chaperone.	Acetylcysteine	29-32	heat shock protein 5	Mus musculus	116-121
23353715-9	2013	In addition, NAC blocked the Cd-induced activation of testicular X binding protein (XBP)-1, indicating that NAC attenuates the Cd-induced ER stress and the unfolded protein response (UPR).	Acetylcysteine	13-16	X-box binding protein 1	Mus musculus	65-90
23353715-9	2013	In addition, NAC blocked the Cd-induced activation of testicular X binding protein (XBP)-1, indicating that NAC attenuates the Cd-induced ER stress and the unfolded protein response (UPR).	Acetylcysteine	108-111	X-box binding protein 1	Mus musculus	65-90
23113536-7	2013	The effect of SKi on androgen receptor expression was reversed by N-acetylcysteine, which was used to scavenge reactive oxygen species.	Acetylcysteine	66-82	androgen receptor	Homo sapiens	21-38
23083489-7	2013	These effects on PDI were mimicked by exogenous 4-HNE and prevented by the carbonyl-scavengers N-acetylcysteine and pyridoxamine, which reduced CHOP expression and toxicity by oxLDLs.	Acetylcysteine	95-111	DNA damage inducible transcript 3	Homo sapiens	144-148
23292300-8	2013	However, the quenching of ROS generation with antioxidant N-acetyl-L-cysteine conferred significant protection against cordycepin-elicited ROS generation, disruption of the MMP, modulation of Bcl-2 and IAP family proteins, caspase-3 and -9 activation and apoptosis.	Acetylcysteine	58-77	caspase 3	Homo sapiens	223-239
23328933-7	2013	Inhibition of endosomal NOX by the anion channel blocker niflumic acid or capture of superoxide by the radical scavenger N-acetylcysteine blocks TF induction by aPL.	Acetylcysteine	121-137	coagulation factor III	Mus musculus	145-147
23284002-6	2013	Treatment with TSA and the Nrf2-ARE activator resulted in increased inhibition of the TGF-beta-induced myofibroblast differentiation as compared with treatment with DPI or NAC.	Acetylcysteine	172-175	NFE2 like bZIP transcription factor 2	Homo sapiens	27-31
23268108-7	2013	We showed that NF-kappaB inhibitor N-acetyl-L-cysteine (NAC) effectively attenuates the expression of LPS-stimulated iNOS, COX-2 and TNF-alpha.	Acetylcysteine	35-54	nitric oxide synthase 2, inducible	Mus musculus	117-121
23268108-7	2013	We showed that NF-kappaB inhibitor N-acetyl-L-cysteine (NAC) effectively attenuates the expression of LPS-stimulated iNOS, COX-2 and TNF-alpha.	Acetylcysteine	35-54	tumor necrosis factor	Mus musculus	133-142
23268108-7	2013	We showed that NF-kappaB inhibitor N-acetyl-L-cysteine (NAC) effectively attenuates the expression of LPS-stimulated iNOS, COX-2 and TNF-alpha.	Acetylcysteine	56-59	nitric oxide synthase 2, inducible	Mus musculus	117-121
23268108-7	2013	We showed that NF-kappaB inhibitor N-acetyl-L-cysteine (NAC) effectively attenuates the expression of LPS-stimulated iNOS, COX-2 and TNF-alpha.	Acetylcysteine	56-59	tumor necrosis factor	Mus musculus	133-142
23559643-7	2013	n-Acetyl-l-cysteine pretreatment showed that changes in the intracellular free [Ca(2+)] and caspase-3 activity were independent of ROS formation.	Acetylcysteine	0-19	caspase 3	Homo sapiens	92-101
23281030-6	2013	Moreover, antioxidants, N-acetyl-cysteine and desferioxamine, prevented OTA-mediated enhancement of ROS generation, and TGFbeta expression.	Acetylcysteine	24-41	transforming growth factor beta 1	Homo sapiens	120-127
23233130-11	2013	Western blot analysis showed that the G6PDH expression was stimulated by PEG6000 and buthionine sulfoximine (BSO, glutathione biosynthesis inhibitor), and blocked by Glucm, DPI and N-acetyl-L-cysteine (NAC, GSH precursor) in both cultivars.	Acetylcysteine	181-200	glucose-6-phosphate dehydrogenase	Glycine max	38-43
23233130-11	2013	Western blot analysis showed that the G6PDH expression was stimulated by PEG6000 and buthionine sulfoximine (BSO, glutathione biosynthesis inhibitor), and blocked by Glucm, DPI and N-acetyl-L-cysteine (NAC, GSH precursor) in both cultivars.	Acetylcysteine	202-205	glucose-6-phosphate dehydrogenase	Glycine max	38-43
23014887-6	2013	The ROS scavenger, N-acetyl-L-cysteine, and the ROS inhibitor, diphenyleneiodonium, also impaired P2X7-induced ROS formation, but use of enzyme-specific ROS inhibitors failed to identify the intracellular source of P2X7-induced ROS formation.	Acetylcysteine	19-38	purinergic receptor P2X, ligand-gated ion channel, 7	Mus musculus	98-102
23449454-6	2013	Statin-induced cytotoxic effects, DNA fragmentation and changes of activation of caspase-3, Akt, Erk and p38 were blocked by antioxidant (N-acetylcysteine) and metabolic products of the HMG-CoA reductase reaction, such as mevalonate, farnesyl pyrophosphate (FPP) and geranylgeranyl pyrophosphate (GGPP).	Acetylcysteine	138-154	thymoma viral proto-oncogene 1	Mus musculus	92-95
22676837-6	2013	And the antioxidant N-acetyl-l-cysteine inhibited induction of both GRP78 and CHOP by alpha-TOS transcriptionally and translationally.	Acetylcysteine	20-39	heat shock protein family A (Hsp70) member 5	Homo sapiens	68-73
22676837-6	2013	And the antioxidant N-acetyl-l-cysteine inhibited induction of both GRP78 and CHOP by alpha-TOS transcriptionally and translationally.	Acetylcysteine	20-39	DNA damage inducible transcript 3	Homo sapiens	78-82
23449454-6	2013	Statin-induced cytotoxic effects, DNA fragmentation and changes of activation of caspase-3, Akt, Erk and p38 were blocked by antioxidant (N-acetylcysteine) and metabolic products of the HMG-CoA reductase reaction, such as mevalonate, farnesyl pyrophosphate (FPP) and geranylgeranyl pyrophosphate (GGPP).	Acetylcysteine	138-154	mitogen-activated protein kinase 1	Mus musculus	97-100
25206699-4	2013	The antioxidant N-acetylcysteine significantly inhibited reactive oxygen species production and reduced hypoxia-inducible factor-1alpha mRNA expression in normoxic and hypoxic groups, especially in the latter group.	Acetylcysteine	16-32	hypoxia inducible factor 1 subunit alpha	Homo sapiens	104-135
23379731-5	2013	The inhibitory effects of GSH and NAC on the biological activities of CySSR were correlated with a glutaredoxin (Grx)-dependent intracellular reduction of CySSR to generate cysteine and RSH, which were secreted into the extracellular medium.	Acetylcysteine	34-37	glutaredoxin	Mus musculus	99-111
23379731-5	2013	The inhibitory effects of GSH and NAC on the biological activities of CySSR were correlated with a glutaredoxin (Grx)-dependent intracellular reduction of CySSR to generate cysteine and RSH, which were secreted into the extracellular medium.	Acetylcysteine	34-37	glutaredoxin	Mus musculus	113-116
25206699-5	2013	These findings indicate that hypoxia induces reactive oxygen species production and hypoxia-inducible factor-1alpha mRNA expression in human SHG-44 glioma cells, and that the antioxidant N-acetylcysteine can inhibit these changes.	Acetylcysteine	187-203	hypoxia inducible factor 1 subunit alpha	Homo sapiens	84-115
22944050-0	2013	N-acetylcysteine (NAC) inhibits cell growth by mediating the EGFR/Akt/HMG box-containing protein 1 (HBP1) signaling pathway in invasive oral cancer.	Acetylcysteine	0-16	epidermal growth factor receptor	Homo sapiens	61-65
23363008-9	2013	Pretreatment with the antioxidant N-acetylcysteine (NAC) significantly blocked cell death and changes of Akt and MAPK signalings induced by chicoric acid.	Acetylcysteine	34-50	AKT serine/threonine kinase 1	Homo sapiens	105-108
23363008-9	2013	Pretreatment with the antioxidant N-acetylcysteine (NAC) significantly blocked cell death and changes of Akt and MAPK signalings induced by chicoric acid.	Acetylcysteine	34-50	mitogen-activated protein kinase 3	Homo sapiens	113-117
23363008-9	2013	Pretreatment with the antioxidant N-acetylcysteine (NAC) significantly blocked cell death and changes of Akt and MAPK signalings induced by chicoric acid.	Acetylcysteine	52-55	AKT serine/threonine kinase 1	Homo sapiens	105-108
23363008-9	2013	Pretreatment with the antioxidant N-acetylcysteine (NAC) significantly blocked cell death and changes of Akt and MAPK signalings induced by chicoric acid.	Acetylcysteine	52-55	mitogen-activated protein kinase 3	Homo sapiens	113-117
22833345-6	2013	NAC abrogated activation of HIF-1alpha and NF-kappaB, both of which were found to play an active role in hypoxia-induced EMT.	Acetylcysteine	0-3	hypoxia inducible factor 1 subunit alpha	Homo sapiens	28-38
23175375-7	2013	In addition, NAC inhibited KSHV infection-induced translocation of alphaVbeta3 integrin into lipid rafts, actin-dependent membrane perturbations, such as blebs, observed during macropinocytosis, and activation of the signal molecules ephrin-A2 receptor, FAK, Src, and Rac1.	Acetylcysteine	13-16	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	259-262
23124852-5	2013	After scavenging ROS with N-acetylcysteine, Wnt/beta-catenin signaling-induced MSC aging was significantly attenuated and the DNA damage and the expression of p16(INK4A), p53, and p21 were reduced in MSCs.	Acetylcysteine	26-42	cyclin dependent kinase inhibitor 2A	Homo sapiens	163-168
23124852-5	2013	After scavenging ROS with N-acetylcysteine, Wnt/beta-catenin signaling-induced MSC aging was significantly attenuated and the DNA damage and the expression of p16(INK4A), p53, and p21 were reduced in MSCs.	Acetylcysteine	26-42	tumor protein p53	Homo sapiens	171-174
22944050-0	2013	N-acetylcysteine (NAC) inhibits cell growth by mediating the EGFR/Akt/HMG box-containing protein 1 (HBP1) signaling pathway in invasive oral cancer.	Acetylcysteine	18-21	epidermal growth factor receptor	Homo sapiens	61-65
22944050-0	2013	N-acetylcysteine (NAC) inhibits cell growth by mediating the EGFR/Akt/HMG box-containing protein 1 (HBP1) signaling pathway in invasive oral cancer.	Acetylcysteine	0-16	AKT serine/threonine kinase 1	Homo sapiens	66-69
22944050-0	2013	N-acetylcysteine (NAC) inhibits cell growth by mediating the EGFR/Akt/HMG box-containing protein 1 (HBP1) signaling pathway in invasive oral cancer.	Acetylcysteine	18-21	AKT serine/threonine kinase 1	Homo sapiens	66-69
22944050-3	2013	The objective of this study is to investigate the role of NAC in EGFR-overexpressing oral cancer.	Acetylcysteine	58-61	epidermal growth factor receptor	Homo sapiens	65-69
22944050-5	2013	RESULTS: NAC treatment suppressed cell growth, with concomitantly increased expression of HMG box-containing protein 1 (HBP1), a transcription suppressor, and decreased EGFR/Akt activation, in EGFR-overexpressing HSC-3 oral cancer cells.	Acetylcysteine	9-12	epidermal growth factor receptor	Homo sapiens	169-173
22944050-5	2013	RESULTS: NAC treatment suppressed cell growth, with concomitantly increased expression of HMG box-containing protein 1 (HBP1), a transcription suppressor, and decreased EGFR/Akt activation, in EGFR-overexpressing HSC-3 oral cancer cells.	Acetylcysteine	9-12	AKT serine/threonine kinase 1	Homo sapiens	174-177
22944050-5	2013	RESULTS: NAC treatment suppressed cell growth, with concomitantly increased expression of HMG box-containing protein 1 (HBP1), a transcription suppressor, and decreased EGFR/Akt activation, in EGFR-overexpressing HSC-3 oral cancer cells.	Acetylcysteine	9-12	epidermal growth factor receptor	Homo sapiens	193-197
22944050-7	2013	Lastly, NAC and AG1478, an EGFR inhibitor, additively suppressed colony formation in HSC-3 cells.	Acetylcysteine	8-11	epidermal growth factor receptor	Homo sapiens	27-31
22944050-8	2013	CONCLUSION: Taken together, our data indicate that NAC exerts its growth-inhibitory function through modulating EGFR/Akt signaling and HBP1 expression in EGFR-overexpressing oral cancer.	Acetylcysteine	51-54	epidermal growth factor receptor	Homo sapiens	112-116
22944050-8	2013	CONCLUSION: Taken together, our data indicate that NAC exerts its growth-inhibitory function through modulating EGFR/Akt signaling and HBP1 expression in EGFR-overexpressing oral cancer.	Acetylcysteine	51-54	AKT serine/threonine kinase 1	Homo sapiens	117-120
22944050-8	2013	CONCLUSION: Taken together, our data indicate that NAC exerts its growth-inhibitory function through modulating EGFR/Akt signaling and HBP1 expression in EGFR-overexpressing oral cancer.	Acetylcysteine	51-54	epidermal growth factor receptor	Homo sapiens	154-158
23322302-7	2013	Concordantly, H(2)O(2) preferentially promoted apoptosis in RBF1-depleted tissues, and the sensitivity of RBF1-depleted animals to fasting was specifically suppressed by either a glutamine supplement or the antioxidant N-acetyl-cysteine.	Acetylcysteine	219-236	Retinoblastoma-family protein	Drosophila melanogaster	60-64
23159886-7	2013	Similarly, MB and/or PQ-mediated histopathological symptoms and changes in the catalytic activities/expressions of CYP1A2, CYP2E1, iNOS, TNF-alpha, and IL-1beta were alleviated by NAC and SIL.	Acetylcysteine	180-183	cytochrome P450, family 2, subfamily e, polypeptide 1	Rattus norvegicus	123-129
23159886-7	2013	Similarly, MB and/or PQ-mediated histopathological symptoms and changes in the catalytic activities/expressions of CYP1A2, CYP2E1, iNOS, TNF-alpha, and IL-1beta were alleviated by NAC and SIL.	Acetylcysteine	180-183	nitric oxide synthase 2	Rattus norvegicus	131-135
23159886-7	2013	Similarly, MB and/or PQ-mediated histopathological symptoms and changes in the catalytic activities/expressions of CYP1A2, CYP2E1, iNOS, TNF-alpha, and IL-1beta were alleviated by NAC and SIL.	Acetylcysteine	180-183	tumor necrosis factor	Rattus norvegicus	137-146
23159886-7	2013	Similarly, MB and/or PQ-mediated histopathological symptoms and changes in the catalytic activities/expressions of CYP1A2, CYP2E1, iNOS, TNF-alpha, and IL-1beta were alleviated by NAC and SIL.	Acetylcysteine	180-183	interleukin 1 beta	Rattus norvegicus	152-160
23322302-7	2013	Concordantly, H(2)O(2) preferentially promoted apoptosis in RBF1-depleted tissues, and the sensitivity of RBF1-depleted animals to fasting was specifically suppressed by either a glutamine supplement or the antioxidant N-acetyl-cysteine.	Acetylcysteine	219-236	Retinoblastoma-family protein	Drosophila melanogaster	106-110
23319318-10	2013	TNF-alpha-induced MCP-1 mRNA expression was inhibited by N-acetylcysteine (NAC), Syk inhibitor, Syk-siRNA and MPA.	Acetylcysteine	75-78	tumor necrosis factor	Homo sapiens	0-9
23267148-5	2013	Likewise, NAC prevented the CDDO-Me-caused binding of fluorescein isothiocyanate (FITC)-tagged annexin V, cleavage of poly ADP-ribose polymerase-1 (PARP-1), procaspases-3, -8 and -9 and loss of mitochondrial membrane potential.	Acetylcysteine	10-13	caspase 3	Homo sapiens	157-181
23319318-10	2013	TNF-alpha-induced MCP-1 mRNA expression was inhibited by N-acetylcysteine (NAC), Syk inhibitor, Syk-siRNA and MPA.	Acetylcysteine	57-73	tumor necrosis factor	Homo sapiens	0-9
23103613-9	2013	Pretreatment with NAC and specific p38-MAPK inhibitor (SB203580), but not JNK inhibitor (SP600125) effectively abrogated the phosphorylation of p38-MAPK and attenuated the apoptotic signals (including: decrease in cytotoxicity, caspase-3/-7 activation, the cytosolic cytochrome c release, and the reversed alteration of Bcl-2 and Bax mRNA) in CA-treated Neuro-2a cells.	Acetylcysteine	18-21	B cell leukemia/lymphoma 2	Mus musculus	320-325
23267148-5	2013	Likewise, NAC prevented the CDDO-Me-caused binding of fluorescein isothiocyanate (FITC)-tagged annexin V, cleavage of poly ADP-ribose polymerase-1 (PARP-1), procaspases-3, -8 and -9 and loss of mitochondrial membrane potential.	Acetylcysteine	10-13	poly(ADP-ribose) polymerase 1	Homo sapiens	118-146
23267148-5	2013	Likewise, NAC prevented the CDDO-Me-caused binding of fluorescein isothiocyanate (FITC)-tagged annexin V, cleavage of poly ADP-ribose polymerase-1 (PARP-1), procaspases-3, -8 and -9 and loss of mitochondrial membrane potential.	Acetylcysteine	10-13	poly(ADP-ribose) polymerase 1	Homo sapiens	148-154
23841076-5	2013	Similarly, pretreatment with the antioxidant N-acetyl-cysteine (NAC) markedly inhibited both the autophagy and the apoptosis triggered by DHA, indicating that mitochondrial ROS mediate the cytotoxicity of DHA in mutant p53 cells.	Acetylcysteine	45-62	tumor protein p53	Homo sapiens	219-222
23841076-5	2013	Similarly, pretreatment with the antioxidant N-acetyl-cysteine (NAC) markedly inhibited both the autophagy and the apoptosis triggered by DHA, indicating that mitochondrial ROS mediate the cytotoxicity of DHA in mutant p53 cells.	Acetylcysteine	64-67	tumor protein p53	Homo sapiens	219-222
24329505-1	2013	AIM: To investigate the effects of L-carnitine (LCAR) and N-acetylcysteine (NAC) on carbon tetrachloride (CCl4)-induced acute liver damage in rats.	Acetylcysteine	76-79	C-C motif chemokine ligand 4	Rattus norvegicus	106-110
24329505-15	2013	CONCLUSION: LCAR and NAC were concluded to have beneficial effects on the acute liver damage induced by CCl4 administration (Tab.	Acetylcysteine	21-24	C-C motif chemokine ligand 4	Rattus norvegicus	104-108
23723006-9	2013	Notably, normalization of cardiac function and oxidant/antioxidant level after N-acetylcysteine (NAC)-treatment of diabetic rats resulted with a significant restoration in the expression levels of miR-499, miR-1, miR-133a, and miR-133b in the myocardium.	Acetylcysteine	79-95	microRNA 133b	Rattus norvegicus	227-235
23723006-9	2013	Notably, normalization of cardiac function and oxidant/antioxidant level after N-acetylcysteine (NAC)-treatment of diabetic rats resulted with a significant restoration in the expression levels of miR-499, miR-1, miR-133a, and miR-133b in the myocardium.	Acetylcysteine	97-100	microRNA 133b	Rattus norvegicus	227-235
24356372-11	2013	The pretreatment of H9c2 cells with N-acetyl-L-cysteine (NAC), a scavenger of reactive oxygen species (ROS) prior to exposure to DOX depressed the phosphorylation of NF-kappaB p65 induced by DOX.	Acetylcysteine	36-55	synaptotagmin 1	Rattus norvegicus	176-179
24356372-11	2013	The pretreatment of H9c2 cells with N-acetyl-L-cysteine (NAC), a scavenger of reactive oxygen species (ROS) prior to exposure to DOX depressed the phosphorylation of NF-kappaB p65 induced by DOX.	Acetylcysteine	57-60	synaptotagmin 1	Rattus norvegicus	176-179
23319318-13	2013	TNF-alpha increased ROS generation, which was inhibited by NAC and MPA, but not by Syk inhibitor.	Acetylcysteine	59-62	tumor necrosis factor	Homo sapiens	0-9
23319318-14	2013	TNF-alpha increased tyrosine phosphorylation of Syk, which was attenuated by NAC and MPA.	Acetylcysteine	77-80	tumor necrosis factor	Homo sapiens	0-9
24021937-11	2013	N-acetylcysteine antagonized Ang II-induced CRP expression.	Acetylcysteine	0-16	angiotensinogen	Homo sapiens	29-35
24021937-11	2013	N-acetylcysteine antagonized Ang II-induced CRP expression.	Acetylcysteine	0-16	C-reactive protein	Homo sapiens	44-47
24021937-12	2013	Losartan and N-acetylcysteine inhibited Ang II-activated ERK1/2.	Acetylcysteine	13-29	angiotensinogen	Homo sapiens	40-46
24021937-12	2013	Losartan and N-acetylcysteine inhibited Ang II-activated ERK1/2.	Acetylcysteine	13-29	mitogen-activated protein kinase 3	Homo sapiens	57-63
23222262-7	2013	Removal of intracellular reactive oxygen species by N-acetyl-cysteine reduced the activation of AMP-activated protein kinase, extracellular signal-regulated kinase and Jun N-terminal kinase, and interleukin-8 induction.	Acetylcysteine	52-69	mitogen-activated protein kinase 8	Homo sapiens	168-189
23092328-11	2013	Also cells treated with the anti-oxidants N-acetylcysteine or HO-effector molecule bilirubin showed protection against heme insults, which may explain the increased protection by HO-1 compared to BCRP.	Acetylcysteine	42-58	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	196-200
23615310-10	2013	Growth retardation, degeneration of lens fibers, and an increased number of osteoclasts in the Ggt1(dwg/dwg) mice were reversed by administration of N-acetyl-L-cysteine, a precursor of GSH synthesis.	Acetylcysteine	149-168	gamma-glutamyltransferase 1	Mus musculus	95-99
23063000-7	2013	In addition, most of the genes, known to be inducible by NF-kappaB or JNK following cytokines stimulation, were less induced by SCE when endothelial cells were pretreated with the antioxidant N-Acetylcysteine (NAC), suggesting a role of ROS in endothelial cell activation by SCE.	Acetylcysteine	192-208	mitogen-activated protein kinase 8	Homo sapiens	70-73
23063000-7	2013	In addition, most of the genes, known to be inducible by NF-kappaB or JNK following cytokines stimulation, were less induced by SCE when endothelial cells were pretreated with the antioxidant N-Acetylcysteine (NAC), suggesting a role of ROS in endothelial cell activation by SCE.	Acetylcysteine	210-213	mitogen-activated protein kinase 8	Homo sapiens	70-73
23128467-0	2013	N-acetylcysteine potentiates doxorubicin-induced ATM and p53 activation             in ovarian cancer cells.	Acetylcysteine	0-16	tumor protein p53	Homo sapiens	57-60
23063593-6	2013	Furthermore, the addition of a ROS inhibitor (N-Acetyl-l-cysteine, NAC) significantly attenuated the apoptosis induced by HER and also blocked the expression of PGC-1alpha protein.	Acetylcysteine	46-65	PPARG coactivator 1 alpha	Homo sapiens	161-171
24002405-10	2013	Supplementation with omega-3 fatty acids, alpha-lipoic acid and N-acetylcysteine is considered to have an anti-inflammatory and antioxidant effect and to improve dyslipidemia and insulin sensitivity in PCOS women.	Acetylcysteine	64-80	insulin	Homo sapiens	179-186
23128467-9	2013	Pretreatment of CaOV3 cells with antioxidant N-acetylcysteine (NAC),             but not pyrrolidine dithiocarbamate (PDTC) potentiates doxorubicin-induced phosphorylation             of p53 and ATM.	Acetylcysteine	45-61	tumor protein p53	Homo sapiens	187-190
23128467-9	2013	Pretreatment of CaOV3 cells with antioxidant N-acetylcysteine (NAC),             but not pyrrolidine dithiocarbamate (PDTC) potentiates doxorubicin-induced phosphorylation             of p53 and ATM.	Acetylcysteine	63-66	tumor protein p53	Homo sapiens	187-190
23782641-10	2013	NAC also attenuated the ratio of sub-G1, the generation of DNA fragmentation and the expression of Bcl-2, Bax, caspase-3, and caspase-9.	Acetylcysteine	0-3	BCL2 apoptosis regulator	Homo sapiens	99-104
23853776-7	2013	NAC normalized tissue and plasma levels of 15-F2t-isoprostane, significantly increased cardiac Brg1, HO-1 and p-STAT3 protein expression levels and reduced TNF-alpha and IL-6, resulting in improved cardiac function.	Acetylcysteine	0-3	tumor necrosis factor	Rattus norvegicus	156-165
23853776-7	2013	NAC normalized tissue and plasma levels of 15-F2t-isoprostane, significantly increased cardiac Brg1, HO-1 and p-STAT3 protein expression levels and reduced TNF-alpha and IL-6, resulting in improved cardiac function.	Acetylcysteine	0-3	interleukin 6	Rattus norvegicus	170-174
23782641-10	2013	NAC also attenuated the ratio of sub-G1, the generation of DNA fragmentation and the expression of Bcl-2, Bax, caspase-3, and caspase-9.	Acetylcysteine	0-3	BCL2 associated X, apoptosis regulator	Homo sapiens	106-109
23782641-10	2013	NAC also attenuated the ratio of sub-G1, the generation of DNA fragmentation and the expression of Bcl-2, Bax, caspase-3, and caspase-9.	Acetylcysteine	0-3	caspase 3	Homo sapiens	111-120
23431238-9	2013	The ROS scavenger N-acetyl-L-cysteine impaired both P2X7-induced EOC13 ROS formation and cell death, suggesting that ROS mediate P2X7-induced EOC13 death.	Acetylcysteine	18-37	purinergic receptor P2X, ligand-gated ion channel, 7	Mus musculus	52-56
23431238-9	2013	The ROS scavenger N-acetyl-L-cysteine impaired both P2X7-induced EOC13 ROS formation and cell death, suggesting that ROS mediate P2X7-induced EOC13 death.	Acetylcysteine	18-37	purinergic receptor P2X, ligand-gated ion channel, 7	Mus musculus	129-133
23124098-8	2013	Furthermore, additional experiments indicated that the inhibitory effect of curcumin on LPS-induced MCP-1 expression was significantly attenuated in the presence of N-acetylcysteine (an effective ROS scavenger).	Acetylcysteine	165-181	toll-like receptor 4	Mus musculus	88-91
23682786-4	2013	Further, treatment of TOCO and NAC either alone or in combination to AO/TPA- or SANG/TPA-induced mice significantly decreased lipid peroxidation, along with significant revival in glutathione (GSH) content and activities of tyrosinase, histidase, catalase, SOD, GSH peroxidase, and GSH reductase in skin.	Acetylcysteine	31-34	histidine ammonia lyase	Mus musculus	236-245
23682786-4	2013	Further, treatment of TOCO and NAC either alone or in combination to AO/TPA- or SANG/TPA-induced mice significantly decreased lipid peroxidation, along with significant revival in glutathione (GSH) content and activities of tyrosinase, histidase, catalase, SOD, GSH peroxidase, and GSH reductase in skin.	Acetylcysteine	31-34	catalase	Mus musculus	247-255
24096134-8	2013	Hsp70 levels were higher in MG132-treated cells when N-acetyl cysteine was applied.	Acetylcysteine	53-70	heat shock protein 1B	Mus musculus	0-5
24096134-10	2013	Inhibition of Hsp70/Hsc70 activity with VER 155008 attenuated the protection afforded by N-acetyl cysteine in a dose-responsive manner.	Acetylcysteine	89-106	heat shock protein 1B	Mus musculus	14-19
24096134-12	2013	Consistent with the chaperone functions of Hsp70, VER 155008 also prevented the reduction in ubiquitin-conjugated proteins by N-acetyl cysteine.	Acetylcysteine	126-143	heat shock protein 1B	Mus musculus	43-48
23682786-5	2013	In vitro studies showed that TOCO and/or NAC significantly decreased the AO and SANG induced cell proliferation and activation of ERK, p38, JNK MAPKs and NF-kappaB signaling in HaCaT cells.	Acetylcysteine	41-44	mitogen-activated protein kinase 14	Homo sapiens	135-138
23405080-7	2013	Furthermore, exposure to Cd induced the phosphorylations of c-jun N-terminal kinases (JNK), extracellular signal-regulated kinases (ERK)1/2, and p38-mitogen-activated protein kinase (MAPK), which was prevented by NAC.	Acetylcysteine	213-216	mitogen-activated protein kinase 8	Homo sapiens	60-84
23577223-4	2013	The results of western blot showed that NAC preincubation affected Cd-activated MAPK pathways, p38 and ERK phosphorylation.	Acetylcysteine	40-43	Eph receptor B1	Rattus norvegicus	103-106
23555559-11	2013	N-acetylcysteine (NAC), an antioxidant reagent, reduced both the increase in cellular H2O2 levels and AKT phosphorylation induced by glucose deprivation.	Acetylcysteine	0-16	AKT serine/threonine kinase 1	Homo sapiens	102-105
23555559-11	2013	N-acetylcysteine (NAC), an antioxidant reagent, reduced both the increase in cellular H2O2 levels and AKT phosphorylation induced by glucose deprivation.	Acetylcysteine	18-21	AKT serine/threonine kinase 1	Homo sapiens	102-105
23405080-7	2013	Furthermore, exposure to Cd induced the phosphorylations of c-jun N-terminal kinases (JNK), extracellular signal-regulated kinases (ERK)1/2, and p38-mitogen-activated protein kinase (MAPK), which was prevented by NAC.	Acetylcysteine	213-216	mitogen-activated protein kinase 14	Homo sapiens	145-181
22986110-5	2013	Rd10 mice were treated with an antioxidant NAC, and its effect on retinal inflammation and photoreceptor apoptosis were examined by immunohistochemistry.	Acetylcysteine	43-46	phosphodiesterase 6B, cGMP, rod receptor, beta polypeptide	Mus musculus	0-4
23536773-1	2013	BACKGROUND: The aim of this study was to investigate the molecular mechanisms involved in the production of Th1 cytokines, namely IL-12 and IL-27, when the intra-macrophage redox state was altered by different chemical entities such as GSH-C4, which is reduced glutathione carrying an aliphatic chain, or I-152, a pro-drug of N-acetyl-cysteine (NAC) and beta-mercaptoethylamine.	Acetylcysteine	326-343	negative elongation factor complex member C/D, Th1l	Mus musculus	108-111
23536773-1	2013	BACKGROUND: The aim of this study was to investigate the molecular mechanisms involved in the production of Th1 cytokines, namely IL-12 and IL-27, when the intra-macrophage redox state was altered by different chemical entities such as GSH-C4, which is reduced glutathione carrying an aliphatic chain, or I-152, a pro-drug of N-acetyl-cysteine (NAC) and beta-mercaptoethylamine.	Acetylcysteine	345-348	negative elongation factor complex member C/D, Th1l	Mus musculus	108-111
23405080-7	2013	Furthermore, exposure to Cd induced the phosphorylations of c-jun N-terminal kinases (JNK), extracellular signal-regulated kinases (ERK)1/2, and p38-mitogen-activated protein kinase (MAPK), which was prevented by NAC.	Acetylcysteine	213-216	mitogen-activated protein kinase 3	Homo sapiens	92-139
24112955-4	2013	RESULTS: NAC treatment inhibited fat accumulation and reduced the expression of obesity-related proteins, including monoamine oxidase A, heat shock protein 70 (HSP70), aminoacylase -1 (ACY-1), and transketolase.	Acetylcysteine	9-12	transketolase	Homo sapiens	197-210
23560513-12	2013	RESULTS: NAC and NAC + OT significantly decreased MDA and TNF-alpha levels and increased IL-10 levels and GPx activities.	Acetylcysteine	9-12	tumor necrosis factor	Rattus norvegicus	58-67
23560513-12	2013	RESULTS: NAC and NAC + OT significantly decreased MDA and TNF-alpha levels and increased IL-10 levels and GPx activities.	Acetylcysteine	17-20	tumor necrosis factor	Rattus norvegicus	58-67
22664745-13	2013	Serum nitrite/nitrate and IL-6 were also significantly lower in the NAC group.	Acetylcysteine	68-71	interleukin 6	Rattus norvegicus	26-30
22664745-14	2013	The levels of lung cytoplasmic p-IkappaB-alpha expression was mitigated by NAC, and NF-kappaB p65 DNA binding activity was also significantly decreased in the NAC group.	Acetylcysteine	159-162	synaptotagmin 1	Rattus norvegicus	94-97
22982566-4	2012	However, hypoxia further increased the susceptibility of mutant p53 breast cancer SKBR3 cells to lower PRIMA-1 levels, possibly through oxidative stress since this was counteracted by N-acetylcysteine.	Acetylcysteine	184-200	tumor protein p53	Homo sapiens	64-67
24120238-4	2013	ROS scavengers N-acetylcysteine (NAC) and dithiothreitol (DTT) abolish not only collagen, thrombin, and A23187 induced ROS production, but also GPIbalpha ectodomain shedding.	Acetylcysteine	15-31	coagulation factor II, thrombin	Homo sapiens	90-98
24120238-4	2013	ROS scavengers N-acetylcysteine (NAC) and dithiothreitol (DTT) abolish not only collagen, thrombin, and A23187 induced ROS production, but also GPIbalpha ectodomain shedding.	Acetylcysteine	33-36	coagulation factor II, thrombin	Homo sapiens	90-98
24398995-0	2013	Valproic acid substantially downregulated genes folr1, IGF2R, RGS2, COL6A3, EDNRB, KLF6, and pax-3, N-acetylcysteine alleviated most of the induced gene alterations in chicken embryo model.	Acetylcysteine	100-116	folate receptor 1	Gallus gallus	48-53
24398995-0	2013	Valproic acid substantially downregulated genes folr1, IGF2R, RGS2, COL6A3, EDNRB, KLF6, and pax-3, N-acetylcysteine alleviated most of the induced gene alterations in chicken embryo model.	Acetylcysteine	100-116	regulator of G-protein signaling 2	Gallus gallus	62-66
22985912-6	2013	N-acetylcysteine prevented morphologic and oxidative derangements, and significantly reduced proinflammatory product secretion (P range&lt;0.0001 to&lt;0.00001 for TNFalpha, VCAM-1, MCP-1, and IL-6); rosuvastatin inhibited morphology and oxidative modifications only.	Acetylcysteine	0-16	tumor necrosis factor	Homo sapiens	164-172
22985912-6	2013	N-acetylcysteine prevented morphologic and oxidative derangements, and significantly reduced proinflammatory product secretion (P range&lt;0.0001 to&lt;0.00001 for TNFalpha, VCAM-1, MCP-1, and IL-6); rosuvastatin inhibited morphology and oxidative modifications only.	Acetylcysteine	0-16	vascular cell adhesion molecule 1	Homo sapiens	174-180
22985912-6	2013	N-acetylcysteine prevented morphologic and oxidative derangements, and significantly reduced proinflammatory product secretion (P range&lt;0.0001 to&lt;0.00001 for TNFalpha, VCAM-1, MCP-1, and IL-6); rosuvastatin inhibited morphology and oxidative modifications only.	Acetylcysteine	0-16	interleukin 6	Homo sapiens	193-197
23085515-6	2012	The effect of TNF-alpha on MST1 activation was reversed by the reducing agent N-acetyl-l-cysteine.	Acetylcysteine	78-97	tumor necrosis factor	Homo sapiens	14-23
23000247-7	2012	Moreover, the antioxidant N-acetylcysteine reduced the protective effect of CPN-9 against oxidative stress-induced cell death with concomitant diminishing of Nrf2 nuclear translocation.	Acetylcysteine	26-42	NFE2 like bZIP transcription factor 2	Homo sapiens	158-162
23007278-8	2012	Pretreatment with the c-Jun N-terminal kinase (JNK) inhibitor SP600125 and the reactive oxygen species (ROS) scavenger N-acetylcysteine reduced the SVT and TRAIL-induced upregulation of DR4 and DR5 expression, expression of the apoptosis related protein such as caspase-3 and-9, as well as cell growth inhibitory effects.	Acetylcysteine	119-135	TNF superfamily member 10	Homo sapiens	156-161
23007278-8	2012	Pretreatment with the c-Jun N-terminal kinase (JNK) inhibitor SP600125 and the reactive oxygen species (ROS) scavenger N-acetylcysteine reduced the SVT and TRAIL-induced upregulation of DR4 and DR5 expression, expression of the apoptosis related protein such as caspase-3 and-9, as well as cell growth inhibitory effects.	Acetylcysteine	119-135	caspase 3	Homo sapiens	262-277
23210443-5	2012	AA treatment induced upregulation of LFA-1 and pretreatment of monocytes with NAC or an inhibitor to p38 MAPK inhibited this upregulation in monocytes.	Acetylcysteine	78-81	integrin subunit beta 2	Homo sapiens	37-42
22562160-9	2012	Co-incubation of NCCIT cells with bleomycin and 10 mM NAC abolished bleomycin-induced increases in caspase-3 and caspase-9 activities, Bax, and Cyt-c levels and bleomycin-induced decrease in Bcl-2 level.	Acetylcysteine	54-57	caspase 3	Homo sapiens	99-108
23986968-6	2012	On the other hand, addition of N-acetyl cysteine (NAC), an antioxidant, blocked the curcumin-induced ROS production and rescued malignant cells from curcumin-induced apoptosis through caspase-3 deactivation.	Acetylcysteine	31-48	caspase 3	Homo sapiens	184-193
23986968-6	2012	On the other hand, addition of N-acetyl cysteine (NAC), an antioxidant, blocked the curcumin-induced ROS production and rescued malignant cells from curcumin-induced apoptosis through caspase-3 deactivation.	Acetylcysteine	50-53	caspase 3	Homo sapiens	184-193
22495438-8	2012	The restoration of glutathione levels by N-acetylcysteine opposed Cox-2 expression and preserved the integrity of endothelial monolayers.	Acetylcysteine	41-57	prostaglandin-endoperoxide synthase 2	Homo sapiens	66-71
22939972-7	2012	Addition of glutathione monoethyl ester, which is cleaved intracellularly to GSH, prevented attenuation of LIF-induced JAK1 and STAT3 activation, as did the reductant N-acetyl-cysteine.	Acetylcysteine	167-184	signal transducer and activator of transcription 3	Homo sapiens	128-133
22562160-9	2012	Co-incubation of NCCIT cells with bleomycin and 10 mM NAC abolished bleomycin-induced increases in caspase-3 and caspase-9 activities, Bax, and Cyt-c levels and bleomycin-induced decrease in Bcl-2 level.	Acetylcysteine	54-57	BCL2 associated X, apoptosis regulator	Homo sapiens	135-138
22562160-9	2012	Co-incubation of NCCIT cells with bleomycin and 10 mM NAC abolished bleomycin-induced increases in caspase-3 and caspase-9 activities, Bax, and Cyt-c levels and bleomycin-induced decrease in Bcl-2 level.	Acetylcysteine	54-57	cytochrome c, somatic	Homo sapiens	144-149
22562160-9	2012	Co-incubation of NCCIT cells with bleomycin and 10 mM NAC abolished bleomycin-induced increases in caspase-3 and caspase-9 activities, Bax, and Cyt-c levels and bleomycin-induced decrease in Bcl-2 level.	Acetylcysteine	54-57	BCL2 apoptosis regulator	Homo sapiens	191-196
22878643-8	2012	Western blot analysis showed that CI-IB-MECA induced the down-regulation of extracellular signal-regulated kinases (ERK) and Akt, which was prevented by EGTA, NAC, and the A3AR antagonist MRS1191.	Acetylcysteine	159-162	mitogen-activated protein kinase 1	Homo sapiens	76-114
22878643-8	2012	Western blot analysis showed that CI-IB-MECA induced the down-regulation of extracellular signal-regulated kinases (ERK) and Akt, which was prevented by EGTA, NAC, and the A3AR antagonist MRS1191.	Acetylcysteine	159-162	mitogen-activated protein kinase 1	Homo sapiens	116-119
22898295-5	2012	Treatment with NAC and DFX also increased the activity of the antioxidant enzymes, superoxide dismutase and catalase in the same brain areas.	Acetylcysteine	15-18	catalase	Rattus norvegicus	108-116
22878643-8	2012	Western blot analysis showed that CI-IB-MECA induced the down-regulation of extracellular signal-regulated kinases (ERK) and Akt, which was prevented by EGTA, NAC, and the A3AR antagonist MRS1191.	Acetylcysteine	159-162	AKT serine/threonine kinase 1	Homo sapiens	125-128
22922338-7	2012	CHOP induction was also reactive oxygen species (ROS)-dependent, as shown by capsazepine"s ability to induce ROS and by the quenching of ROS by N-acetylcysteine or glutathione, which prevented induction of CHOP and DR5 and consequent sensitization to TRAIL.	Acetylcysteine	144-160	DNA damage inducible transcript 3	Homo sapiens	0-4
24977134-11	2013	The magnitude of GFR improvement after N-acetylcysteine administration was less pronounced in the group treated with high-flux biocompatible membranes: +0.17 +- 0.56 mL/min/1.73 m(2) in treatment group and +0.65 +- 0.53 mL/min/1.73 m(2) in control group (P &lt; 0.05).	Acetylcysteine	39-55	CD59 molecule (CD59 blood group)	Homo sapiens	169-174
24977134-11	2013	The magnitude of GFR improvement after N-acetylcysteine administration was less pronounced in the group treated with high-flux biocompatible membranes: +0.17 +- 0.56 mL/min/1.73 m(2) in treatment group and +0.65 +- 0.53 mL/min/1.73 m(2) in control group (P &lt; 0.05).	Acetylcysteine	39-55	CD59 molecule (CD59 blood group)	Homo sapiens	223-228
23009681-3	2012	5HT formed three adducts with N-acetylcysteine (NAC) when it was incubated with myeloperoxidase, xanthine oxidase, and acetaldehyde.	Acetylcysteine	30-46	myeloperoxidase	Homo sapiens	80-95
23009681-3	2012	5HT formed three adducts with N-acetylcysteine (NAC) when it was incubated with myeloperoxidase, xanthine oxidase, and acetaldehyde.	Acetylcysteine	48-51	myeloperoxidase	Homo sapiens	80-95
23027866-4	2012	Recently, it was reported that the antioxidant N-acetylcysteine (NAC) decreased DMXAA-induced TNF-alpha and IL-6, suggesting that oxidative stress may play a role.	Acetylcysteine	47-63	tumor necrosis factor	Mus musculus	94-103
23027866-4	2012	Recently, it was reported that the antioxidant N-acetylcysteine (NAC) decreased DMXAA-induced TNF-alpha and IL-6, suggesting that oxidative stress may play a role.	Acetylcysteine	47-63	interleukin 6	Mus musculus	108-112
23027866-4	2012	Recently, it was reported that the antioxidant N-acetylcysteine (NAC) decreased DMXAA-induced TNF-alpha and IL-6, suggesting that oxidative stress may play a role.	Acetylcysteine	65-68	tumor necrosis factor	Mus musculus	94-103
23027866-4	2012	Recently, it was reported that the antioxidant N-acetylcysteine (NAC) decreased DMXAA-induced TNF-alpha and IL-6, suggesting that oxidative stress may play a role.	Acetylcysteine	65-68	interleukin 6	Mus musculus	108-112
22922338-7	2012	CHOP induction was also reactive oxygen species (ROS)-dependent, as shown by capsazepine"s ability to induce ROS and by the quenching of ROS by N-acetylcysteine or glutathione, which prevented induction of CHOP and DR5 and consequent sensitization to TRAIL.	Acetylcysteine	144-160	DNA damage inducible transcript 3	Homo sapiens	206-210
22922338-7	2012	CHOP induction was also reactive oxygen species (ROS)-dependent, as shown by capsazepine"s ability to induce ROS and by the quenching of ROS by N-acetylcysteine or glutathione, which prevented induction of CHOP and DR5 and consequent sensitization to TRAIL.	Acetylcysteine	144-160	TNF superfamily member 10	Homo sapiens	251-256
23026832-9	2012	Furthermore, the addition of a ROS inhibitor (N-acetyl cysteine, NAC) or iNOS inhibitor (N-[3-(aminomethyl) benzyl] acetamidine, dihydrochloride, 1400W) significantly diminished the apoptosis induced by ISO and also blocked the phosphorylation of Akt.	Acetylcysteine	46-63	AKT serine/threonine kinase 1	Homo sapiens	247-250
23042187-5	2012	Heme oxygenase 1 protein induced by J2, Delta, and 15d was inhibited by the transcriptional inhibitor, actinomycin (Act) D; the translational inhibitor, cycloheximide; and the antioxidant, N-acetyl cysteine (NAC).	Acetylcysteine	189-206	heme oxygenase 1	Mus musculus	0-16
22917563-7	2012	Finally, the antioxidant N-acetyl cysteine antagonized 6-OHDA-induced activation of AMPK, p38 and autophagy.	Acetylcysteine	25-42	mitogen-activated protein kinase 14	Homo sapiens	90-93
22618532-7	2012	NAC-mediated neuroprotection was attributed to the direct scavenging of reactive oxygen species and was mediated by targeting the hypoxia-inducible factor-1alpha pathway via the BNIP3 and PI3K/Akt/mTOR pathways.	Acetylcysteine	0-3	thymoma viral proto-oncogene 1	Mus musculus	193-196
22825625-9	2012	In addition, pretreatment with PM or N-acetyl cysteine resulted in inhibition of nuclear NF-kappaB activation.	Acetylcysteine	37-54	nuclear factor kappa B subunit 1	Homo sapiens	89-98
22744860-10	2012	The antioxidant N-acetylcysteine and the NADPH inhibitor partially blunted sustained adenosine-induced JNK activation but were ineffective in attenuation of p38 activation or barrier dysfunction.	Acetylcysteine	16-32	mitogen-activated protein kinase 8	Homo sapiens	103-106
22923157-6	2012	Interestingly such pro-apoptosis effect in LNCaP cells was associated with reduced c-Flip levels through proteasomal degradation via increased reactive oxygen species production and p38 activation; such c-Flip reduction was reversed in the presence of either the proteasome inhibitor MG132 or the reactive oxygen species scavenger N-acetyl-cysteine.	Acetylcysteine	331-348	CASP8 and FADD like apoptosis regulator	Homo sapiens	83-89
22923157-6	2012	Interestingly such pro-apoptosis effect in LNCaP cells was associated with reduced c-Flip levels through proteasomal degradation via increased reactive oxygen species production and p38 activation; such c-Flip reduction was reversed in the presence of either the proteasome inhibitor MG132 or the reactive oxygen species scavenger N-acetyl-cysteine.	Acetylcysteine	331-348	CASP8 and FADD like apoptosis regulator	Homo sapiens	203-209
22692000-6	2012	Pre-treatment with the scavenger for H(2)O(2), dimethylthiourea (DMTU) and antioxidant, N-acetyl cysteine (NAC), effectively inhibited the activities of caspase-3 and caspase-9, eventually blocked Cd-induced DNA fragmentation and the appearance of markers for apoptotic cell death.	Acetylcysteine	88-105	caspase 3	Homo sapiens	153-162
22692000-6	2012	Pre-treatment with the scavenger for H(2)O(2), dimethylthiourea (DMTU) and antioxidant, N-acetyl cysteine (NAC), effectively inhibited the activities of caspase-3 and caspase-9, eventually blocked Cd-induced DNA fragmentation and the appearance of markers for apoptotic cell death.	Acetylcysteine	107-110	caspase 3	Homo sapiens	153-162
23042187-5	2012	Heme oxygenase 1 protein induced by J2, Delta, and 15d was inhibited by the transcriptional inhibitor, actinomycin (Act) D; the translational inhibitor, cycloheximide; and the antioxidant, N-acetyl cysteine (NAC).	Acetylcysteine	208-211	heme oxygenase 1	Mus musculus	0-16
22854047-6	2012	Modulating the redox-state using decomposing peroxynitrite (FeTPPS, 2.5 microM) or the GSH-precursor [N-acetylcysteine (NAC), 1 mM] caused a positive-shift of the redox-state and prevented VEGF-mediated S-glutathionylation and oxidative inhibition of LMW-PTP.	Acetylcysteine	102-118	vascular endothelial growth factor A	Homo sapiens	189-193
23000044-7	2012	In contrast, antioxidant N-acetyl cysteine protected Nrf2-KD MIN6 cells against acute cytotoxicity of iAs3+.	Acetylcysteine	25-42	nuclear factor, erythroid derived 2, like 2	Mus musculus	53-60
22917661-8	2012	The addition of n-acetylcysteine (NAC) suppressed CoCl(2)-induced reactive oxygen species (ROS) formation and completely negated CoCl(2)-induced FGF21 loss.	Acetylcysteine	16-32	fibroblast growth factor 21	Homo sapiens	145-150
22917661-8	2012	The addition of n-acetylcysteine (NAC) suppressed CoCl(2)-induced reactive oxygen species (ROS) formation and completely negated CoCl(2)-induced FGF21 loss.	Acetylcysteine	34-37	fibroblast growth factor 21	Homo sapiens	145-150
22906494-9	2012	N-acetyl cysteine prevents GSH depletion and blocks menadione-induced complex dissociation, JNK activation and inhibits menadione-induced cytotoxicity.	Acetylcysteine	0-17	mitogen-activated protein kinase 8	Homo sapiens	92-95
22854047-6	2012	Modulating the redox-state using decomposing peroxynitrite (FeTPPS, 2.5 microM) or the GSH-precursor [N-acetylcysteine (NAC), 1 mM] caused a positive-shift of the redox-state and prevented VEGF-mediated S-glutathionylation and oxidative inhibition of LMW-PTP.	Acetylcysteine	120-123	vascular endothelial growth factor A	Homo sapiens	189-193
22743636-5	2012	At 3 days after TNFalpha stimulation, 30 muM telmisartan or 20 mM NAC administered before and during TNFalpha stimulation prevented the enhancement of LPC content in LDL and monocyte chemoattractant protein-1 mRNA by LDL incubation with TNFalpha-stimulated HUVEC.	Acetylcysteine	66-69	tumor necrosis factor	Homo sapiens	101-109
22809665-0	2012	Inflammation-induced dysfunction of the low-density lipoprotein receptor-related protein-1 at the blood-brain barrier: protection by the antioxidant N-acetylcysteine.	Acetylcysteine	149-165	LDL receptor related protein 1	Homo sapiens	40-90
22743636-0	2012	Telmisartan and N-acetylcysteine suppress group V secretory phospholipase A2 expression in TNFalpha-stimulated human endothelial cells and reduce associated atherogenicity.	Acetylcysteine	16-32	tumor necrosis factor	Homo sapiens	91-99
22842544-6	2012	Pretreatment with N-acetyl-l-cysteine (NAC) partly recovered the expression levels of c-FLIPL and c-FLIPs proteins were downregulated by the AMA treatment, suggesting that AMA appears to be partially dependent on the generation of ROS for downregulation of c-FLIPL and c-FLIPs.	Acetylcysteine	18-37	CASP8 and FADD like apoptosis regulator	Homo sapiens	86-93
22842544-6	2012	Pretreatment with N-acetyl-l-cysteine (NAC) partly recovered the expression levels of c-FLIPL and c-FLIPs proteins were downregulated by the AMA treatment, suggesting that AMA appears to be partially dependent on the generation of ROS for downregulation of c-FLIPL and c-FLIPs.	Acetylcysteine	18-37	CASP8 and FADD like apoptosis regulator	Homo sapiens	98-105
22842544-6	2012	Pretreatment with N-acetyl-l-cysteine (NAC) partly recovered the expression levels of c-FLIPL and c-FLIPs proteins were downregulated by the AMA treatment, suggesting that AMA appears to be partially dependent on the generation of ROS for downregulation of c-FLIPL and c-FLIPs.	Acetylcysteine	18-37	CASP8 and FADD like apoptosis regulator	Homo sapiens	257-264
22842544-6	2012	Pretreatment with N-acetyl-l-cysteine (NAC) partly recovered the expression levels of c-FLIPL and c-FLIPs proteins were downregulated by the AMA treatment, suggesting that AMA appears to be partially dependent on the generation of ROS for downregulation of c-FLIPL and c-FLIPs.	Acetylcysteine	18-37	CASP8 and FADD like apoptosis regulator	Homo sapiens	269-276
22743636-3	2012	Telmisartan or NAC administered before and during TNFalpha stimulation diminished the increase of sPLA2-V mRNA in HUVEC and reduced TNFalpha-induced sPLA2-V protein at 3 days after TNFalpha stimulation.	Acetylcysteine	15-18	tumor necrosis factor	Homo sapiens	50-58
22743636-3	2012	Telmisartan or NAC administered before and during TNFalpha stimulation diminished the increase of sPLA2-V mRNA in HUVEC and reduced TNFalpha-induced sPLA2-V protein at 3 days after TNFalpha stimulation.	Acetylcysteine	15-18	phospholipase A2 group X	Homo sapiens	98-103
22743636-3	2012	Telmisartan or NAC administered before and during TNFalpha stimulation diminished the increase of sPLA2-V mRNA in HUVEC and reduced TNFalpha-induced sPLA2-V protein at 3 days after TNFalpha stimulation.	Acetylcysteine	15-18	tumor necrosis factor	Homo sapiens	132-140
22743636-3	2012	Telmisartan or NAC administered before and during TNFalpha stimulation diminished the increase of sPLA2-V mRNA in HUVEC and reduced TNFalpha-induced sPLA2-V protein at 3 days after TNFalpha stimulation.	Acetylcysteine	15-18	phospholipase A2 group X	Homo sapiens	149-154
22743636-3	2012	Telmisartan or NAC administered before and during TNFalpha stimulation diminished the increase of sPLA2-V mRNA in HUVEC and reduced TNFalpha-induced sPLA2-V protein at 3 days after TNFalpha stimulation.	Acetylcysteine	15-18	tumor necrosis factor	Homo sapiens	132-140
22743636-5	2012	At 3 days after TNFalpha stimulation, 30 muM telmisartan or 20 mM NAC administered before and during TNFalpha stimulation prevented the enhancement of LPC content in LDL and monocyte chemoattractant protein-1 mRNA by LDL incubation with TNFalpha-stimulated HUVEC.	Acetylcysteine	66-69	tumor necrosis factor	Homo sapiens	101-109
22732512-10	2012	Treatment of HCV replicon cells with the antioxidant N-acetylcysteine resulted in reduction of PGC-1alpha levels, suggesting that HCV-induced oxidative stress promoted PGC-1alpha upregulation.	Acetylcysteine	53-69	PPARG coactivator 1 alpha	Homo sapiens	95-105
22732512-10	2012	Treatment of HCV replicon cells with the antioxidant N-acetylcysteine resulted in reduction of PGC-1alpha levels, suggesting that HCV-induced oxidative stress promoted PGC-1alpha upregulation.	Acetylcysteine	53-69	PPARG coactivator 1 alpha	Homo sapiens	168-178
22819282-22	2012	Nuclear immunostaining for COX2 was significantly lower after NAC treatment compared to control mares (P &lt; 0.05).	Acetylcysteine	62-65	prostaglandin-endoperoxide synthase 2	Equus caballus	27-31
22773008-10	2012	In all groups, NAC decreased the synthesis of interferon-gamma and nitric oxide, while increasing the levels of interleukin-10, but it did not influence the production of interleukin-4.	Acetylcysteine	15-18	interferon gamma	Mus musculus	46-62
22773008-10	2012	In all groups, NAC decreased the synthesis of interferon-gamma and nitric oxide, while increasing the levels of interleukin-10, but it did not influence the production of interleukin-4.	Acetylcysteine	15-18	interleukin 10	Mus musculus	112-126
22800716-5	2012	Bay11-7085 (an inhibitor of NF-kappaB pathway) inhibited the up-regulation of HIF-2alpha, and N-acetyl-l-cysteine (a ROS scavenger) inhibited both the decrease of IkappaB-alpha and the up-regulation of HIF-2alpha.	Acetylcysteine	94-113	nuclear factor of kappa light polypeptide gene enhancer in B cells inhibitor, alpha	Mus musculus	163-176
22718889-11	2012	This increase in MnSOD protein apparently depends on the elevation of ROS since it is eliminated by the antioxidant N-acetylcysteine, and it occurs without raising osmolality when ROS are elevated by antimycin A or xanthine oxidase plus xanthine.	Acetylcysteine	116-132	superoxide dismutase 2, mitochondrial	Mus musculus	17-22
22892127-3	2012	Our Western-Blot results in primary cultured human skin keratinocytes and in HaCaT cell line demonstrated that UVB radiation and hydrogen peroxide (H(2)O(2)) induced Cyp-D expression, which was inhibited by anti-oxidant N-acetyl cysteine (NAC).	Acetylcysteine	220-237	peptidylprolyl isomerase F	Homo sapiens	166-171
22892127-3	2012	Our Western-Blot results in primary cultured human skin keratinocytes and in HaCaT cell line demonstrated that UVB radiation and hydrogen peroxide (H(2)O(2)) induced Cyp-D expression, which was inhibited by anti-oxidant N-acetyl cysteine (NAC).	Acetylcysteine	239-242	peptidylprolyl isomerase F	Homo sapiens	166-171
22871220-4	2012	Our resultant data indicated that the expression of HDAC2 in liver increased after CCl(4) exposure, which was attenuated by antioxidants N-acetyl-L-cysteine or alpha-lipoic acid.	Acetylcysteine	137-156	histone deacetylase 2	Mus musculus	52-57
22824464-8	2012	Moreover, it was found that antioxidant N-acetylcysteine (NAC) blocked the induction of apoptosis and partly reversed the activation of JNK and p38, up-regulation of Bax, down-regulation of Bcl-2 and the activation of caspase-3 in NG-treated cells.	Acetylcysteine	40-56	mitogen-activated protein kinase 8	Homo sapiens	136-139
22824464-8	2012	Moreover, it was found that antioxidant N-acetylcysteine (NAC) blocked the induction of apoptosis and partly reversed the activation of JNK and p38, up-regulation of Bax, down-regulation of Bcl-2 and the activation of caspase-3 in NG-treated cells.	Acetylcysteine	40-56	mitogen-activated protein kinase 1	Homo sapiens	144-147
22824464-8	2012	Moreover, it was found that antioxidant N-acetylcysteine (NAC) blocked the induction of apoptosis and partly reversed the activation of JNK and p38, up-regulation of Bax, down-regulation of Bcl-2 and the activation of caspase-3 in NG-treated cells.	Acetylcysteine	40-56	BCL2 associated X, apoptosis regulator	Homo sapiens	166-169
22824464-8	2012	Moreover, it was found that antioxidant N-acetylcysteine (NAC) blocked the induction of apoptosis and partly reversed the activation of JNK and p38, up-regulation of Bax, down-regulation of Bcl-2 and the activation of caspase-3 in NG-treated cells.	Acetylcysteine	40-56	BCL2 apoptosis regulator	Homo sapiens	190-195
22824464-8	2012	Moreover, it was found that antioxidant N-acetylcysteine (NAC) blocked the induction of apoptosis and partly reversed the activation of JNK and p38, up-regulation of Bax, down-regulation of Bcl-2 and the activation of caspase-3 in NG-treated cells.	Acetylcysteine	40-56	caspase 3	Homo sapiens	218-227
22824464-8	2012	Moreover, it was found that antioxidant N-acetylcysteine (NAC) blocked the induction of apoptosis and partly reversed the activation of JNK and p38, up-regulation of Bax, down-regulation of Bcl-2 and the activation of caspase-3 in NG-treated cells.	Acetylcysteine	58-61	mitogen-activated protein kinase 8	Homo sapiens	136-139
22824464-8	2012	Moreover, it was found that antioxidant N-acetylcysteine (NAC) blocked the induction of apoptosis and partly reversed the activation of JNK and p38, up-regulation of Bax, down-regulation of Bcl-2 and the activation of caspase-3 in NG-treated cells.	Acetylcysteine	58-61	mitogen-activated protein kinase 1	Homo sapiens	144-147
22824464-8	2012	Moreover, it was found that antioxidant N-acetylcysteine (NAC) blocked the induction of apoptosis and partly reversed the activation of JNK and p38, up-regulation of Bax, down-regulation of Bcl-2 and the activation of caspase-3 in NG-treated cells.	Acetylcysteine	58-61	BCL2 associated X, apoptosis regulator	Homo sapiens	166-169
22824464-8	2012	Moreover, it was found that antioxidant N-acetylcysteine (NAC) blocked the induction of apoptosis and partly reversed the activation of JNK and p38, up-regulation of Bax, down-regulation of Bcl-2 and the activation of caspase-3 in NG-treated cells.	Acetylcysteine	58-61	BCL2 apoptosis regulator	Homo sapiens	190-195
22824464-8	2012	Moreover, it was found that antioxidant N-acetylcysteine (NAC) blocked the induction of apoptosis and partly reversed the activation of JNK and p38, up-regulation of Bax, down-regulation of Bcl-2 and the activation of caspase-3 in NG-treated cells.	Acetylcysteine	58-61	caspase 3	Homo sapiens	218-227
23351387-2	2012	OBJECTIVE: To evaluate the role of prophylactic ibuprofen and N-acetylcysteine (NAC) on the levels of tumor necrosis factor alpha (TNF- alpha), interleukin- 6(IL-6) and IL-17 and post-treatment pain level in chronic periapical lesions.	Acetylcysteine	62-78	tumor necrosis factor	Homo sapiens	102-129
23351387-2	2012	OBJECTIVE: To evaluate the role of prophylactic ibuprofen and N-acetylcysteine (NAC) on the levels of tumor necrosis factor alpha (TNF- alpha), interleukin- 6(IL-6) and IL-17 and post-treatment pain level in chronic periapical lesions.	Acetylcysteine	80-83	tumor necrosis factor	Homo sapiens	102-129
23351387-2	2012	OBJECTIVE: To evaluate the role of prophylactic ibuprofen and N-acetylcysteine (NAC) on the levels of tumor necrosis factor alpha (TNF- alpha), interleukin- 6(IL-6) and IL-17 and post-treatment pain level in chronic periapical lesions.	Acetylcysteine	80-83	interleukin 6	Homo sapiens	144-158
22781707-9	2012	The upregulated EGFR expression by indoxyl sulfate was suppressed by the antioxidant, N-acetylcysteine.	Acetylcysteine	86-102	epidermal growth factor receptor	Homo sapiens	16-20
22867088-15	2012	In addition, pretreatment of HBEC with the antioxidant N-acetyl cysteine significantly inhibited DEP-induced ERK and Akt phosphorylation, and subsequent IL-8 and IL-1beta expression.	Acetylcysteine	55-72	mitogen-activated protein kinase 1	Homo sapiens	109-112
22564156-8	2012	Additionally, N-acetylcysteine and Tiron inhibited zinc-induced HO-1 upregulation and also nuclear translocation of nuclear factor erythroid 2-related factor 2 (Nrf2).	Acetylcysteine	14-30	NFE2 like bZIP transcription factor 2	Homo sapiens	116-159
22564156-8	2012	Additionally, N-acetylcysteine and Tiron inhibited zinc-induced HO-1 upregulation and also nuclear translocation of nuclear factor erythroid 2-related factor 2 (Nrf2).	Acetylcysteine	14-30	NFE2 like bZIP transcription factor 2	Homo sapiens	161-165
22683510-6	2012	In addition, N-acetyl cysteine (NAC), an ROS scavenger, blocked cell cycle G2/M arrest and phosphorylation of ERK1/2 and Cdc25cSer(216) in U87 cells.	Acetylcysteine	13-30	mitogen-activated protein kinase 3	Homo sapiens	110-116
22683510-6	2012	In addition, N-acetyl cysteine (NAC), an ROS scavenger, blocked cell cycle G2/M arrest and phosphorylation of ERK1/2 and Cdc25cSer(216) in U87 cells.	Acetylcysteine	32-35	mitogen-activated protein kinase 3	Homo sapiens	110-116
22549432-10	2012	NAC increased Deltapsim (P = 0.0001) in all T cells, profoundly reduced mTOR activity (P = 0.0009), enhanced apoptosis (P = 0.0004), reversed expansion of CD4-CD8- T cells (mean +- SEM 1.35 +- 0.12-fold change; P = 0.008), stimulated FoxP3 expression in CD4+CD25+ T cells (P = 0.045), and reduced anti-DNA production (P = 0.049).	Acetylcysteine	0-3	mechanistic target of rapamycin kinase	Homo sapiens	72-76
22549432-10	2012	NAC increased Deltapsim (P = 0.0001) in all T cells, profoundly reduced mTOR activity (P = 0.0009), enhanced apoptosis (P = 0.0004), reversed expansion of CD4-CD8- T cells (mean +- SEM 1.35 +- 0.12-fold change; P = 0.008), stimulated FoxP3 expression in CD4+CD25+ T cells (P = 0.045), and reduced anti-DNA production (P = 0.049).	Acetylcysteine	0-3	CD4 molecule	Homo sapiens	155-158
22549432-10	2012	NAC increased Deltapsim (P = 0.0001) in all T cells, profoundly reduced mTOR activity (P = 0.0009), enhanced apoptosis (P = 0.0004), reversed expansion of CD4-CD8- T cells (mean +- SEM 1.35 +- 0.12-fold change; P = 0.008), stimulated FoxP3 expression in CD4+CD25+ T cells (P = 0.045), and reduced anti-DNA production (P = 0.049).	Acetylcysteine	0-3	CD4 molecule	Homo sapiens	254-257
22549432-11	2012	CONCLUSION: This pilot study suggests that NAC safely improves lupus disease activity by blocking mTOR in T lymphocytes.	Acetylcysteine	43-46	mechanistic target of rapamycin kinase	Homo sapiens	98-102
22351438-5	2012	This raised basal expression of NRF2 appeared to be a response to on-going production of ROS, since treatment with the antioxidant and GSH precursor N-acetylcysteine (NAC) reduced NRF2 expression.	Acetylcysteine	149-165	NFE2 like bZIP transcription factor 2	Homo sapiens	32-36
22351438-5	2012	This raised basal expression of NRF2 appeared to be a response to on-going production of ROS, since treatment with the antioxidant and GSH precursor N-acetylcysteine (NAC) reduced NRF2 expression.	Acetylcysteine	149-165	NFE2 like bZIP transcription factor 2	Homo sapiens	180-184
22351438-5	2012	This raised basal expression of NRF2 appeared to be a response to on-going production of ROS, since treatment with the antioxidant and GSH precursor N-acetylcysteine (NAC) reduced NRF2 expression.	Acetylcysteine	167-170	NFE2 like bZIP transcription factor 2	Homo sapiens	32-36
22351438-5	2012	This raised basal expression of NRF2 appeared to be a response to on-going production of ROS, since treatment with the antioxidant and GSH precursor N-acetylcysteine (NAC) reduced NRF2 expression.	Acetylcysteine	167-170	NFE2 like bZIP transcription factor 2	Homo sapiens	180-184
22710416-7	2012	NAC successfully blocked the inhibition             of HSP70 and HSP90 as well as the activation of caspase-3, suggesting that ROS             is essential in Cr(VI)-induced caspase-3 activation.	Acetylcysteine	0-3	caspase 3	Homo sapiens	100-109
22710416-7	2012	NAC successfully blocked the inhibition             of HSP70 and HSP90 as well as the activation of caspase-3, suggesting that ROS             is essential in Cr(VI)-induced caspase-3 activation.	Acetylcysteine	0-3	caspase 3	Homo sapiens	174-183
22974601-8	2012	Intestinal tissue tumor necrosis factor alpha levels were significantly reduced with NAC treatment in group 3 compared with group 2 (P &lt; .003).	Acetylcysteine	85-88	tumor necrosis factor	Rattus norvegicus	18-45
22825687-11	2012	In the femoral head, co-treatment with NAC and MPSL significantly decreased the expression of TRIM21 at 3 h and significantly increased the expression of interferon (IFN)-alpha at 24 h when compared with the MPSL group.	Acetylcysteine	39-42	tripartite motif containing 21	Homo sapiens	94-100
22825687-11	2012	In the femoral head, co-treatment with NAC and MPSL significantly decreased the expression of TRIM21 at 3 h and significantly increased the expression of interferon (IFN)-alpha at 24 h when compared with the MPSL group.	Acetylcysteine	39-42	interferon alpha 1	Homo sapiens	154-176
23156673-0	2012	N-acetylcysteine enhances neuronal differentiation of P19 embryonic stem cells via Akt and N-cadherin activation.	Acetylcysteine	0-16	AKT serine/threonine kinase 1	Homo sapiens	83-86
23156673-5	2012	Furthermore, NAC-enhanced neuronal differentiation was mediated by activation of Akt.	Acetylcysteine	13-16	AKT serine/threonine kinase 1	Homo sapiens	81-84
22751949-8	2012	An antioxidant, N-acetylcysteine (NAC), attenuated             the generation of ROS and IL-8 mRNA expression in KB and Yumoto cells, and H2O2             increased IL-8 mRNA expression in Yumoto cells, suggesting that ROS generated             by TP caused the increased expression of IL-8 mRNA.	Acetylcysteine	16-32	C-X-C motif chemokine ligand 8	Homo sapiens	89-93
22751949-8	2012	An antioxidant, N-acetylcysteine (NAC), attenuated             the generation of ROS and IL-8 mRNA expression in KB and Yumoto cells, and H2O2             increased IL-8 mRNA expression in Yumoto cells, suggesting that ROS generated             by TP caused the increased expression of IL-8 mRNA.	Acetylcysteine	34-37	C-X-C motif chemokine ligand 8	Homo sapiens	89-93
22751949-8	2012	An antioxidant, N-acetylcysteine (NAC), attenuated             the generation of ROS and IL-8 mRNA expression in KB and Yumoto cells, and H2O2             increased IL-8 mRNA expression in Yumoto cells, suggesting that ROS generated             by TP caused the increased expression of IL-8 mRNA.	Acetylcysteine	34-37	C-X-C motif chemokine ligand 8	Homo sapiens	165-169
22751949-8	2012	An antioxidant, N-acetylcysteine (NAC), attenuated             the generation of ROS and IL-8 mRNA expression in KB and Yumoto cells, and H2O2             increased IL-8 mRNA expression in Yumoto cells, suggesting that ROS generated             by TP caused the increased expression of IL-8 mRNA.	Acetylcysteine	34-37	C-X-C motif chemokine ligand 8	Homo sapiens	165-169
22714038-5	2012	Importantly, N-acetyl cysteine (NAC) treatment effectively blocked apoptosis via the caspase-9 and caspase-3 pathways while NAC attenuated the inhibition of mitochondrial complex I activity as well as the oxidative metabolism of dopamine (DA).	Acetylcysteine	13-30	caspase 9	Rattus norvegicus	85-94
22714038-5	2012	Importantly, N-acetyl cysteine (NAC) treatment effectively blocked apoptosis via the caspase-9 and caspase-3 pathways while NAC attenuated the inhibition of mitochondrial complex I activity as well as the oxidative metabolism of dopamine (DA).	Acetylcysteine	32-35	caspase 9	Rattus norvegicus	85-94
22931549-8	2012	N-acetyl-cysteine (NAC, 5 mM) reduced PM-induced ROS generation in ECs, which further prevented TER decreases and atteneuated ZO-1 degradation.	Acetylcysteine	0-17	tight junction protein 1	Homo sapiens	126-130
22931549-8	2012	N-acetyl-cysteine (NAC, 5 mM) reduced PM-induced ROS generation in ECs, which further prevented TER decreases and atteneuated ZO-1 degradation.	Acetylcysteine	19-22	tight junction protein 1	Homo sapiens	126-130
22696214-10	2012	Furthermore, the administration of N-acetylcysteine also prevented NF-kappaB activation, neutrophil infiltration, hepatocyte apoptosis, and liver damage.	Acetylcysteine	35-51	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	67-76
22867088-15	2012	In addition, pretreatment of HBEC with the antioxidant N-acetyl cysteine significantly inhibited DEP-induced ERK and Akt phosphorylation, and subsequent IL-8 and IL-1beta expression.	Acetylcysteine	55-72	AKT serine/threonine kinase 1	Homo sapiens	117-120
22867088-15	2012	In addition, pretreatment of HBEC with the antioxidant N-acetyl cysteine significantly inhibited DEP-induced ERK and Akt phosphorylation, and subsequent IL-8 and IL-1beta expression.	Acetylcysteine	55-72	C-X-C motif chemokine ligand 8	Homo sapiens	153-157
22867088-15	2012	In addition, pretreatment of HBEC with the antioxidant N-acetyl cysteine significantly inhibited DEP-induced ERK and Akt phosphorylation, and subsequent IL-8 and IL-1beta expression.	Acetylcysteine	55-72	interleukin 1 beta	Homo sapiens	162-170
22564028-8	2012	The ATP-induced MIP-2 production was inhibited by treatment with the antioxidant N-acetyl-l-cysteine.	Acetylcysteine	81-100	chemokine (C-X-C motif) ligand 2	Mus musculus	16-21
22648949-3	2012	H(2)O(2) causes nuclear efflux of HDAC4-GFP or HDAC5-GFP, which is blocked by the ROS scavenger N-acetyl-l-cysteine (NAC).	Acetylcysteine	96-115	histone deacetylase 4	Mus musculus	34-39
22648949-3	2012	H(2)O(2) causes nuclear efflux of HDAC4-GFP or HDAC5-GFP, which is blocked by the ROS scavenger N-acetyl-l-cysteine (NAC).	Acetylcysteine	96-115	histone deacetylase 5	Mus musculus	47-52
22648949-3	2012	H(2)O(2) causes nuclear efflux of HDAC4-GFP or HDAC5-GFP, which is blocked by the ROS scavenger N-acetyl-l-cysteine (NAC).	Acetylcysteine	117-120	histone deacetylase 4	Mus musculus	34-39
22648949-3	2012	H(2)O(2) causes nuclear efflux of HDAC4-GFP or HDAC5-GFP, which is blocked by the ROS scavenger N-acetyl-l-cysteine (NAC).	Acetylcysteine	117-120	histone deacetylase 5	Mus musculus	47-52
22648949-5	2012	During 50-Hz trains, HDAC5-GFP nuclear efflux was completely blocked by NAC, but HDAC4-GFP nuclear efflux was only partially blocked by NAC and partially blocked by the calcium-dependent protein kinase (CaMK) inhibitor KN-62.	Acetylcysteine	72-75	histone deacetylase 5	Mus musculus	21-26
22648949-5	2012	During 50-Hz trains, HDAC5-GFP nuclear efflux was completely blocked by NAC, but HDAC4-GFP nuclear efflux was only partially blocked by NAC and partially blocked by the calcium-dependent protein kinase (CaMK) inhibitor KN-62.	Acetylcysteine	136-139	histone deacetylase 4	Mus musculus	81-86
21953860-6	2012	Pretreatment with antioxidant N-acetyl-L-cysteine, apoptosis signal-regulating kinase 1 inhibitor thioredoxin, and c-Jun NH(2) -terminal kinase inhibitor SP600125 significantly reduced thrombin-induced CCN2 synthesis.	Acetylcysteine	30-49	coagulation factor II, thrombin	Homo sapiens	185-193
22046978-7	2012	NAC administered prior to and after LPS significantly reduced fetal brain IL-6 at E18 and E20 and IL-10 at E20.	Acetylcysteine	0-3	interleukin 6	Rattus norvegicus	74-78
22549117-3	2012	Proton magnetic resonance spectroscopy ((1)H MRS) was used to investigate Glu changes in the dorsal anterior cingulate cortex (dACC) after a single dose of NAC in cocaine-dependent patients and normal controls.	Acetylcysteine	156-159	Acetyl-CoA carboxylase	Drosophila melanogaster	127-131
22554771-9	2012	An antioxidant drug, N-acetyl-l-cysteine significantly inhibited TNF-alpha-induced phosphorylation of p38 and JNK.	Acetylcysteine	21-40	tumor necrosis factor	Rattus norvegicus	65-74
22552773-8	2012	Antioxidants (N-acetyl-cysteine and vitamin C), which blocked oxidative stress induced by chronic ethanol in WT mice and acute ethanol in Cyp2e1  (-/-)   KI mice, also blunted the induction of CYP2A5 and Nrf2 by ethanol but not the induction of CYP2E1 by ethanol.	Acetylcysteine	14-31	nuclear factor, erythroid derived 2, like 2	Mus musculus	204-208
22648416-7	2012	In addition, the potent antioxidant N-acetylcysteine blocked EMT and expression of HIF-1alpha induced by NiCl(2), whereas the DNA methyltransferase inhibitor 5-aza-2"-deoxycytidine restored the down-regulation of E-cadherin induced by NiCl(2).	Acetylcysteine	36-52	hypoxia inducible factor 1 subunit alpha	Homo sapiens	83-93
22648416-7	2012	In addition, the potent antioxidant N-acetylcysteine blocked EMT and expression of HIF-1alpha induced by NiCl(2), whereas the DNA methyltransferase inhibitor 5-aza-2"-deoxycytidine restored the down-regulation of E-cadherin induced by NiCl(2).	Acetylcysteine	36-52	cadherin 1	Homo sapiens	213-223
22575515-8	2012	Meanwhile, results also showed that N-acetylcysteine (a reactive oxygen species scavenger) suppressed the proliferation and the ERK1/2 and JNK activation induced by 5-HT.	Acetylcysteine	36-52	mitogen-activated protein kinase 3	Homo sapiens	128-134
22575515-8	2012	Meanwhile, results also showed that N-acetylcysteine (a reactive oxygen species scavenger) suppressed the proliferation and the ERK1/2 and JNK activation induced by 5-HT.	Acetylcysteine	36-52	mitogen-activated protein kinase 8	Homo sapiens	139-142
22231145-10	2012	IL-1beta-induced cPLA2 expression was mediated through recruitment of activator protein 1 (AP-1) to the cPLA2 promoter region, which was attenuated by NAC and overexpression of HO-1.	Acetylcysteine	151-154	interleukin 1 beta	Mus musculus	0-8
22453841-8	2012	NAC down-regulated MCP-1, CINC and P-selectin in BPDO- but not in NaTc-induced AP.	Acetylcysteine	0-3	selectin P	Rattus norvegicus	35-45
22534037-12	2012	OTC and NAC counteracted the effect of HEMA on GPx1/2, SOD1, and catalase expression.	Acetylcysteine	8-11	superoxide dismutase 1, soluble	Mus musculus	55-59
22534037-12	2012	OTC and NAC counteracted the effect of HEMA on GPx1/2, SOD1, and catalase expression.	Acetylcysteine	8-11	catalase	Mus musculus	65-73
22231145-9	2012	RESULTS: IL-1beta-induced cPLA2 expression was mediated through NOX activation/ROS production, which was attenuated by N-acetylcysteine (NAC; a scavenger of ROS), the inhibitors of NOX (diphenyleneiodonium chloride and apocynin), MEK-1/2 (U0126), and JNK-1/2 (SP600125), transfection with the respective siRNAs, and the overexpression of HO-1 in RASFs.	Acetylcysteine	119-135	interleukin 1 beta	Mus musculus	9-17
22231145-9	2012	RESULTS: IL-1beta-induced cPLA2 expression was mediated through NOX activation/ROS production, which was attenuated by N-acetylcysteine (NAC; a scavenger of ROS), the inhibitors of NOX (diphenyleneiodonium chloride and apocynin), MEK-1/2 (U0126), and JNK-1/2 (SP600125), transfection with the respective siRNAs, and the overexpression of HO-1 in RASFs.	Acetylcysteine	119-135	heme oxygenase 1	Mus musculus	338-342
22231145-9	2012	RESULTS: IL-1beta-induced cPLA2 expression was mediated through NOX activation/ROS production, which was attenuated by N-acetylcysteine (NAC; a scavenger of ROS), the inhibitors of NOX (diphenyleneiodonium chloride and apocynin), MEK-1/2 (U0126), and JNK-1/2 (SP600125), transfection with the respective siRNAs, and the overexpression of HO-1 in RASFs.	Acetylcysteine	137-140	interleukin 1 beta	Mus musculus	9-17
22231145-9	2012	RESULTS: IL-1beta-induced cPLA2 expression was mediated through NOX activation/ROS production, which was attenuated by N-acetylcysteine (NAC; a scavenger of ROS), the inhibitors of NOX (diphenyleneiodonium chloride and apocynin), MEK-1/2 (U0126), and JNK-1/2 (SP600125), transfection with the respective siRNAs, and the overexpression of HO-1 in RASFs.	Acetylcysteine	137-140	heme oxygenase 1	Mus musculus	338-342
22161819-11	2012	Treatment of the cells with NAC restored the activity of PTP1B, improved the profile of PDGFR phosphorylation, decreased the numbers of tyrosine-phosphorylated proteins and levels of type I collagen, and scavenged ROS in SSc fibroblasts.	Acetylcysteine	28-31	platelet derived growth factor receptor beta	Homo sapiens	88-93
22471522-5	2012	IL-6 combined with IR or Dex increased early intracellular pro-oxidant levels that were causally related to activation of NF-kappaB (nuclear factor kappaB) as determined by the ability of N-acetylcysteine to suppress both pro-oxidant levels and NF-kappaB activation.	Acetylcysteine	188-204	interleukin 6	Homo sapiens	0-4
22522044-11	2012	Treatment of infected animals with anti-oxidants alpha-lipoic acid and N-acetylcysteine and HO inhibitor stannous protoporphyrin (SnPPIX) showed only selective beneficial effects on HO-1 and COX-2 expression in the liver and spleen and serum levels of KC and MCP-1.	Acetylcysteine	71-87	heme oxygenase 1	Mus musculus	182-186
22546856-8	2012	Addition of GSH or N-acetylcysteine to PBMCs             selectively restored IL-12 and IFN-gamma production and improved bacterial             killing.	Acetylcysteine	19-35	interferon gamma	Homo sapiens	88-97
22622864-8	2012	Furthermore, As(2)O(3) (10 muM) effectively decreased the phosphorylation of Akt, which could be reversed by NAC.	Acetylcysteine	109-112	AKT serine/threonine kinase 1	Homo sapiens	77-80
22581648-9	2012	In addition, an antioxidant N-acetylcysteine mimicked the effects of GIP on RAGE and VCAM-1 gene expression in HUVECs.	Acetylcysteine	28-44	gastric inhibitory polypeptide	Homo sapiens	69-72
22581648-9	2012	In addition, an antioxidant N-acetylcysteine mimicked the effects of GIP on RAGE and VCAM-1 gene expression in HUVECs.	Acetylcysteine	28-44	vascular cell adhesion molecule 1	Homo sapiens	85-91
22137594-10	2012	CONCLUSIONS: The effect of NAC on relapse to cocaine seeking depends on the balance between stimulating mGluR2/3 and mGluR5 in the NAcore, and the efficacy of NAC can be improved by simultaneously inhibiting mGluR5.	Acetylcysteine	27-30	glutamate receptor, metabotropic 2	Mus musculus	104-112
22041018-11	2012	This increase in VEGF and IL6 was blocked by the ROS scavenger N-acetyl cysteine (NAC).	Acetylcysteine	63-80	vascular endothelial growth factor A	Homo sapiens	17-21
22105918-9	2012	Pre-treatment of CRC cells with the antioxidant N-acetylcysteine (NAC) significantly inhibited activation of caspase-4 and altholactone-induced apoptosis.	Acetylcysteine	48-64	caspase 4	Homo sapiens	109-118
22105918-9	2012	Pre-treatment of CRC cells with the antioxidant N-acetylcysteine (NAC) significantly inhibited activation of caspase-4 and altholactone-induced apoptosis.	Acetylcysteine	66-69	caspase 4	Homo sapiens	109-118
22300897-0	2012	TRPM2 channel protective properties of N-acetylcysteine on cytosolic glutathione depletion dependent oxidative stress and Ca2+ influx in rat dorsal root ganglion.	Acetylcysteine	39-55	transient receptor potential cation channel, subfamily M, member 2	Rattus norvegicus	0-5
22300897-4	2012	NAC may have a protective role on calcium influx through regulation of TRPM2 channels in the neurons.	Acetylcysteine	0-3	transient receptor potential cation channel, subfamily M, member 2	Rattus norvegicus	71-76
22300897-5	2012	Therefore, we tested the effects of NAC on TRPM2 channel currents in cytosolic GSH depleted DRG in rats.	Acetylcysteine	36-39	transient receptor potential cation channel, subfamily M, member 2	Rattus norvegicus	43-48
22300897-9	2012	BSO + H(2)O(2)-induced TRPM2 channel gating was totally inhibited by extracellular NAC and partially inhibited by 2-aminoethyl diphenylborinate.	Acetylcysteine	83-86	transient receptor potential cation channel, subfamily M, member 2	Rattus norvegicus	23-28
22300897-11	2012	In conclusion, we observed a modulator role of NAC on Ca(2+) influx through a TRPM2 channel in intracellular GSH depleted DRG neurons.	Acetylcysteine	47-50	transient receptor potential cation channel, subfamily M, member 2	Rattus norvegicus	78-83
22551149-10	2012	Both NAC and alpha-toco protected against caspase-3 induction following PB282 treatment, while only NAC offered protection following SW43 treatment.	Acetylcysteine	5-8	caspase 3	Homo sapiens	42-51
22041018-11	2012	This increase in VEGF and IL6 was blocked by the ROS scavenger N-acetyl cysteine (NAC).	Acetylcysteine	63-80	interleukin 6	Homo sapiens	26-29
22041018-11	2012	This increase in VEGF and IL6 was blocked by the ROS scavenger N-acetyl cysteine (NAC).	Acetylcysteine	82-85	vascular endothelial growth factor A	Homo sapiens	17-21
22041018-11	2012	This increase in VEGF and IL6 was blocked by the ROS scavenger N-acetyl cysteine (NAC).	Acetylcysteine	82-85	interleukin 6	Homo sapiens	26-29
22537194-8	2012	We show that an increment of the intracellular reactive oxygen species (ROS) and p53 is required for MTA-induced cytotoxicity by utilizing N-Acetyl-L-Cysteine (NAC) to blockage of ROS and p53-defective H1299 NSCLC cell line.	Acetylcysteine	139-158	tumor protein p53	Homo sapiens	81-84
22509835-4	2012	A decrease in the p53 protein with increased protein ubiquitination was detected in QUE/As(+3)-treated HaCaT cells, and this was prevented by the addition of NAC.	Acetylcysteine	158-161	tumor protein p53	Homo sapiens	18-21
22325070-7	2012	Increased expression of EGFR and fibrocyte proliferation and transformation were induced by hydrogen peroxide, and these effects were inhibited by N-acetylcysteine.	Acetylcysteine	147-163	epidermal growth factor receptor	Homo sapiens	24-28
22497815-5	2012	Treatments of N-acetylcysteine and glutathione markedly reduced protein levels of both NFAT5 and Hsp72.	Acetylcysteine	14-30	heat shock protein family A (Hsp70) member 1A	Homo sapiens	97-102
22319213-7	2012	Double-strand breaks were reduced when cells were treated with the reactive oxygen species scavenger N-acetyl-cysteine, but this did not rescue the cell proliferation defect, indicating that several classes of endogenously formed DNA lesions require Rev3L for tolerance or repair.	Acetylcysteine	101-118	REV3 like, DNA directed polymerase zeta catalytic subunit	Homo sapiens	250-255
21796654-9	2012	We show that ROS production preceded AR protein loss and that ca27-mediated down-regulation of the AR was attenuated by the antioxidant, N-acetyl cysteine.	Acetylcysteine	137-154	androgen receptor	Homo sapiens	99-101
21978796-8	2012	Plasma IL-6 was lower on days 4-5 (p&lt;0.05), IL-8 on days 4-6 (p&lt;0.05) and IL-10 on days 4-6 (p&lt;0.05) in NAC group.	Acetylcysteine	113-116	interleukin 6	Homo sapiens	7-11
22537194-8	2012	We show that an increment of the intracellular reactive oxygen species (ROS) and p53 is required for MTA-induced cytotoxicity by utilizing N-Acetyl-L-Cysteine (NAC) to blockage of ROS and p53-defective H1299 NSCLC cell line.	Acetylcysteine	139-158	tumor protein p53	Homo sapiens	188-191
22330067-9	2012	Moreover, epirubicin significantly enhanced the phosphorylation of p38 MAPK, and these effects were attenuated by GSH and NAC.	Acetylcysteine	122-125	mitogen-activated protein kinase 14	Homo sapiens	67-70
22781576-12	2012	The level of SOD in the NAC group increased versus the irradiation group (10.7 +- 3.0 vs 8.7 +- 1.3, P &lt; 0.05).	Acetylcysteine	24-27	superoxide dismutase [Mn], mitochondrial	Cavia porcellus	13-16
22389501-6	2012	Phorbol myristate acetate, a known stimulator of NF-kappaB, increased the levels of GRK5 in myocytes whereas treatment of cells with N-acetyl cysteine, a known inhibitor of NF-kappaB, or with SC 514, an inhibitor of IkappaB kinase 2 decreased GRK5.	Acetylcysteine	133-150	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	173-182
22342303-9	2012	Furthermore, NAC treatment abrogated CSE-stimulated Src activation.	Acetylcysteine	13-16	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	52-55
22392142-7	2012	On the other hand, N-acetyl-L-cysteine decreased mRNA stability of ICAM-1 and IL-6 in LPS-treated cells and IL-6 and ICAM-1 in TNF-alpha-treated cells.	Acetylcysteine	19-38	interleukin 6	Homo sapiens	78-82
22318155-7	2012	Angiotensin II also inhibited the anandamide transporter activity concentration-dependently while increased intracellular reactive oxygen species production, which was reversed by pretreatment with losartan or n-acetyl-cysteine.	Acetylcysteine	210-227	angiotensinogen	Rattus norvegicus	0-14
22745145-9	2012	CONCLUSION: short-term oral NAC treatment resulted in reduction of circulating PCT, IL-6, IL-1, C3, sICAM, hsCRP, and TNF- in CAPD patients.	Acetylcysteine	28-31	interleukin 6	Homo sapiens	84-88
22745145-9	2012	CONCLUSION: short-term oral NAC treatment resulted in reduction of circulating PCT, IL-6, IL-1, C3, sICAM, hsCRP, and TNF- in CAPD patients.	Acetylcysteine	28-31	tumor necrosis factor	Homo sapiens	118-121
22294162-5	2012	N-acetylcysteine, a reactive oxygen species scavenger, not only blocked the oridonin-induced increase in hydrogen peroxide and glutathione depletion, but also blocked apoptosis and senescence induced by oridonin, as evidenced by the decrease in Annexin V and senescence-associated beta-galactosidase- positive cells and the inhibition of oridonin-induced upregulation of p53 and p16 and downregulation of c-Myc.	Acetylcysteine	0-16	tumor protein p53	Homo sapiens	371-374
22294162-5	2012	N-acetylcysteine, a reactive oxygen species scavenger, not only blocked the oridonin-induced increase in hydrogen peroxide and glutathione depletion, but also blocked apoptosis and senescence induced by oridonin, as evidenced by the decrease in Annexin V and senescence-associated beta-galactosidase- positive cells and the inhibition of oridonin-induced upregulation of p53 and p16 and downregulation of c-Myc.	Acetylcysteine	0-16	cyclin dependent kinase inhibitor 2A	Homo sapiens	379-382
22284448-12	2012	Experimental results were further supported by density functional theory (DFT) calculations of supermolecular interaction energies (E(inter)) showing a greater interaction of Pb(II) with NACA than NAC.	Acetylcysteine	187-190	submaxillary gland androgen regulated protein 3B	Homo sapiens	175-181
22093110-3	2012	We compared the effects of fluoride-induced changes with those obtained when stimulating HUVECs with TNF-alpha and verified whether N-acetyl cysteine (NAC), well-known antioxidant, can prevent both fluoride- and TNF-alpha-induced alterations.	Acetylcysteine	132-149	tumor necrosis factor	Homo sapiens	212-221
22093110-3	2012	We compared the effects of fluoride-induced changes with those obtained when stimulating HUVECs with TNF-alpha and verified whether N-acetyl cysteine (NAC), well-known antioxidant, can prevent both fluoride- and TNF-alpha-induced alterations.	Acetylcysteine	151-154	tumor necrosis factor	Homo sapiens	212-221
22093110-5	2012	Pre-incubating HUVECs with NAC prevented the effects induced by 5.0 mM of NaF and 0.5 mM of Sn(2) F.	Acetylcysteine	27-30	C-X-C motif chemokine ligand 8	Homo sapiens	74-77
22327021-6	2012	The study corroborates the antidepressant-like effects of NAC in the TST, a model with a well-established predictive value.	Acetylcysteine	58-61	thiosulfate sulfurtransferase, mitochondrial	Mus musculus	69-72
22418739-8	2012	Exposure to the antioxidant N-acetylcysteine reduced oxidative stress and improved survival in the RYR1-related myopathies human myotubes ex vivo and led to significant restoration of aspects of muscle function in the relatively relaxed zebrafish, thereby confirming its efficacy in vivo.	Acetylcysteine	28-44	ryanodine receptor 1	Homo sapiens	99-103
22284448-6	2012	XPS of the Pb 4f orbitals showed that more Pb(II) was chemically bound to NACA than NAC.	Acetylcysteine	74-77	submaxillary gland androgen regulated protein 3B	Homo sapiens	43-49
22392142-7	2012	On the other hand, N-acetyl-L-cysteine decreased mRNA stability of ICAM-1 and IL-6 in LPS-treated cells and IL-6 and ICAM-1 in TNF-alpha-treated cells.	Acetylcysteine	19-38	interleukin 6	Homo sapiens	108-112
22392142-7	2012	On the other hand, N-acetyl-L-cysteine decreased mRNA stability of ICAM-1 and IL-6 in LPS-treated cells and IL-6 and ICAM-1 in TNF-alpha-treated cells.	Acetylcysteine	19-38	tumor necrosis factor	Homo sapiens	127-136
22198183-9	2012	Preincubating RLE-6TN cells with N-acetylcysteine, an antioxidant, abolished the radiation-induced phosphorylation of ERK and altered protein levels of Snail, E-cadherin, and alpha-SMA.	Acetylcysteine	33-49	Eph receptor B1	Rattus norvegicus	118-121
22115526-10	2012	And, the general apoptosis marker-Caspase-3 activation-was also greatly relieved by NAC.	Acetylcysteine	84-87	caspase 3	Homo sapiens	34-43
21997484-8	2012	The inhibition of Src by PP2 and ROS production by N-acetyl cysteine inhibited the disassembly of VE-cadherin-p120-catenin complexes, and attenuated high OxPAPC-induced EC barrier disruption.	Acetylcysteine	51-68	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	18-21
21827635-5	2012	RESULTS: Analysis was conducted on the mitogen-activated protein kinase signalling pathways, demonstrating that NAC infusion blocked the exercise-induced increase in JNK phosphorylation, but not ERK1/2, or p38 MAPK.	Acetylcysteine	112-115	mitogen-activated protein kinase 8	Homo sapiens	166-169
21997484-8	2012	The inhibition of Src by PP2 and ROS production by N-acetyl cysteine inhibited the disassembly of VE-cadherin-p120-catenin complexes, and attenuated high OxPAPC-induced EC barrier disruption.	Acetylcysteine	51-68	cadherin 5	Homo sapiens	98-109
24116290-7	2012	ERK phosphorylation was also increased by scratching cells but it was decreased by the treatment with ROS scavengers, N-acetylcysteine (NAC).	Acetylcysteine	118-134	mitogen-activated protein kinase 1	Mus musculus	0-3
24116290-7	2012	ERK phosphorylation was also increased by scratching cells but it was decreased by the treatment with ROS scavengers, N-acetylcysteine (NAC).	Acetylcysteine	136-139	mitogen-activated protein kinase 1	Mus musculus	0-3
22283740-6	2012	The ROS scavenger N-acetyl cysteine (NAC) attenuated silibinin-induced up-regulation of p-p53 expression, suggesting that p53 might be regulated by ROS and forms a positive feedback loop with ROS.	Acetylcysteine	18-35	tumor protein p53	Homo sapiens	90-93
22166790-5	2012	Pre-treatment with antioxidant vitamin E or N-acetylcysteine (NAC) completely abolished the I6-induced generation of ROS, loss of MMP, release of cytochrome c, activation of caspase-9 and caspase-3, and cleavage of PARP.	Acetylcysteine	44-60	caspase 9	Rattus norvegicus	174-183
22166790-5	2012	Pre-treatment with antioxidant vitamin E or N-acetylcysteine (NAC) completely abolished the I6-induced generation of ROS, loss of MMP, release of cytochrome c, activation of caspase-9 and caspase-3, and cleavage of PARP.	Acetylcysteine	62-65	caspase 9	Rattus norvegicus	174-183
22283740-6	2012	The ROS scavenger N-acetyl cysteine (NAC) attenuated silibinin-induced up-regulation of p-p53 expression, suggesting that p53 might be regulated by ROS and forms a positive feedback loop with ROS.	Acetylcysteine	18-35	tumor protein p53	Homo sapiens	122-125
22283740-6	2012	The ROS scavenger N-acetyl cysteine (NAC) attenuated silibinin-induced up-regulation of p-p53 expression, suggesting that p53 might be regulated by ROS and forms a positive feedback loop with ROS.	Acetylcysteine	37-40	tumor protein p53	Homo sapiens	90-93
22283740-6	2012	The ROS scavenger N-acetyl cysteine (NAC) attenuated silibinin-induced up-regulation of p-p53 expression, suggesting that p53 might be regulated by ROS and forms a positive feedback loop with ROS.	Acetylcysteine	37-40	tumor protein p53	Homo sapiens	122-125
22382681-5	2012	Doxorubicin-induced TG2 activity was suppressed by treatment with caffeine at the early phase, N-acetylcysteine at the mid-phase, and EGTA at the late phase.	Acetylcysteine	95-111	transglutaminase 2	Homo sapiens	20-23
22065336-4	2012	We utilized comprehensive proteomics to identify alterations in liver protein expression during pretreatment with triptolide or N-acetylcysteine (NAC) after LPS/D-GalN injection, 44 proteins were found to be related to oxidative stress, mitochondria, metabolism and signal transduction, and 23 proteins of them seemed to be significantly up- or down-regulated.	Acetylcysteine	128-144	galanin and GMAP prepropeptide	Mus musculus	163-167
22065336-4	2012	We utilized comprehensive proteomics to identify alterations in liver protein expression during pretreatment with triptolide or N-acetylcysteine (NAC) after LPS/D-GalN injection, 44 proteins were found to be related to oxidative stress, mitochondria, metabolism and signal transduction, and 23 proteins of them seemed to be significantly up- or down-regulated.	Acetylcysteine	146-149	galanin and GMAP prepropeptide	Mus musculus	163-167
22245127-8	2012	The regulation of the expression of Bcl-2-family proteins, the release of cytochrome c and the activation of caspases 9, 3 and 6 were inhibited in the presence of NAC.	Acetylcysteine	163-166	BCL2 apoptosis regulator	Homo sapiens	36-41
22245127-8	2012	The regulation of the expression of Bcl-2-family proteins, the release of cytochrome c and the activation of caspases 9, 3 and 6 were inhibited in the presence of NAC.	Acetylcysteine	163-166	cytochrome c, somatic	Homo sapiens	74-86
22318816-8	2012	NAC reduced the expression of p22phox and p67phox, suppressed p67phox membrane translocation, and reduced free 15-F(2t)-isoprostane levels in all tissues.	Acetylcysteine	0-3	cytochrome b-245 alpha chain	Rattus norvegicus	30-37
22241216-11	2012	NAC was effectively significant in preventing TGF-beta and IL-6 expression and further augmented the IL-10 expression.	Acetylcysteine	0-3	interleukin 6	Rattus norvegicus	59-63
22244881-11	2012	Apocynin and/or NAC also mitigated Zn- and PQ-induced alterations in oxidative stress, NADPH oxidase activation and cytochrome c release, caspases-9 and -3 activation and CD11b expression.	Acetylcysteine	16-19	caspase 9	Rattus norvegicus	138-155
22244881-11	2012	Apocynin and/or NAC also mitigated Zn- and PQ-induced alterations in oxidative stress, NADPH oxidase activation and cytochrome c release, caspases-9 and -3 activation and CD11b expression.	Acetylcysteine	16-19	integrin subunit alpha M	Rattus norvegicus	171-176
22139554-7	2012	In accordance, N-acetyl-cysteine and tempol, but not apocynin, inhibited the hypoxic effect and restored PKCepsilon protein and mRNA expression to the control values in foetal hearts and H9c2 cells.	Acetylcysteine	15-32	protein kinase C, epsilon	Rattus norvegicus	105-115
22019695-6	2012	Nrf2 protein levels in both nuclear and whole cell lysates were increased after sulforaphane treatment and were decreased by pretreatment with NAC, actinomycin D and cycloheximide.	Acetylcysteine	143-146	NFE2 like bZIP transcription factor 2	Homo sapiens	0-4
22019695-7	2012	Activation of the Nrf2/HO-1 system after sulforaphane treatment was suppressed by pretreatment with NAC or Ly294002, a PI3K inhibitor.	Acetylcysteine	100-103	NFE2 like bZIP transcription factor 2	Homo sapiens	18-22
22134636-0	2012	Pro-oxidant and antioxidant effects of N-acetylcysteine regulate doxorubicin-induced NF-kappa B activity in leukemic cells.	Acetylcysteine	39-55	nuclear factor kappa B subunit 1	Homo sapiens	85-95
21928347-8	2012	Furthermore, these effects were regulated by redox conditions since antioxidant N-acetylcysteine abolished the HO-1/HMGB1/caspase-3 axis.	Acetylcysteine	80-96	heme oxygenase 1	Mus musculus	111-115
22249458-7	2012	An ERK inhibitor U0126 and an antioxidant N-acetylcysteine prevented the expression and activity of beta-secretase, ERK activation, and reactive oxygen species generation in both neurons and PC12 cells expressing mutant PS2 in a dose-dependent manner.	Acetylcysteine	42-58	Eph receptor B1	Rattus norvegicus	116-119
22249458-7	2012	An ERK inhibitor U0126 and an antioxidant N-acetylcysteine prevented the expression and activity of beta-secretase, ERK activation, and reactive oxygen species generation in both neurons and PC12 cells expressing mutant PS2 in a dose-dependent manner.	Acetylcysteine	42-58	presenilin 2	Rattus norvegicus	220-223
21968809-7	2012	The treatment of tobacco-exposed MI rats with NAC resulted in significantly increased levels of intracardiac mRNA expression of antioxidants, including superoxide dismutase, thioredoxin and nuclear factor-E2-related factor 2, as well as circulating levels of glutathione (7+-0.12 vs 10+-0.18; P&lt;=0.001), where the levels were almost identical to the tobacco-naive sham rats.	Acetylcysteine	46-49	thioredoxin 1	Rattus norvegicus	174-185
22085531-8	2012	Importantly, the ROS scavenger N-acetylcysteine (NAC) could inhibited LPS-induced autophagy and knockdown of p8 by RNA interference inhibited the autophagy, p53 protein level increase, the translocation of p53 into nuclei and the ROS level increase induced by LPS in HUVECs.	Acetylcysteine	49-52	tumor protein p53	Homo sapiens	157-160
22134636-6	2012	We report a functional consequence of NAC supplementation during doxorubicin (Dox) chemotherapy administration via the NF-kappa B (NF-kappaB) signal transduction pathway.	Acetylcysteine	38-41	nuclear factor kappa B subunit 1	Homo sapiens	119-129
22134636-6	2012	We report a functional consequence of NAC supplementation during doxorubicin (Dox) chemotherapy administration via the NF-kappa B (NF-kappaB) signal transduction pathway.	Acetylcysteine	38-41	nuclear factor kappa B subunit 1	Homo sapiens	131-140
22134636-7	2012	The ability of NAC to alter Dox-induced NF-kappaB activity is contingent on the ROS-mediated S-glutathionylation of IKK-beta.	Acetylcysteine	15-18	nuclear factor kappa B subunit 1	Homo sapiens	40-49
22134636-8	2012	Moreover, the NAC-dependent alteration of intracellular glutathione redox balance, through pro-oxidant and antioxidant mechanisms, can be exploited to either promote or inhibit Dox-induced NF-kappaB activity in an NAC-concentration-dependent manner.	Acetylcysteine	14-17	nuclear factor kappa B subunit 1	Homo sapiens	189-198
22134636-8	2012	Moreover, the NAC-dependent alteration of intracellular glutathione redox balance, through pro-oxidant and antioxidant mechanisms, can be exploited to either promote or inhibit Dox-induced NF-kappaB activity in an NAC-concentration-dependent manner.	Acetylcysteine	214-217	nuclear factor kappa B subunit 1	Homo sapiens	189-198
22134636-9	2012	We developed an electron-transfer-based computational model that predicts the effect of NAC pretreatment on Dox-induced NF-kappaB signaling for a range of NAC and Dox treatment combinations.	Acetylcysteine	88-91	nuclear factor kappa B subunit 1	Homo sapiens	120-129
22134636-9	2012	We developed an electron-transfer-based computational model that predicts the effect of NAC pretreatment on Dox-induced NF-kappaB signaling for a range of NAC and Dox treatment combinations.	Acetylcysteine	155-158	nuclear factor kappa B subunit 1	Homo sapiens	120-129
22079975-9	2012	Administration of N-acetyl cysteine, a scavenger of ROS, also resulted in significant inhibition of apoptosis induced by combinatory treatment with J7 and TRAIL.	Acetylcysteine	18-35	TNF superfamily member 10	Homo sapiens	155-160
21660448-9	2012	Pretreatment with N-acetylcysteine (NAC) inhibited DMF-induced upregulation of DR5, CHOP, GPR78, and ATF4 protein expression and blocked the cotreatment-induced apoptosis.	Acetylcysteine	18-34	DNA damage inducible transcript 3	Homo sapiens	84-88
22155089-8	2012	Furthermore, DEHP (10mug/ml) significantly increases ROS levels and reduces the expression and activity of SOD1 compared to DMSO controls, whereas NAC (0.5mM) rescues the effects of DEHP on ROS levels and SOD1.	Acetylcysteine	147-150	superoxide dismutase 1, soluble	Mus musculus	205-209
22791152-5	2012	In addition, the expressions of antioxidant catalase and glutathione peroxidase were abrogated by treatment using LS-1 with or without NAC.	Acetylcysteine	135-138	catalase	Homo sapiens	44-52
21928090-6	2012	Cucurbitacin-sensitized TRAIL-induced cytotoxicity was inhibited by N-acetyl cysteine.	Acetylcysteine	68-85	TNF superfamily member 10	Homo sapiens	24-29
21660448-9	2012	Pretreatment with N-acetylcysteine (NAC) inhibited DMF-induced upregulation of DR5, CHOP, GPR78, and ATF4 protein expression and blocked the cotreatment-induced apoptosis.	Acetylcysteine	36-39	DNA damage inducible transcript 3	Homo sapiens	84-88
22217266-8	2012	The antioxidant N-acetyl-L-cysteine reduced ROS production and STAT1 activity induced by Ang II, indicating that Ang II uses ROS as a second messenger to regulate STAT1 activity.	Acetylcysteine	16-35	angiotensinogen	Homo sapiens	89-95
22217266-8	2012	The antioxidant N-acetyl-L-cysteine reduced ROS production and STAT1 activity induced by Ang II, indicating that Ang II uses ROS as a second messenger to regulate STAT1 activity.	Acetylcysteine	16-35	angiotensinogen	Homo sapiens	113-119
21806545-9	2012	Atorvastatin, SP600125, JNK siRNA (small interfering RNA) and NAC (N-acetylcysteine) completely attenuated the leptin and phospho-JNK protein expression induced by Ang II.	Acetylcysteine	62-65	mitogen-activated protein kinase 8	Homo sapiens	130-133
21806545-9	2012	Atorvastatin, SP600125, JNK siRNA (small interfering RNA) and NAC (N-acetylcysteine) completely attenuated the leptin and phospho-JNK protein expression induced by Ang II.	Acetylcysteine	67-83	mitogen-activated protein kinase 8	Homo sapiens	130-133
21826188-6	2012	The ATO/CMEMM-induced activation of caspase-3 and caspase-9 can be blocked by NAC.	Acetylcysteine	78-81	caspase 3	Homo sapiens	36-45
22701509-5	2012	An increase in intracellular reactive oxygen species (ROS) was observed in AC-treated cells, whereas antioxidant N-acetylcysteine (NAC) significantly prevented AC induced HER-2/neu depletion and cell death, which directly indicates that AC-induced HER-2/neu depletion and cell death was mediated by ROS generation.	Acetylcysteine	113-129	erb-b2 receptor tyrosine kinase 2	Homo sapiens	171-176
22701509-5	2012	An increase in intracellular reactive oxygen species (ROS) was observed in AC-treated cells, whereas antioxidant N-acetylcysteine (NAC) significantly prevented AC induced HER-2/neu depletion and cell death, which directly indicates that AC-induced HER-2/neu depletion and cell death was mediated by ROS generation.	Acetylcysteine	113-129	erb-b2 receptor tyrosine kinase 2	Homo sapiens	248-253
22701509-5	2012	An increase in intracellular reactive oxygen species (ROS) was observed in AC-treated cells, whereas antioxidant N-acetylcysteine (NAC) significantly prevented AC induced HER-2/neu depletion and cell death, which directly indicates that AC-induced HER-2/neu depletion and cell death was mediated by ROS generation.	Acetylcysteine	131-134	erb-b2 receptor tyrosine kinase 2	Homo sapiens	171-176
22701509-5	2012	An increase in intracellular reactive oxygen species (ROS) was observed in AC-treated cells, whereas antioxidant N-acetylcysteine (NAC) significantly prevented AC induced HER-2/neu depletion and cell death, which directly indicates that AC-induced HER-2/neu depletion and cell death was mediated by ROS generation.	Acetylcysteine	131-134	erb-b2 receptor tyrosine kinase 2	Homo sapiens	248-253
22419868-7	2012	Moreover, inhibition of reactive oxygen species with an antioxidant, N-acetyl-L-cysteine, clearly suppressed upregulation of Fas, conformational activation of Bax, and subsequent apoptotic cell death in response to combination treatment using TiO(2) (P25-70) and ultraviolet A irradiation.	Acetylcysteine	69-88	BCL2 associated X, apoptosis regulator	Homo sapiens	159-162
23319348-10	2012	NAC administration also improved hematopoietic differentiation of iPSCs in terms of production of CD34, CD45 and CD43 positive cells.	Acetylcysteine	0-3	CD34 molecule	Homo sapiens	98-102
23319348-10	2012	NAC administration also improved hematopoietic differentiation of iPSCs in terms of production of CD34, CD45 and CD43 positive cells.	Acetylcysteine	0-3	sialophorin	Homo sapiens	113-117
21627650-7	2012	Hypoxia-induced increase in urotensin II protein and ROS was significantly attenuated after the addition of SP600125, JNK siRNA or N-acetylcysteine before hypoxia treatment.	Acetylcysteine	131-147	urotensin 2	Rattus norvegicus	28-40
22946344-6	2012	Likewise, NAC prevented the induction of apoptosis (annexin V-FITC binding and cleavage of PARP-1 and procaspases-3,-8 and -9) and reversed the loss of mitochondrial membrane potential and release of cytochrome c from mitochondria by CDDO-Me.	Acetylcysteine	10-13	poly(ADP-ribose) polymerase 1	Homo sapiens	91-125
22694287-9	2012	ISL treatment increased the degradation of PARP, which was counteracted by antioxidants (NAC or CAT), whereas the combination treatment of ISL and pro-oxidant (BSO) enhanced the PARP degradation induced by ISL.	Acetylcysteine	89-92	poly(ADP-ribose) polymerase 1	Homo sapiens	43-47
22946344-6	2012	Likewise, NAC prevented the induction of apoptosis (annexin V-FITC binding and cleavage of PARP-1 and procaspases-3,-8 and -9) and reversed the loss of mitochondrial membrane potential and release of cytochrome c from mitochondria by CDDO-Me.	Acetylcysteine	10-13	cytochrome c, somatic	Homo sapiens	200-212
22946344-7	2012	CDDO-Me down-regulated p-Akt, p-mTOR and NF-kappaB (p65) but increased the activation of Erk1/2 and NAC blocked the modulation of these cell signaling proteins by CDDO-Me.	Acetylcysteine	100-103	AKT serine/threonine kinase 1	Homo sapiens	25-28
22946344-7	2012	CDDO-Me down-regulated p-Akt, p-mTOR and NF-kappaB (p65) but increased the activation of Erk1/2 and NAC blocked the modulation of these cell signaling proteins by CDDO-Me.	Acetylcysteine	100-103	mechanistic target of rapamycin kinase	Homo sapiens	32-36
22946344-7	2012	CDDO-Me down-regulated p-Akt, p-mTOR and NF-kappaB (p65) but increased the activation of Erk1/2 and NAC blocked the modulation of these cell signaling proteins by CDDO-Me.	Acetylcysteine	100-103	mitogen-activated protein kinase 3	Homo sapiens	89-95
22001128-8	2012	Ancillary antioxidant measures - phase 2 inducing phytochemicals, melatonin, N-acetylcysteine, and astaxanthin - may also aid cox-2 down-regulation.	Acetylcysteine	77-93	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	126-131
20798331-10	2012	RESULTS: The levels of adiponectin in plasma and spent dialysate were significantly downregulated by PDS and this effect was suppressed by NAC.	Acetylcysteine	139-142	adiponectin, C1Q and collagen domain containing	Homo sapiens	23-34
22078209-0	2012	Modulation of CD40-activated B lymphocytes by N-acetylcysteine involves decreased phosphorylation of STAT3.	Acetylcysteine	46-62	signal transducer and activator of transcription 3	Homo sapiens	101-106
22078209-7	2012	Mechanistically, a 24h exposure of B lymphocytes with NAC is sufficient to show strong inhibition of STAT3 phosphorylation.	Acetylcysteine	54-57	signal transducer and activator of transcription 3	Homo sapiens	101-106
22078209-8	2012	Besides, the treatment of B lymphocytes with the STAT3 inhibitor VI increases viability and decreases proliferation and secretion as in NAC-treated cells thus showing a role for STAT3 in these NAC-induced phenotypes.	Acetylcysteine	136-139	signal transducer and activator of transcription 3	Homo sapiens	49-54
22078209-8	2012	Besides, the treatment of B lymphocytes with the STAT3 inhibitor VI increases viability and decreases proliferation and secretion as in NAC-treated cells thus showing a role for STAT3 in these NAC-induced phenotypes.	Acetylcysteine	136-139	signal transducer and activator of transcription 3	Homo sapiens	178-183
22078209-8	2012	Besides, the treatment of B lymphocytes with the STAT3 inhibitor VI increases viability and decreases proliferation and secretion as in NAC-treated cells thus showing a role for STAT3 in these NAC-induced phenotypes.	Acetylcysteine	193-196	signal transducer and activator of transcription 3	Homo sapiens	49-54
22078209-8	2012	Besides, the treatment of B lymphocytes with the STAT3 inhibitor VI increases viability and decreases proliferation and secretion as in NAC-treated cells thus showing a role for STAT3 in these NAC-induced phenotypes.	Acetylcysteine	193-196	signal transducer and activator of transcription 3	Homo sapiens	178-183
22701598-0	2012	The ROS scavenger, NAC, regulates hepatic Valpha14iNKT cells signaling during Fas mAb-dependent fulminant liver failure.	Acetylcysteine	19-22	T cell receptor alpha, variable 14	Mus musculus	42-50
23251571-9	2012	ROS accumulation followed E2F1 induction and treatment with the antioxidant N-acetylcysteine, inhibited E2F1-induced Bax translocation to mitochondria and subsequent apoptosis.	Acetylcysteine	76-92	BCL2 associated X, apoptosis regulator	Homo sapiens	117-120
23094067-14	2012	NAC also inhibited the overexpression of p-STAT3 and VEGF in CNV and in RPE cells.	Acetylcysteine	0-3	signal transducer and activator of transcription 3	Mus musculus	43-48
22701598-2	2012	In this study, we demonstrate that treatment of mice with N-acetylcysteine (NAC), an ROS scavenger and glutathione (GSH) precursor, almost completely abolished Fas mAb-induced FLF through suppression of Valpha14iNKT cell activation, IFN-gamma signaling, apoptosis and nitrotyrosine formation in liver.	Acetylcysteine	58-74	T cell receptor alpha, variable 14	Mus musculus	203-211
22701695-9	2012	The free radical scavenger N-acetyl-cysteine (NAC) was able to completely suppress cell death induced by jacaranone as it blocked Akt downregulation, p38 MAPK activation as well as upregulation of proapoptotic Bax.	Acetylcysteine	27-44	thymoma viral proto-oncogene 1	Mus musculus	130-133
22701695-9	2012	The free radical scavenger N-acetyl-cysteine (NAC) was able to completely suppress cell death induced by jacaranone as it blocked Akt downregulation, p38 MAPK activation as well as upregulation of proapoptotic Bax.	Acetylcysteine	46-49	thymoma viral proto-oncogene 1	Mus musculus	130-133
22701598-2	2012	In this study, we demonstrate that treatment of mice with N-acetylcysteine (NAC), an ROS scavenger and glutathione (GSH) precursor, almost completely abolished Fas mAb-induced FLF through suppression of Valpha14iNKT cell activation, IFN-gamma signaling, apoptosis and nitrotyrosine formation in liver.	Acetylcysteine	58-74	interferon gamma	Mus musculus	233-242
22701598-2	2012	In this study, we demonstrate that treatment of mice with N-acetylcysteine (NAC), an ROS scavenger and glutathione (GSH) precursor, almost completely abolished Fas mAb-induced FLF through suppression of Valpha14iNKT cell activation, IFN-gamma signaling, apoptosis and nitrotyrosine formation in liver.	Acetylcysteine	76-79	T cell receptor alpha, variable 14	Mus musculus	203-211
22701598-2	2012	In this study, we demonstrate that treatment of mice with N-acetylcysteine (NAC), an ROS scavenger and glutathione (GSH) precursor, almost completely abolished Fas mAb-induced FLF through suppression of Valpha14iNKT cell activation, IFN-gamma signaling, apoptosis and nitrotyrosine formation in liver.	Acetylcysteine	76-79	interferon gamma	Mus musculus	233-242
22701598-5	2012	Therefore, our study provides critical new insights into how NAC, a ROS scavenger, regulates Th1 signaling in intrahepatic Valpha14iNKT cells to impact inflammatory and pathological responses.	Acetylcysteine	61-64	negative elongation factor complex member C/D, Th1l	Mus musculus	93-96
22701598-5	2012	Therefore, our study provides critical new insights into how NAC, a ROS scavenger, regulates Th1 signaling in intrahepatic Valpha14iNKT cells to impact inflammatory and pathological responses.	Acetylcysteine	61-64	T cell receptor alpha, variable 14	Mus musculus	123-131
23006535-8	2012	Consistently, NAC partially attenuated pulmonary fibrosis and inhibited TGF-beta(1) and alpha-SMA expression in this model.	Acetylcysteine	14-17	transforming growth factor, beta 1	Rattus norvegicus	72-83
22666346-7	2012	However, N-acetyl cysteine significantly reduced the enhanced apoptosis observed with the combination of DHA and Apo2L/TRAIL.	Acetylcysteine	9-26	TNF superfamily member 10	Homo sapiens	113-118
22666346-7	2012	However, N-acetyl cysteine significantly reduced the enhanced apoptosis observed with the combination of DHA and Apo2L/TRAIL.	Acetylcysteine	9-26	TNF superfamily member 10	Homo sapiens	119-124
22606295-10	2012	NRG induced elevation in JNK phosphorylation that was inhibited by NAC.	Acetylcysteine	67-70	mitogen-activated protein kinase 8	Homo sapiens	25-28
22442667-4	2012	In glial C6 cells, NAC promoted phosphorylation of ERK induced by (s)-3,5-dihydroxy-phenylglycine (DHPG), an agonist of group I mGlus.	Acetylcysteine	19-22	Eph receptor B1	Rattus norvegicus	51-54
22442667-6	2012	Moreover, in rotenone-treated MN9D cells and PD rat model, NAC protected against group I mGlus-induced toxicity by compromising the decrease in phosphorylation of ERK, phosphorylation or expression level of TH.	Acetylcysteine	59-62	Eph receptor B1	Rattus norvegicus	163-166
22530011-7	2012	N-acetylcysteine (NAC), a pharmacological antioxidant, increased T-cell proliferation and IL-2 production by TCR and ConA stimulated splenocytes but had no effect on the response to PHA in primary porcine splenocytes confirming that PHA-induced T-cell activation is insensitive to the redox status.	Acetylcysteine	0-16	interleukin 2	Homo sapiens	90-94
22530011-7	2012	N-acetylcysteine (NAC), a pharmacological antioxidant, increased T-cell proliferation and IL-2 production by TCR and ConA stimulated splenocytes but had no effect on the response to PHA in primary porcine splenocytes confirming that PHA-induced T-cell activation is insensitive to the redox status.	Acetylcysteine	18-21	interleukin 2	Homo sapiens	90-94
22403609-7	2012	Both pathways were critical for senescence as was proven by p21 and Rb knock-down and by quenching ROS with N-Acetyl cysteine and p63 silencing also mimicked AR-induced senescence.	Acetylcysteine	108-125	androgen receptor	Homo sapiens	158-160
21903093-11	2011	Pretreatment with N-acetyl-L-cysteine and glutathione inhibited GGS-induced ER-stress, and CHOP and DR5 upregulation and almost completely blocked GGS/TRAIL-induced apoptosis.	Acetylcysteine	18-37	DNA damage inducible transcript 3	Homo sapiens	91-95
22111911-10	2011	The PS-NH(2)-mediated proinflammatory macrophage activation could be antagonized by the radical scavenger N-acetyl-L-cysteine, which prevented mitochondrial damage, caspase-1 activation, and the subsequent release of IL-1beta.	Acetylcysteine	106-125	caspase 1	Homo sapiens	165-174
22111911-10	2011	The PS-NH(2)-mediated proinflammatory macrophage activation could be antagonized by the radical scavenger N-acetyl-L-cysteine, which prevented mitochondrial damage, caspase-1 activation, and the subsequent release of IL-1beta.	Acetylcysteine	106-125	interleukin 1 beta	Homo sapiens	217-225
21903093-11	2011	Pretreatment with N-acetyl-L-cysteine and glutathione inhibited GGS-induced ER-stress, and CHOP and DR5 upregulation and almost completely blocked GGS/TRAIL-induced apoptosis.	Acetylcysteine	18-37	TNF superfamily member 10	Homo sapiens	151-156
22122305-13	2011	NAC also inhibited the transcription of NFkappaB, IL-6, TNF-alpha and COX2 usually induced by LPS.	Acetylcysteine	0-3	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	40-48
22122305-13	2011	NAC also inhibited the transcription of NFkappaB, IL-6, TNF-alpha and COX2 usually induced by LPS.	Acetylcysteine	0-3	interleukin 6	Mus musculus	50-54
22122305-13	2011	NAC also inhibited the transcription of NFkappaB, IL-6, TNF-alpha and COX2 usually induced by LPS.	Acetylcysteine	0-3	tumor necrosis factor	Mus musculus	56-65
21833842-8	2011	Moreover, NAC attenuated the CA-induced phosphorylation of p38.	Acetylcysteine	10-13	mitogen-activated protein kinase 1	Homo sapiens	59-62
21719110-6	2011	METHOD: This study reports data on the treatment of 149 individuals with moderate depression during the 2 month open label phase of a randomised placebo controlled clinical trial of the efficacy of 1g BID of NAC that examined the use of NAC as a maintenance treatment for bipolar disorder.	Acetylcysteine	208-211	BH3 interacting domain death agonist	Homo sapiens	201-204
21985290-3	2011	The HO-1 inhibitor or CO scavenger significantly reversed the inhibitory effect of Alk-8/9 on TNF-alpha expression, whereas N-acetyl-L-cysteine was observed to reduce Alk-8/9-induced HO-1 expression in LPS-treated macrophages.	Acetylcysteine	124-143	heme oxygenase 1	Mus musculus	183-187
21934138-9	2011	Increased oxidative stress and urothelial cell hyperplasia with evidence of activated p44/42 MAPK (ERK1/2) and cyclin D1 were found in the DMA(V) and NAC (high dose) cotreated group.	Acetylcysteine	150-153	cyclin D1	Rattus norvegicus	111-120
21937425-7	2011	The PRC-dependent inflammatory response was inhibited by N-acetylcysteine, suggesting that PRC may contribute to the inflammatory microenvironment linked to oxidant signaling.	Acetylcysteine	57-73	PPARG related coactivator 1	Homo sapiens	4-7
21958470-9	2011	Moreover, pretreatment of rats with the antioxidant N-acetylcysteine (NAC; 150 mg/kg) prevented the increase of non-activated platelet adhesion, and significantly reduced the inhibitory effect of LPS on thrombin-stimulated adhesion.	Acetylcysteine	52-68	coagulation factor II	Rattus norvegicus	203-211
21958470-9	2011	Moreover, pretreatment of rats with the antioxidant N-acetylcysteine (NAC; 150 mg/kg) prevented the increase of non-activated platelet adhesion, and significantly reduced the inhibitory effect of LPS on thrombin-stimulated adhesion.	Acetylcysteine	70-73	coagulation factor II	Rattus norvegicus	203-211
21937425-7	2011	The PRC-dependent inflammatory response was inhibited by N-acetylcysteine, suggesting that PRC may contribute to the inflammatory microenvironment linked to oxidant signaling.	Acetylcysteine	57-73	PPARG related coactivator 1	Homo sapiens	91-94
21981804-3	2011	The LPS-inducible TNFalpha was significantly suppressed by pretreatment with the O(2)(-) scavenger N-acetyl cysteine (NAC), but not by the NO scavenger 2-(4-Carboxyphenyl)-4,4,5,5-tetramethyl imidazoline-1-oxyl 3-oxide, suggesting the close association of O(2)(-) with TNFalpha induction.	Acetylcysteine	99-116	tumor necrosis factor	Rattus norvegicus	18-26
21981804-3	2011	The LPS-inducible TNFalpha was significantly suppressed by pretreatment with the O(2)(-) scavenger N-acetyl cysteine (NAC), but not by the NO scavenger 2-(4-Carboxyphenyl)-4,4,5,5-tetramethyl imidazoline-1-oxyl 3-oxide, suggesting the close association of O(2)(-) with TNFalpha induction.	Acetylcysteine	99-116	tumor necrosis factor	Rattus norvegicus	269-277
21981804-3	2011	The LPS-inducible TNFalpha was significantly suppressed by pretreatment with the O(2)(-) scavenger N-acetyl cysteine (NAC), but not by the NO scavenger 2-(4-Carboxyphenyl)-4,4,5,5-tetramethyl imidazoline-1-oxyl 3-oxide, suggesting the close association of O(2)(-) with TNFalpha induction.	Acetylcysteine	118-121	tumor necrosis factor	Rattus norvegicus	18-26
21981804-3	2011	The LPS-inducible TNFalpha was significantly suppressed by pretreatment with the O(2)(-) scavenger N-acetyl cysteine (NAC), but not by the NO scavenger 2-(4-Carboxyphenyl)-4,4,5,5-tetramethyl imidazoline-1-oxyl 3-oxide, suggesting the close association of O(2)(-) with TNFalpha induction.	Acetylcysteine	118-121	tumor necrosis factor	Rattus norvegicus	269-277
21981804-4	2011	NAC strongly depressed phosphorylation of p38 mitogen-activated protein kinase (p38 MAPK), which is necessary for inducing TNFalpha in microglia.	Acetylcysteine	0-3	tumor necrosis factor	Rattus norvegicus	123-131
21843581-10	2011	As expected, NAC suppressed the expression of iNOS, COX-2, and TNF-alpha by blocking proteasome-mediated degradation.	Acetylcysteine	13-16	nitric oxide synthase 2, inducible	Mus musculus	46-50
21843499-5	2011	We found the treatment of SP600125 or NAC could decrease the activation of Ask1 during ischemia/reperfusion and suppress the assembly of the Fas Daxx Ask1 signaling module, and in succession inhibit JNK activation and c-Jun phosphorylation.	Acetylcysteine	38-41	mitogen-activated protein kinase kinase kinase 5	Rattus norvegicus	75-79
21843499-5	2011	We found the treatment of SP600125 or NAC could decrease the activation of Ask1 during ischemia/reperfusion and suppress the assembly of the Fas Daxx Ask1 signaling module, and in succession inhibit JNK activation and c-Jun phosphorylation.	Acetylcysteine	38-41	mitogen-activated protein kinase kinase kinase 5	Rattus norvegicus	150-154
21831508-10	2011	The effects of metformin and NAC on insulin sensitivity are not associated with TNF-alpha.	Acetylcysteine	29-32	insulin	Homo sapiens	36-43
21854768-8	2011	Interestingly, pretreatment with an antioxidant, N-acetylcysteine (NAC), inhibited not only CHOP and DR5 up-regulation but also the cell death induced by acrolein plus TRAIL.	Acetylcysteine	49-65	DNA damage inducible transcript 3	Homo sapiens	92-96
21854768-8	2011	Interestingly, pretreatment with an antioxidant, N-acetylcysteine (NAC), inhibited not only CHOP and DR5 up-regulation but also the cell death induced by acrolein plus TRAIL.	Acetylcysteine	49-65	TNF superfamily member 10	Homo sapiens	168-173
21854768-8	2011	Interestingly, pretreatment with an antioxidant, N-acetylcysteine (NAC), inhibited not only CHOP and DR5 up-regulation but also the cell death induced by acrolein plus TRAIL.	Acetylcysteine	67-70	DNA damage inducible transcript 3	Homo sapiens	92-96
21854768-8	2011	Interestingly, pretreatment with an antioxidant, N-acetylcysteine (NAC), inhibited not only CHOP and DR5 up-regulation but also the cell death induced by acrolein plus TRAIL.	Acetylcysteine	67-70	TNF superfamily member 10	Homo sapiens	168-173
21832251-4	2011	Indoxyl sulfate induced phosphorylation of NF-kappaB p65 on Ser-276, which was suppressed by N-acetylcysteine, an antioxidant.	Acetylcysteine	93-109	nuclear factor kappa B subunit 1	Homo sapiens	43-52
21832251-4	2011	Indoxyl sulfate induced phosphorylation of NF-kappaB p65 on Ser-276, which was suppressed by N-acetylcysteine, an antioxidant.	Acetylcysteine	93-109	synaptotagmin 1	Rattus norvegicus	53-56
21615775-14	2011	Antioxidants such as acetylcysteine and salicylate might be beneficial through free radical scavenging, anti-inflammatory and NF-kappaB inhibitory actions.	Acetylcysteine	21-35	nuclear factor kappa B subunit 1	Homo sapiens	126-135
21394639-0	2011	Effect of N-acetyl-cysteine and hyperoxia on erythropoietin production.	Acetylcysteine	10-27	erythropoietin	Homo sapiens	45-59
21394639-1	2011	Previous studies in healthy subjects have shown an increase in erythropoietin (EPO) production after administration of N-acetyl-cysteine (NAC).	Acetylcysteine	119-136	erythropoietin	Homo sapiens	63-77
21394639-1	2011	Previous studies in healthy subjects have shown an increase in erythropoietin (EPO) production after administration of N-acetyl-cysteine (NAC).	Acetylcysteine	119-136	erythropoietin	Homo sapiens	79-82
21394639-1	2011	Previous studies in healthy subjects have shown an increase in erythropoietin (EPO) production after administration of N-acetyl-cysteine (NAC).	Acetylcysteine	138-141	erythropoietin	Homo sapiens	63-77
21394639-1	2011	Previous studies in healthy subjects have shown an increase in erythropoietin (EPO) production after administration of N-acetyl-cysteine (NAC).	Acetylcysteine	138-141	erythropoietin	Homo sapiens	79-82
21394639-2	2011	These authors hypothesized that NAC increases intracellular reduced glutathione, decreasing reactive oxygen species and enabling EPO production.	Acetylcysteine	32-35	erythropoietin	Homo sapiens	129-132
21394639-3	2011	We investigated if EPO production could be stimulated with a single dose of NAC, after 90 min of pure oxygen breathing.	Acetylcysteine	76-79	erythropoietin	Homo sapiens	19-22
21394639-7	2011	The EPO concentrations of the NAC group decreased significantly at T1, followed by a significant increase compared to baseline, which was obvious until T4.	Acetylcysteine	30-33	erythropoietin	Homo sapiens	4-7
21394639-9	2011	In this study, a significant increase of EPO production was observed after a short-term hyperoxic stimulus only when preceded with the administration of a single dose of NAC.	Acetylcysteine	170-173	erythropoietin	Homo sapiens	41-44
21843581-10	2011	As expected, NAC suppressed the expression of iNOS, COX-2, and TNF-alpha by blocking proteasome-mediated degradation.	Acetylcysteine	13-16	tumor necrosis factor	Mus musculus	63-72
22065904-10	2011	Induction of the Nrf2/HO-1 after SFN treatment was potently suppressed by pretreatment with NAC.	Acetylcysteine	92-95	NFE2 like bZIP transcription factor 2	Homo sapiens	17-21
21704193-7	2011	3,4,5-Tricaffeoylquinic acid, Bay 11-7085, Akt inhibitor and N-acetylcysteine inhibited the TNF-alpha-induced activation of NF-kappaB, activation of Akt, and formation of reactive oxygen and nitrogen species.	Acetylcysteine	61-77	tumor necrosis factor	Homo sapiens	92-101
21704193-7	2011	3,4,5-Tricaffeoylquinic acid, Bay 11-7085, Akt inhibitor and N-acetylcysteine inhibited the TNF-alpha-induced activation of NF-kappaB, activation of Akt, and formation of reactive oxygen and nitrogen species.	Acetylcysteine	61-77	nuclear factor kappa B subunit 1	Homo sapiens	124-133
21704193-7	2011	3,4,5-Tricaffeoylquinic acid, Bay 11-7085, Akt inhibitor and N-acetylcysteine inhibited the TNF-alpha-induced activation of NF-kappaB, activation of Akt, and formation of reactive oxygen and nitrogen species.	Acetylcysteine	61-77	AKT serine/threonine kinase 1	Homo sapiens	149-152
21683791-12	2011	An anti-oxidant, N-acetyl-L-cysteine blocked the TNF-alpha-induced activation of NF-kappaB, PKCtheta and expression of ICAM-1.	Acetylcysteine	17-36	tumor necrosis factor	Rattus norvegicus	49-58
21775771-6	2011	In the presence of nicotine, NAC decreased active MMP-2 protein levels and reversed the nicotine-induced increase in collagen staining.	Acetylcysteine	29-32	72 kDa type IV collagenase	Cavia porcellus	50-55
21801798-10	2011	Treatment of the cells with a specific p38 inhibitor (SB203580) or the antioxidant N-acetylcysteine (NAC) was able to prevent the toluene/benzene/styrene-dependent COX-2 activation, and subsequent increased PGE(2) and PGF(2alpha) secretion.	Acetylcysteine	83-99	prostaglandin-endoperoxide synthase 2	Homo sapiens	164-169
21801798-10	2011	Treatment of the cells with a specific p38 inhibitor (SB203580) or the antioxidant N-acetylcysteine (NAC) was able to prevent the toluene/benzene/styrene-dependent COX-2 activation, and subsequent increased PGE(2) and PGF(2alpha) secretion.	Acetylcysteine	101-104	prostaglandin-endoperoxide synthase 2	Homo sapiens	164-169
21770721-13	2011	Moreover, these findings can contribute to others" research, regarding the utilization of NAC to ALA-D activity restoration in the kidneys.	Acetylcysteine	90-93	aminolevulinate dehydratase	Rattus norvegicus	97-102
21658841-4	2011	AHA-induced cell death was found to be: (i) associated with the release of cytochrome c, (ii) suppressed by the overexpression of Bcl-x(L), (iii) amplified by inhibition of extracellular signal-regulated kinases (ERKs) 1/2 and c-jun NH(2)-terminal kinases/stress activated protein kinases (JNK/SAPK) signaling, and (iv) completely abrogated by the free-radical scavenger N-acetyl-l-cysteine.	Acetylcysteine	371-390	BCL2 like 1	Homo sapiens	130-135
21751261-12	2011	Reflecting changes in GSH, HNE-induced EGFR phosphorylation was suppressed by NAC, whereas it was promoted by BSO.	Acetylcysteine	78-81	epidermal growth factor receptor	Homo sapiens	39-43
21767632-3	2011	The TNF-alpha-induced expression of VCAM-1 was significantly reduced by respectively 38+-7 or 34+-16% when HUVECs were pretreated with 10 or 30muM viscolin, as shown by Western blotting, and was also significantly reduced by pretreatment with the antioxidants N-acetylcysteine, diphenylene iodonium chloride, and apocynin.	Acetylcysteine	260-276	tumor necrosis factor	Homo sapiens	4-13
21767632-3	2011	The TNF-alpha-induced expression of VCAM-1 was significantly reduced by respectively 38+-7 or 34+-16% when HUVECs were pretreated with 10 or 30muM viscolin, as shown by Western blotting, and was also significantly reduced by pretreatment with the antioxidants N-acetylcysteine, diphenylene iodonium chloride, and apocynin.	Acetylcysteine	260-276	vascular cell adhesion molecule 1	Homo sapiens	36-42
21833601-6	2011	Indeed, the free radical inducer menadione caused a decrease in cyt c that was reversed by N-acetylcysteine.	Acetylcysteine	91-107	cytochrome c, somatic	Homo sapiens	64-69
21762691-8	2011	We then showed that luteolin induced accumulation of reactive oxygen species and that the anti-oxidant N-acetylcysteine reduced luteolin-induced cell death and expression of CHOP and GRP78.	Acetylcysteine	103-119	heat shock protein 5	Mus musculus	183-188
21722752-10	2011	The P450 2E1 inhibitor diallyl sulphide (DAS), N-acetylcysteine (NAC), and reduced glutathione (GSH) antioxidants also regulated processes, including ApoB expression and lipid accumulation in CCl(4)-treated animals.	Acetylcysteine	65-68	apolipoprotein B	Rattus norvegicus	150-154
21384399-7	2011	Pretreatment with N-acetyl cysteine, a scavenger of reactive oxygen species, suppressed MnCl(2) -induced Nrf2 activation, increase in Nrf2-ARE binding and subsequent upregulation of HO-1 expression.	Acetylcysteine	18-35	NFE2 like bZIP transcription factor 2	Rattus norvegicus	105-109
21384399-7	2011	Pretreatment with N-acetyl cysteine, a scavenger of reactive oxygen species, suppressed MnCl(2) -induced Nrf2 activation, increase in Nrf2-ARE binding and subsequent upregulation of HO-1 expression.	Acetylcysteine	18-35	NFE2 like bZIP transcription factor 2	Rattus norvegicus	134-138
22092168-8	2011	RESULTS: NAC infusion patients had significantly lower post-operative concentrations of myocardial-specific protein [cTnI, CPK-MB] and pro-inflammatory cytokines [TNF-alpha, IL-1beta].	Acetylcysteine	9-12	tumor necrosis factor	Homo sapiens	163-172
21265612-7	2011	Likewise, the hypoxia-induced proliferation and migration of ASCs were reversed by N-acetyl-cysteine and diphenyleneiodonium treatment, suggesting the involvement of ROS generation in ASC stimulation.	Acetylcysteine	83-100	PYD and CARD domain containing	Homo sapiens	61-64
21777666-13	2011	Pretreatment of cells with N-acetyl-l-cysteine (NAC) attenuated intracellular ROS generation, the Bax/Bcl-2 protein expression, and apoptosis.	Acetylcysteine	27-46	BCL2 associated X, apoptosis regulator	Homo sapiens	98-101
21777666-13	2011	Pretreatment of cells with N-acetyl-l-cysteine (NAC) attenuated intracellular ROS generation, the Bax/Bcl-2 protein expression, and apoptosis.	Acetylcysteine	27-46	BCL2 apoptosis regulator	Homo sapiens	102-107
22092168-8	2011	RESULTS: NAC infusion patients had significantly lower post-operative concentrations of myocardial-specific protein [cTnI, CPK-MB] and pro-inflammatory cytokines [TNF-alpha, IL-1beta].	Acetylcysteine	9-12	interleukin 1 beta	Homo sapiens	174-182
21620964-7	2011	Pretreatment with anti-oxidants (N-acetylcysteine (NAC) or glutathione) significantly reduced Bay-induced HO-1 mRNA/protein expression, nuclear translocation of Nrf2 and phosphorylation of Akt.	Acetylcysteine	33-49	NFE2 like bZIP transcription factor 2	Homo sapiens	161-165
20919940-4	2011	Pretreatment with apocynin (NADPH oxidase inhibitor) or N-acetyl cysteine (antioxidant) significantly attenuated OSS-induced JNK activation.	Acetylcysteine	56-73	mitogen-activated protein kinase 8	Homo sapiens	125-128
21544615-6	2011	The TNF-alpha-induced upregulation of LOX-1 was also attenuated by the NF-kappaB inhibitor N-acetyl-L-cysteine.	Acetylcysteine	91-110	tumor necrosis factor	Mus musculus	4-13
21544615-6	2011	The TNF-alpha-induced upregulation of LOX-1 was also attenuated by the NF-kappaB inhibitor N-acetyl-L-cysteine.	Acetylcysteine	91-110	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	71-80
21635667-5	2011	Reactive oxygen species generation and p38 MAPK activity both increased in a dose-dependent manner and were prevented by SB203580, an inhibitor of p38 MAPK, and N-acetylcysteine (NAC), a ROS scavenger.	Acetylcysteine	161-177	mitogen-activated protein kinase 14	Homo sapiens	39-42
21635667-5	2011	Reactive oxygen species generation and p38 MAPK activity both increased in a dose-dependent manner and were prevented by SB203580, an inhibitor of p38 MAPK, and N-acetylcysteine (NAC), a ROS scavenger.	Acetylcysteine	179-182	mitogen-activated protein kinase 14	Homo sapiens	39-42
21239607-6	2011	The exacerbation of bleomycin-induced pulmonary inflammation and fibrosis in Prx I-deficient mice was inhibited by treatment with N-acetyl-L-cysteine, a radical scavenger, or with (S,R)-3-(4-hydroxyphenyl)-4,5-dihydro-5-isoxazole acetic acid methyl ester, a tautomerase inhibitor of macrophage migration inhibitory factor.	Acetylcysteine	130-149	macrophage migration inhibitory factor (glycosylation-inhibiting factor)	Mus musculus	283-321
21620964-7	2011	Pretreatment with anti-oxidants (N-acetylcysteine (NAC) or glutathione) significantly reduced Bay-induced HO-1 mRNA/protein expression, nuclear translocation of Nrf2 and phosphorylation of Akt.	Acetylcysteine	33-49	AKT serine/threonine kinase 1	Homo sapiens	189-192
21620964-7	2011	Pretreatment with anti-oxidants (N-acetylcysteine (NAC) or glutathione) significantly reduced Bay-induced HO-1 mRNA/protein expression, nuclear translocation of Nrf2 and phosphorylation of Akt.	Acetylcysteine	51-54	NFE2 like bZIP transcription factor 2	Homo sapiens	161-165
21620964-7	2011	Pretreatment with anti-oxidants (N-acetylcysteine (NAC) or glutathione) significantly reduced Bay-induced HO-1 mRNA/protein expression, nuclear translocation of Nrf2 and phosphorylation of Akt.	Acetylcysteine	51-54	AKT serine/threonine kinase 1	Homo sapiens	189-192
21229292-8	2011	Instead, the free radical scavenger N-acetyl-L: -cysteine (NAC) completely blocked the effect on TRAIL-induced apoptosis caused by curcumin, oridonin, and PDTC.	Acetylcysteine	36-57	TNF superfamily member 10	Homo sapiens	97-102
21630435-2	2011	By modifying PDMS using short- and long-chain mono-functional polyethylene glycol (PEG604 and PEG5K, respectively) and N-acetyl-L-cysteine via adsorption and covalent binding (NAC and NAC/EDC/NHS, respectively), we increased surface wettability.	Acetylcysteine	119-138	NHS actin remodeling regulator	Homo sapiens	192-195
21229292-8	2011	Instead, the free radical scavenger N-acetyl-L: -cysteine (NAC) completely blocked the effect on TRAIL-induced apoptosis caused by curcumin, oridonin, and PDTC.	Acetylcysteine	59-62	TNF superfamily member 10	Homo sapiens	97-102
20407854-5	2011	N-acetyl-L cysteine (NAC) blocked the pro-apoptotic effects of SOD1 knockdown, suggesting the antioxidant effects of SOD1 was essential for the resistance of CD34+ cells to imatinib therapy.	Acetylcysteine	0-19	superoxide dismutase 1	Homo sapiens	63-67
20407854-5	2011	N-acetyl-L cysteine (NAC) blocked the pro-apoptotic effects of SOD1 knockdown, suggesting the antioxidant effects of SOD1 was essential for the resistance of CD34+ cells to imatinib therapy.	Acetylcysteine	0-19	superoxide dismutase 1	Homo sapiens	117-121
20407854-5	2011	N-acetyl-L cysteine (NAC) blocked the pro-apoptotic effects of SOD1 knockdown, suggesting the antioxidant effects of SOD1 was essential for the resistance of CD34+ cells to imatinib therapy.	Acetylcysteine	0-19	CD34 molecule	Homo sapiens	158-162
21777978-9	2011	The antioxidant N-acetylcysteine almost totally inhibits ROS production and Src kinase activation in ATO-pre-treated cells.	Acetylcysteine	16-32	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	76-79
21708263-10	2011	Interestingly, pre-incubation with N-acetylcysteine, a precursor of glutathione synthesis, protected neurons from UCB-induced oxidative stress and necrotic cell death, preventing DJ-1 down-regulation and neuritic impairment.	Acetylcysteine	35-51	Parkinsonism associated deglycase	Rattus norvegicus	179-183
21728338-7	2011	Pharmacologic inhibition or siRNA knockdown of Akt, the target of phosphoinositide 3-kinase (PI3-K), attenuated 15d-PGJ(2)-induced Nrf2 activation and GCLC expression, and NAC treatment inhibited phosphorylation of Akt, and subsequently Nrf2 activation and GCLC upregulation.	Acetylcysteine	172-175	AKT serine/threonine kinase 1	Homo sapiens	47-50
21861928-8	2011	ROS scavenger (N-acetyl-L-cysteine, NAC) blocked the PPCSE-induced ROS generation and HO-1 expression.	Acetylcysteine	15-34	heme oxygenase 1	Mus musculus	86-90
21728338-6	2011	The reactive oxygen species (ROS) scavenger N-acetylcysteine (NAC) abolished the 15d-PGJ2-induced Nrf2 activation and GCLC expression.	Acetylcysteine	44-60	NFE2 like bZIP transcription factor 2	Homo sapiens	98-102
21453688-4	2011	An increase in the intracellular ROS level by EPO1 was observed in the DCHF-DA analysis, and EPO1-induced apoptosis and caspase 3 protein cleavage were prevented by adding the antioxidant, N-acetyl-cysteine (NAC), with decreased ROS production elicited by EPO1.	Acetylcysteine	189-206	caspase 3	Homo sapiens	120-129
21453688-4	2011	An increase in the intracellular ROS level by EPO1 was observed in the DCHF-DA analysis, and EPO1-induced apoptosis and caspase 3 protein cleavage were prevented by adding the antioxidant, N-acetyl-cysteine (NAC), with decreased ROS production elicited by EPO1.	Acetylcysteine	208-211	caspase 3	Homo sapiens	120-129
21453688-5	2011	Activation of ERK and JNK, but not p38, via phosphorylation induction was identified in EPO1- but not EPO- or EPO2-treated U87 and C6 cells, and this was blocked by adding NAC.	Acetylcysteine	172-175	mitogen-activated protein kinase 1	Homo sapiens	14-17
21453688-5	2011	Activation of ERK and JNK, but not p38, via phosphorylation induction was identified in EPO1- but not EPO- or EPO2-treated U87 and C6 cells, and this was blocked by adding NAC.	Acetylcysteine	172-175	mitogen-activated protein kinase 8	Homo sapiens	22-25
21453688-5	2011	Activation of ERK and JNK, but not p38, via phosphorylation induction was identified in EPO1- but not EPO- or EPO2-treated U87 and C6 cells, and this was blocked by adding NAC.	Acetylcysteine	172-175	erythropoietin	Homo sapiens	88-91
21728338-6	2011	The reactive oxygen species (ROS) scavenger N-acetylcysteine (NAC) abolished the 15d-PGJ2-induced Nrf2 activation and GCLC expression.	Acetylcysteine	62-65	NFE2 like bZIP transcription factor 2	Homo sapiens	98-102
21391979-10	2011	Generation of ROS induced phosphorylation of p42/p44 mitogen-activated protein kinase (MAPK), p38 MAPK and JNK1/2, which was attenuated by DPI and APO and the ROS scavenger N-acetylcysteine.	Acetylcysteine	173-189	mitogen-activated protein kinase 14	Homo sapiens	94-97
21252047-10	2011	Both N-acetyl cysteine and diphenylene iodonium, a NADP(H) inhibitor, inhibited the expression of HIF-1alpha and VEGF stimulated by leptin or PDGF.	Acetylcysteine	5-22	hypoxia inducible factor 1 subunit alpha	Homo sapiens	98-108
21252047-10	2011	Both N-acetyl cysteine and diphenylene iodonium, a NADP(H) inhibitor, inhibited the expression of HIF-1alpha and VEGF stimulated by leptin or PDGF.	Acetylcysteine	5-22	vascular endothelial growth factor A	Homo sapiens	113-117
21722651-11	2011	Furthermore, treatment with NAC blocked the transcriptional activation of CREB, and the expression of dominant-negative mutants of CREB inhibited adipocyte differentiation.	Acetylcysteine	28-31	cAMP responsive element binding protein 1	Mus musculus	74-78
21810225-10	2011	The initiation of the AA pathway due to MAF02 particle exposure was demonstrated to depend on the formation of ROS since the presence of the antioxidant N-acetyl-cysteine (NAC) prevented the MAF02-mediated enhancement of free AA, the subsequent conversion to PGE2/TXB2 via the induction of COX-2 and the ERK1/2 and JNK1/2 phosphorylation.	Acetylcysteine	153-170	rolled	Drosophila melanogaster	304-310
21810225-10	2011	The initiation of the AA pathway due to MAF02 particle exposure was demonstrated to depend on the formation of ROS since the presence of the antioxidant N-acetyl-cysteine (NAC) prevented the MAF02-mediated enhancement of free AA, the subsequent conversion to PGE2/TXB2 via the induction of COX-2 and the ERK1/2 and JNK1/2 phosphorylation.	Acetylcysteine	172-175	rolled	Drosophila melanogaster	304-310
21391979-10	2011	Generation of ROS induced phosphorylation of p42/p44 mitogen-activated protein kinase (MAPK), p38 MAPK and JNK1/2, which was attenuated by DPI and APO and the ROS scavenger N-acetylcysteine.	Acetylcysteine	173-189	mitogen-activated protein kinase 8	Homo sapiens	107-113
21519330-6	2011	Furthermore, the introduction of the antioxidant N-acetyl cysteine was able to abrogate the induction of apoptosis observed with VOPP1 knockdown in a dose-responsive manner.	Acetylcysteine	49-66	VOPP1 WW domain binding protein	Homo sapiens	129-134
21604367-6	2011	Reduced ALP activity and OPN mRNA expression by TEGDMA were partially recovered via cotreatment with NAC.	Acetylcysteine	101-104	alkaline phosphatase, placental	Homo sapiens	8-11
21574020-10	2011	The results from immunohistochemical staining demonstrated that NAC suppressed the expression of IL-1beta and TNF-alpha in the periodontal ligament tissues compared to the vehicle-treated group.	Acetylcysteine	64-67	interleukin 1 beta	Rattus norvegicus	97-105
21574020-10	2011	The results from immunohistochemical staining demonstrated that NAC suppressed the expression of IL-1beta and TNF-alpha in the periodontal ligament tissues compared to the vehicle-treated group.	Acetylcysteine	64-67	tumor necrosis factor	Rattus norvegicus	110-119
21712056-10	2011	The ability of BRS-3 to regulate EGFR transactivation in NCI-H1299-BRS-3 cells was reduced by AG1478 or gefitinib (EGFR tyrosine kinase inhibitors), GM6001 (matrix metalloprotease inhibitor), PP2 (Src inhibitor), N-acetylcysteine (anti-oxidant), Tiron (superoxide scavenger) and DPI (NADPH oxidase inhibitor).	Acetylcysteine	215-229	epidermal growth factor receptor	Homo sapiens	33-37
21385609-9	2011	The antioxidant N-acetylcysteine prevented JNK activation by trans-2-hexadecenal.	Acetylcysteine	16-32	mitogen-activated protein kinase 8	Homo sapiens	43-46
21600978-7	2011	Consistent with the above, Zn deficiency-induced tubulin-mediated alterations in transcription factor NF-kappaB nuclear translocation were prevented by treating IMR-32 cells with LA and NAC.	Acetylcysteine	186-189	nuclear factor kappa B subunit 1	Homo sapiens	102-111
21600978-8	2011	Binding of the NF-kappaB protein p50, dynein, and karyopherin alpha (components of the NF-kappaB transport complex) to beta-tubulin as well as the expression of NF-kappaB-dependent genes (Bcl-2, cyclin D1, and c-myc) was also restored by the addition of LA and NAC to Zn-deficient cells.	Acetylcysteine	261-264	nuclear factor kappa B subunit 1	Homo sapiens	15-24
21521714-4	2011	Restoring TR4 or supplying the antioxidant N-acetyl-l-cysteine (NAC) to TR4(-/-) MEFs reduced the DNA damage and slowed down cellular growth arrest.	Acetylcysteine	43-62	nuclear receptor subfamily 2, group C, member 2	Mus musculus	72-75
21521714-4	2011	Restoring TR4 or supplying the antioxidant N-acetyl-l-cysteine (NAC) to TR4(-/-) MEFs reduced the DNA damage and slowed down cellular growth arrest.	Acetylcysteine	64-67	nuclear receptor subfamily 2, group C, member 2	Mus musculus	72-75
21532338-8	2011	N-acetyl-cysteine (NAC; 10 mM) pre-treatment rescued cell viability of RKS262 (23 microM)-treated SMSKCNR cells, and pre-treatment with ascorbic acid (100 muM) and a MAPK inhibitor SB203580 (20 muM) reversed SAPK/JNK, caspase-3 activation, PARP-1 cleavage, and suppression of IGF-1R, PI3K, and PKC phosphorylation.	Acetylcysteine	0-17	mitogen-activated protein kinase 8	Homo sapiens	213-216
23554696-7	2011	Interestingly, EGF could induce a significant production of ROS, and N-acetyl-L-cysteine, a scavenger of ROS which abolished the EGF-induced ROS generation, cell migration, as well as activation of PI3K/Akt and PAK, but not Rac1.	Acetylcysteine	69-88	AKT serine/threonine kinase 1	Homo sapiens	203-206
22214156-11	2011	CONCLUSION: The intervention with high dose N-acetylcysteine can significantly reduce the alveolitis and the TNF-alpha and IL-8 levels in the BALF, therefore, inhibit and delay the development of pulmonary fibrosis of rats exposed to silicon dioxide.	Acetylcysteine	44-60	tumor necrosis factor	Rattus norvegicus	109-118
21624350-6	2011	Moreover, when the free radical (ROS) generating capacity of the compounds was studied by 2",7"-dichlorofluorescein-diacetate assay using flow cytometry, we found that a known antioxidant N-acetyl-cysteine almost completely abrogated the H2AX((S139)) phosphorylations and the caspase 3 cleavage and activation.	Acetylcysteine	188-205	caspase 3	Homo sapiens	276-285
21424515-4	2011	OBJECTIVE: To evaluate the anti-inflammatory effect of N-acetylcysteine (NAC) on the expression and secretion of inflammatory cytokines and interleukin (IL)-10 in lipopolysaccharide (LPS)-activated THP-1 macrophages under mild oxidative conditions.	Acetylcysteine	55-71	GLI family zinc finger 2	Homo sapiens	198-203
21424515-4	2011	OBJECTIVE: To evaluate the anti-inflammatory effect of N-acetylcysteine (NAC) on the expression and secretion of inflammatory cytokines and interleukin (IL)-10 in lipopolysaccharide (LPS)-activated THP-1 macrophages under mild oxidative conditions.	Acetylcysteine	73-76	GLI family zinc finger 2	Homo sapiens	198-203
21424515-7	2011	RESULTS: NAC inhibits the inflammatory cytokines TNFalpha, IL-1beta and IL-6 in LPS-activated macrophages under mild oxidative conditions.	Acetylcysteine	9-12	tumor necrosis factor	Homo sapiens	49-57
21424515-7	2011	RESULTS: NAC inhibits the inflammatory cytokines TNFalpha, IL-1beta and IL-6 in LPS-activated macrophages under mild oxidative conditions.	Acetylcysteine	9-12	interleukin 1 beta	Homo sapiens	59-67
21424515-7	2011	RESULTS: NAC inhibits the inflammatory cytokines TNFalpha, IL-1beta and IL-6 in LPS-activated macrophages under mild oxidative conditions.	Acetylcysteine	9-12	interleukin 6	Homo sapiens	72-76
21268136-6	2011	Furthermore, pretreatment of cells with N-acetylcysteine inhibited GSE-induced ERK1/2 phosphorylation as well as p21 upregulation, suggesting the involvement of GSE-induced oxidative stress as an upstream event.	Acetylcysteine	40-56	mitogen-activated protein kinase 3	Homo sapiens	79-85
21268136-6	2011	Furthermore, pretreatment of cells with N-acetylcysteine inhibited GSE-induced ERK1/2 phosphorylation as well as p21 upregulation, suggesting the involvement of GSE-induced oxidative stress as an upstream event.	Acetylcysteine	40-56	cyclin dependent kinase inhibitor 1A	Homo sapiens	113-116
21536676-6	2011	15(S)-HETE induced the production of H(2)O(2) via an NADPH oxidase-dependent manner and its scavengers, N-acetyl cysteine (NAC) and catalase suppressed 15(S)-HETE-stimulated EGFR, Src, Jak2, and STAT3 phosphorylation and MCP-1 expression.	Acetylcysteine	104-121	signal transducer and activator of transcription 3	Mus musculus	195-200
21532338-8	2011	N-acetyl-cysteine (NAC; 10 mM) pre-treatment rescued cell viability of RKS262 (23 microM)-treated SMSKCNR cells, and pre-treatment with ascorbic acid (100 muM) and a MAPK inhibitor SB203580 (20 muM) reversed SAPK/JNK, caspase-3 activation, PARP-1 cleavage, and suppression of IGF-1R, PI3K, and PKC phosphorylation.	Acetylcysteine	0-17	caspase 3	Homo sapiens	218-227
21532338-8	2011	N-acetyl-cysteine (NAC; 10 mM) pre-treatment rescued cell viability of RKS262 (23 microM)-treated SMSKCNR cells, and pre-treatment with ascorbic acid (100 muM) and a MAPK inhibitor SB203580 (20 muM) reversed SAPK/JNK, caspase-3 activation, PARP-1 cleavage, and suppression of IGF-1R, PI3K, and PKC phosphorylation.	Acetylcysteine	0-17	poly(ADP-ribose) polymerase 1	Homo sapiens	240-246
21532338-8	2011	N-acetyl-cysteine (NAC; 10 mM) pre-treatment rescued cell viability of RKS262 (23 microM)-treated SMSKCNR cells, and pre-treatment with ascorbic acid (100 muM) and a MAPK inhibitor SB203580 (20 muM) reversed SAPK/JNK, caspase-3 activation, PARP-1 cleavage, and suppression of IGF-1R, PI3K, and PKC phosphorylation.	Acetylcysteine	19-22	mitogen-activated protein kinase 8	Homo sapiens	213-216
21532338-8	2011	N-acetyl-cysteine (NAC; 10 mM) pre-treatment rescued cell viability of RKS262 (23 microM)-treated SMSKCNR cells, and pre-treatment with ascorbic acid (100 muM) and a MAPK inhibitor SB203580 (20 muM) reversed SAPK/JNK, caspase-3 activation, PARP-1 cleavage, and suppression of IGF-1R, PI3K, and PKC phosphorylation.	Acetylcysteine	19-22	caspase 3	Homo sapiens	218-227
21532338-8	2011	N-acetyl-cysteine (NAC; 10 mM) pre-treatment rescued cell viability of RKS262 (23 microM)-treated SMSKCNR cells, and pre-treatment with ascorbic acid (100 muM) and a MAPK inhibitor SB203580 (20 muM) reversed SAPK/JNK, caspase-3 activation, PARP-1 cleavage, and suppression of IGF-1R, PI3K, and PKC phosphorylation.	Acetylcysteine	19-22	poly(ADP-ribose) polymerase 1	Homo sapiens	240-246
21306579-5	2011	CSE-evoked VEGF release was mimicked by its component acrolein at concentrations (10-100 microM) found in CSE, and prevented by the antioxidant and alpha,beta-unsaturated aldehyde scavenger, N-acetylcysteine (NAC).	Acetylcysteine	191-207	vascular endothelial growth factor A	Homo sapiens	11-15
21421815-9	2011	Mitochondrial PTEN protein levels were decreased by NAC and increased by H(2)O(2).	Acetylcysteine	52-55	phosphatase and tensin homolog	Mus musculus	14-18
21306579-5	2011	CSE-evoked VEGF release was mimicked by its component acrolein at concentrations (10-100 microM) found in CSE, and prevented by the antioxidant and alpha,beta-unsaturated aldehyde scavenger, N-acetylcysteine (NAC).	Acetylcysteine	209-212	vascular endothelial growth factor A	Homo sapiens	11-15
21306579-8	2011	CSE-evoked VEGF release was accompanied by rapid and lasting phosphorylation of p38 MAPK (mitogen-activated protein kinase), which was abolished by NAC and mimicked by acrolein.	Acetylcysteine	148-151	vascular endothelial growth factor A	Homo sapiens	11-15
21306579-8	2011	CSE-evoked VEGF release was accompanied by rapid and lasting phosphorylation of p38 MAPK (mitogen-activated protein kinase), which was abolished by NAC and mimicked by acrolein.	Acetylcysteine	148-151	mitogen-activated protein kinase 14	Homo sapiens	80-83
21424539-7	2011	RESULTS: High-glucose-induced HPR1 production and heparan sulphate degradation in three human endothelial cell lines, both of which were blocked by ROS scavengers, glutathione and N-acetylcysteine.	Acetylcysteine	180-196	heparanase	Homo sapiens	30-34
21778551-1	2011	The effect of N- acetylcysteine on the level of tumor necrosis factor-a (TNF-alpha) and liver parenchyma injury in an experimental rat model of obstructive jaundice were investigated.	Acetylcysteine	14-31	tumor necrosis factor	Rattus norvegicus	73-82
21376115-5	2011	Removal of intracellular ROS by N-acetylcysteine reduced the AMPK activation and IL-8 induction.	Acetylcysteine	32-48	C-X-C motif chemokine ligand 8	Homo sapiens	81-85
21778551-6	2011	N-Acetylcysteine can be useful in decreasing the parenchymal damage in the liver and suppress the plasma TNF-alpha level in experimental obstructive jaundice.	Acetylcysteine	0-16	tumor necrosis factor	Rattus norvegicus	105-114
21569548-9	2011	JNK phosphorylation induced by celastrol was suppressed by NAC and JNK inhibitor SP600125 (SP).	Acetylcysteine	59-62	mitogen-activated protein kinase 8	Homo sapiens	0-3
21524888-5	2011	The expression of postconfluence-induced NQO-1 was stimulated by 0.1 mM H(2)O(2), but attenuated by 5 mM N-acetylcysteine, implying that reactive oxygen species (ROS) are implicated in the expression of NQO-1 in differentiated KCs.	Acetylcysteine	105-121	NAD(P)H quinone dehydrogenase 1	Homo sapiens	41-46
21563917-0	2011	Thyroid hormone administration induces rat liver Nrf2 activation: suppression by N-acetylcysteine pretreatment.	Acetylcysteine	81-97	NFE2 like bZIP transcription factor 2	Rattus norvegicus	49-53
21563917-4	2011	MATERIALS AND METHODS: The effect of T(3) administration in the presence and absence of N-acetylcysteine (NAC) on cytosol-to-nuclear translocation of Nrf2 was evaluated, with inhibition of this process by NAC taken as evidence that the process was redox mediated.	Acetylcysteine	88-104	NFE2 like bZIP transcription factor 2	Rattus norvegicus	150-154
21563917-4	2011	MATERIALS AND METHODS: The effect of T(3) administration in the presence and absence of N-acetylcysteine (NAC) on cytosol-to-nuclear translocation of Nrf2 was evaluated, with inhibition of this process by NAC taken as evidence that the process was redox mediated.	Acetylcysteine	106-109	NFE2 like bZIP transcription factor 2	Rattus norvegicus	150-154
21563917-4	2011	MATERIALS AND METHODS: The effect of T(3) administration in the presence and absence of N-acetylcysteine (NAC) on cytosol-to-nuclear translocation of Nrf2 was evaluated, with inhibition of this process by NAC taken as evidence that the process was redox mediated.	Acetylcysteine	205-208	NFE2 like bZIP transcription factor 2	Rattus norvegicus	150-154
21563917-14	2011	In the group of rats pretreated with NAC, the increase in cytosol-to-nuclear translocation of Nrf2 was only 28% that induced by T(3).	Acetylcysteine	37-40	NFE2 like bZIP transcription factor 2	Rattus norvegicus	94-98
21382479-11	2011	The reactive oxygen species (ROS) scavenger N-acetylcysteine decreased the Cav-1-Fas interaction.	Acetylcysteine	44-60	caveolin 1	Homo sapiens	75-80
21569548-13	2011	NAC completely inhibited celastrol-induced decrease of HSP90 client proteins, catalase and thioredoxin.	Acetylcysteine	0-3	catalase	Homo sapiens	78-86
21600014-7	2011	Critically, NAC inhibited thrombin- and ADP-induced platelet aggregation in vitro.	Acetylcysteine	12-15	coagulation factor II, thrombin	Homo sapiens	26-34
21595915-10	2011	The results showed that BSO pretreatment down-regulated HIF-1alpha and the effect was concentration-dependent, on the other hand, the increases of intracellular GSH contents by NAC could partly elevate the levels of HIF-1alpha expression.	Acetylcysteine	177-180	hypoxia inducible factor 1 subunit alpha	Homo sapiens	56-66
21595915-10	2011	The results showed that BSO pretreatment down-regulated HIF-1alpha and the effect was concentration-dependent, on the other hand, the increases of intracellular GSH contents by NAC could partly elevate the levels of HIF-1alpha expression.	Acetylcysteine	177-180	hypoxia inducible factor 1 subunit alpha	Homo sapiens	216-226
21325641-10	2011	NAC pretreatment blunted IRB-induced cytokine upregulation in the diaphragm and resulted in decreased ERK1/2, P38, and NF-kappaB/p65 phosphorylation.	Acetylcysteine	0-3	synaptotagmin 1	Rattus norvegicus	129-132
21131132-9	2011	Expression of CD11a (p &lt; 0.05), CD18 (p &lt; 0.05) and CD97 (p &lt; 0.01) on the granulocytes were significantly lower in the NAC treated group, similarly to lymphocyte CD 49d (p &lt; 0.05) and monocyte CD 49d (p &lt; 0.01) and CD 97 (p &lt; 0.05) expression.	Acetylcysteine	129-132	integrin subunit beta 2	Homo sapiens	35-39
21401696-15	2011	Furthermore, NAC treatment increased eNOS protein expression, but decreased iNOS expression, in lung tissues after infection.	Acetylcysteine	13-16	nitric oxide synthase 2	Rattus norvegicus	76-80
21401696-19	2011	The results suggest that this effect maybe due to regulation of iNOS and eNOS protein expression by NAC.	Acetylcysteine	100-103	nitric oxide synthase 2	Rattus norvegicus	64-68
21713097-11	2011	There was decrease in C-reactive protein (CRP) from 1.03+-0.72 mg/dL to 0.52+-0.22 mg/dL and that of malondialdehyde (MDA) from 11.20+-4.07 nmol/mL to 8.81+-2.79 nmol/mL with N-acetylcysteine treatment (P &lt; 0.05).	Acetylcysteine	175-191	C-reactive protein	Homo sapiens	22-40
21713097-16	2011	There was decrease in CRP (a marker of inflammation) and MDA after treatment with N-acetylcysteine suggesting improvement in endothelial dysfunction.	Acetylcysteine	82-98	C-reactive protein	Homo sapiens	22-25
21540553-6	2011	N-acetyl-cysteine (NAC), an antioxidant that restores intracellular glutathione (GSH) concentrations, prevented the IL-6-induced inhibitory effect on D1- and D2-mediated T3 production, which suggests that IL-6 might function by depleting an intracellular thiol cofactor, perhaps GSH.	Acetylcysteine	0-17	interleukin 6	Homo sapiens	116-120
21540553-6	2011	N-acetyl-cysteine (NAC), an antioxidant that restores intracellular glutathione (GSH) concentrations, prevented the IL-6-induced inhibitory effect on D1- and D2-mediated T3 production, which suggests that IL-6 might function by depleting an intracellular thiol cofactor, perhaps GSH.	Acetylcysteine	0-17	interleukin 6	Homo sapiens	205-209
21540553-6	2011	N-acetyl-cysteine (NAC), an antioxidant that restores intracellular glutathione (GSH) concentrations, prevented the IL-6-induced inhibitory effect on D1- and D2-mediated T3 production, which suggests that IL-6 might function by depleting an intracellular thiol cofactor, perhaps GSH.	Acetylcysteine	19-22	interleukin 6	Homo sapiens	116-120
21540553-6	2011	N-acetyl-cysteine (NAC), an antioxidant that restores intracellular glutathione (GSH) concentrations, prevented the IL-6-induced inhibitory effect on D1- and D2-mediated T3 production, which suggests that IL-6 might function by depleting an intracellular thiol cofactor, perhaps GSH.	Acetylcysteine	19-22	interleukin 6	Homo sapiens	205-209
21378396-7	2011	Iron or N-acetylcysteine supplementation reversed Dp44mT-induced up-regulation of phospho-JNK, but only iron was able to reverse the effect of DFO on JNK.	Acetylcysteine	8-24	mitogen-activated protein kinase 8	Homo sapiens	90-93
21320508-5	2011	N-acetylcysteine, the superoxide dismutase mimetic MnTMPyP, and apocynin significantly attenuated ET-1-mediated inotropic effect, which was accompanied by inhibition of extracellular signal regulated kinase 1/2 (ERK1/2) phosphorylation.	Acetylcysteine	0-16	endothelin 1	Rattus norvegicus	98-102
21320508-8	2011	In contrast to ET-1 stimulation, the positive inotropic effect of beta(1)-adrenergic receptor agonist dobutamine (250nmol/L) was significantly augmented by N-acetylcysteine and apocynin.	Acetylcysteine	156-172	adrenoceptor beta 1	Rattus norvegicus	66-93
21236267-5	2011	Irbesartan or an anti-oxidant N-acetylcysteine inhibited the AGE-induced increase in reactive oxygen species (ROS) generation and subsequently blocked up-regulation of VCAM-1 mRNA levels in glomerular ECs.	Acetylcysteine	30-46	vascular cell adhesion molecule 1	Homo sapiens	168-174
21372137-10	2011	Furthermore, Mct-1 siRNA lowered the level of ROS generated after 15-h exposure to IL-1beta, whereas a ROS scavenger, N-acetylcysteine, suppressed both late phase degradation of IkappaBalpha and Nox-2 expression.	Acetylcysteine	118-134	nuclear factor of kappa light polypeptide gene enhancer in B cells inhibitor, alpha	Mus musculus	178-190
21303669-10	2011	NAC also up-regulated Bcl-2 and Xiap.	Acetylcysteine	0-3	BCL2 apoptosis regulator	Homo sapiens	22-27
20938377-8	2011	The tissue levels of lipid hydroperoxides and caspase 3 in the kidney of NAC-treated animals were significantly lower than those of H/R controls.	Acetylcysteine	73-76	caspase 3	Sus scrofa	46-55
21258765-8	2011	In addition, NAC increased Mn-SOD activity and decreased ROS levels in FCCP-treated As4.1 cells.	Acetylcysteine	13-16	superoxide dismutase 2, mitochondrial	Mus musculus	27-33
21217061-6	2011	High-glucose-induced upregulation of NQO1, GCLC, and HMOX1 was also prevented by pretreatment with polyethylene glycol (PEG)-catalase or N-acetylcysteine, whereas administration of H(2)O(2) mimicked the effect of high glucose.	Acetylcysteine	137-153	heme oxygenase 1	Mus musculus	53-58
20836702-8	2011	Selective inhibition of the NADPH oxidase or N-acetyl L-cysteine also prevented the enhanced translocation of p65 in hippocampal cells, while N-acetyl L-cysteine abolished the increase in RyR2 protein content induced by high frequency stimulation.	Acetylcysteine	142-161	ryanodine receptor 2	Homo sapiens	188-192
21237301-5	2011	The effect of eugenol and N-acetylcysteine on the release of Th1 cytokines (TNF-alpha, IL-12) and Th2 cytokines (IL-10, TGF-beta) was measured by ELISA, and the expression of these cytokines at mRNA level were analyzed by real-time PCR.	Acetylcysteine	26-42	negative elongation factor complex member C/D, Th1l	Mus musculus	61-64
21237301-5	2011	The effect of eugenol and N-acetylcysteine on the release of Th1 cytokines (TNF-alpha, IL-12) and Th2 cytokines (IL-10, TGF-beta) was measured by ELISA, and the expression of these cytokines at mRNA level were analyzed by real-time PCR.	Acetylcysteine	26-42	tumor necrosis factor	Mus musculus	76-85
21237301-9	2011	Eugenol and N-acetylcysteine were found to down regulate the Th1 cytokines in nicotine treated macrophages with concurrent activation of Th2 responses.	Acetylcysteine	12-28	negative elongation factor complex member C/D, Th1l	Mus musculus	61-64
21448585-6	2011	Further investigation revealed that wogonin activated ERK and p38 MAPKs, which was inhibited by N-acetyl cysteine (NAC), a ROS scavenger, indicating that wogonin-induced ROS are associated with MAPKs activation.	Acetylcysteine	96-113	mitogen-activated protein kinase 14	Homo sapiens	62-65
21448585-6	2011	Further investigation revealed that wogonin activated ERK and p38 MAPKs, which was inhibited by N-acetyl cysteine (NAC), a ROS scavenger, indicating that wogonin-induced ROS are associated with MAPKs activation.	Acetylcysteine	115-118	mitogen-activated protein kinase 14	Homo sapiens	62-65
21345685-6	2011	N-acetylcysteine (NAC) treatment abolished p38 phosphorylation as well as HO-1 induction caused by SC-1, indicating that ROS are upstream signals of p38 in Nrf2/ARE activation by SC-1.	Acetylcysteine	0-16	NFE2 like bZIP transcription factor 2	Rattus norvegicus	156-160
21345685-6	2011	N-acetylcysteine (NAC) treatment abolished p38 phosphorylation as well as HO-1 induction caused by SC-1, indicating that ROS are upstream signals of p38 in Nrf2/ARE activation by SC-1.	Acetylcysteine	18-21	NFE2 like bZIP transcription factor 2	Rattus norvegicus	156-160
21195169-5	2011	Cd induction of ROS contributed to the activation of mTOR signaling, as pretreatment with N-acetyl-l-cysteine (NAC), a ROS scavenger, prevented this event.	Acetylcysteine	90-109	mechanistic target of rapamycin kinase	Homo sapiens	53-57
21195169-5	2011	Cd induction of ROS contributed to the activation of mTOR signaling, as pretreatment with N-acetyl-l-cysteine (NAC), a ROS scavenger, prevented this event.	Acetylcysteine	111-114	mechanistic target of rapamycin kinase	Homo sapiens	53-57
21173077-6	2011	The antioxidants N-acetylcysteine and glutathione monoethyl ester inhibited both RA + TPA and RA + TGF-beta-stimulated secretion of VEGF, as well as RA-induced ROS production.	Acetylcysteine	17-33	transforming growth factor beta 1	Homo sapiens	99-107
21610364-11	2011	SOD and GSH activities in the control group were found to be increased significantly, whereas SOD and GSH activities in IPC and NAC groups did not change significantly after reperfusion.	Acetylcysteine	128-131	superoxide dismutase 1	Homo sapiens	94-97
21610364-16	2011	NAC and IPC had protective effect on occurrence of oxidative stress resulting from IR period by preventing MDA, SOD, GSH-Px, TAC, and TOS changes in routine arthroscopic knee surgery.	Acetylcysteine	0-3	superoxide dismutase 1	Homo sapiens	112-115
21173077-6	2011	The antioxidants N-acetylcysteine and glutathione monoethyl ester inhibited both RA + TPA and RA + TGF-beta-stimulated secretion of VEGF, as well as RA-induced ROS production.	Acetylcysteine	17-33	vascular endothelial growth factor A	Homo sapiens	132-136
21148404-6	2011	Treatment of the cells with hydrogen peroxide scavengers, catalase and N-acetylcysteine, promoted Cav-1 downregulation and anoikis during cell detachment, indicating that produced hydrogen peroxide plays a primary role in preventing anoikis by stabilizing Cav-1 protein.	Acetylcysteine	71-87	caveolin 1	Homo sapiens	98-103
21148404-6	2011	Treatment of the cells with hydrogen peroxide scavengers, catalase and N-acetylcysteine, promoted Cav-1 downregulation and anoikis during cell detachment, indicating that produced hydrogen peroxide plays a primary role in preventing anoikis by stabilizing Cav-1 protein.	Acetylcysteine	71-87	caveolin 1	Homo sapiens	256-261
21148404-7	2011	Catalase and N-acetylcysteine promoted ubiquitination and proteasomal degradation of Cav-1, which is a major pathway of its downregulation during cell anoikis.	Acetylcysteine	13-29	caveolin 1	Homo sapiens	85-90
20795947-9	2011	Resistin siRNA and NAC (N-acetylcysteine) significantly reduced resistin protein and mRNA expression induced by balloon injury.	Acetylcysteine	19-22	resistin	Rattus norvegicus	64-72
21082355-9	2011	ROS scavenger-N-acetyl cysteine, mitochondrial stabilizer-cyclosporin-A, and broad spectrum caspase inhibitor Z-VAD-FMK inhibited the OA induced caspase-3 activation, DNA damage and cell death but caspase-8 inhibitor had no effect.	Acetylcysteine	14-31	caspase 3	Homo sapiens	145-154
20946208-8	2011	The percentage of the ALP-positive area was consistently 7% or less on CM and DFDB at days 7 and 14, which was restored by NAC pretreatment up to 60% or more.	Acetylcysteine	123-126	alkaline phosphatase, placental	Homo sapiens	22-25
21131394-10	2011	The changes in oxidant/antioxidant enzymes and IL-6 release were reversed by the antioxidants N-acetyl-cysteine (NAC) and ebselen through inhibition of Smad3 phosphorylation, indicating redox-dependent activation of Smad3 by TGF-beta.	Acetylcysteine	94-111	interleukin 6	Homo sapiens	47-51
21131394-10	2011	The changes in oxidant/antioxidant enzymes and IL-6 release were reversed by the antioxidants N-acetyl-cysteine (NAC) and ebselen through inhibition of Smad3 phosphorylation, indicating redox-dependent activation of Smad3 by TGF-beta.	Acetylcysteine	94-111	transforming growth factor beta 1	Homo sapiens	225-233
21131394-10	2011	The changes in oxidant/antioxidant enzymes and IL-6 release were reversed by the antioxidants N-acetyl-cysteine (NAC) and ebselen through inhibition of Smad3 phosphorylation, indicating redox-dependent activation of Smad3 by TGF-beta.	Acetylcysteine	113-116	interleukin 6	Homo sapiens	47-51
21131394-10	2011	The changes in oxidant/antioxidant enzymes and IL-6 release were reversed by the antioxidants N-acetyl-cysteine (NAC) and ebselen through inhibition of Smad3 phosphorylation, indicating redox-dependent activation of Smad3 by TGF-beta.	Acetylcysteine	113-116	transforming growth factor beta 1	Homo sapiens	225-233
21131394-11	2011	Moreover, these findings suggest a potential role for NAC in preventing TGF-beta-mediated pro-oxidant and proinflammatory responses in ASMCs.	Acetylcysteine	54-57	transforming growth factor beta 1	Homo sapiens	72-80
20795947-9	2011	Resistin siRNA and NAC (N-acetylcysteine) significantly reduced resistin protein and mRNA expression induced by balloon injury.	Acetylcysteine	24-40	resistin	Rattus norvegicus	64-72
20978740-10	2011	Furthermore, LRP6 stability was increased by HNE and decreased by NAC.	Acetylcysteine	66-69	LDL receptor related protein 6	Rattus norvegicus	13-17
20978740-13	2011	NAC treatment reduced HNE and 3-nitrotyrosine levels and attenuated the upregulation of LRP6, beta-catenin and CTGF in diabetic rat retina.	Acetylcysteine	0-3	LDL receptor related protein 6	Rattus norvegicus	88-92
21170508-5	2011	Pretreatment with N-acetyl-L-cysteine (NAC) significantly inhibited the cell death induced by the combined treatment with BBR and TRAIL as well as recovered the expression levels of c-FLIP and Mcl-1 downregulated by treatment with BBR.	Acetylcysteine	18-37	TNF superfamily member 10	Homo sapiens	130-135
21537415-8	2011	Of note, there was nucleocytoplasmic translocation of Pdx1, which was partially prevented by treatment with an antioxidant, N-acetyl-L-cysteine.	Acetylcysteine	124-143	pancreatic and duodenal homeobox 1	Rattus norvegicus	54-58
20954832-6	2011	Ex vivo studies revealed that GSH and NAC effectively scavenged N-chloramines in sputum and inhibited sputum MPO activity with potency exquisitely dependent upon MPO activity levels.	Acetylcysteine	38-41	myeloperoxidase	Homo sapiens	109-112
20954832-6	2011	Ex vivo studies revealed that GSH and NAC effectively scavenged N-chloramines in sputum and inhibited sputum MPO activity with potency exquisitely dependent upon MPO activity levels.	Acetylcysteine	38-41	myeloperoxidase	Homo sapiens	162-165
20954832-7	2011	Detailed kinetic analyses revealed that NAC and GSH inhibit MPO by distinct mechanisms.	Acetylcysteine	40-43	myeloperoxidase	Homo sapiens	60-63
20954832-9	2011	The findings reveal that MPO activity and its reactive products represent useful predictors of the doses of inhaled thiol antioxidants required to ameliorate airway oxidative stress and inflammation in CF patients and provide mechanistic insight into the antioxidative/anti-inflammatory mechanisms of action of GSH and NAC when administered into the CF lung.	Acetylcysteine	319-322	myeloperoxidase	Homo sapiens	25-28
21170508-5	2011	Pretreatment with N-acetyl-L-cysteine (NAC) significantly inhibited the cell death induced by the combined treatment with BBR and TRAIL as well as recovered the expression levels of c-FLIP and Mcl-1 downregulated by treatment with BBR.	Acetylcysteine	18-37	CASP8 and FADD like apoptosis regulator	Homo sapiens	182-188
21266777-0	2011	N-acetylcysteine reduces the size and activity of von Willebrand factor in human plasma and mice.	Acetylcysteine	0-16	von Willebrand factor	Homo sapiens	50-71
21266777-5	2011	Here, we examined whether NAC could reduce vWF multimers, which polymerize in a manner similar to mucins.	Acetylcysteine	26-29	von Willebrand factor	Homo sapiens	43-46
21266777-6	2011	In vitro, NAC reduced soluble plasma-type vWF multimers in a concentration-dependent manner and rapidly degraded ULVWF multimer strings extruded from activated ECs.	Acetylcysteine	10-13	von Willebrand factor	Homo sapiens	42-45
21266777-8	2011	NAC also inhibited vWF-dependent platelet aggregation and collagen binding.	Acetylcysteine	0-3	von Willebrand factor	Homo sapiens	19-22
21266777-9	2011	Injection of NAC into ADAMTS13-deficient mice led to the rapid resolution of thrombi produced by ionophore treatment of the mesenteric venules and reduced plasma vWF multimers.	Acetylcysteine	13-16	a disintegrin-like and metallopeptidase (reprolysin type) with thrombospondin type 1 motif, 13	Mus musculus	22-30
21254278-0	2011	N-acetyl-L-cysteine counteracts oxidative stress and prevents H2O2 induced germ cell apoptosis through down-regulation of caspase-9 and JNK/c-Jun.	Acetylcysteine	0-19	mitogen-activated protein kinase 8	Homo sapiens	136-139
20847117-9	2011	Pretreatment with the specific NF-kappaB inhibitor DHMEQ or the antioxidant NAC significantly reduced corneal angiogenesis by downregulating the NF-kappaB pathway (P&lt;0.01) in both WT and SOD-1-/- mice.	Acetylcysteine	76-79	superoxide dismutase 1, soluble	Mus musculus	190-195
21283817-7	2011	Furthermore, chronic CSE treatment was found to increase ROS (reactive oxygen species) production, and application of the ROS scavengers N-acetylcysteine abrogated the expression of PDK2 and HIF1alpha.	Acetylcysteine	137-153	hypoxia inducible factor 1 subunit alpha	Homo sapiens	191-200
21372386-12	2011	NAC and glutathione highly stimulated the hepatic expression of cytokines, particularly interleukin-6, which might be involved in the alleviation of APAP hepatotoxicity.	Acetylcysteine	0-3	interleukin 6	Mus musculus	88-101
21029048-3	2011	The antioxidant NAC (N-acetyl-L-cysteine) and the flavoprotein enzyme NAD(P)H oxidase inhibitor DPI (diphenyleneiodonium) prevented BMP-2-stimulated alkaline phosphatase expression and mineralized bone nodule formation in mouse 2T3 pre-osteoblasts.	Acetylcysteine	16-19	bone morphogenetic protein 2	Mus musculus	132-137
21029048-3	2011	The antioxidant NAC (N-acetyl-L-cysteine) and the flavoprotein enzyme NAD(P)H oxidase inhibitor DPI (diphenyleneiodonium) prevented BMP-2-stimulated alkaline phosphatase expression and mineralized bone nodule formation in mouse 2T3 pre-osteoblasts.	Acetylcysteine	21-40	bone morphogenetic protein 2	Mus musculus	132-137
21029048-5	2011	NAC and DPI inhibited BMP-2-induced ROS production and NAD(P)H oxidase activity respectively.	Acetylcysteine	0-3	bone morphogenetic protein 2	Mus musculus	22-27
21029048-11	2011	NAC and DPI significantly blocked BMP-2-stimulated expression of BMP2 mRNA and protein due to a decrease in BMP2 gene transcription.	Acetylcysteine	0-3	bone morphogenetic protein 2	Mus musculus	34-39
21029048-11	2011	NAC and DPI significantly blocked BMP-2-stimulated expression of BMP2 mRNA and protein due to a decrease in BMP2 gene transcription.	Acetylcysteine	0-3	bone morphogenetic protein 2	Mus musculus	65-69
21029048-11	2011	NAC and DPI significantly blocked BMP-2-stimulated expression of BMP2 mRNA and protein due to a decrease in BMP2 gene transcription.	Acetylcysteine	0-3	bone morphogenetic protein 2	Mus musculus	108-112
20868662-4	2011	Carnosine exhibited better protection against MDA-induced cell injury than antioxidant N-acetyl-cysteine (NAC) with its multi-potency, which alleviated MDA-induced protein cross-linking, Deltapsim decrease, reactive oxygen species burst, JNK and ERK activation.	Acetylcysteine	87-104	mitogen-activated protein kinase 8	Homo sapiens	238-241
20868662-4	2011	Carnosine exhibited better protection against MDA-induced cell injury than antioxidant N-acetyl-cysteine (NAC) with its multi-potency, which alleviated MDA-induced protein cross-linking, Deltapsim decrease, reactive oxygen species burst, JNK and ERK activation.	Acetylcysteine	87-104	mitogen-activated protein kinase 1	Homo sapiens	246-249
20868662-4	2011	Carnosine exhibited better protection against MDA-induced cell injury than antioxidant N-acetyl-cysteine (NAC) with its multi-potency, which alleviated MDA-induced protein cross-linking, Deltapsim decrease, reactive oxygen species burst, JNK and ERK activation.	Acetylcysteine	106-109	mitogen-activated protein kinase 8	Homo sapiens	238-241
20868662-4	2011	Carnosine exhibited better protection against MDA-induced cell injury than antioxidant N-acetyl-cysteine (NAC) with its multi-potency, which alleviated MDA-induced protein cross-linking, Deltapsim decrease, reactive oxygen species burst, JNK and ERK activation.	Acetylcysteine	106-109	mitogen-activated protein kinase 1	Homo sapiens	246-249
20868662-6	2011	Carnosine alleviated all these alterations induced by MDA, but NAC merely inhibited Bcl-2 family-related activation of JNK and ERK.	Acetylcysteine	63-66	BCL2 apoptosis regulator	Homo sapiens	84-89
20868662-6	2011	Carnosine alleviated all these alterations induced by MDA, but NAC merely inhibited Bcl-2 family-related activation of JNK and ERK.	Acetylcysteine	63-66	mitogen-activated protein kinase 8	Homo sapiens	119-122
20868662-6	2011	Carnosine alleviated all these alterations induced by MDA, but NAC merely inhibited Bcl-2 family-related activation of JNK and ERK.	Acetylcysteine	63-66	mitogen-activated protein kinase 1	Homo sapiens	127-130
21093414-6	2011	The ROS scavenger, N-acetyl cysteine partially reversed Snail-mediated EMT after 7 days characterized by increased E-cadherin levels and decreased ERK activity, while treatment with the MEK inhibitor, UO126, resulted in a more marked effect by 3 days, characterized by cells returning back to the epithelial morphology and increased E-cadherin.	Acetylcysteine	19-36	snail family transcriptional repressor 1	Homo sapiens	56-61
21093414-6	2011	The ROS scavenger, N-acetyl cysteine partially reversed Snail-mediated EMT after 7 days characterized by increased E-cadherin levels and decreased ERK activity, while treatment with the MEK inhibitor, UO126, resulted in a more marked effect by 3 days, characterized by cells returning back to the epithelial morphology and increased E-cadherin.	Acetylcysteine	19-36	cadherin 1	Homo sapiens	115-125
21093414-6	2011	The ROS scavenger, N-acetyl cysteine partially reversed Snail-mediated EMT after 7 days characterized by increased E-cadherin levels and decreased ERK activity, while treatment with the MEK inhibitor, UO126, resulted in a more marked effect by 3 days, characterized by cells returning back to the epithelial morphology and increased E-cadherin.	Acetylcysteine	19-36	mitogen-activated protein kinase 1	Homo sapiens	147-150
21093414-6	2011	The ROS scavenger, N-acetyl cysteine partially reversed Snail-mediated EMT after 7 days characterized by increased E-cadherin levels and decreased ERK activity, while treatment with the MEK inhibitor, UO126, resulted in a more marked effect by 3 days, characterized by cells returning back to the epithelial morphology and increased E-cadherin.	Acetylcysteine	19-36	cadherin 1	Homo sapiens	333-343
20955365-8	2011	Glutamate-induced p53 activation was preceded by accumulation of reactive oxygen species, and co-treatment with N-acetyl-cysteine prevented glutamate-induced p53 activation and GADD45alpha expression.	Acetylcysteine	112-129	growth arrest and DNA-damage-inducible 45 alpha	Mus musculus	177-188
21804221-4	2011	Pre-treatment with N-acetylcysteine (NAC) significantly suppressed the ROS production and down-regulation of EC-SOD.	Acetylcysteine	19-35	superoxide dismutase 3	Homo sapiens	109-115
21804221-4	2011	Pre-treatment with N-acetylcysteine (NAC) significantly suppressed the ROS production and down-regulation of EC-SOD.	Acetylcysteine	37-40	superoxide dismutase 3	Homo sapiens	109-115
21963500-8	2011	The expression rate of Hex-EGFP clearly increased by treatment with radical scavengers, propyl gallate and butylated hydroxyanisole, slightly increased with a caspase inhibitor, zVAD-fmk, and was not affected by N-acetyl cysteine in ATDC5 cells.	Acetylcysteine	212-229	hematopoietically expressed homeobox	Mus musculus	23-26
21778718-7	2011	NAC reduced the paclitaxel-induced increase in activated caspase-10 levels, but potentiated that for caspase-3.	Acetylcysteine	0-3	caspase 3	Homo sapiens	101-110
21106878-11	2011	Cotreatment with N-acetyl cysteine or ascorbic acid also preserved IGF-I sensitivity and mTOR activity.	Acetylcysteine	17-34	insulin like growth factor 1	Homo sapiens	67-72
21106878-11	2011	Cotreatment with N-acetyl cysteine or ascorbic acid also preserved IGF-I sensitivity and mTOR activity.	Acetylcysteine	17-34	mechanistic target of rapamycin kinase	Homo sapiens	89-93
19592481-6	2011	Treatment with the antioxidant N-acetyl-cysteine (NAC), a ROS scavenger, inhibited ROS generation and Bax translocation and led to a significant protection against bufalin-induced apoptosis.	Acetylcysteine	31-48	BCL2 associated X, apoptosis regulator	Homo sapiens	102-105
19592481-6	2011	Treatment with the antioxidant N-acetyl-cysteine (NAC), a ROS scavenger, inhibited ROS generation and Bax translocation and led to a significant protection against bufalin-induced apoptosis.	Acetylcysteine	50-53	BCL2 associated X, apoptosis regulator	Homo sapiens	102-105
19592481-7	2011	Our results also revealed that bufalin induced a prominent increase of caspase-3 activation blocked potently by NAC.	Acetylcysteine	112-115	caspase 3	Homo sapiens	71-80
20845026-8	2011	NAC exhibited no significant effect on biochemical parameters but reduced renal tissue SOD level and reversed immunocytochemical staining of inducible nitric oxide synthase (i-NOS) and neurotrophin-3.	Acetylcysteine	0-3	nitric oxide synthase 2	Rattus norvegicus	141-172
21212636-0	2011	Effects of 4-hydroxy-2-nonenal, a major lipid peroxidation-derived aldehyde, and N-acetylcysteine on the cyclooxygenase-2 expression in human uterine myometrium.	Acetylcysteine	81-97	prostaglandin-endoperoxide synthase 2	Homo sapiens	105-121
21212636-5	2011	We also examined the effect of N-acetylcysteine (NAC) on 4-HNE-induced COX-2 expression.	Acetylcysteine	31-47	prostaglandin-endoperoxide synthase 2	Homo sapiens	71-76
21212636-5	2011	We also examined the effect of N-acetylcysteine (NAC) on 4-HNE-induced COX-2 expression.	Acetylcysteine	49-52	prostaglandin-endoperoxide synthase 2	Homo sapiens	71-76
21212636-13	2011	NAC inhibited 4-HNE-induced COX-2 expression.	Acetylcysteine	0-3	prostaglandin-endoperoxide synthase 2	Homo sapiens	28-33
22072928-6	2011	NAC also inhibited both adipogenic transcription factors CCAAT/enhancer binding protein beta (C/EBP beta) and peroxisomal proliferator activated receptor gamma (PPAR gamma) expression; we suggested that intracellular GSH content could be responsible for these effects.	Acetylcysteine	0-3	peroxisome proliferator activated receptor gamma	Homo sapiens	110-159
22072928-6	2011	NAC also inhibited both adipogenic transcription factors CCAAT/enhancer binding protein beta (C/EBP beta) and peroxisomal proliferator activated receptor gamma (PPAR gamma) expression; we suggested that intracellular GSH content could be responsible for these effects.	Acetylcysteine	0-3	peroxisome proliferator activated receptor gamma	Homo sapiens	161-171
22114506-8	2011	The effects of iron oxide nanoparticles on interferon-gamma and glutathione were attenuated by the presence of N-acetyl-L-cysteine, a precursor of glutathione.	Acetylcysteine	111-130	interferon gamma	Homo sapiens	43-59
20845026-8	2011	NAC exhibited no significant effect on biochemical parameters but reduced renal tissue SOD level and reversed immunocytochemical staining of inducible nitric oxide synthase (i-NOS) and neurotrophin-3.	Acetylcysteine	0-3	nitric oxide synthase 2	Rattus norvegicus	174-179
20845026-10	2011	Additionally, NAC significantly reduced the immunostaining of endothelial NOS (e-NOS) and i-NOS in the lung tissue.	Acetylcysteine	14-17	nitric oxide synthase 2	Rattus norvegicus	90-95
21873804-0	2011	The antioxidant N-acetylcysteine promotes atherosclerotic plaque stabilization through suppression of RAGE, MMPs and NF-kappaB in ApoE-deficient mice.	Acetylcysteine	16-32	advanced glycosylation end product-specific receptor	Mus musculus	102-106
21873804-0	2011	The antioxidant N-acetylcysteine promotes atherosclerotic plaque stabilization through suppression of RAGE, MMPs and NF-kappaB in ApoE-deficient mice.	Acetylcysteine	16-32	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	117-126
21873804-8	2011	RESULTS: ApoE(-/-) mice administrated with NAC displayed reduced serum MDA level and impaired ROS generation in aortic root.	Acetylcysteine	43-46	apolipoprotein E	Mus musculus	9-13
21873804-0	2011	The antioxidant N-acetylcysteine promotes atherosclerotic plaque stabilization through suppression of RAGE, MMPs and NF-kappaB in ApoE-deficient mice.	Acetylcysteine	16-32	apolipoprotein E	Mus musculus	130-134
21873804-10	2011	Analysis of plaque composition showed decreased amounts of macrophages, lipid deposition, but not smooth muscle cells, and increased collagen content in atherosclerotic lesions in apoE(-/-) mice administered with NAC.	Acetylcysteine	213-216	apolipoprotein E	Mus musculus	180-184
21873804-11	2011	Moreover, we found that NAC down-regulated the expression of VCAM-1, MMP2 and MMP9, accompanied by inhibition of NF-kappaB activation and reduced expression of RAGE.	Acetylcysteine	24-27	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	113-122
22129737-4	2011	The effects of anti-oxidative enzymes and reagents including N-acetyl-L-cysteine, alpha-tocopherol, and lecithinized-superoxide dismutase (SOD) on TGFbeta1-induced expression of alphaSMA were also examined.	Acetylcysteine	61-80	transforming growth factor beta 1	Homo sapiens	147-155
21873804-11	2011	Moreover, we found that NAC down-regulated the expression of VCAM-1, MMP2 and MMP9, accompanied by inhibition of NF-kappaB activation and reduced expression of RAGE.	Acetylcysteine	24-27	advanced glycosylation end product-specific receptor	Mus musculus	160-164
21873804-12	2011	CONCLUSION: In the present study, we show novel data to suggest that NAC promotes atherosclerotic plaque stabilization through suppression of RAGE, MMPs and NF-kappaB in apoE(-/-) mice.	Acetylcysteine	69-72	advanced glycosylation end product-specific receptor	Mus musculus	142-146
21873804-12	2011	CONCLUSION: In the present study, we show novel data to suggest that NAC promotes atherosclerotic plaque stabilization through suppression of RAGE, MMPs and NF-kappaB in apoE(-/-) mice.	Acetylcysteine	69-72	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	157-166
21873804-12	2011	CONCLUSION: In the present study, we show novel data to suggest that NAC promotes atherosclerotic plaque stabilization through suppression of RAGE, MMPs and NF-kappaB in apoE(-/-) mice.	Acetylcysteine	69-72	apolipoprotein E	Mus musculus	170-174
20625996-5	2011	A ROS scavenger, N-acetyl cysteine (NAC), significantly inhibited the IFN-gamma-induced production of chemokines as well as the activation of I kappa-B (IkappaB)-nuclear factor-kappa B (NF-kappaB).	Acetylcysteine	17-34	interferon gamma	Homo sapiens	70-79
20625996-5	2011	A ROS scavenger, N-acetyl cysteine (NAC), significantly inhibited the IFN-gamma-induced production of chemokines as well as the activation of I kappa-B (IkappaB)-nuclear factor-kappa B (NF-kappaB).	Acetylcysteine	17-34	nuclear factor kappa B subunit 1	Homo sapiens	186-195
20625996-5	2011	A ROS scavenger, N-acetyl cysteine (NAC), significantly inhibited the IFN-gamma-induced production of chemokines as well as the activation of I kappa-B (IkappaB)-nuclear factor-kappa B (NF-kappaB).	Acetylcysteine	36-39	interferon gamma	Homo sapiens	70-79
20625996-5	2011	A ROS scavenger, N-acetyl cysteine (NAC), significantly inhibited the IFN-gamma-induced production of chemokines as well as the activation of I kappa-B (IkappaB)-nuclear factor-kappa B (NF-kappaB).	Acetylcysteine	36-39	nuclear factor kappa B subunit 1	Homo sapiens	186-195
20625996-9	2011	However, IFN-gamma-stimulated activation of IkappaB and NF-kappaB was suppressed by NAC but enhanced by BSO.	Acetylcysteine	84-87	interferon gamma	Homo sapiens	9-18
20625996-9	2011	However, IFN-gamma-stimulated activation of IkappaB and NF-kappaB was suppressed by NAC but enhanced by BSO.	Acetylcysteine	84-87	nuclear factor kappa B subunit 1	Homo sapiens	56-65
22129741-4	2011	Immunohistochemical analysis showed that the glutathione-S-transferase placental form (GST-P) positive foci promoted by I3C were suppressed by the administration of NAC.	Acetylcysteine	165-168	glutathione S-transferase pi 1	Rattus norvegicus	45-92
22129741-5	2011	The mRNAs of members of the phase II nuclear factor, erythroid derived 2, like 2 (Nrf2) gene batteries, whose promoter region is called as antioxidant response element (ARE), were down-regulated in the DEN-I3C-NAC group compared to the DEN-I3C group, but Cyp1a1 was not suppressed in the DEN-I3C-NAC group compared to the DEN-I3C group.	Acetylcysteine	210-213	NFE2 like bZIP transcription factor 2	Rattus norvegicus	82-86
22129741-5	2011	The mRNAs of members of the phase II nuclear factor, erythroid derived 2, like 2 (Nrf2) gene batteries, whose promoter region is called as antioxidant response element (ARE), were down-regulated in the DEN-I3C-NAC group compared to the DEN-I3C group, but Cyp1a1 was not suppressed in the DEN-I3C-NAC group compared to the DEN-I3C group.	Acetylcysteine	296-299	NFE2 like bZIP transcription factor 2	Rattus norvegicus	82-86
21912612-8	2011	ALP enhanced the effects of NAC in restoring cardiac AdipoR2 and phosphorylation of Akt, STAT3 and eNOS in diabetic rats.	Acetylcysteine	28-31	AKT serine/threonine kinase 1	Rattus norvegicus	84-87
21035514-6	2011	Treatment with Bay 11-7085 (an inhibitor of NF-kappaB activation) and oxidant scavengers, including N-acetylcysteine, prevented the 7-ketocholesterol-induced formation of reactive oxygen species, activation of NF-kappaB, Akt and apoptosis-related proteins, and cell death.	Acetylcysteine	100-116	AKT serine/threonine kinase 1	Rattus norvegicus	221-224
21980400-8	2011	N-acetyl-L-cysteine, a scavenger of ROS, inhibited hypoxia-induced ROS generation, PI3K, ERK and Rac1 activation as well as HIF-1alpha expression.	Acetylcysteine	0-19	mitogen-activated protein kinase 1	Homo sapiens	89-92
21980400-8	2011	N-acetyl-L-cysteine, a scavenger of ROS, inhibited hypoxia-induced ROS generation, PI3K, ERK and Rac1 activation as well as HIF-1alpha expression.	Acetylcysteine	0-19	hypoxia inducible factor 1 subunit alpha	Homo sapiens	124-134
21209852-8	2010	Moreover, in the breast cancer cell, LPA treatment resulted in remarkable production of reactive oxygen species (ROS), while LPA-induced ROS generation, PI3K/PAK1/ERK activation and cell migration could be inhibited by N-acetyl-L-Cysteine, a scavenger of ROS.	Acetylcysteine	219-238	mitogen-activated protein kinase 1	Homo sapiens	163-166
21858089-7	2011	Furthermore, it was found that ROS scavenging by N-acetylcysteine (NAC) and inhibition of p53 activation by pifithrin-alpha or knockdown of p53 using siRNA, respectively, delayed autophagy impairment-induced premature senescence and restored the expression levels of components in the mTOR and autophagy pathways.	Acetylcysteine	67-70	mechanistic target of rapamycin kinase	Homo sapiens	285-289
20937831-7	2010	Furthermore, treatment with the NAD(P)H oxidase inhibitor apocynin and the glutathione donor N-acetylcysteine inhibited indoxyl sulfate-induced enhancement of THP-1 adhesion to HUVEC.	Acetylcysteine	93-109	GLI family zinc finger 2	Homo sapiens	159-164
20804741-11	2010	TNF-alpha-induced expression of uPA and activation of beta-catenin signaling appear to be mediated by ROS in MCF-10A cells, as both events were blocked by the antioxidant N-acetylcysteine.	Acetylcysteine	171-187	tumor necrosis factor	Homo sapiens	0-9
20804741-11	2010	TNF-alpha-induced expression of uPA and activation of beta-catenin signaling appear to be mediated by ROS in MCF-10A cells, as both events were blocked by the antioxidant N-acetylcysteine.	Acetylcysteine	171-187	plasminogen activator, urokinase	Homo sapiens	32-35
21078900-5	2010	CD70-induced apoptosis was inhibited by pretreatment with the ER stress inhibitor salubrinal, ROS quencher N-acetylcysteine, and Ca(2+) chelator BAPTA.	Acetylcysteine	107-123	CD70 molecule	Homo sapiens	0-4
21078900-6	2010	We supposed that ROS generation might be the first event of CD70-induced apoptosis because N-acetylcysteine blocked increases of ROS and Ca(2+), but BAPTA did not block ROS generation.	Acetylcysteine	91-107	CD70 molecule	Homo sapiens	60-64
21203535-9	2010	Accompanied with the hemodynamic improvement, NAC-treated piglets had significantly lower plasma cardiac troponin-I, myocardial lipid hydroperoxides, activated caspase-3 and lactate levels (vs. H-R controls).	Acetylcysteine	46-49	caspase 3	Sus scrofa	160-169
20836655-7	2010	NAC treatment only slightly restored Akt phosphorylation impaired by ox-LDL in the cells.	Acetylcysteine	0-3	AKT serine/threonine kinase 1	Rattus norvegicus	37-40
20920557-5	2010	The same results were obtained in the cells treated with N-acetyl-L-cysteine, suggesting that the prolonged activation of JNK and p38 by ISA is mediated by reactive oxygen species generated from mitochondria.	Acetylcysteine	57-76	mitogen-activated protein kinase 8	Homo sapiens	122-125
20920557-5	2010	The same results were obtained in the cells treated with N-acetyl-L-cysteine, suggesting that the prolonged activation of JNK and p38 by ISA is mediated by reactive oxygen species generated from mitochondria.	Acetylcysteine	57-76	mitogen-activated protein kinase 14	Homo sapiens	130-133
20674153-4	2010	In addition, icariin provoked the generation of reactive oxygen species (ROS) in SMMC-7721 cells, while the antioxidant N-acetyl cysteine almost completely blocked icariin-induced JNK activation and apoptosis.	Acetylcysteine	120-137	mitogen-activated protein kinase 8	Homo sapiens	180-183
20408853-10	2010	CONCLUSIONS: A mouse model of incisional wound treated with NAC resulted in lower levels of tissue oxidative stress, higher levels of tissue glutathione, and downregulation of iNOS expression coupled with upregulation of VEGF expression, producing an overall favourable clinical outcome of higher WBS and a shorter wound-healing period both in diabetic and nondiabetic mice.	Acetylcysteine	60-63	nitric oxide synthase 2, inducible	Mus musculus	176-180
22416658-17	2010	Renal antioxidant defense system was re-enforced by NAC, leading to increase in the activities of SOD, CAT, GST and decreases in GSH depletion and MDA level.	Acetylcysteine	52-55	catalase	Rattus norvegicus	103-106
20639439-8	2010	This Ca2(+)- and MLC20 phosphorylation-independent contraction was mimicked by hydrogen peroxide and inhibited by N-acetyl cysteine.	Acetylcysteine	114-131	myosin light chain 12B	Homo sapiens	17-22
20698855-6	2010	CSE-induced ET(B) expression was attenuated by bosentan, the ET(B) receptor antagonist BQ788, the Rho kinase antagonist Y27632 and the antioxidant N-acetylcysteine.	Acetylcysteine	147-163	endothelin receptor type B	Homo sapiens	12-17
21121367-6	2010	SWCNT induced nuclear NF-kB/P65 translocation can be inhibited by N-acetylcysteine, indicating elevated ICAM-1 and VCAM-1 expression is mediated by oxidative stress in RAECs, and may play important inflammatory roles in SWCNT-induced vascular endothelium damage.	Acetylcysteine	66-82	synaptotagmin 1	Rattus norvegicus	28-31
20388917-8	2010	In the NAC group, the levels of ALP, GGT, WBC, CRP, and NE% decreased significantly (P &lt; .001), whereas a significant decrease did not occur in the placebo group.	Acetylcysteine	7-10	alkaline phosphatase, placental	Homo sapiens	32-35
20388917-8	2010	In the NAC group, the levels of ALP, GGT, WBC, CRP, and NE% decreased significantly (P &lt; .001), whereas a significant decrease did not occur in the placebo group.	Acetylcysteine	7-10	C-reactive protein	Homo sapiens	47-50
20954712-11	2010	VE-cadherin and ZO-1 disruptions were also diminished by N-acetyl cysteine and the VEGF antibody.	Acetylcysteine	57-74	cadherin 5	Mus musculus	0-11
20833869-8	2010	The activation and cytoplasmic localization of p38 in H(2)O(2)-treated KGN cells were blocked by N-acetylcysteine and SB203580.	Acetylcysteine	97-113	mitogen-activated protein kinase 14	Homo sapiens	47-50
21221209-11	2010	N-Acetylcysteine, a potent antioxidant, inhibited ROS production, Cyt c release, caspase-3 activation, and apoptosis induction in DMC-treated cells.	Acetylcysteine	0-16	cytochrome c, somatic	Homo sapiens	66-71
21221209-11	2010	N-Acetylcysteine, a potent antioxidant, inhibited ROS production, Cyt c release, caspase-3 activation, and apoptosis induction in DMC-treated cells.	Acetylcysteine	0-16	caspase 3	Homo sapiens	81-90
20956556-9	2010	N-Acetyl cysteine (NAC) treatment restored insulin signaling in late-passage primary fibroblasts.	Acetylcysteine	0-17	insulin	Homo sapiens	43-50
20956556-9	2010	N-Acetyl cysteine (NAC) treatment restored insulin signaling in late-passage primary fibroblasts.	Acetylcysteine	19-22	insulin	Homo sapiens	43-50
20816907-7	2010	Reduction of oxidative stress by NAC, as shown by normalization of reduced glutathione levels and attenuation of endothelial heme oxygenase-1 and nitric oxide synthase expression, resulted in prevention of the up-regulation of caveolin-1 in TD.	Acetylcysteine	33-36	heme oxygenase 1	Mus musculus	125-141
20816907-8	2010	Normalization of caveolin-1 levels by NAC was accompanied by a reduction in BBB breakdown, indicated by decreased IgG extravasation, normalization of occludin levels and prevention of matrix metalloproteinase-9 up-regulation.	Acetylcysteine	38-41	occludin	Mus musculus	150-158
20932751-5	2010	Pretreatment with the antioxidant N-acetyl-L-cysteine (NAC) markedly inhibited the CWJ-081-induced JNK activation and apoptosis.	Acetylcysteine	34-53	mitogen-activated protein kinase 8	Homo sapiens	99-102
20939553-9	2010	One major metabolite, M3, was also produced by HLM as determined by trapping with NAC.	Acetylcysteine	82-85	oxysterol binding protein 2	Homo sapiens	47-50
20954712-11	2010	VE-cadherin and ZO-1 disruptions were also diminished by N-acetyl cysteine and the VEGF antibody.	Acetylcysteine	57-74	tight junction protein 1	Mus musculus	16-20
20932820-8	2010	In addition, co-treatment of rats with TD and N-acetylcysteine prevented the increase in CD11b/c and CD68, but did not alter the onset of neurological impairment.	Acetylcysteine	46-62	integrin subunit alpha M	Rattus norvegicus	89-94
20833961-9	2010	Antioxidants (N-acetyl-l-cysteine and diphenyleneiodonium) abolished ANG II- and ET-1-increased B(1)R protein expression.	Acetylcysteine	14-33	angiotensinogen	Rattus norvegicus	69-75
20958190-10	2010	Macrophage and neutrophil recruitment were inhibited and the levels of MCP-1, CXCL1, VEGF, and VEGFR-1 were also lower in NAC-treated mice compared to vehicle-treated mice.	Acetylcysteine	122-125	chemokine (C-X-C motif) ligand 1	Mus musculus	78-83
20613681-8	2010	NAC pretreatment attenuated the increases in TNF-alpha and IL-6 levels, but augmented IL-10 levels at 2 h post-LPS.	Acetylcysteine	0-3	tumor necrosis factor	Mus musculus	45-54
20822922-13	2010	Reverse transcription polymerase chain reaction for IL-8 messenger RNA was significantly higher in controls during the reperfusion period than in the NAC group (p = 0.001).	Acetylcysteine	150-153	C-X-C motif chemokine ligand 8	Homo sapiens	52-56
20822922-14	2010	The amount of lung tissue nuclear NF-kappaB (p50 sub-unit) was significantly higher in controls than in NAC pigs (p = 0.03).	Acetylcysteine	104-107	nuclear factor kappa B subunit 1	Homo sapiens	45-48
20631980-9	2010	Adenoviral overexpression of RAGE or AGE treatment decreased cell surface AT2 expression, in association with increasing superoxide generation; both were reversed using antioxidants N-acetylcysteine and apocynin, and soluble RAGE in primary mesangial cells.	Acetylcysteine	182-198	advanced glycosylation end product-specific receptor	Mus musculus	29-33
20951298-6	2010	RESULTS: NAC enhanced ALP activity and mRNA expression of dentin sialophosphoprotein gene, whereas extracts of dentin bonding agents inhibited the induction of ALP activity.	Acetylcysteine	9-12	alkaline phosphatase, placental	Homo sapiens	22-25
20951298-9	2010	The disruption of ALP activity and matrix mineralization in pulp cells was partially reversed by NAC only in Prime &amp; Bond NT-treated cells.	Acetylcysteine	97-100	alkaline phosphatase, placental	Homo sapiens	18-21
20613681-8	2010	NAC pretreatment attenuated the increases in TNF-alpha and IL-6 levels, but augmented IL-10 levels at 2 h post-LPS.	Acetylcysteine	0-3	interleukin 6	Mus musculus	59-63
20613681-8	2010	NAC pretreatment attenuated the increases in TNF-alpha and IL-6 levels, but augmented IL-10 levels at 2 h post-LPS.	Acetylcysteine	0-3	interleukin 10	Mus musculus	86-91
20613681-8	2010	NAC pretreatment attenuated the increases in TNF-alpha and IL-6 levels, but augmented IL-10 levels at 2 h post-LPS.	Acetylcysteine	0-3	toll-like receptor 4	Mus musculus	111-114
20674558-6	2010	DP increased the levels of reactive oxygen species (ROS) in HepG2 cells, and antioxidant N-acetylcysteine (NAC) completely blocked DP-induced ROS accumulation and the disruption of the balance between Bax and Bcl-2 proteins, and effectively blocked the decreased MMP and apoptosis, but had no effect on the activation of caspase-8 and the up-regulations of DR4 and DR5 induced by DP.	Acetylcysteine	89-105	BCL2 associated X, apoptosis regulator	Homo sapiens	201-204
20954279-9	2010	However, treatment with ROS scavenger N-acetyl cysteine can reverse PTEN to a reduced form.	Acetylcysteine	38-55	phosphatase and tensin homolog	Mus musculus	68-72
20674558-6	2010	DP increased the levels of reactive oxygen species (ROS) in HepG2 cells, and antioxidant N-acetylcysteine (NAC) completely blocked DP-induced ROS accumulation and the disruption of the balance between Bax and Bcl-2 proteins, and effectively blocked the decreased MMP and apoptosis, but had no effect on the activation of caspase-8 and the up-regulations of DR4 and DR5 induced by DP.	Acetylcysteine	89-105	BCL2 apoptosis regulator	Homo sapiens	209-214
20674558-6	2010	DP increased the levels of reactive oxygen species (ROS) in HepG2 cells, and antioxidant N-acetylcysteine (NAC) completely blocked DP-induced ROS accumulation and the disruption of the balance between Bax and Bcl-2 proteins, and effectively blocked the decreased MMP and apoptosis, but had no effect on the activation of caspase-8 and the up-regulations of DR4 and DR5 induced by DP.	Acetylcysteine	107-110	BCL2 associated X, apoptosis regulator	Homo sapiens	201-204
20674558-6	2010	DP increased the levels of reactive oxygen species (ROS) in HepG2 cells, and antioxidant N-acetylcysteine (NAC) completely blocked DP-induced ROS accumulation and the disruption of the balance between Bax and Bcl-2 proteins, and effectively blocked the decreased MMP and apoptosis, but had no effect on the activation of caspase-8 and the up-regulations of DR4 and DR5 induced by DP.	Acetylcysteine	107-110	BCL2 apoptosis regulator	Homo sapiens	209-214
20649480-7	2010	Post-resuscitation NAC treatment also significantly attenuated the increase in cortical caspase-3 and lipid hydroperoxide concentrations.	Acetylcysteine	19-22	caspase 3	Sus scrofa	88-97
20802176-5	2010	Further, vascular endothelial growth factor led to heightened generation of reactive oxygen species from cultured human choroidal endothelial cells, which was prevented by the NADPH oxidase inhibitors, apocynin and diphenyleneiodonium, or the antioxidant, N-acetyl-L-cysteine.	Acetylcysteine	256-275	vascular endothelial growth factor A	Homo sapiens	9-43
20637250-8	2010	In the groups, which were administered N-acetylcysteine prior to sodium fluoride, however, it was observed that, after sodium fluoride administration, plasma MDA levels and erythrocyte SOD and CAT activities drew closer to the values of the control group.	Acetylcysteine	39-55	catalase	Mus musculus	193-196
20638463-11	2010	When the participants were grouped by GST M1/T1 genotypes, the NAC effect was only significant among workers with null genotypes in both GSTM1 and GSTT1 (p = 0.004).	Acetylcysteine	63-66	glutathione S-transferase mu 1	Homo sapiens	137-142
20638463-13	2010	The protective effect of NAC was more prominent in subjects with both GSTM1-null and GSTT1-null genotypes.	Acetylcysteine	25-28	glutathione S-transferase mu 1	Homo sapiens	70-75
20981856-7	2010	Pretreatment with N-acetylcysteine (NAC), an antioxidant, attenuated caspase-3 activation by ACN, as evidenced by a reduction in proteolysis of PARP, a known caspase-3 substrate, as well as in the number of sub-G1 apoptotic cells.	Acetylcysteine	18-34	caspase 3	Homo sapiens	69-78
20981856-7	2010	Pretreatment with N-acetylcysteine (NAC), an antioxidant, attenuated caspase-3 activation by ACN, as evidenced by a reduction in proteolysis of PARP, a known caspase-3 substrate, as well as in the number of sub-G1 apoptotic cells.	Acetylcysteine	18-34	poly(ADP-ribose) polymerase 1	Homo sapiens	144-148
20981856-7	2010	Pretreatment with N-acetylcysteine (NAC), an antioxidant, attenuated caspase-3 activation by ACN, as evidenced by a reduction in proteolysis of PARP, a known caspase-3 substrate, as well as in the number of sub-G1 apoptotic cells.	Acetylcysteine	18-34	caspase 3	Homo sapiens	158-167
20981856-7	2010	Pretreatment with N-acetylcysteine (NAC), an antioxidant, attenuated caspase-3 activation by ACN, as evidenced by a reduction in proteolysis of PARP, a known caspase-3 substrate, as well as in the number of sub-G1 apoptotic cells.	Acetylcysteine	36-39	caspase 3	Homo sapiens	69-78
20981856-7	2010	Pretreatment with N-acetylcysteine (NAC), an antioxidant, attenuated caspase-3 activation by ACN, as evidenced by a reduction in proteolysis of PARP, a known caspase-3 substrate, as well as in the number of sub-G1 apoptotic cells.	Acetylcysteine	36-39	poly(ADP-ribose) polymerase 1	Homo sapiens	144-148
20981856-7	2010	Pretreatment with N-acetylcysteine (NAC), an antioxidant, attenuated caspase-3 activation by ACN, as evidenced by a reduction in proteolysis of PARP, a known caspase-3 substrate, as well as in the number of sub-G1 apoptotic cells.	Acetylcysteine	36-39	caspase 3	Homo sapiens	158-167
20981856-8	2010	Moreover, induction of Bax by ACN was abolished by NAC.	Acetylcysteine	51-54	BCL2 associated X, apoptosis regulator	Homo sapiens	23-26
20846156-9	2010	The addition of NAC, curcumin, PD98059, and staurosporine markedly inhibited the arecoline-induced HIF-1alpha expression (P&lt;0.05).	Acetylcysteine	16-19	hypoxia inducible factor 1 subunit alpha	Homo sapiens	99-109
20846156-10	2010	CONCLUSIONS: Hypoxia inducible factor-1alpha expression is significantly upregulated in areca quid chewing-associated OSCC and HIF-1alpha expression induced by arecoline is downregulated by NAC, curcumin, PD98059, and staurosporine.	Acetylcysteine	190-193	hypoxia inducible factor 1 subunit alpha	Homo sapiens	127-137
19220795-2	2010	Concentrations of NAC and its synthetic derivative, NAC-amide (NACA) were evaluated for effects on nuclear maturation, fertilization success and embryo development.	Acetylcysteine	18-21	nascent polypeptide associated complex subunit alpha	Homo sapiens	63-67
20970637-6	2010	pH levels, which were determined using a radiometer ABL77 (Copenhagen, Denmark), were significantly lower among the NAC than the placebo group at I-4 (P=.027) and I-5 (P=.031).	Acetylcysteine	116-119	PPP1R2C family member C	Homo sapiens	146-149
20443032-5	2010	At the same time, ERK and c-Jun N-terminal kinase (JNK) as well as cell division control protein 2 homolog (Cdc2) were found to be highly phosphorylated, which could be counteracted with the antioxidant N-acetylcysteine (NAC).	Acetylcysteine	203-219	mitogen-activated protein kinase 1	Homo sapiens	18-21
20583210-10	2010	Inclusion of N-acetyl-L-cysteine, a known antioxidant and NF-kappaB inhibitor, in the drinking water led to complete abolition of tumorigenesis in DEN-exposed beta-cat KO.	Acetylcysteine	13-32	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	58-67
20583212-11	2010	The treatment of cells with the ROS scavenger N-acetyl-L-cysteine, or silencing of the NOX4 gene, rescued p21(Cip1) and p15(Ink4b) accumulation as well as the growth arrest in response to TGF-beta.	Acetylcysteine	46-65	cyclin dependent kinase inhibitor 1A	Homo sapiens	106-109
20583212-11	2010	The treatment of cells with the ROS scavenger N-acetyl-L-cysteine, or silencing of the NOX4 gene, rescued p21(Cip1) and p15(Ink4b) accumulation as well as the growth arrest in response to TGF-beta.	Acetylcysteine	46-65	cyclin dependent kinase inhibitor 1A	Homo sapiens	110-114
20583212-11	2010	The treatment of cells with the ROS scavenger N-acetyl-L-cysteine, or silencing of the NOX4 gene, rescued p21(Cip1) and p15(Ink4b) accumulation as well as the growth arrest in response to TGF-beta.	Acetylcysteine	46-65	cyclin dependent kinase inhibitor 2B	Homo sapiens	120-123
20583212-11	2010	The treatment of cells with the ROS scavenger N-acetyl-L-cysteine, or silencing of the NOX4 gene, rescued p21(Cip1) and p15(Ink4b) accumulation as well as the growth arrest in response to TGF-beta.	Acetylcysteine	46-65	cyclin dependent kinase inhibitor 2B	Homo sapiens	124-129
20583212-11	2010	The treatment of cells with the ROS scavenger N-acetyl-L-cysteine, or silencing of the NOX4 gene, rescued p21(Cip1) and p15(Ink4b) accumulation as well as the growth arrest in response to TGF-beta.	Acetylcysteine	46-65	transforming growth factor beta 1	Homo sapiens	188-196
20576917-9	2010	Alcohol treatment inactivated HNF-4alpha, which was prevented by N-acetyl-cysteine or zinc.	Acetylcysteine	65-82	hepatocyte nuclear factor 4 alpha	Homo sapiens	30-40
20443032-5	2010	At the same time, ERK and c-Jun N-terminal kinase (JNK) as well as cell division control protein 2 homolog (Cdc2) were found to be highly phosphorylated, which could be counteracted with the antioxidant N-acetylcysteine (NAC).	Acetylcysteine	203-219	mitogen-activated protein kinase 8	Homo sapiens	26-49
20443032-5	2010	At the same time, ERK and c-Jun N-terminal kinase (JNK) as well as cell division control protein 2 homolog (Cdc2) were found to be highly phosphorylated, which could be counteracted with the antioxidant N-acetylcysteine (NAC).	Acetylcysteine	203-219	mitogen-activated protein kinase 8	Homo sapiens	51-54
20432471-3	2010	Pretreatment with BAPTA-AM (Ca(2+) chelator) and N-acetylcysteine (ROS scavenger) abolished caffeine-induced ERK inactivation and p38 MPAK activation.	Acetylcysteine	49-65	mitogen-activated protein kinase 1	Homo sapiens	109-112
20443032-5	2010	At the same time, ERK and c-Jun N-terminal kinase (JNK) as well as cell division control protein 2 homolog (Cdc2) were found to be highly phosphorylated, which could be counteracted with the antioxidant N-acetylcysteine (NAC).	Acetylcysteine	221-224	mitogen-activated protein kinase 1	Homo sapiens	18-21
20432471-3	2010	Pretreatment with BAPTA-AM (Ca(2+) chelator) and N-acetylcysteine (ROS scavenger) abolished caffeine-induced ERK inactivation and p38 MPAK activation.	Acetylcysteine	49-65	mitogen-activated protein kinase 14	Homo sapiens	130-133
20443032-5	2010	At the same time, ERK and c-Jun N-terminal kinase (JNK) as well as cell division control protein 2 homolog (Cdc2) were found to be highly phosphorylated, which could be counteracted with the antioxidant N-acetylcysteine (NAC).	Acetylcysteine	221-224	mitogen-activated protein kinase 8	Homo sapiens	26-49
20443032-5	2010	At the same time, ERK and c-Jun N-terminal kinase (JNK) as well as cell division control protein 2 homolog (Cdc2) were found to be highly phosphorylated, which could be counteracted with the antioxidant N-acetylcysteine (NAC).	Acetylcysteine	221-224	mitogen-activated protein kinase 8	Homo sapiens	51-54
20045538-9	2010	On the other hand, treatment with the antioxidant N-acetyl cysteine suppressed the decrease in the expression and secretion of AGT in the hypertrophied 3T3-L1 adipocytes.	Acetylcysteine	50-67	angiotensinogen (serpin peptidase inhibitor, clade A, member 8)	Mus musculus	127-130
20045538-10	2010	Finally, treatment of obese db/db mice with N-acetyl cysteine augmented the expression of AGT in the adipose tissue, but not in the liver.	Acetylcysteine	44-61	angiotensinogen (serpin peptidase inhibitor, clade A, member 8)	Mus musculus	90-93
20594983-5	2010	Moreover, fucoxanthin-induced the cleavage of caspases -3 and -7, and poly-ADP-ribose polymerase (PARP) and a decrease of Bcl-xL levels, whereas NAC pre-treatment significantly inhibited caspase-3, -7, and PARP cleavage and the reduction in Bcl-xL levels.	Acetylcysteine	145-148	caspase 3	Homo sapiens	187-196
21038848-10	2010	N-Acetylcysteine (NAC), a known antioxidant, also decreased ROS generation, effectively blocked apoptosis, and decreased DADS-induced phosphorylated JNK levels.	Acetylcysteine	0-16	mitogen-activated protein kinase 8	Homo sapiens	149-152
21038848-10	2010	N-Acetylcysteine (NAC), a known antioxidant, also decreased ROS generation, effectively blocked apoptosis, and decreased DADS-induced phosphorylated JNK levels.	Acetylcysteine	18-21	mitogen-activated protein kinase 8	Homo sapiens	149-152
20594983-5	2010	Moreover, fucoxanthin-induced the cleavage of caspases -3 and -7, and poly-ADP-ribose polymerase (PARP) and a decrease of Bcl-xL levels, whereas NAC pre-treatment significantly inhibited caspase-3, -7, and PARP cleavage and the reduction in Bcl-xL levels.	Acetylcysteine	145-148	BCL2 like 1	Homo sapiens	241-247
20493918-6	2010	We also found that antioxidants such as N-acetylcysteine and glutathione blocked TG- and BFA-induced cell death and the expression of CHOP and GRP78.	Acetylcysteine	40-56	heat shock protein 5	Mus musculus	143-148
20594983-5	2010	Moreover, fucoxanthin-induced the cleavage of caspases -3 and -7, and poly-ADP-ribose polymerase (PARP) and a decrease of Bcl-xL levels, whereas NAC pre-treatment significantly inhibited caspase-3, -7, and PARP cleavage and the reduction in Bcl-xL levels.	Acetylcysteine	145-148	poly(ADP-ribose) polymerase 1	Homo sapiens	206-210
20637781-8	2010	The increased level of HIF-1alpha by TB4P was reduced by the treatment with N-acetylcysteine (NAC), a well-known ROS scavenger.	Acetylcysteine	76-92	hypoxia inducible factor 1 subunit alpha	Homo sapiens	23-33
20206441-5	2010	IGF-1-mediated cellular proliferation was also inhibited by N-acetylcysteine, which implicates reactive oxygen species generation.	Acetylcysteine	60-76	insulin like growth factor 1	Homo sapiens	0-5
20637781-8	2010	The increased level of HIF-1alpha by TB4P was reduced by the treatment with N-acetylcysteine (NAC), a well-known ROS scavenger.	Acetylcysteine	94-97	hypoxia inducible factor 1 subunit alpha	Homo sapiens	23-33
20808797-6	2010	Despite the transient nature of the impact of NAC on brain glutathione, the loss of dopaminergic terminals at 1 year associated with SNCA overexpression was significantly attenuated by NAC supplementation, as measured by immunoreactivity for tyrosine hydroxylase in the striatum (p = 0.007; unpaired, two-tailed t-test), with a similar but nonsignificant trend for dopamine transporter (DAT) immunoreactivity.	Acetylcysteine	185-188	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	365-385
20808797-6	2010	Despite the transient nature of the impact of NAC on brain glutathione, the loss of dopaminergic terminals at 1 year associated with SNCA overexpression was significantly attenuated by NAC supplementation, as measured by immunoreactivity for tyrosine hydroxylase in the striatum (p = 0.007; unpaired, two-tailed t-test), with a similar but nonsignificant trend for dopamine transporter (DAT) immunoreactivity.	Acetylcysteine	185-188	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	387-390
20808797-8	2010	This was associated with a decrease in nuclear NFkappaB localization and an increase in cytoplasmic localization of NFkappaB in the NAC-treated transgenics.	Acetylcysteine	132-135	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	116-124
20388507-7	2010	The transactivation of the EGF receptor and the increase in reactive oxygen species caused by NMB-like peptides was inhibited by N-acetylcysteine (NAC) or Tiron.	Acetylcysteine	129-145	epidermal growth factor receptor	Homo sapiens	27-39
20570722-5	2010	Cell-free as well as intracellular particle-induced ROS generation was assessed and related to the induced Akt and ERK1/2 phosphorylation by inhibiting oxidative stress with catalase, superoxide dismutase, and N-acetylcysteine.	Acetylcysteine	210-226	AKT serine/threonine kinase 1	Homo sapiens	107-110
20570722-5	2010	Cell-free as well as intracellular particle-induced ROS generation was assessed and related to the induced Akt and ERK1/2 phosphorylation by inhibiting oxidative stress with catalase, superoxide dismutase, and N-acetylcysteine.	Acetylcysteine	210-226	mitogen-activated protein kinase 3	Homo sapiens	115-121
20815772-4	2010	The effects of ROS on both BRAK and IL-8 expression were attenuated by pre-treatment with N-acetyl-L-cysteine (NAC), epidermal growth factor receptor (EGFR), and mitogen-activated protein kinase (MAPK) inhibitors.	Acetylcysteine	90-109	C-X-C motif chemokine ligand 14	Homo sapiens	27-31
20815772-4	2010	The effects of ROS on both BRAK and IL-8 expression were attenuated by pre-treatment with N-acetyl-L-cysteine (NAC), epidermal growth factor receptor (EGFR), and mitogen-activated protein kinase (MAPK) inhibitors.	Acetylcysteine	90-109	C-X-C motif chemokine ligand 8	Homo sapiens	36-40
20653475-6	2010	CONCLUSIONS: NAC prevents the increased expression levels of p53 and CASP8 induced by long-term maintained hypoxia.	Acetylcysteine	13-16	tumor protein p53	Homo sapiens	61-64
20632440-14	2010	Peak JNK activation occurred at 12 h post-treatment and this activation persisted for up to 24 h. The expression of phosphorylated JNK and c-Jun protein after 12 h with BrMC-treated cells was inhibited by N-acetylcysteine and SP600125 pre-treatment, but GW9662 had no effect.	Acetylcysteine	205-221	mitogen-activated protein kinase 8	Homo sapiens	5-8
20632440-14	2010	Peak JNK activation occurred at 12 h post-treatment and this activation persisted for up to 24 h. The expression of phosphorylated JNK and c-Jun protein after 12 h with BrMC-treated cells was inhibited by N-acetylcysteine and SP600125 pre-treatment, but GW9662 had no effect.	Acetylcysteine	205-221	mitogen-activated protein kinase 8	Homo sapiens	131-134
20632440-16	2010	N-acetylcysteine and GW9662 also attenuated induction of cell death and caspase-3 activation in HepG2 cells treated with BrMC.	Acetylcysteine	0-16	caspase 3	Homo sapiens	72-81
20653470-0	2010	N-acetylcysteine protects alveolar epithelial cells from hydrogen peroxide-induced apoptosis through scavenging reactive oxygen species and suppressing c-Jun N-terminal kinase.	Acetylcysteine	0-16	mitogen-activated protein kinase 8	Homo sapiens	152-175
21113238-6	2010	Lowering ROS levels by treatment with N-acetyl cysteine limited cisplatin toxicity, resulting in higher cell numbers and decreased cleavage of the apoptotic proteins PARP and caspase 3.	Acetylcysteine	38-55	poly(ADP-ribose) polymerase 1	Homo sapiens	166-170
21113238-6	2010	Lowering ROS levels by treatment with N-acetyl cysteine limited cisplatin toxicity, resulting in higher cell numbers and decreased cleavage of the apoptotic proteins PARP and caspase 3.	Acetylcysteine	38-55	caspase 3	Homo sapiens	175-184
20211185-7	2010	Indeed, treatment with n-acetylcysteine (NAC) or with the p38 MAPK inhibitor SB203580 inhibits IL-10 responses and significantly restores IL-12p70 responses to IFNgamma/LPS in HE-conditioned BMDM.	Acetylcysteine	23-39	interleukin 10	Mus musculus	95-100
20211185-7	2010	Indeed, treatment with n-acetylcysteine (NAC) or with the p38 MAPK inhibitor SB203580 inhibits IL-10 responses and significantly restores IL-12p70 responses to IFNgamma/LPS in HE-conditioned BMDM.	Acetylcysteine	23-39	interferon gamma	Mus musculus	160-168
20211185-7	2010	Indeed, treatment with n-acetylcysteine (NAC) or with the p38 MAPK inhibitor SB203580 inhibits IL-10 responses and significantly restores IL-12p70 responses to IFNgamma/LPS in HE-conditioned BMDM.	Acetylcysteine	41-44	interleukin 10	Mus musculus	95-100
20211185-7	2010	Indeed, treatment with n-acetylcysteine (NAC) or with the p38 MAPK inhibitor SB203580 inhibits IL-10 responses and significantly restores IL-12p70 responses to IFNgamma/LPS in HE-conditioned BMDM.	Acetylcysteine	41-44	interferon gamma	Mus musculus	160-168
20557081-10	2010	Additionally, pretreatment of Huh7 cells with antioxidants ascorbic acid and N-acetyl cysteine markedly attenuated the MAA-induced apoptosis by upregulation of Bax, Bak, and PUMA, mitochondrial translocation of cofilin, activation of caspase-3, and cell death.	Acetylcysteine	77-94	BCL2 associated X, apoptosis regulator	Homo sapiens	160-163
20398749-6	2010	Moreover, pretreatment with the ROS scavenger N-acetylcysteine abolishes flavokawain B-induced ROS generation, GADD153 up-regulation, and apoptosis.	Acetylcysteine	46-62	DNA damage inducible transcript 3	Homo sapiens	111-118
20388507-7	2010	The transactivation of the EGF receptor and the increase in reactive oxygen species caused by NMB-like peptides was inhibited by N-acetylcysteine (NAC) or Tiron.	Acetylcysteine	147-150	epidermal growth factor receptor	Homo sapiens	27-39
20489144-5	2010	Vitreous-driven activation of PDGFRalpha and cellular responses intrinsic to PVR (contraction of collagen gels and cell proliferation) were blocked by concentrations of NAC that were well below the maximum tolerated dose.	Acetylcysteine	169-172	platelet derived growth factor receptor alpha	Homo sapiens	30-40
20489149-7	2010	In vitro, NAC not only reduced ROS production below control levels, but further decreased the expression of thyroid-specific proteins in addition to IL-1alpha/IFNgamma-inhibitory effects.	Acetylcysteine	10-13	interferon gamma	Homo sapiens	159-167
19929443-7	2010	Pretreatment with nitric oxide scavenger (PTIO), reactive oxygen species scavengers (combination of SOD with catalase), and N-acetyl-L-cysteine, significantly attenuated the CSE-induced impairment of VEGF-mediated Akt and eNOS phosphorylation.	Acetylcysteine	124-143	vascular endothelial growth factor A	Homo sapiens	200-204
20138622-6	2010	N-acetylcysteine that downregulated TNF-alpha-induced reactive oxygen species (ROS) inhibited JNK activation, but not p38 MAPK.	Acetylcysteine	0-16	tumor necrosis factor	Homo sapiens	36-45
20138622-6	2010	N-acetylcysteine that downregulated TNF-alpha-induced reactive oxygen species (ROS) inhibited JNK activation, but not p38 MAPK.	Acetylcysteine	0-16	mitogen-activated protein kinase 8	Homo sapiens	94-97
20463052-5	2010	Moreover, the iPLA(2)beta inhibitor bromoenol lactone caused mitochondrial membrane peroxidation and cytochrome c release, and these effects were reversed by N-acetyl cysteine.	Acetylcysteine	158-175	phospholipase A2, group VI	Mus musculus	14-25
20138622-7	2010	N-acetylcysteine, SP600125 (JNK inhibitor) and SB203580 (p38 MAPK inhibitor) attenuated TNF-alpha-induced DNA-binding activities of both AP-1 and NF-kappaB.	Acetylcysteine	0-16	tumor necrosis factor	Homo sapiens	88-97
20204677-6	2010	Our results shows that TGF-beta1 stimulation of uPA and MMP-9 expression involve NOXs-dependent ROS and NFkappaB, activation, demonstrated by using DPI, NOXs inhibitor, ROS scavenger N-acetylcysteine and SN50, an NFkb inhibitor.	Acetylcysteine	183-199	transforming growth factor beta 1	Homo sapiens	23-32
20204677-6	2010	Our results shows that TGF-beta1 stimulation of uPA and MMP-9 expression involve NOXs-dependent ROS and NFkappaB, activation, demonstrated by using DPI, NOXs inhibitor, ROS scavenger N-acetylcysteine and SN50, an NFkb inhibitor.	Acetylcysteine	183-199	plasminogen activator, urokinase	Homo sapiens	48-51
20171194-7	2010	NAC subsequently inhibited BEL-induced activation of p38 and p53 in LNCaP cells.	Acetylcysteine	0-3	mitogen-activated protein kinase 14	Homo sapiens	53-56
20171194-7	2010	NAC subsequently inhibited BEL-induced activation of p38 and p53 in LNCaP cells.	Acetylcysteine	0-3	tumor protein p53	Homo sapiens	61-64
20456495-8	2010	The effects of curcuminoids on keratinocytes mirrored some aspects of UVB and could be inhibited by N-acetylcysteine, suggesting that these compounds activate p38 through a mechanism that involves glutathione depletion.	Acetylcysteine	100-116	mitogen-activated protein kinase 14	Homo sapiens	159-162
20392701-0	2010	Molecular identification of NAT8 as the enzyme that acetylates cysteine S-conjugates to mercapturic acids.	Acetylcysteine	88-105	N-acetyltransferase 8 (putative)	Homo sapiens	28-32
20194814-11	2010	Treatment of mycotoxin-exposed DCs with the antioxidants N-acetylcysteine or glutathione ethyl ester restored IL-12 secretion and pretreatment of exposed mice with N-acetylcysteine prevented the mycotoxin-induced increase of airway inflammation and AHR.	Acetylcysteine	57-73	aryl-hydrocarbon receptor	Mus musculus	249-252
20194814-11	2010	Treatment of mycotoxin-exposed DCs with the antioxidants N-acetylcysteine or glutathione ethyl ester restored IL-12 secretion and pretreatment of exposed mice with N-acetylcysteine prevented the mycotoxin-induced increase of airway inflammation and AHR.	Acetylcysteine	164-180	aryl-hydrocarbon receptor	Mus musculus	249-252
20144638-5	2010	BAPTA-AM or NAC abrogated CMS-9-elicited p38 MAPK and JNK activation, and rescued viability of CMS-9-treated K562 cells.	Acetylcysteine	12-15	mitogen-activated protein kinase 14	Homo sapiens	41-44
20144638-5	2010	BAPTA-AM or NAC abrogated CMS-9-elicited p38 MAPK and JNK activation, and rescued viability of CMS-9-treated K562 cells.	Acetylcysteine	12-15	mitogen-activated protein kinase 8	Homo sapiens	54-57
20392701-2	2010	The almost exclusive expression of NAT8 in kidney and liver and its predicted association with the endoplasmic reticulum suggested that it was cysteinyl-S-conjugate N-acetyltransferase, the microsomal enzyme that catalyzes the last step of mercapturic acid formation.	Acetylcysteine	240-256	N-acetyltransferase 8 (putative)	Homo sapiens	35-39
20392701-8	2010	Taken together, these findings indicate that NAT8 is involved in mercapturic acid formation and confirm that NAT8B is an inactive gene in humans.	Acetylcysteine	65-81	N-acetyltransferase 8 (putative)	Homo sapiens	45-49
19597128-6	2010	The H(2)O(2)-augmented IL-8 release was inhibited by treatment with N-acetylcysteine.	Acetylcysteine	68-84	C-X-C motif chemokine ligand 8	Homo sapiens	23-27
20088848-7	2010	MBMC treatment rapidly and transiently decreased glutathione (GSH) levels, and treatment with GSH-Et (cell permeable form of GSH) or N-acetylcysteine (precursor of GSH) counteracted the HO-1 and Nrf2 expression elicited by MBMC, indicating that MBMC-induced HO-1 expression requires transient depletion of GSH.	Acetylcysteine	133-149	heme oxygenase 1	Mus musculus	186-190
20088848-7	2010	MBMC treatment rapidly and transiently decreased glutathione (GSH) levels, and treatment with GSH-Et (cell permeable form of GSH) or N-acetylcysteine (precursor of GSH) counteracted the HO-1 and Nrf2 expression elicited by MBMC, indicating that MBMC-induced HO-1 expression requires transient depletion of GSH.	Acetylcysteine	133-149	nuclear factor, erythroid derived 2, like 2	Mus musculus	195-199
20088848-7	2010	MBMC treatment rapidly and transiently decreased glutathione (GSH) levels, and treatment with GSH-Et (cell permeable form of GSH) or N-acetylcysteine (precursor of GSH) counteracted the HO-1 and Nrf2 expression elicited by MBMC, indicating that MBMC-induced HO-1 expression requires transient depletion of GSH.	Acetylcysteine	133-149	heme oxygenase 1	Mus musculus	258-262
20590572-6	2010	The AEA- or HU210-induced cell death and MAPK activation were attenuated by CB(1) antagonists [SR141716 (rimonabant) and AM281], inhibitors of p38 and JNK-MAPKs or the antioxidant N-acetylcysteine.	Acetylcysteine	180-196	cannabinoid receptor 1	Homo sapiens	76-81
20590572-8	2010	In contrast, in combination with CB(1) antagonists, N-acetylcysteine completely prevented these effects.	Acetylcysteine	52-68	cannabinoid receptor 1	Homo sapiens	33-38
20185348-10	2010	Furthermore, preincubation of adipocytes with an antioxidant, N-acetyl-cysteine (NAC) restored the IGF-I-induced attenuation of insulin-dependent glucose uptake; this indicates that IGF-I induces insulin resistance via ROS.	Acetylcysteine	62-79	insulin like growth factor 1	Homo sapiens	99-104
20185348-12	2010	Further, NAC restored these changes induced by IGF-I on both serine and tyrosine phosphorylation of IRS-1.	Acetylcysteine	9-12	insulin like growth factor 1	Homo sapiens	47-52
20332008-4	2010	The aim of this work is to study the possible protective role of NAC against BCNU-induced myelotoxicity through evaluation of apoptosis, lipid peroxidation, antioxidant enzymes (superoxide dismutase (SOD), glutathione peroxidase (GPx) and catalase(CAT)) as well as glutathione (GSH) content in bone marrow cells of rats.	Acetylcysteine	65-68	catalase	Rattus norvegicus	239-252
20185348-10	2010	Furthermore, preincubation of adipocytes with an antioxidant, N-acetyl-cysteine (NAC) restored the IGF-I-induced attenuation of insulin-dependent glucose uptake; this indicates that IGF-I induces insulin resistance via ROS.	Acetylcysteine	62-79	insulin	Homo sapiens	128-135
20185348-10	2010	Furthermore, preincubation of adipocytes with an antioxidant, N-acetyl-cysteine (NAC) restored the IGF-I-induced attenuation of insulin-dependent glucose uptake; this indicates that IGF-I induces insulin resistance via ROS.	Acetylcysteine	62-79	insulin like growth factor 1	Homo sapiens	182-187
20185348-10	2010	Furthermore, preincubation of adipocytes with an antioxidant, N-acetyl-cysteine (NAC) restored the IGF-I-induced attenuation of insulin-dependent glucose uptake; this indicates that IGF-I induces insulin resistance via ROS.	Acetylcysteine	62-79	insulin	Homo sapiens	196-203
20185348-10	2010	Furthermore, preincubation of adipocytes with an antioxidant, N-acetyl-cysteine (NAC) restored the IGF-I-induced attenuation of insulin-dependent glucose uptake; this indicates that IGF-I induces insulin resistance via ROS.	Acetylcysteine	81-84	insulin like growth factor 1	Homo sapiens	99-104
20185348-10	2010	Furthermore, preincubation of adipocytes with an antioxidant, N-acetyl-cysteine (NAC) restored the IGF-I-induced attenuation of insulin-dependent glucose uptake; this indicates that IGF-I induces insulin resistance via ROS.	Acetylcysteine	81-84	insulin	Homo sapiens	128-135
20185348-10	2010	Furthermore, preincubation of adipocytes with an antioxidant, N-acetyl-cysteine (NAC) restored the IGF-I-induced attenuation of insulin-dependent glucose uptake; this indicates that IGF-I induces insulin resistance via ROS.	Acetylcysteine	81-84	insulin like growth factor 1	Homo sapiens	182-187
20185348-10	2010	Furthermore, preincubation of adipocytes with an antioxidant, N-acetyl-cysteine (NAC) restored the IGF-I-induced attenuation of insulin-dependent glucose uptake; this indicates that IGF-I induces insulin resistance via ROS.	Acetylcysteine	81-84	insulin	Homo sapiens	196-203
23675187-4	2010	In addition, N-acetyl cysteine, a scavenger of reactive oxygen species, inhibits activation of NF-kappaB and induction of interleukin-6 by tumor necrosis factor alpha, being ineffective on interleukin-1 beta activity.	Acetylcysteine	13-30	interleukin 6	Homo sapiens	122-135
20384467-0	2010	N-acetylcysteine attenuates phosgene-induced acute lung injury via up-regulation of Nrf2 expression.	Acetylcysteine	0-16	NFE2 like bZIP transcription factor 2	Homo sapiens	84-88
20384467-8	2010	However, NAC administration elevated Nrf2 expression significantly.	Acetylcysteine	9-12	NFE2 like bZIP transcription factor 2	Homo sapiens	37-41
20384467-10	2010	NAC protected against oxidative stress through acting on this newly disclosed Nrf2/GR/GSH pathway, by which NAC elevated the biosynthesis of protective GSH to repair and reconstitute the defense system destroyed by phosgene.	Acetylcysteine	0-3	NFE2 like bZIP transcription factor 2	Homo sapiens	78-82
20384467-10	2010	NAC protected against oxidative stress through acting on this newly disclosed Nrf2/GR/GSH pathway, by which NAC elevated the biosynthesis of protective GSH to repair and reconstitute the defense system destroyed by phosgene.	Acetylcysteine	108-111	NFE2 like bZIP transcription factor 2	Homo sapiens	78-82
23675187-4	2010	In addition, N-acetyl cysteine, a scavenger of reactive oxygen species, inhibits activation of NF-kappaB and induction of interleukin-6 by tumor necrosis factor alpha, being ineffective on interleukin-1 beta activity.	Acetylcysteine	13-30	tumor necrosis factor	Homo sapiens	139-166
20356045-7	2010	Pretreatment with N-acetyl-l-cysteine (NAC) attenuated 6-DG-induced DR5 expression and inhibited TRAIL-induced apoptosis.	Acetylcysteine	18-37	TNF superfamily member 10	Homo sapiens	97-102
20013880-7	2010	Moreover, the induction of GSTP by methionine restriction and BSO was reversed by GSH monoethyl ester and N-acetylcysteine.	Acetylcysteine	106-122	glutathione S-transferase pi 1	Rattus norvegicus	27-31
20504369-9	2010	CSE effects on IFN-gamma-induced Stat1 activation, antiviral protein expression, and inhibition of RSV infection were decreased by glutathione augmentation of epithelial cells using N-acetylcysteine or glutathione monoethyl ester, providing one strategy to alter cigarette smoke effects.	Acetylcysteine	182-198	interferon gamma	Homo sapiens	15-24
20862209-5	2010	Release of IL-1beta from macrophages was suppressed by the reactive oxygen species (ROS) scavenger N-acetyl cysteine (NAC) and high extracellular K(+), which are two agents known to inhibit NALP3/cryopyrin/CIAS1 inflammasome formation.	Acetylcysteine	99-116	interleukin 1 beta	Mus musculus	11-19
20862209-5	2010	Release of IL-1beta from macrophages was suppressed by the reactive oxygen species (ROS) scavenger N-acetyl cysteine (NAC) and high extracellular K(+), which are two agents known to inhibit NALP3/cryopyrin/CIAS1 inflammasome formation.	Acetylcysteine	118-121	interleukin 1 beta	Mus musculus	11-19
20356045-7	2010	Pretreatment with N-acetyl-l-cysteine (NAC) attenuated 6-DG-induced DR5 expression and inhibited TRAIL-induced apoptosis.	Acetylcysteine	39-42	TNF superfamily member 10	Homo sapiens	97-102
20439172-7	2010	Antioxidants, such as N-acetyl cysteine and superoxide dismutase, but not catalase, protected against As-induced inactivation of the LKB1-AMPK pathway and reversed the inhibitory effect of As on neurite outgrowth.	Acetylcysteine	22-39	serine/threonine kinase 11	Mus musculus	133-137
20439172-7	2010	Antioxidants, such as N-acetyl cysteine and superoxide dismutase, but not catalase, protected against As-induced inactivation of the LKB1-AMPK pathway and reversed the inhibitory effect of As on neurite outgrowth.	Acetylcysteine	22-39	protein kinase, AMP-activated, alpha 1 catalytic subunit	Mus musculus	138-142
20200986-6	2010	Coadministration of the antioxidant N-acetylcysteine (NAC) was able to block bone loss and downregulation of the bone-formation markers alkaline phosphatase and osteocalcin in serum and gene expression in bone.	Acetylcysteine	36-52	bone gamma-carboxyglutamate protein	Rattus norvegicus	161-172
20200986-6	2010	Coadministration of the antioxidant N-acetylcysteine (NAC) was able to block bone loss and downregulation of the bone-formation markers alkaline phosphatase and osteocalcin in serum and gene expression in bone.	Acetylcysteine	54-57	bone gamma-carboxyglutamate protein	Rattus norvegicus	161-172
20167675-3	2010	In spontaneously breathing rats, CS evoked a CSLVA-mediated reflex bradypnea that was prevented by N-acetyl-L-cysteine (NAC; an antioxidant), HC-030031 [a transient receptor potential ankyrin 1 (TRPA1) receptor antagonist], and iso-pyridoxalphosphate-6-azophenyl-2",5"-disulfonate (iso-PPADS; a P2X receptor antagonist).	Acetylcysteine	99-118	transient receptor potential cation channel, subfamily A, member 1	Rattus norvegicus	155-193
20037173-10	2010	However, NAC pretreatment significantly improved renal function and decreased the activation of ERK, JNK, Bax and Bad, whereas it increased Bcl-2 and Bcl-xL.	Acetylcysteine	9-12	Eph receptor B1	Rattus norvegicus	96-99
20167675-3	2010	In spontaneously breathing rats, CS evoked a CSLVA-mediated reflex bradypnea that was prevented by N-acetyl-L-cysteine (NAC; an antioxidant), HC-030031 [a transient receptor potential ankyrin 1 (TRPA1) receptor antagonist], and iso-pyridoxalphosphate-6-azophenyl-2",5"-disulfonate (iso-PPADS; a P2X receptor antagonist).	Acetylcysteine	99-118	transient receptor potential cation channel, subfamily A, member 1	Rattus norvegicus	195-200
20167675-3	2010	In spontaneously breathing rats, CS evoked a CSLVA-mediated reflex bradypnea that was prevented by N-acetyl-L-cysteine (NAC; an antioxidant), HC-030031 [a transient receptor potential ankyrin 1 (TRPA1) receptor antagonist], and iso-pyridoxalphosphate-6-azophenyl-2",5"-disulfonate (iso-PPADS; a P2X receptor antagonist).	Acetylcysteine	120-123	transient receptor potential cation channel, subfamily A, member 1	Rattus norvegicus	155-193
20167675-3	2010	In spontaneously breathing rats, CS evoked a CSLVA-mediated reflex bradypnea that was prevented by N-acetyl-L-cysteine (NAC; an antioxidant), HC-030031 [a transient receptor potential ankyrin 1 (TRPA1) receptor antagonist], and iso-pyridoxalphosphate-6-azophenyl-2",5"-disulfonate (iso-PPADS; a P2X receptor antagonist).	Acetylcysteine	120-123	transient receptor potential cation channel, subfamily A, member 1	Rattus norvegicus	195-200
20214734-8	2010	Six-month treatment with the anti-oxidant N-acetyl cysteine dramatically reduced hepatic steatosis in transgenic mice fed the excess-iron diet through decreased expression of unspliced and spliced XBP-1, p-eIF2alpha, and CHOP.	Acetylcysteine	42-59	X-box binding protein 1	Mus musculus	197-202
20037173-0	2010	N-acetylcysteine attenuates glycerol-induced acute kidney injury by regulating MAPKs and Bcl-2 family proteins.	Acetylcysteine	0-16	BCL2, apoptosis regulator	Rattus norvegicus	89-94
20142804-4	2010	N-acetyl-L-cysteine (NAC), a scavenger of reactive oxygen species (ROS), blocked H(2)O(2) inhibition of mTOR signaling.	Acetylcysteine	0-19	mechanistic target of rapamycin kinase	Homo sapiens	104-108
20142804-4	2010	N-acetyl-L-cysteine (NAC), a scavenger of reactive oxygen species (ROS), blocked H(2)O(2) inhibition of mTOR signaling.	Acetylcysteine	21-24	mechanistic target of rapamycin kinase	Homo sapiens	104-108
20037173-10	2010	However, NAC pretreatment significantly improved renal function and decreased the activation of ERK, JNK, Bax and Bad, whereas it increased Bcl-2 and Bcl-xL.	Acetylcysteine	9-12	BCL2, apoptosis regulator	Rattus norvegicus	140-145
20190028-11	2010	CONCLUSION: Short-term oral NAC treatment resulted in reduction of circulating IL-6, suggesting that such treatment could be a useful strategy in blunting the inflammatory response in PD patients.	Acetylcysteine	28-31	interleukin 6	Homo sapiens	79-83
20005956-9	2010	Further, angiotensin II was found to up-regulate NPC1L1 mRNA and protein levels in Caco-2 cells, which were completely blocked by an angiotensin II type 1 receptor blocker or an anti-oxidant, N-acetylcysteine.	Acetylcysteine	192-208	angiotensinogen	Homo sapiens	9-23
20716947-10	2010	Akt was slowly phosphorylated after treatment with DA, while NAC clearly inhibited the DA-induced Akt activation.	Acetylcysteine	61-64	thymoma viral proto-oncogene 1	Mus musculus	98-101
20716947-14	2010	Moreover, NAC effectively protects against DA-induced melanocyte death via inhibition of DA-induced Akt activation.	Acetylcysteine	10-13	thymoma viral proto-oncogene 1	Mus musculus	100-103
20654106-10	2010	The band density ratio of pp38 and p38 was significantly upregulated in H/R group (13.4 vs. 3.89), the mRNA and protein expressions of bcl2 were significantly lower and bax expressions were significantly higher in H/R group than those in control group and these changes could also be attenuated by NAC.	Acetylcysteine	298-301	BCL2, apoptosis regulator	Rattus norvegicus	135-139
20177149-2	2010	In the present study, we found that the co-treatment with hepatocyte growth factor (HGF) and TGF-beta1 resulted in enhanced migration of HaCaT cells compared with either growth factor alone, and that N-acetylcysteine, an antioxidant agent, was the most effective among several inhibitors tested, suggesting the involvement of reactive oxygen species (ROS).	Acetylcysteine	200-216	transforming growth factor beta 1	Homo sapiens	93-102
19903460-8	2010	Induction of OPN expression by FGF-2 was inhibited not only by PD98059 (MEK1 inhibitor) and PP1 (c-Src inhibitor), but also by an antioxidant, N-acetyl cysteine.	Acetylcysteine	143-160	fibroblast growth factor 2	Homo sapiens	31-36
20420656-3	2010	METHODS: Ovalbumin (OVA)-sensitized mice were exposed to EC-UFP (507 microg/m(3) for 24 h) or filtered air immediately prior to allergen challenge and systemically treated with N-acetylcysteine (NAC) or vehicle prior and during EC-UFP inhalation.	Acetylcysteine	177-193	serine (or cysteine) peptidase inhibitor, clade B, member 1, pseudogene	Mus musculus	9-18
22312380-7	2010	A reduction in catalase (CAT) activity and an increase in glutathione concentration were statistically significant in the NAC group (P &lt; 0.05).	Acetylcysteine	122-125	catalase	Homo sapiens	15-23
20089932-4	2010	Hypoxia-induced phosphorylation of p38 mitogen-activated protein kinase (MAPK) and stress-activated protein kinase/c-Jun NH(2)-terminal kinase (SAPK/JNK) were inhibited by the antioxidant (N-acetylcysteine, NAC, 10(-6) M) and (taurine, 4x10(-6) M).	Acetylcysteine	189-205	mitogen-activated protein kinase 14	Homo sapiens	35-71
19520919-7	2010	Furthermore, PM induced p38 MAPK activation and HSP27 phosphorylation, events that were both attenuated by NAC.	Acetylcysteine	107-110	mitogen-activated protein kinase 14	Homo sapiens	24-27
19751964-5	2010	Pretreatment of N-acetyl cysteine abolished TGFbeta(1)-induced H(2)O(2) induction and EGFR activation.	Acetylcysteine	16-33	transforming growth factor beta 1	Homo sapiens	44-54
19751964-5	2010	Pretreatment of N-acetyl cysteine abolished TGFbeta(1)-induced H(2)O(2) induction and EGFR activation.	Acetylcysteine	16-33	epidermal growth factor receptor	Homo sapiens	86-90
20121705-6	2010	Spermine-induced JNK activation was prevented by 200 microg/ml of both NAC and F1, while iNOS induction was blocked only by F1.	Acetylcysteine	71-74	mitogen-activated protein kinase 8	Homo sapiens	17-20
20002787-8	2010	Fibrinopeptides A and B (FPA and FPB, respectively) were released after fibrinogen cleavage by L-FCN-MASPs complexes captured on N-acetylcysteine-Sepharose.	Acetylcysteine	129-145	fibrinogen beta chain	Homo sapiens	72-82
20006595-5	2010	However, the increase in both uPA expression and activity was greatly reduced or alleviated by treatment with either ROS scavenger N-acetylcysteine or extracellular signal-regulated kinase (ERK) inhibitor PD98059.	Acetylcysteine	131-147	plasminogen activator, urokinase	Homo sapiens	30-33
22312380-7	2010	A reduction in catalase (CAT) activity and an increase in glutathione concentration were statistically significant in the NAC group (P &lt; 0.05).	Acetylcysteine	122-125	catalase	Homo sapiens	25-28
20198323-6	2010	Moreover, pre-treatment of transfected cells with N-acetyl L-cysteine blocked the silencing of uPA and uPAR, which further confirmed the oxidative damage-mediated downregulation.	Acetylcysteine	50-69	proline rich acidic protein 1	Homo sapiens	95-98
20179891-6	2010	Furthermore, NAC increased the protein expression of p-ERK, while inhibited protein expression of p-JNK, NF-kappaB in gastric mucosa.	Acetylcysteine	13-16	Eph receptor B1	Rattus norvegicus	55-58
20138851-8	2010	In addition, co-treatment of the Bv-2 cells with LPS and NAC surprisingly further increased the iNOS expression, an effect also found to be mediated through the JNK MAPK pathway.	Acetylcysteine	57-60	nitric oxide synthase 2, inducible	Mus musculus	96-100
20138851-8	2010	In addition, co-treatment of the Bv-2 cells with LPS and NAC surprisingly further increased the iNOS expression, an effect also found to be mediated through the JNK MAPK pathway.	Acetylcysteine	57-60	mitogen-activated protein kinase 1	Mus musculus	165-169
20138851-9	2010	The level of phosphorylated JNK MAPK (p46) was strongly increased by LPS alone and was further increased when combined with NAC.	Acetylcysteine	124-127	mitogen-activated protein kinase 1	Mus musculus	32-36
20112989-7	2010	Scavenging of nickel-induced ROS by NAC or catalase attenuated Akt, ASK1, and p38 MAPK activation and apoptosis, which implies involvement of ROS in the Akt/ASK1/p38 pathway.	Acetylcysteine	36-39	AKT serine/threonine kinase 1	Homo sapiens	63-66
20112989-7	2010	Scavenging of nickel-induced ROS by NAC or catalase attenuated Akt, ASK1, and p38 MAPK activation and apoptosis, which implies involvement of ROS in the Akt/ASK1/p38 pathway.	Acetylcysteine	36-39	mitogen-activated protein kinase 14	Homo sapiens	78-81
20112989-7	2010	Scavenging of nickel-induced ROS by NAC or catalase attenuated Akt, ASK1, and p38 MAPK activation and apoptosis, which implies involvement of ROS in the Akt/ASK1/p38 pathway.	Acetylcysteine	36-39	AKT serine/threonine kinase 1	Homo sapiens	153-156
20112989-7	2010	Scavenging of nickel-induced ROS by NAC or catalase attenuated Akt, ASK1, and p38 MAPK activation and apoptosis, which implies involvement of ROS in the Akt/ASK1/p38 pathway.	Acetylcysteine	36-39	mitogen-activated protein kinase 14	Homo sapiens	162-165
20009026-7	2010	In soleus muscles of AMPK-KD and WT mice, NAC prevented contraction-stimulated glucose uptake and l-NMMA had no effect.	Acetylcysteine	42-45	protein kinase, AMP-activated, alpha 2 catalytic subunit	Mus musculus	21-25
20354834-1	2010	The aim of this study was to follow up whether the modification of pro-antioxidant status by 8-day oral application of N-acetylcysteine (NAC) in healthy men affects the haematological response, whether there is a direct relationship between antioxidant defences and erythropoietin (EPO) secretion and whether NAC intake enhances exercise performance.	Acetylcysteine	137-140	erythropoietin	Homo sapiens	266-280
20354834-1	2010	The aim of this study was to follow up whether the modification of pro-antioxidant status by 8-day oral application of N-acetylcysteine (NAC) in healthy men affects the haematological response, whether there is a direct relationship between antioxidant defences and erythropoietin (EPO) secretion and whether NAC intake enhances exercise performance.	Acetylcysteine	137-140	erythropoietin	Homo sapiens	282-285
20354834-6	2010	NAC noticeably affected the plasma level of EPO (+26%), haemoglobin (+9%), haematocrit (+9%) and erythrocytes (-6%) at rest and after exercise.	Acetylcysteine	0-3	erythropoietin	Homo sapiens	44-47
20179891-7	2010	NAC also decreased the expression of TNF-alpha mRNA and Caspase-3 mRNA in gastric mucosa.	Acetylcysteine	0-3	tumor necrosis factor	Rattus norvegicus	37-46
19965809-9	2010	In the presence of ex vivo apoptotic cells, alveolar macrophages exposed to LPS or LPS + NAC had reduced tumor necrosis factor-alpha levels and increased transforming growth factor-beta1 levels.	Acetylcysteine	89-92	tumor necrosis factor	Mus musculus	105-132
19954742-7	2010	However, the phosphorylation of JNK rather than ERK1/2 activation by surfactin was blocked by NAC/catalase.	Acetylcysteine	94-97	mitogen-activated protein kinase 8	Homo sapiens	32-35
20117097-13	2010	Pre-treatment with NAC suppressed both MUC5AC production and p38 activation.	Acetylcysteine	19-22	mitogen-activated protein kinase 14	Homo sapiens	61-64
19954742-7	2010	However, the phosphorylation of JNK rather than ERK1/2 activation by surfactin was blocked by NAC/catalase.	Acetylcysteine	94-97	catalase	Homo sapiens	98-106
21577291-8	2010	NAC is also capable of reducing the activation of transcription factors especially sensitive to the cellular redox state, such as Nuclear factor-kappaB, signal transducer and activator of transcription-3 and mitogen-activated protein kinase.	Acetylcysteine	0-3	signal transducer and activator of transcription 3	Homo sapiens	153-203
20068565-10	2010	Brucein D-mediated activation of p38-MAPK was also inhibited by NAC.	Acetylcysteine	64-67	mitogen-activated protein kinase 14	Homo sapiens	33-36
20068565-10	2010	Brucein D-mediated activation of p38-MAPK was also inhibited by NAC.	Acetylcysteine	64-67	mitogen-activated protein kinase 14	Homo sapiens	37-41
20044024-6	2010	Furthermore, thiol-containing compounds such as N-acetylcysteine, l-cysteine and monothioglycerol prevented Cyt C release, and hence induction of apoptosis.	Acetylcysteine	48-64	cytochrome c, somatic	Homo sapiens	108-113
19935767-3	2010	Treatment with an antioxidant (N-acetyl cysteine) or Nox inhibitors strongly inhibited the expression of MMPs by LPS and inhibited cell migration.	Acetylcysteine	31-48	toll-like receptor 4	Mus musculus	113-116
20133848-4	2010	Here, we report that reduction of LDHA by siRNA or its inhibition by a small-molecule inhibitor (FX11 [3-dihydroxy-6-methyl-7-(phenylmethyl)-4-propylnaphthalene-1-carboxylic acid]) reduced ATP levels and induced significant oxidative stress and cell death that could be partially reversed by the antioxidant N-acetylcysteine.	Acetylcysteine	308-324	lactate dehydrogenase A	Homo sapiens	34-38
19782051-7	2010	Pretreatment with NAC blocked annexin V-binding, cleavage of PARP-1 and procaspases-3, -8, -9, loss of mitochondrial membrane potential and release of cytochrome c by CDDO-Me.	Acetylcysteine	18-21	poly(ADP-ribose) polymerase 1	Homo sapiens	61-93
19782051-7	2010	Pretreatment with NAC blocked annexin V-binding, cleavage of PARP-1 and procaspases-3, -8, -9, loss of mitochondrial membrane potential and release of cytochrome c by CDDO-Me.	Acetylcysteine	18-21	cytochrome c, somatic	Homo sapiens	151-163
19782051-8	2010	NAC also prevented the inhibition of constitutively active Akt, NF-kappaB and mTOR by CDDO-Me.	Acetylcysteine	0-3	AKT serine/threonine kinase 1	Homo sapiens	59-62
19782051-8	2010	NAC also prevented the inhibition of constitutively active Akt, NF-kappaB and mTOR by CDDO-Me.	Acetylcysteine	0-3	mechanistic target of rapamycin kinase	Homo sapiens	78-82
19947928-7	2010	Moreover immunocytochemistry and Western blot experiments revealed expression of CFTR channel on CFBE cells after treatment with 10 mM NAC.	Acetylcysteine	135-138	CF transmembrane conductance regulator	Homo sapiens	81-85
19565658-8	2010	Treatment of TD rats with N-acetylcysteine prevented the downregulation of EAAT2 in the medial thalamus, and ameliorated the loss of several other astrocyte proteins, concomitant with increased neuronal survival.	Acetylcysteine	26-42	solute carrier family 1 member 2	Rattus norvegicus	75-80
19837105-11	2010	The cytoprotective properties of NAC were related to the recovery of intracellular Ca2+ concentration, NOS-3 expression and NO production induced by GCDCA-treated HepG2 cells.	Acetylcysteine	33-36	nitric oxide synthase 3	Homo sapiens	103-108
19837105-12	2010	The increase of NO production by Ca2+-dependent NOS-3 expression during NAC administration reduces cell death in GCDCA-treated hepatocytes.	Acetylcysteine	72-75	nitric oxide synthase 3	Homo sapiens	48-53
19802001-3	2010	In this study, Twist1, a member of basic helix-loop-helix transcription factors as well as AR was upregulated in response to hydrogen peroxide, and the response to which was abolished by an addition of N-acetyl-L-cysteine and Twist1 knockdown.	Acetylcysteine	202-221	twist family bHLH transcription factor 1	Homo sapiens	15-21
19968960-3	2010	TGF-beta1-induced reduction of Grx1 expression caused an increase of intracellular reactive oxygen species (ROS) in EpRas cells, and pre-treatment of the ROS scavenger N-acetylcysteine (NAC) inhibited TGF-beta1-induced EMT.	Acetylcysteine	168-184	glutaredoxin	Mus musculus	31-35
19837105-3	2010	The study evaluated the involvement of Ca2+ on the regulation of NO synthase (NOS)-3 expression during N-acetylcysteine (NAC) cytoprotection against GCDCA-induced cell death in hepatocytes.	Acetylcysteine	103-119	nitric oxide synthase 3	Homo sapiens	65-84
19837105-3	2010	The study evaluated the involvement of Ca2+ on the regulation of NO synthase (NOS)-3 expression during N-acetylcysteine (NAC) cytoprotection against GCDCA-induced cell death in hepatocytes.	Acetylcysteine	121-124	nitric oxide synthase 3	Homo sapiens	65-84
19968960-3	2010	TGF-beta1-induced reduction of Grx1 expression caused an increase of intracellular reactive oxygen species (ROS) in EpRas cells, and pre-treatment of the ROS scavenger N-acetylcysteine (NAC) inhibited TGF-beta1-induced EMT.	Acetylcysteine	186-189	glutaredoxin	Mus musculus	31-35
19951696-8	2010	The phosphorylation of P70S6K, downstream of mTOR signaling, and AKT were further reduced by pretreatment with N-acetyl-l-cysteine (NAC), an ROS scavenger, whereas the phosphorylation of ERK1/2 and the conversion of LC3 I to LC3 II were further enhanced.	Acetylcysteine	111-130	mechanistic target of rapamycin kinase	Homo sapiens	45-49
19951696-8	2010	The phosphorylation of P70S6K, downstream of mTOR signaling, and AKT were further reduced by pretreatment with N-acetyl-l-cysteine (NAC), an ROS scavenger, whereas the phosphorylation of ERK1/2 and the conversion of LC3 I to LC3 II were further enhanced.	Acetylcysteine	132-135	mechanistic target of rapamycin kinase	Homo sapiens	45-49
19189384-6	2010	The bone cement extract-induced, downregulated expression of osteoblastic genes, such as alkaline phosphatase, collagen I, and osteocalcin, was also restored to the baseline level by cotreatment with NAC.	Acetylcysteine	200-203	bone gamma-carboxyglutamate protein	Rattus norvegicus	127-138
19951696-8	2010	The phosphorylation of P70S6K, downstream of mTOR signaling, and AKT were further reduced by pretreatment with N-acetyl-l-cysteine (NAC), an ROS scavenger, whereas the phosphorylation of ERK1/2 and the conversion of LC3 I to LC3 II were further enhanced.	Acetylcysteine	132-135	AKT serine/threonine kinase 1	Homo sapiens	65-68
19951696-8	2010	The phosphorylation of P70S6K, downstream of mTOR signaling, and AKT were further reduced by pretreatment with N-acetyl-l-cysteine (NAC), an ROS scavenger, whereas the phosphorylation of ERK1/2 and the conversion of LC3 I to LC3 II were further enhanced.	Acetylcysteine	132-135	mitogen-activated protein kinase 3	Homo sapiens	187-193
19717140-6	2010	We also examined the affect of ceftriaxone (previously shown to increase GLT-1) and N-acetylcysteine treatment on the expression of GLT-1 and xCT.	Acetylcysteine	84-100	solute carrier family 1 member 2	Homo sapiens	132-137
19717140-10	2010	N-acetylcysteine also restored GLT-1 and xCT levels.	Acetylcysteine	0-16	solute carrier family 1 member 2	Homo sapiens	31-36
20061637-0	2010	N-acetylcysteine prevents 4-hydroxynonenal- and amyloid-beta-induced modification and inactivation of neprilysin in SH-SY5Y cells.	Acetylcysteine	0-16	membrane metalloendopeptidase	Homo sapiens	102-112
19951696-8	2010	The phosphorylation of P70S6K, downstream of mTOR signaling, and AKT were further reduced by pretreatment with N-acetyl-l-cysteine (NAC), an ROS scavenger, whereas the phosphorylation of ERK1/2 and the conversion of LC3 I to LC3 II were further enhanced.	Acetylcysteine	111-130	AKT serine/threonine kinase 1	Homo sapiens	65-68
19951696-8	2010	The phosphorylation of P70S6K, downstream of mTOR signaling, and AKT were further reduced by pretreatment with N-acetyl-l-cysteine (NAC), an ROS scavenger, whereas the phosphorylation of ERK1/2 and the conversion of LC3 I to LC3 II were further enhanced.	Acetylcysteine	111-130	mitogen-activated protein kinase 3	Homo sapiens	187-193
20460760-7	2010	Furthermore, NAC attenuated shikonin-induced ERK phosphorylation.	Acetylcysteine	13-16	mitogen-activated protein kinase 1	Homo sapiens	45-48
20054154-9	2010	The protective effect of NAC against CdCl(2) induced MT1X, HSP70 and HMOX-1 genes, demonstrates an anti-oxidant effect of NAC in addition to Cd chelation.	Acetylcysteine	25-28	metallothionein 1X	Homo sapiens	53-57
20054154-9	2010	The protective effect of NAC against CdCl(2) induced MT1X, HSP70 and HMOX-1 genes, demonstrates an anti-oxidant effect of NAC in addition to Cd chelation.	Acetylcysteine	122-125	metallothionein 1X	Homo sapiens	53-57
20606481-6	2010	When the erythropoietin dosage was stable throughout, only the NAC group had a significant increase in hematocrit, accompanied with a decrease in plasma levels of 8-isoprostane and oxidized low-density lipoprotein.	Acetylcysteine	63-66	erythropoietin	Homo sapiens	9-23
19910455-9	2010	Although the precise mechanism(s) of the RA effect remains to be defined, it appears to be mediated by reactive oxygen species; the antioxidant N-acetylcysteine inhibited RA+TPA-stimulated secretion of VEGF by more than 80%.	Acetylcysteine	144-160	vascular endothelial growth factor A	Homo sapiens	202-206
20358478-14	2010	Western blot analysis showed that treatment of MF extracts caused an increase in Bax expression, which was inhibited by the antioxidant N-acetylcysteine (NAC).	Acetylcysteine	136-152	BCL2 associated X, apoptosis regulator	Homo sapiens	81-84
20358478-14	2010	Western blot analysis showed that treatment of MF extracts caused an increase in Bax expression, which was inhibited by the antioxidant N-acetylcysteine (NAC).	Acetylcysteine	154-157	BCL2 associated X, apoptosis regulator	Homo sapiens	81-84
20358478-16	2010	MF extracts induced cytochrome c release, which was inhibited by NAC.	Acetylcysteine	65-68	cytochrome c, somatic	Homo sapiens	20-32
19815813-10	2010	Blocking tyrosine nitration of PI 3-kinase with epicatechin or NAC restored Akt phosphorylation, and inhibited vaso-obliteration at p12 and neovascularization at p17 comparable with FeTPPS.	Acetylcysteine	63-66	AKT serine/threonine kinase 1	Homo sapiens	76-79
19815813-10	2010	Blocking tyrosine nitration of PI 3-kinase with epicatechin or NAC restored Akt phosphorylation, and inhibited vaso-obliteration at p12 and neovascularization at p17 comparable with FeTPPS.	Acetylcysteine	63-66	DNA polymerase epsilon 4, accessory subunit	Homo sapiens	132-135
20562516-7	2010	An antioxidant drug, N-acetyl-L-cysteine (NAC) inhibited TNF-induced VCAM-1.	Acetylcysteine	21-40	tumor necrosis factor	Rattus norvegicus	57-60
20562516-7	2010	An antioxidant drug, N-acetyl-L-cysteine (NAC) inhibited TNF-induced VCAM-1.	Acetylcysteine	42-45	tumor necrosis factor	Rattus norvegicus	57-60
20562516-8	2010	NAC also inhibited TNF-induced phosphorylation of Akt and NF-kappaB.	Acetylcysteine	0-3	tumor necrosis factor	Rattus norvegicus	19-22
20562516-8	2010	NAC also inhibited TNF-induced phosphorylation of Akt and NF-kappaB.	Acetylcysteine	0-3	AKT serine/threonine kinase 1	Rattus norvegicus	50-53
20402656-10	2010	ERK activation was inhibited by PD98059, Wortmanin and the ROS scavenger NAC (N-acetyl cysteine).	Acetylcysteine	73-76	mitogen-activated protein kinase 1	Homo sapiens	0-3
20402656-10	2010	ERK activation was inhibited by PD98059, Wortmanin and the ROS scavenger NAC (N-acetyl cysteine).	Acetylcysteine	78-95	mitogen-activated protein kinase 1	Homo sapiens	0-3
19722195-3	2010	We found that glucose-regulated protein 78 (GRP78) was upregulated in HeLa cells following treatment with NAC or PEN.	Acetylcysteine	106-109	heat shock protein family A (Hsp70) member 5	Homo sapiens	14-42
19722195-3	2010	We found that glucose-regulated protein 78 (GRP78) was upregulated in HeLa cells following treatment with NAC or PEN.	Acetylcysteine	106-109	heat shock protein family A (Hsp70) member 5	Homo sapiens	44-49
19722195-6	2010	Furthermore, the PERK-ATF4 pathway, which also induces the expression of CHOP, was activated in NAC-treated cells.	Acetylcysteine	96-99	DNA damage inducible transcript 3	Homo sapiens	73-77
19722195-7	2010	The role of the ER stress pathway was further confirmed through the small interfering RNA (siRNA)-mediated knockdown of CHOP, which attenuated NAC and PEN-induced apoptosis.	Acetylcysteine	143-146	DNA damage inducible transcript 3	Homo sapiens	120-124
20360623-0	2010	N-acetylcysteine inhibits IL-8 and MMP-9 release and ICAM-1 expression by bronchoalveolar cells from interstitial lung disease patients.	Acetylcysteine	0-16	C-X-C motif chemokine ligand 8	Homo sapiens	26-30
20360623-7	2010	NAC exerted a dose-dependent inhibitory effect on IL-8 and MMP-9 release and ICAM- expression by BAL macrophages and lymphocytes from patients with IPF and sarcoidosis.	Acetylcysteine	0-3	C-X-C motif chemokine ligand 8	Homo sapiens	50-54
19720122-5	2009	Pretreatment with BAPTA-AM or NAC abrogated p38 MAPK activation and restored ERK activation.	Acetylcysteine	30-33	mitogen-activated protein kinase 14	Homo sapiens	44-47
19796678-7	2009	These results support the hypothesis that exposure of exponentially growing human breast and prostate epithelial cells to PCBs causes increased steady-state levels of intracellular O(2)(*-) and H(2)O(2), induction of MnSOD or CuZnSOD activity, and clonogenic cell killing that could be inhibited by a clinically relevant thiol antioxidant, NAC, as well as by catalase and superoxide dismutase after PCB exposure.	Acetylcysteine	340-343	pyruvate carboxylase	Homo sapiens	122-125
19747498-8	2009	Finally, co-incubation of the JB6(+/+) cells with N-acetyl-cysteine decreased AP-1 activation and phosphorylation of ERKs, p38 kinase, and JNKs, thus suggesting that oxidative stress is involved in WC-Co-induced toxicity and AP-1 activation.	Acetylcysteine	50-67	mitogen-activated protein kinase 14	Homo sapiens	123-126
20056085-0	2010	[N-acetylcysteine antagonizes the Interleukin-18-induced expression of TNF-alpha and IL-6 in mouse vascular smooth muscle cells].	Acetylcysteine	1-17	tumor necrosis factor	Mus musculus	71-80
20056085-0	2010	[N-acetylcysteine antagonizes the Interleukin-18-induced expression of TNF-alpha and IL-6 in mouse vascular smooth muscle cells].	Acetylcysteine	1-17	interleukin 6	Mus musculus	85-89
20056085-1	2010	AIM: To explore the effect of N-acetylcysteine(NAC)on the interleukin(IL)18-induced expression of tumor necrosis factor (TNF) alpha and interleukin(IL) 6 in mouse vascular smooth muscle cells(VSMC).	Acetylcysteine	30-46	tumor necrosis factor	Mus musculus	98-131
20056085-7	2010	CONCLUSION: N-acetylcysteine antagonizes the production of TNF-alpha and IL-6 induced by IL-18 in VSMC.	Acetylcysteine	12-28	tumor necrosis factor	Mus musculus	59-68
20056085-7	2010	CONCLUSION: N-acetylcysteine antagonizes the production of TNF-alpha and IL-6 induced by IL-18 in VSMC.	Acetylcysteine	12-28	interleukin 6	Mus musculus	73-77
19878651-6	2009	The pro-drug N-acetylcysteine (NAC) that promotes T-helper type 1 responses was also shown to mediate the reduction of IL-4 disulfides.	Acetylcysteine	13-29	interleukin 4	Homo sapiens	119-123
19878651-6	2009	The pro-drug N-acetylcysteine (NAC) that promotes T-helper type 1 responses was also shown to mediate the reduction of IL-4 disulfides.	Acetylcysteine	31-34	interleukin 4	Homo sapiens	119-123
19796678-6	2009	Finally, treatment with either N-acetylcysteine (NAC) or the combination of polyethylene glycol (PEG)-conjugated CuZnSOD and PEG-catalase added 1 h after PCBs significantly protected these cells from PCB toxicity.	Acetylcysteine	31-47	pyruvate carboxylase	Homo sapiens	154-157
19720122-5	2009	Pretreatment with BAPTA-AM or NAC abrogated p38 MAPK activation and restored ERK activation.	Acetylcysteine	30-33	mitogen-activated protein kinase 1	Homo sapiens	77-80
19944371-11	2009	The reduction in BKN-dependent relaxation was prevented by treatment for 1 month with the antioxidant N-acetylcysteine (1 g.kg.day), or losartan, an Ang II type 1 receptor blocker (10 mg.kg.day).	Acetylcysteine	102-118	kininogen 1	Homo sapiens	17-20
19703426-14	2009	CONCLUSIONS: ethanol causes a shift towards apoptosis in both cNCC and tNCC, a shift, which is diminished by NAC treatment.	Acetylcysteine	109-112	troponin C1, slow skeletal and cardiac type	Rattus norvegicus	71-75
19460788-10	2009	Apoptosis induced by TN is driven by oxidative stress and cell exposure to sulfydryl donors, such as glutathione monoethylester and l-N-acetylcysteine, significantly reduced pro-apoptotic effects and Akt inhibition.	Acetylcysteine	132-150	AKT serine/threonine kinase 1	Homo sapiens	200-203
19864306-11	2009	PTX3 concentrations were lower in cells co-treated with antioxidants (all P&lt;0.05), associated with lower nuclear factor kappaB expression for NAC and trolox (P&lt;0.05).	Acetylcysteine	145-148	pentraxin 3	Homo sapiens	0-4
19467570-4	2009	The p38 MAPK activation by dihydrotanshinone was inhibited by N-acetyl cysteine pretreatment.	Acetylcysteine	62-79	mitogen-activated protein kinase 14	Homo sapiens	4-7
19626645-10	2009	Additionally, the antioxidant N-acetyl-L-cysteine could obviously abrogate p53 stabilization triggered by oroxylin A.	Acetylcysteine	30-49	tumor protein p53	Homo sapiens	75-78
19755521-6	2009	Apocynin, an NAD(P)H oxidase inhibitor, and N-acetyl cysteine (NAC), an ROS scavenger, both inhibited EGFR transactivation induced by U-II.	Acetylcysteine	44-61	urotensin 2	Rattus norvegicus	134-138
19755521-6	2009	Apocynin, an NAD(P)H oxidase inhibitor, and N-acetyl cysteine (NAC), an ROS scavenger, both inhibited EGFR transactivation induced by U-II.	Acetylcysteine	63-66	urotensin 2	Rattus norvegicus	134-138
19755521-11	2009	SHP-2, but not PTP 1B, was transiently oxidized during U-II treatment, which could be repressed by NAC treatment.	Acetylcysteine	99-102	protein tyrosine phosphatase, non-receptor type 11	Rattus norvegicus	0-5
19755521-11	2009	SHP-2, but not PTP 1B, was transiently oxidized during U-II treatment, which could be repressed by NAC treatment.	Acetylcysteine	99-102	urotensin 2	Rattus norvegicus	55-59
19393328-0	2009	N-acetyl-L-cysteine inhibits TGF-beta1-induced profibrotic responses in fibroblasts.	Acetylcysteine	0-19	transforming growth factor beta 1	Homo sapiens	29-38
19393328-3	2009	OBJECTIVES: The aim of this study was to evaluate whether the antioxidant N-acetyl-l-cysteine (NAC) can affect TGF-beta(1)-mediated tissue remodeling in fibroblasts or modulate the production of fibronectin and vascular endothelial growth factor (VEGF) which are believed to be important mediators of tissue repair and remodeling.	Acetylcysteine	74-93	transforming growth factor beta 1	Homo sapiens	111-121
19393328-3	2009	OBJECTIVES: The aim of this study was to evaluate whether the antioxidant N-acetyl-l-cysteine (NAC) can affect TGF-beta(1)-mediated tissue remodeling in fibroblasts or modulate the production of fibronectin and vascular endothelial growth factor (VEGF) which are believed to be important mediators of tissue repair and remodeling.	Acetylcysteine	74-93	fibronectin 1	Homo sapiens	195-206
19393328-3	2009	OBJECTIVES: The aim of this study was to evaluate whether the antioxidant N-acetyl-l-cysteine (NAC) can affect TGF-beta(1)-mediated tissue remodeling in fibroblasts or modulate the production of fibronectin and vascular endothelial growth factor (VEGF) which are believed to be important mediators of tissue repair and remodeling.	Acetylcysteine	74-93	vascular endothelial growth factor A	Homo sapiens	211-245
19393328-3	2009	OBJECTIVES: The aim of this study was to evaluate whether the antioxidant N-acetyl-l-cysteine (NAC) can affect TGF-beta(1)-mediated tissue remodeling in fibroblasts or modulate the production of fibronectin and vascular endothelial growth factor (VEGF) which are believed to be important mediators of tissue repair and remodeling.	Acetylcysteine	74-93	vascular endothelial growth factor A	Homo sapiens	247-251
19765584-0	2009	Differential effects of the antioxidant n-acetylcysteine on the production of catabolic mediators in IL-1beta-stimulated human osteoarthritic synoviocytes and chondrocytes.	Acetylcysteine	40-56	interleukin 1 beta	Homo sapiens	101-109
19765584-5	2009	While NAC significantly diminished PGE(2) release and the expression of both COX-2 and MMP-13 protein in IL-1beta-stimulated synoviocytes, it failed to modify their production in stimulated chondrocytes.	Acetylcysteine	6-9	matrix metallopeptidase 13	Homo sapiens	87-93
19765584-5	2009	While NAC significantly diminished PGE(2) release and the expression of both COX-2 and MMP-13 protein in IL-1beta-stimulated synoviocytes, it failed to modify their production in stimulated chondrocytes.	Acetylcysteine	6-9	interleukin 1 beta	Homo sapiens	105-113
19765584-6	2009	Likewise, NAC only inhibited IL-1beta-stimulated NF-kappaB activation in synoviocytes.	Acetylcysteine	10-13	interleukin 1 beta	Homo sapiens	29-37
19765584-6	2009	Likewise, NAC only inhibited IL-1beta-stimulated NF-kappaB activation in synoviocytes.	Acetylcysteine	10-13	nuclear factor kappa B subunit 1	Homo sapiens	49-58
19648289-2	2009	We investigated the effects of N-acetylcysteine (NAC) on TGF-beta1-induced EMT in a rat epithelial cell line (RLE-6TN) and in primary rat alveolar epithelial cells (AEC).	Acetylcysteine	31-47	transforming growth factor, beta 1	Rattus norvegicus	57-66
19762915-9	2009	In osteoarthritic chondrocytes, the antioxidants Mn(III) tetrakis(4-benzoic acid)porphyrin and N-acetylcysteine increased the ratio of Akt to ERK phosphorylation and promoted IGF-I-mediated proteoglycan synthesis.	Acetylcysteine	95-111	AKT serine/threonine kinase 1	Homo sapiens	135-138
19762915-9	2009	In osteoarthritic chondrocytes, the antioxidants Mn(III) tetrakis(4-benzoic acid)porphyrin and N-acetylcysteine increased the ratio of Akt to ERK phosphorylation and promoted IGF-I-mediated proteoglycan synthesis.	Acetylcysteine	95-111	mitogen-activated protein kinase 1	Homo sapiens	142-145
19762915-9	2009	In osteoarthritic chondrocytes, the antioxidants Mn(III) tetrakis(4-benzoic acid)porphyrin and N-acetylcysteine increased the ratio of Akt to ERK phosphorylation and promoted IGF-I-mediated proteoglycan synthesis.	Acetylcysteine	95-111	insulin like growth factor 1	Homo sapiens	175-180
19648289-2	2009	We investigated the effects of N-acetylcysteine (NAC) on TGF-beta1-induced EMT in a rat epithelial cell line (RLE-6TN) and in primary rat alveolar epithelial cells (AEC).	Acetylcysteine	49-52	transforming growth factor, beta 1	Rattus norvegicus	57-66
19648289-4	2009	These changes were inhibited by NAC, which also prevented Smad3 phosphorylation.	Acetylcysteine	32-35	SMAD family member 3	Rattus norvegicus	58-63
19648289-5	2009	Similarly, primary alveolar epithelial type II cells exposed to TGF-beta1 also underwent EMT that was prevented by NAC.	Acetylcysteine	115-118	transforming growth factor, beta 1	Rattus norvegicus	64-73
19648289-6	2009	TGF-beta1 decreased cellular GSH levels by 50-80%, whereas NAC restored them to approximately 150% of those found in TGF-beta1-treated cells.	Acetylcysteine	59-62	transforming growth factor, beta 1	Rattus norvegicus	117-126
19648289-8	2009	Consistent with its role as an antioxidant and cellular redox stabilizer, NAC dramatically reduced intracellular reactive oxygen species production in the presence of TGF-beta1.	Acetylcysteine	74-77	transforming growth factor, beta 1	Rattus norvegicus	167-176
19648289-10	2009	We conclude that NAC prevents EMT in AEC in vitro, at least in part through replenishment of intracellular GSH stores and limitation of TGF-beta1-induced intracellular ROS generation.	Acetylcysteine	17-20	transforming growth factor, beta 1	Rattus norvegicus	136-145
19737348-7	2009	Additionally, Akt, p70 ribosomal protein S6 kinase, and S6 ribosomal protein were also phosphorylated upon sPLA(2)-IIA treatment, effect that was abrogated by N-acetylcysteine or LY294002 treatment indicating that ROS and phosphatidylinositol 3 kinase are upstream signaling regulators.	Acetylcysteine	159-175	AKT serine/threonine kinase 1	Homo sapiens	14-17
19464387-5	2009	Relative to unsheared controls, NEP mRNA and protein were substantially down-regulated by LSS (&gt;or=50%), events which could be prevented by treatment of BAECs with either N-acetylcysteine, superoxide dismutase, or catalase, implicating reactive oxygen species (ROS) involvement.	Acetylcysteine	174-190	membrane metalloendopeptidase	Bos taurus	32-35
20104683-8	2009	The level of TNF-alpha and ALT declined significantly in the group pretreated by NAC.	Acetylcysteine	81-84	tumor necrosis factor	Mus musculus	13-22
19729059-6	2009	Importantly, blockade of ROS by preincubation of cells with the general ROS scavenger N-acetyl-l-cysteine (NAC) or the NADPH oxidase inhibitor DPI significantly reduced M. bovis BCG-induced up-regulation of cathelicidin LL-37 mRNA expression as determined by semi-quantitative RT-PCR or real-time PCR.	Acetylcysteine	86-105	cathelicidin antimicrobial peptide	Homo sapiens	220-225
19729059-6	2009	Importantly, blockade of ROS by preincubation of cells with the general ROS scavenger N-acetyl-l-cysteine (NAC) or the NADPH oxidase inhibitor DPI significantly reduced M. bovis BCG-induced up-regulation of cathelicidin LL-37 mRNA expression as determined by semi-quantitative RT-PCR or real-time PCR.	Acetylcysteine	107-110	cathelicidin antimicrobial peptide	Homo sapiens	220-225
19729059-9	2009	In addition, M. bovis BCG-induced cathelicidin LL-37 protein secretion was inhibited by the addition of NAC, DPI, and the selective inhibitor of NADPH oxidase apocynin.	Acetylcysteine	104-107	cathelicidin antimicrobial peptide	Homo sapiens	47-52
19917357-9	2009	Serum lactate dehydrogenase also indicated a significant decrease in the NAC group at 24 hours posttransplantation (P = .02) Serum tumor necrosis factor-alpha and interleukin-1 concentrations which rapidly increased postoperatively were reduced by administration of NAC.	Acetylcysteine	73-76	tumor necrosis factor	Rattus norvegicus	131-158
19917357-9	2009	Serum lactate dehydrogenase also indicated a significant decrease in the NAC group at 24 hours posttransplantation (P = .02) Serum tumor necrosis factor-alpha and interleukin-1 concentrations which rapidly increased postoperatively were reduced by administration of NAC.	Acetylcysteine	266-269	tumor necrosis factor	Rattus norvegicus	131-158
20104683-9	2009	CONCLUSION: N-acetylcysteine can inhibit the activation of TLR2/4 and reduce TNF-alpha secretion resulted from I/R injury it might abate liver and lung injury following partial hepatic ischemia-reperfusion in mice.	Acetylcysteine	12-28	tumor necrosis factor	Mus musculus	77-86
19699266-6	2009	Finally, we showed that OA reduced reactive oxygen species (ROS) accumulation and an anti-oxidant N-acetylcysteine inhibited NF-kappaB transactivation and phosphorylation of IKK and Akt in LPS-stimulated BV2 cells.	Acetylcysteine	98-114	thymoma viral proto-oncogene 1	Mus musculus	182-185
20137606-9	2009	However, NAC significantly decreased the BDNF and increased the TrkB mRNA and protein expression in rat hippocampal neuron after MG induction.	Acetylcysteine	9-12	neurotrophic receptor tyrosine kinase 2	Rattus norvegicus	64-68
20310085-5	2009	The specific p38 MAPK (mitogen-activated protein kinase) inhibitor SB203580, the antioxidant N-acetylcysteine and p38 MAPK siRNA (small interfering RNA) attenuated the induction of resistin protein by cyclic stretch.	Acetylcysteine	93-109	resistin	Rattus norvegicus	181-189
20310085-9	2009	Pre-treatment with SB203580 and N-acetylcysteine significantly attenuated resistin promoter activity induced by cyclic stretch.	Acetylcysteine	32-48	resistin	Rattus norvegicus	74-82
19625608-6	2009	The HOCl-mediated induction of Nrf2 or HO-1 was blocked by the glutathione donor N-acetyl-l-cysteine but was unaffected by ascorbic or uric acid.	Acetylcysteine	81-100	NFE2 like bZIP transcription factor 2	Homo sapiens	31-35
19767766-10	2009	Furthermore, atorvastatin inhibited Hcy-induced phosphorylation of p38 MAPK (1.7+/-0.1 vs 2.22+/-0.25, P&lt;0.05), similar effects occurred with DPI, NAC and SB203580.	Acetylcysteine	150-153	mitogen-activated protein kinase 14	Homo sapiens	67-75
19668088-3	2009	The impact of NAC pretreatment (2 hours) on aggregation of platelets from healthy volunteers in response to thrombin and adenosine diphosphate and on platelet-derived nitric oxide (NO) was examined.	Acetylcysteine	14-17	coagulation factor II, thrombin	Homo sapiens	108-116
19809176-6	2009	Glutathione ethyl ester and N-acetyl-L-cysteine prevented the growth inhibitory effect of SMO.	Acetylcysteine	28-47	smoothened, frizzled class receptor	Rattus norvegicus	90-93
19808019-4	2009	The increased insulin sensitivity in Gpx1(-/-) mice was attributed to insulin-induced phosphatidylinositol-3-kinase/Akt signaling and glucose uptake in muscle and could be reversed by the antioxidant N-acetylcysteine.	Acetylcysteine	200-216	thymoma viral proto-oncogene 1	Mus musculus	116-119
19668088-7	2009	Finally, NAC significantly reduced both thrombin-induced and adenosine diphosphate-induced platelet aggregation.	Acetylcysteine	9-12	coagulation factor II, thrombin	Homo sapiens	40-48
19553350-8	2009	Interestingly, hydrogen peroxide increased HDAC-2 activity, and the treatment with an antioxidant, N-acetylcysteine, almost completely reduced TGF-beta1-induced activation of HDAC-2.	Acetylcysteine	99-115	transforming growth factor, beta 1	Rattus norvegicus	143-152
19615393-11	2009	NAC co-treatment restored follicle growth and expression of Ccnd2 and Cdk4.	Acetylcysteine	0-3	cyclin-dependent kinase 4	Mus musculus	70-74
19559059-7	2009	N-Acetylcysteine (NAC) intervention promotes neuroprotection of cutaneous sensory neurons through considerable upregulation of Bcl-2 and downregulation of both Bax and caspase-3 mRNA.	Acetylcysteine	0-16	BCL2, apoptosis regulator	Rattus norvegicus	127-132
19559059-7	2009	N-Acetylcysteine (NAC) intervention promotes neuroprotection of cutaneous sensory neurons through considerable upregulation of Bcl-2 and downregulation of both Bax and caspase-3 mRNA.	Acetylcysteine	18-21	BCL2, apoptosis regulator	Rattus norvegicus	127-132
19633358-4	2009	ROS are required for VEGF-induced permeability as treatment with the free radical scavenger, N-acetylcysteine, inhibited this effect.	Acetylcysteine	93-109	vascular endothelial growth factor A	Homo sapiens	21-25
19482076-6	2009	Our data also reveal that 4-HPR-mediated ROS evoke Akt conformational change by forming an intramolecular disulfide bond; N-acetylcysteine and glutathione, as thiol antioxidants, significantly abate the ROS generation in 4-HPR-exposed cells.	Acetylcysteine	122-138	AKT serine/threonine kinase 1	Homo sapiens	51-54
19269634-6	2009	NAD(P)H oxidase inhibitor apocynin and ROS scavenger N-acetylcysteine (NAC) inhibited the EGFR transactivation induced by U-II.	Acetylcysteine	53-69	urotensin 2	Rattus norvegicus	122-126
19269634-6	2009	NAD(P)H oxidase inhibitor apocynin and ROS scavenger N-acetylcysteine (NAC) inhibited the EGFR transactivation induced by U-II.	Acetylcysteine	71-74	urotensin 2	Rattus norvegicus	122-126
19269634-11	2009	SHP-2 was oxidized during U-II treatment; and this oxidization could be repressed by NAC treatment.	Acetylcysteine	85-88	protein tyrosine phosphatase, non-receptor type 11	Rattus norvegicus	0-5
19269634-11	2009	SHP-2 was oxidized during U-II treatment; and this oxidization could be repressed by NAC treatment.	Acetylcysteine	85-88	urotensin 2	Rattus norvegicus	26-30
19560222-11	2009	Inhibition of radiation-induced HNE generation by acetyl-cysteine blocked radiation-induced src activation and EGFR phosphorylation.	Acetylcysteine	50-65	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	92-95
19560222-11	2009	Inhibition of radiation-induced HNE generation by acetyl-cysteine blocked radiation-induced src activation and EGFR phosphorylation.	Acetylcysteine	50-65	epidermal growth factor receptor	Homo sapiens	111-115
19540902-4	2009	N-Acetylcysteine (ROS scavenger) pretreatment reduced the dissipation of DeltaPsim, but insignificantly affected AA-induced p38 MAPK and JNK activation.	Acetylcysteine	0-16	mitogen-activated protein kinase 8	Homo sapiens	137-140
19553346-6	2009	Moreover, AGE-induced extracellular signal-regulated kinase/c-Jun N-terminal kinase/p38 mitogen-activated protein kinase activation was markedly blocked by antireceptor for AGE (RAGE), SNAP, SNP, NAC, and taurine.	Acetylcysteine	196-199	mitogen-activated protein kinase 14	Homo sapiens	84-87
19553346-7	2009	The abilities of NO and antioxidants to inhibit AGE/RAGE-induced hypertrophic growth were verified by the observation that SNAP, SNP, NAC, and taurine inhibited fibronectin, p21(Waf1/Cip1), and RAGE expression.	Acetylcysteine	134-137	fibronectin 1	Homo sapiens	161-172
19553346-7	2009	The abilities of NO and antioxidants to inhibit AGE/RAGE-induced hypertrophic growth were verified by the observation that SNAP, SNP, NAC, and taurine inhibited fibronectin, p21(Waf1/Cip1), and RAGE expression.	Acetylcysteine	134-137	cyclin dependent kinase inhibitor 1A	Homo sapiens	174-177
19398917-0	2009	N-acetylcysteine prevents carbon tetrachloride-induced liver cirrhosis: role of liver transforming growth factor-beta and oxidative stress.	Acetylcysteine	0-16	transforming growth factor beta 1	Homo sapiens	86-117
19468286-3	2009	The reducing agent, N-acetylcysteine (NAC), effectively inhibited the sustained activation of JNK, release of Endo G, and cell death in Jurkat cells treated by AD5-10.	Acetylcysteine	20-36	mitogen-activated protein kinase 8	Homo sapiens	94-97
19468286-3	2009	The reducing agent, N-acetylcysteine (NAC), effectively inhibited the sustained activation of JNK, release of Endo G, and cell death in Jurkat cells treated by AD5-10.	Acetylcysteine	38-41	mitogen-activated protein kinase 8	Homo sapiens	94-97
18830972-9	2009	Expression changes of HO-1 and iNOS were markedly blocked when Jurkat cells were preincubated with NAC, suggesting that ROS resulted in HO-1 and iNOS dysfunction in Jurkat cells.	Acetylcysteine	99-102	nitric oxide synthase 2	Homo sapiens	31-35
18830972-9	2009	Expression changes of HO-1 and iNOS were markedly blocked when Jurkat cells were preincubated with NAC, suggesting that ROS resulted in HO-1 and iNOS dysfunction in Jurkat cells.	Acetylcysteine	99-102	nitric oxide synthase 2	Homo sapiens	145-149
19409983-5	2009	Treatment with the ROS inhibitor N-acetylcysteine blocked manumycin-induced apoptosis, caspase-3 activity, and PARP expression, indicating the involvement of increased ROS in the proapoptotic activity of manumycin.	Acetylcysteine	33-49	caspase 3	Homo sapiens	87-96
19409983-5	2009	Treatment with the ROS inhibitor N-acetylcysteine blocked manumycin-induced apoptosis, caspase-3 activity, and PARP expression, indicating the involvement of increased ROS in the proapoptotic activity of manumycin.	Acetylcysteine	33-49	poly(ADP-ribose) polymerase 1	Homo sapiens	111-115
19701261-12	2009	Despite early administration of N-acetylcysteine, serum AST/ALT peaked at 384 and 541 IU/L on day 3 with normal coagulation profile.	Acetylcysteine	32-48	solute carrier family 17 member 5	Homo sapiens	56-59
19438509-6	2009	N-acetylcysteine (NAC), an antioxidant, inhibited ROS generation and synergistic interaction between TRAIL and wogonin.	Acetylcysteine	0-16	TNF superfamily member 10	Homo sapiens	101-106
19438509-6	2009	N-acetylcysteine (NAC), an antioxidant, inhibited ROS generation and synergistic interaction between TRAIL and wogonin.	Acetylcysteine	18-21	TNF superfamily member 10	Homo sapiens	101-106
19034653-0	2009	Effect of N-acetylcysteine on the murine model of colitis induced by dextran sodium sulfate through up-regulating PON1 activity.	Acetylcysteine	10-26	paraoxonase 1	Mus musculus	114-118
19034653-8	2009	However, NAC significantly decreased colonic MPO activity, ROS, TNF-alpha and IL-1 beta levels and increased PON1 activity and GSH concentration.	Acetylcysteine	9-12	tumor necrosis factor	Mus musculus	64-73
19034653-8	2009	However, NAC significantly decreased colonic MPO activity, ROS, TNF-alpha and IL-1 beta levels and increased PON1 activity and GSH concentration.	Acetylcysteine	9-12	interleukin 1 beta	Mus musculus	78-87
19034653-8	2009	However, NAC significantly decreased colonic MPO activity, ROS, TNF-alpha and IL-1 beta levels and increased PON1 activity and GSH concentration.	Acetylcysteine	9-12	paraoxonase 1	Mus musculus	109-113
19034653-10	2009	These results suggest that NAC may be effective in the treatment of colitis through its up-regulating PON1 and scavenging oxygen-derived free radicals.	Acetylcysteine	27-30	paraoxonase 1	Mus musculus	102-106
19398917-12	2009	Western blots revealed a four-fold increase in TGF-beta in the group receiving CCl4, NAC cotreatment abolished TGF-beta signal (P&lt;0.05).	Acetylcysteine	85-88	transforming growth factor beta 1	Homo sapiens	47-55
19398917-12	2009	Western blots revealed a four-fold increase in TGF-beta in the group receiving CCl4, NAC cotreatment abolished TGF-beta signal (P&lt;0.05).	Acetylcysteine	85-88	transforming growth factor beta 1	Homo sapiens	111-119
19398917-13	2009	CONCLUSION: Our results strongly suggest that NAC prevents experimental cirrhosis by two mechanisms: by preventing oxidative stress and by downregulating the profibrogenic cytokine TGF-beta.	Acetylcysteine	46-49	transforming growth factor beta 1	Homo sapiens	181-189
19398917-1	2009	OBJECTIVES: N-acetylcysteine (NAC) is an antioxidant, a precursor of reduced glutathione, and an inhibitor of the profibrotic cytokine liver transforming growth factor-beta (TGF-beta).	Acetylcysteine	12-28	transforming growth factor beta 1	Homo sapiens	141-172
19398917-1	2009	OBJECTIVES: N-acetylcysteine (NAC) is an antioxidant, a precursor of reduced glutathione, and an inhibitor of the profibrotic cytokine liver transforming growth factor-beta (TGF-beta).	Acetylcysteine	12-28	transforming growth factor beta 1	Homo sapiens	174-182
19398917-1	2009	OBJECTIVES: N-acetylcysteine (NAC) is an antioxidant, a precursor of reduced glutathione, and an inhibitor of the profibrotic cytokine liver transforming growth factor-beta (TGF-beta).	Acetylcysteine	30-33	transforming growth factor beta 1	Homo sapiens	141-172
19398917-1	2009	OBJECTIVES: N-acetylcysteine (NAC) is an antioxidant, a precursor of reduced glutathione, and an inhibitor of the profibrotic cytokine liver transforming growth factor-beta (TGF-beta).	Acetylcysteine	30-33	transforming growth factor beta 1	Homo sapiens	174-182
19464389-6	2009	Bay 11-7085 (an inhibitor of NF-kappaB activation) and anti-oxidant N-acetylcysteine attenuated the TNF-alpha-induced formation of inflammatory mediators and reactive species.	Acetylcysteine	68-84	tumor necrosis factor	Homo sapiens	100-109
20187293-7	2009	Noticeably, pre-treatment with N-acetylcysteine or rotenone eliminated markedly ROS accompanied with reduction in p38 MAPK activation.	Acetylcysteine	31-47	mitogen-activated protein kinase 14	Homo sapiens	114-117
19450605-5	2009	More importantly, the sex difference in TNF-alpha expression was abrogated by Rac1 knockout or gp91(phox) knockout and by administration of apocynin or N-acetylcysteine in LPS-stimulated mice.	Acetylcysteine	152-168	tumor necrosis factor	Mus musculus	40-49
19463931-8	2009	PAMAM-(COOH)(46)-(NAC)(18) conjugate was non-toxic, and significantly reduced ROS, NO and TNF-alpha release by activated microglial cells after 24 h and 72 h stimulation of LPS following 3h pre-treatment when compared to the same concentration of free NAC (P&lt;0.05 or P&lt;0.01).	Acetylcysteine	18-21	tumor necrosis factor	Mus musculus	90-99
20560295-0	2009	N-acetylcysteine inhibits TNF-alpha, sTNFR, and TGF-beta1 release by alveolar macrophages in idiopathic pulmonary fibrosis in vitro.	Acetylcysteine	0-16	transforming growth factor beta 1	Homo sapiens	48-57
19411311-8	2009	Treating CFTR-deficient cells with N-acetyl-cysteine (NAC) increases HDAC2 expression to near control levels.	Acetylcysteine	35-52	CF transmembrane conductance regulator	Homo sapiens	9-13
19411311-8	2009	Treating CFTR-deficient cells with N-acetyl-cysteine (NAC) increases HDAC2 expression to near control levels.	Acetylcysteine	35-52	histone deacetylase 2	Homo sapiens	69-74
19411311-8	2009	Treating CFTR-deficient cells with N-acetyl-cysteine (NAC) increases HDAC2 expression to near control levels.	Acetylcysteine	54-57	CF transmembrane conductance regulator	Homo sapiens	9-13
19411311-8	2009	Treating CFTR-deficient cells with N-acetyl-cysteine (NAC) increases HDAC2 expression to near control levels.	Acetylcysteine	54-57	histone deacetylase 2	Homo sapiens	69-74
19207719-13	2009	Pretreatment of cardiac fibroblasts with N-acetylcysteine (5 mmol/L) for 30 min prior to exposure to U-II resulted in inhibition of U-II increased ROS formation.	Acetylcysteine	41-57	urotensin 2	Rattus norvegicus	101-105
19207719-13	2009	Pretreatment of cardiac fibroblasts with N-acetylcysteine (5 mmol/L) for 30 min prior to exposure to U-II resulted in inhibition of U-II increased ROS formation.	Acetylcysteine	41-57	urotensin 2	Rattus norvegicus	132-136
19523979-7	2009	In contrast, the anti-oxidant N-acetyl cysteine blocked caspase-3 activation and significantly protected OLPs from cadmium-induced cell death.	Acetylcysteine	30-47	caspase 3	Homo sapiens	56-65
19574996-7	2009	RESULTS: We obtained a high percentage of MAP2-positive neurons derived from embryoid bodies (EBs) induced by RA by administering 1 mmol/L NAC at differentiation day 0.	Acetylcysteine	139-142	microtubule-associated protein 2	Mus musculus	42-46
19574996-8	2009	On differentiation day 8, the expression of MAP2 protein was strongly upregulated in the presence of NAC.	Acetylcysteine	101-104	microtubule-associated protein 2	Mus musculus	44-48
19575001-9	2009	NAC treatment also decreased the pulmonary protein content at 48 and 72 h and the lung wet/dry weight ratio at 24 and 48 h. Additionally, NAC enhanced pulmonary production of TNF-alpha and IL-10 at 24 h and 48 h. CONCLUSION: In combination with antifungal therapy, NAC treatment can alleviate oxidative stress and lung injury associated with IPA in neutropenic mice.Acta Pharmacologica Sinica (2009) 30: 980-986; doi: 10.1038/aps.2009.83.	Acetylcysteine	0-3	tumor necrosis factor	Mus musculus	175-184
19575001-9	2009	NAC treatment also decreased the pulmonary protein content at 48 and 72 h and the lung wet/dry weight ratio at 24 and 48 h. Additionally, NAC enhanced pulmonary production of TNF-alpha and IL-10 at 24 h and 48 h. CONCLUSION: In combination with antifungal therapy, NAC treatment can alleviate oxidative stress and lung injury associated with IPA in neutropenic mice.Acta Pharmacologica Sinica (2009) 30: 980-986; doi: 10.1038/aps.2009.83.	Acetylcysteine	0-3	interleukin 10	Mus musculus	189-194
19575001-9	2009	NAC treatment also decreased the pulmonary protein content at 48 and 72 h and the lung wet/dry weight ratio at 24 and 48 h. Additionally, NAC enhanced pulmonary production of TNF-alpha and IL-10 at 24 h and 48 h. CONCLUSION: In combination with antifungal therapy, NAC treatment can alleviate oxidative stress and lung injury associated with IPA in neutropenic mice.Acta Pharmacologica Sinica (2009) 30: 980-986; doi: 10.1038/aps.2009.83.	Acetylcysteine	138-141	tumor necrosis factor	Mus musculus	175-184
19575001-9	2009	NAC treatment also decreased the pulmonary protein content at 48 and 72 h and the lung wet/dry weight ratio at 24 and 48 h. Additionally, NAC enhanced pulmonary production of TNF-alpha and IL-10 at 24 h and 48 h. CONCLUSION: In combination with antifungal therapy, NAC treatment can alleviate oxidative stress and lung injury associated with IPA in neutropenic mice.Acta Pharmacologica Sinica (2009) 30: 980-986; doi: 10.1038/aps.2009.83.	Acetylcysteine	138-141	interleukin 10	Mus musculus	189-194
19575001-9	2009	NAC treatment also decreased the pulmonary protein content at 48 and 72 h and the lung wet/dry weight ratio at 24 and 48 h. Additionally, NAC enhanced pulmonary production of TNF-alpha and IL-10 at 24 h and 48 h. CONCLUSION: In combination with antifungal therapy, NAC treatment can alleviate oxidative stress and lung injury associated with IPA in neutropenic mice.Acta Pharmacologica Sinica (2009) 30: 980-986; doi: 10.1038/aps.2009.83.	Acetylcysteine	138-141	tumor necrosis factor	Mus musculus	175-184
19575001-9	2009	NAC treatment also decreased the pulmonary protein content at 48 and 72 h and the lung wet/dry weight ratio at 24 and 48 h. Additionally, NAC enhanced pulmonary production of TNF-alpha and IL-10 at 24 h and 48 h. CONCLUSION: In combination with antifungal therapy, NAC treatment can alleviate oxidative stress and lung injury associated with IPA in neutropenic mice.Acta Pharmacologica Sinica (2009) 30: 980-986; doi: 10.1038/aps.2009.83.	Acetylcysteine	138-141	interleukin 10	Mus musculus	189-194
19604316-7	2009	PAAF-mediated MCP-1 up-regulation was completely suppressed by Dx and NAC.	Acetylcysteine	70-73	mast cell protease 1-like 1	Rattus norvegicus	14-19
19604316-10	2009	Both downstream pathways were targeted by Dx and NAC to repress the PAAF-mediated acinar MCP-1 up-regulation.	Acetylcysteine	49-52	mast cell protease 1-like 1	Rattus norvegicus	89-94
20560295-0	2009	N-acetylcysteine inhibits TNF-alpha, sTNFR, and TGF-beta1 release by alveolar macrophages in idiopathic pulmonary fibrosis in vitro.	Acetylcysteine	0-16	tumor necrosis factor	Homo sapiens	26-35
20560295-3	2009	OBJECTIVE: In this study we investigated the effect of NAC on the production of tumor necrosis factor (TNF)-alpha, interleukin (IL)-1beta, IL-6, IL-8, IL-10, IL-12 (p70), IL-18, transforming growth factor (TGF)-beta1, and the soluble TNF receptors (sTNFR1 and sTNFR2) by alveolar macrophages (AM) in IPF patients.	Acetylcysteine	55-58	tumor necrosis factor	Homo sapiens	80-113
20560295-5	2009	RESULTS: NAC suppressed the production of TNF-alpha, its soluble receptors, and TGF-beta1 by AMs in a dose-dependent manner.	Acetylcysteine	9-12	tumor necrosis factor	Homo sapiens	42-51
20560295-5	2009	RESULTS: NAC suppressed the production of TNF-alpha, its soluble receptors, and TGF-beta1 by AMs in a dose-dependent manner.	Acetylcysteine	9-12	transforming growth factor beta 1	Homo sapiens	80-89
20560295-6	2009	At the highest concentration of NAC (10 mM), the spontaneous or LPS-stimulated production ofTNF-alpha, sTNFR1, sTNFR2, and TGF-beta1 were significantly reduced.	Acetylcysteine	32-35	transforming growth factor beta 1	Homo sapiens	123-132
20560295-7	2009	The LPS-stimulated IL-1beta production was also suppressed by 10 mM NAC.	Acetylcysteine	68-71	interleukin 1 beta	Homo sapiens	19-27
20560295-8	2009	CONCLUSIONS: NAC has the potential to down-regulate the production of TNF-alpha and their soluble receptors, as well as TGF-beta1 and LPS-stimulated IL-1beta, by AM in IPF in vitro.	Acetylcysteine	13-16	tumor necrosis factor	Homo sapiens	70-79
19563648-4	2009	The patients were randomly assigned to receive either oral NAC (600 mg BID, starting 24 h before the procedure) or placebo, in adjunct to hydration.	Acetylcysteine	59-62	BH3 interacting domain death agonist	Homo sapiens	71-74
19558798-6	2009	NO production induced by MAPKs and NF-kappaB was similarly reduced by inhibitors of ERK (PD98059), p38 (SB203580), NF-kappaB (N-acetylcysteine), and NSA9.	Acetylcysteine	126-142	nuclear factor kappa B subunit 1	Homo sapiens	35-44
19344884-7	2009	NAC before LPS significantly reduced the fetal IL-6 and IL-1 beta response.	Acetylcysteine	0-3	interleukin 6	Rattus norvegicus	47-51
19211687-7	2009	In experiments designed to unravel the mechanisms underlying BSA-induced ER stress, BSA stimulated the production of cellular reactive oxygen species (ROS), and antioxidants such as ascorbic acid or N-acetylcysteine (NAC) blocked BSA-induced increases in GRP78 activation, eIF2alpha phosphorylation, SGLT expression, and alpha-MG uptake.	Acetylcysteine	199-215	heat shock protein family A (Hsp70) member 5	Homo sapiens	255-260
19211687-7	2009	In experiments designed to unravel the mechanisms underlying BSA-induced ER stress, BSA stimulated the production of cellular reactive oxygen species (ROS), and antioxidants such as ascorbic acid or N-acetylcysteine (NAC) blocked BSA-induced increases in GRP78 activation, eIF2alpha phosphorylation, SGLT expression, and alpha-MG uptake.	Acetylcysteine	217-220	heat shock protein family A (Hsp70) member 5	Homo sapiens	255-260
21977284-10	2009	However, median CRP decreased from 2.35 to 2.14 mg/L during NAC therapy (p=0.04), while it increased from 2.24 to 2.65 mg/L with placebo.	Acetylcysteine	60-63	C-reactive protein	Homo sapiens	16-19
21977284-13	2009	However, NAC therapy decreased CRP levels, suggesting that this compound may have some efficacy in reducing systemic inflammation.	Acetylcysteine	9-12	C-reactive protein	Homo sapiens	31-34
19379726-6	2009	In contrast, other NF-kappaB inhibitors, such as fenofibrate, N-acetylcysteine and MG132, decreased MMP expression in IL-1beta-stimulated FLSs.	Acetylcysteine	62-78	nuclear factor kappa B subunit 1	Homo sapiens	19-28
19379726-6	2009	In contrast, other NF-kappaB inhibitors, such as fenofibrate, N-acetylcysteine and MG132, decreased MMP expression in IL-1beta-stimulated FLSs.	Acetylcysteine	62-78	interleukin 1 beta	Homo sapiens	118-126
19464570-6	2009	Furthermore, N-acetylcysteine, a ROS production inhibitor, partly reversed the activation of JNK and p38 and the induction of apoptosis in GA-treated cells.	Acetylcysteine	13-29	mitogen-activated protein kinase 14	Homo sapiens	101-104
19264975-4	2009	METHODS: Ovalbumin-sensitized mice were exposed to EC-UFPs (504 microg/m(3) for 24 h) or filtered air immediately before allergen challenge and systemically treated with N-acetylcysteine or vehicle before and during EC-UFP inhalation.	Acetylcysteine	170-186	serine (or cysteine) peptidase inhibitor, clade B, member 1, pseudogene	Mus musculus	9-18
19344884-7	2009	NAC before LPS significantly reduced the fetal IL-6 and IL-1 beta response.	Acetylcysteine	0-3	interleukin 1 beta	Rattus norvegicus	56-65
19450459-10	2009	Compared with the group not treated with N-acetylcysteine, catalase activity was increased significantly in the group treated with 20 mM N-acetylcysteine.	Acetylcysteine	137-153	catalase	Oryctolagus cuniculus	59-67
19326266-8	2009	In SHP-2 knockdown cells, UII-induced phosphorylation of EGFR was less influenced by NAC, and significantly suppressed by heparin binding (HB)-EGF neutralizing antibody.	Acetylcysteine	85-88	protein tyrosine phosphatase, non-receptor type 11	Rattus norvegicus	3-8
19326266-8	2009	In SHP-2 knockdown cells, UII-induced phosphorylation of EGFR was less influenced by NAC, and significantly suppressed by heparin binding (HB)-EGF neutralizing antibody.	Acetylcysteine	85-88	urotensin 2	Rattus norvegicus	26-29
19350554-7	2009	In contrast, N-acetylcysteine, a potent cysteine reductive compound, significantly prevents up-regulation of HMOX1, GCLM, and CXCL2 genes, and repression of MMP9 and CCL22 genes induced by As(2)O(3).	Acetylcysteine	13-29	glutamate-cysteine ligase modifier subunit	Homo sapiens	116-120
19433777-3	2009	Treatment of renin-expressing As4.1 cells with the potent cytokine tumor necrosis factor-alpha caused an increase in the steady-state levels of cellular reactive oxygen species, which was reversed by the antioxidant N-acetylcysteine.	Acetylcysteine	216-232	tumor necrosis factor	Mus musculus	67-94
19433777-6	2009	The tumor necrosis factor-alpha-induced decrease in renin mRNA was partially reversed by either N-acetylcysteine or panepoxydone, a nuclear factor kappaB (NFkappaB) inhibitor.	Acetylcysteine	96-112	tumor necrosis factor	Mus musculus	4-31
19433777-6	2009	The tumor necrosis factor-alpha-induced decrease in renin mRNA was partially reversed by either N-acetylcysteine or panepoxydone, a nuclear factor kappaB (NFkappaB) inhibitor.	Acetylcysteine	96-112	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	132-153
18791914-5	2009	The DEP-induced increases in peribronchial eosinophils and mucous goblet cells in the lung tissues, and of IL-5 and IL-13 in the BAL fluid, were significantly attenuated by the antioxidant N-acetylcysteine.	Acetylcysteine	189-205	interleukin 13	Mus musculus	116-121
19234337-12	2009	Studies using human ECs demonstrated that TNF-alpha-induced CCL2 production was also inhibited by the NAD(P)H oxidase inhibitor DPI, the antioxidant N-acetyl-L-cysteine, or the superoxide scavenger Tiron, further indicating that inhibition occurs through the NAD(P)H/ROS pathway.	Acetylcysteine	149-168	tumor necrosis factor	Homo sapiens	42-51
19393651-6	2009	The antioxidant N-acetyl-cysteine inhibits activation of p38 and cell death induced by hypoxia, indicating that reactive oxygen species (ROS) are responsible for p38 activation.	Acetylcysteine	16-33	mitogen-activated protein kinase 14	Homo sapiens	57-60
19454702-9	2009	In addition, pharmacological blockage of ERK and scavenging of reactive oxygen species with N-acetylcysteine reduced HO-1 gene expression in p38(-/-) MEF, respectively.	Acetylcysteine	92-108	heme oxygenase 1	Mus musculus	117-121
19210339-11	2009	Cigarette smoke condensate-stimulated urokinase production was dependent on the activity of ERK/JNK pathways and was inhibited by the reactive oxygen species scavenger, N-acetyl cysteine.	Acetylcysteine	169-186	mitogen-activated protein kinase 1	Homo sapiens	92-95
19210339-11	2009	Cigarette smoke condensate-stimulated urokinase production was dependent on the activity of ERK/JNK pathways and was inhibited by the reactive oxygen species scavenger, N-acetyl cysteine.	Acetylcysteine	169-186	mitogen-activated protein kinase 8	Homo sapiens	96-99
19404261-4	2009	Furthermore, many of the deficiencies normally observed in Bmi1(-/-) mice improve after either pharmacological treatment with the antioxidant N-acetylcysteine or genetic disruption of the DNA damage response pathway by Chk2 (also known as Chek2) deletion.	Acetylcysteine	142-158	Bmi1 polycomb ring finger oncogene	Mus musculus	59-63
19393651-6	2009	The antioxidant N-acetyl-cysteine inhibits activation of p38 and cell death induced by hypoxia, indicating that reactive oxygen species (ROS) are responsible for p38 activation.	Acetylcysteine	16-33	mitogen-activated protein kinase 14	Homo sapiens	162-165
18716872-4	2009	Furthermore, NAC plus 5-ASA reduced nitrate generation, an expression of inducible nitric oxide synthase (iNOS) activity, to basal levels and these results were significantly lower than those observed with either NAC or 5-ASA alone.	Acetylcysteine	13-16	nitric oxide synthase 2	Rattus norvegicus	73-104
19337996-7	2009	This inhibitory effect of IFN-gamma on iTreg generation was significantly abrogated after N-acetyl-L-cysteine treatment both in vitro and in vivo, indicating that IFN-gamma regulation of iTreg generation is dependent on ROS-mediated apoptosis.	Acetylcysteine	90-109	interferon gamma	Mus musculus	26-35
19337996-7	2009	This inhibitory effect of IFN-gamma on iTreg generation was significantly abrogated after N-acetyl-L-cysteine treatment both in vitro and in vivo, indicating that IFN-gamma regulation of iTreg generation is dependent on ROS-mediated apoptosis.	Acetylcysteine	90-109	interferon gamma	Mus musculus	163-172
19061877-7	2009	Furthermore, reactive oxygen species inhibitors N-acetylcysteine and nitric oxide synthase inhibitor aminoguanidine increased the expression of CFTR.	Acetylcysteine	48-64	CF transmembrane conductance regulator	Homo sapiens	144-148
19117669-3	2009	Post-irradiation treatment with N-acetyl-L-cysteine (NAC) inhibited cytochrome c release from mitochondria but did not affect expression levels of Bcl-2, Bcl-X(L) and Bax, suggesting that late production of ROS triggered cytochrome c release.	Acetylcysteine	32-51	cytochrome c, somatic	Homo sapiens	68-80
19117669-3	2009	Post-irradiation treatment with N-acetyl-L-cysteine (NAC) inhibited cytochrome c release from mitochondria but did not affect expression levels of Bcl-2, Bcl-X(L) and Bax, suggesting that late production of ROS triggered cytochrome c release.	Acetylcysteine	32-51	cytochrome c, somatic	Homo sapiens	221-233
19286926-4	2009	CSE-evoked IL-8 release was mimicked by acrolein and crotonaldehyde at concentrations (3-60 microM each) found in CSE and fully prevented by 1 mM alpha,beta-unsaturated aldehydes scavengers N-acetylcysteine (NAC) or sodium 2-mercaptoethanesulfonate.	Acetylcysteine	190-206	C-X-C motif chemokine ligand 8	Homo sapiens	11-15
19286926-4	2009	CSE-evoked IL-8 release was mimicked by acrolein and crotonaldehyde at concentrations (3-60 microM each) found in CSE and fully prevented by 1 mM alpha,beta-unsaturated aldehydes scavengers N-acetylcysteine (NAC) or sodium 2-mercaptoethanesulfonate.	Acetylcysteine	208-211	C-X-C motif chemokine ligand 8	Homo sapiens	11-15
19286926-8	2009	CSE-evoked p38 and ERK1/2 phosphorylation was mimicked by acrolein and inhibited by NAC.	Acetylcysteine	84-87	mitogen-activated protein kinase 1	Homo sapiens	11-14
19286926-8	2009	CSE-evoked p38 and ERK1/2 phosphorylation was mimicked by acrolein and inhibited by NAC.	Acetylcysteine	84-87	mitogen-activated protein kinase 3	Homo sapiens	19-25
19420723-4	2009	Me(2)S(4) combined with beta-carotene and assisted by UVA significantly inhibited the cell viability, and enhanced the caspase-3 activity which was completely inhibited by N-acety-L-cysteine.	Acetylcysteine	172-190	caspase 3	Homo sapiens	119-128
19264484-7	2009	We further investigated the mechanism involved in the neuroprotective effects of NAC on rat brain tissue and found that NAC significantly increased CuZn-SOD and GSH-Px activity and decreased MDA content in the SAH brain.	Acetylcysteine	120-123	superoxide dismutase 1	Rattus norvegicus	148-156
19342982-7	2009	During ATO/PTL-mediated apoptosis, the collapse of mitochondrial transmembrane potential occurred with cytochrome c release, which was reversed by L-N-acetylcysteine.	Acetylcysteine	147-165	cytochrome c, somatic	Homo sapiens	103-115
19336887-9	2009	The antioxidant N-acetylcysteine (NAC) also showed the same effects as HT on LPS-induced ROS and NO generation, change of GSH level, and NF-kappaB activation.	Acetylcysteine	16-32	nuclear factor kappa B subunit 1	Homo sapiens	137-146
19336887-9	2009	The antioxidant N-acetylcysteine (NAC) also showed the same effects as HT on LPS-induced ROS and NO generation, change of GSH level, and NF-kappaB activation.	Acetylcysteine	34-37	nuclear factor kappa B subunit 1	Homo sapiens	137-146
18716872-4	2009	Furthermore, NAC plus 5-ASA reduced nitrate generation, an expression of inducible nitric oxide synthase (iNOS) activity, to basal levels and these results were significantly lower than those observed with either NAC or 5-ASA alone.	Acetylcysteine	13-16	nitric oxide synthase 2	Rattus norvegicus	106-110
19734276-8	2009	NAC administration normalized antioxidant enzyme activities (superoxide dismutase and catalase) and reduced malondialdehyde content (indicator of lipid peroxidation) in hyperoxaluric rat"s red blood cell (RBC) lysate.	Acetylcysteine	0-3	catalase	Rattus norvegicus	86-94
19292871-5	2009	ROS in turn exerted feedback regulation on JNK activation, as shown by the observations that cyclosporin A and the antioxidant N-acetylcysteine significantly inhibited the phosphorylation of JNK induced by morphine.	Acetylcysteine	127-143	mitogen-activated protein kinase 8	Homo sapiens	43-46
19292871-5	2009	ROS in turn exerted feedback regulation on JNK activation, as shown by the observations that cyclosporin A and the antioxidant N-acetylcysteine significantly inhibited the phosphorylation of JNK induced by morphine.	Acetylcysteine	127-143	mitogen-activated protein kinase 8	Homo sapiens	191-194
18389381-7	2009	NAC inhibits the pro-inflammatory factors expressions (TNF-alphaand IL-1beta) stimulated by ISO.	Acetylcysteine	0-3	tumor necrosis factor	Rattus norvegicus	55-58
19179647-7	2009	In contrast, NF-kappaB activation was significantly inhibited by N-acetylcysteine and did not depend on ERK1/2 stimulation, as shown by the lack of effect of the upstream ERK inhibitor U-0126.	Acetylcysteine	65-81	nuclear factor kappa B subunit 1	Homo sapiens	13-22
19714806-7	2009	Intraperitoneal NAC administration prior to the final OVA challenge inhibited Yml/Ym2, SP-D, and FIZZ1 expression in BALF and lung tissue.	Acetylcysteine	16-19	surfactant associated protein D	Mus musculus	87-91
19714806-7	2009	Intraperitoneal NAC administration prior to the final OVA challenge inhibited Yml/Ym2, SP-D, and FIZZ1 expression in BALF and lung tissue.	Acetylcysteine	16-19	resistin like alpha	Mus musculus	97-102
18389381-7	2009	NAC inhibits the pro-inflammatory factors expressions (TNF-alphaand IL-1beta) stimulated by ISO.	Acetylcysteine	0-3	interleukin 1 beta	Rattus norvegicus	68-76
19255346-7	2009	Treatment with N-acetylcysteine restored oxidized to total glutathione ratio, normalized levels of glutathiolated cardiac alpha-actin, reversed cardiac and myocyte hypertrophy and interstitial fibrosis, reduced the propensity for ventricular arrhythmias, prevented cardiac dysfunction, restored myocardial levels of active protein kinase G, and dephosphorylated NFATc1 and phospho-p38.	Acetylcysteine	15-31	nuclear factor of activated T-cells, cytoplasmic 1	Oryctolagus cuniculus	362-368
19176594-0	2009	N-acetyl cysteine mediates protection from 2-hydroxyethyl methacrylate induced apoptosis via nuclear factor kappa B-dependent and independent pathways: potential involvement of JNK.	Acetylcysteine	0-17	mitogen-activated protein kinase 8	Homo sapiens	177-180
19176594-4	2009	NAC also prevented HEMA mediated decrease in vascular endothelial growth factor secretion.	Acetylcysteine	0-3	vascular endothelial growth factor A	Homo sapiens	45-79
19176594-5	2009	The protective effect of NAC was partly related to its ability to induce NF-kappaB in the cells, since HEMA mediated inhibition of nuclear NF-kappaB expression and function was significantly blocked in the presence of NAC treatment.	Acetylcysteine	25-28	nuclear factor kappa B subunit 1	Homo sapiens	73-82
19176594-5	2009	The protective effect of NAC was partly related to its ability to induce NF-kappaB in the cells, since HEMA mediated inhibition of nuclear NF-kappaB expression and function was significantly blocked in the presence of NAC treatment.	Acetylcysteine	25-28	nuclear factor kappa B subunit 1	Homo sapiens	139-148
19176594-5	2009	The protective effect of NAC was partly related to its ability to induce NF-kappaB in the cells, since HEMA mediated inhibition of nuclear NF-kappaB expression and function was significantly blocked in the presence of NAC treatment.	Acetylcysteine	218-221	nuclear factor kappa B subunit 1	Homo sapiens	73-82
19176594-5	2009	The protective effect of NAC was partly related to its ability to induce NF-kappaB in the cells, since HEMA mediated inhibition of nuclear NF-kappaB expression and function was significantly blocked in the presence of NAC treatment.	Acetylcysteine	218-221	nuclear factor kappa B subunit 1	Homo sapiens	139-148
19176594-7	2009	In addition, since NAC was capable of rescuing close to 50% of NF-kappaB knockdown cells from HEMA mediated cell death, there is, therefore, an NF-kappaB independent pathway of protection from HEMA mediated cell death by NAC.	Acetylcysteine	19-22	nuclear factor kappa B subunit 1	Homo sapiens	63-72
19176594-7	2009	In addition, since NAC was capable of rescuing close to 50% of NF-kappaB knockdown cells from HEMA mediated cell death, there is, therefore, an NF-kappaB independent pathway of protection from HEMA mediated cell death by NAC.	Acetylcysteine	221-224	nuclear factor kappa B subunit 1	Homo sapiens	63-72
19176594-7	2009	In addition, since NAC was capable of rescuing close to 50% of NF-kappaB knockdown cells from HEMA mediated cell death, there is, therefore, an NF-kappaB independent pathway of protection from HEMA mediated cell death by NAC.	Acetylcysteine	221-224	nuclear factor kappa B subunit 1	Homo sapiens	144-153
19176594-8	2009	NAC mediated prevention of HEMA induced cell death in NF-kappaB knockdown cells was correlated with a decreased induction of c-Jun N-terminal kinase (JNK) activity since NAC inhibited HEMA mediated increase in JNK levels.	Acetylcysteine	0-3	nuclear factor kappa B subunit 1	Homo sapiens	54-63
19176594-8	2009	NAC mediated prevention of HEMA induced cell death in NF-kappaB knockdown cells was correlated with a decreased induction of c-Jun N-terminal kinase (JNK) activity since NAC inhibited HEMA mediated increase in JNK levels.	Acetylcysteine	0-3	mitogen-activated protein kinase 8	Homo sapiens	125-148
19176594-8	2009	NAC mediated prevention of HEMA induced cell death in NF-kappaB knockdown cells was correlated with a decreased induction of c-Jun N-terminal kinase (JNK) activity since NAC inhibited HEMA mediated increase in JNK levels.	Acetylcysteine	0-3	mitogen-activated protein kinase 8	Homo sapiens	150-153
19176594-8	2009	NAC mediated prevention of HEMA induced cell death in NF-kappaB knockdown cells was correlated with a decreased induction of c-Jun N-terminal kinase (JNK) activity since NAC inhibited HEMA mediated increase in JNK levels.	Acetylcysteine	0-3	mitogen-activated protein kinase 8	Homo sapiens	210-213
19176594-8	2009	NAC mediated prevention of HEMA induced cell death in NF-kappaB knockdown cells was correlated with a decreased induction of c-Jun N-terminal kinase (JNK) activity since NAC inhibited HEMA mediated increase in JNK levels.	Acetylcysteine	170-173	nuclear factor kappa B subunit 1	Homo sapiens	54-63
19176594-8	2009	NAC mediated prevention of HEMA induced cell death in NF-kappaB knockdown cells was correlated with a decreased induction of c-Jun N-terminal kinase (JNK) activity since NAC inhibited HEMA mediated increase in JNK levels.	Acetylcysteine	170-173	mitogen-activated protein kinase 8	Homo sapiens	125-148
19176594-8	2009	NAC mediated prevention of HEMA induced cell death in NF-kappaB knockdown cells was correlated with a decreased induction of c-Jun N-terminal kinase (JNK) activity since NAC inhibited HEMA mediated increase in JNK levels.	Acetylcysteine	170-173	mitogen-activated protein kinase 8	Homo sapiens	150-153
19176594-8	2009	NAC mediated prevention of HEMA induced cell death in NF-kappaB knockdown cells was correlated with a decreased induction of c-Jun N-terminal kinase (JNK) activity since NAC inhibited HEMA mediated increase in JNK levels.	Acetylcysteine	170-173	mitogen-activated protein kinase 8	Homo sapiens	210-213
19176594-10	2009	Therefore, NAC protects oral keratinocytes from the toxic effects of HEMA through NF-kappaB dependent and independent pathways.	Acetylcysteine	11-14	nuclear factor kappa B subunit 1	Homo sapiens	82-91
19176594-11	2009	Moreover, our data suggest the potential involvement of JNK pathway in NAC mediated protection.	Acetylcysteine	71-74	mitogen-activated protein kinase 8	Homo sapiens	56-59
19264704-6	2009	Treatment with sPLA(2) increases reactive oxygen species (ROS) production, and an antioxidant, N-acetylcysteine, inhibits sPLA(2)-induced cellular senescence.	Acetylcysteine	95-111	phospholipase A2 group X	Homo sapiens	122-129
19159629-9	2009	NAC was also able to normalize DeltaPsim, inhibit cytochrome c release, increase Bcl-2 and decrease Bax expression and procaspase-9 activation.	Acetylcysteine	0-3	BCL2, apoptosis regulator	Rattus norvegicus	81-86
19153832-0	2009	N-acetyl cysteine enhances imatinib-induced apoptosis of Bcr-Abl+ cells by endothelial nitric oxide synthase-mediated production of nitric oxide.	Acetylcysteine	0-17	nitric oxide synthase 3	Homo sapiens	75-108
19153832-8	2009	NAC-mediated enhanced killing correlated with cleavage of caspases, PARP and up-regulation and down regulation of pro- and anti-apoptotic family of proteins, respectively.	Acetylcysteine	0-3	poly(ADP-ribose) polymerase 1	Homo sapiens	68-72
19153832-9	2009	Co-treatment with NAC leads to enhanced production of nitric oxide (NO) by endothelial nitric oxide synthase (eNOS).	Acetylcysteine	18-21	nitric oxide synthase 3	Homo sapiens	75-108
19153832-12	2009	CONCLUSION: NAC enhances imatinib-induced apoptosis of Bcr-Abl(+) cells by endothelial nitric oxide synthase-mediated production of nitric oxide.	Acetylcysteine	12-15	nitric oxide synthase 3	Homo sapiens	75-108
19220841-6	2009	Anti-oxidant N-acetyl-L-cysteine (NAC) abolished U18666A-induced TNF-alpha production.	Acetylcysteine	13-32	tumor necrosis factor	Mus musculus	65-74
19220841-6	2009	Anti-oxidant N-acetyl-L-cysteine (NAC) abolished U18666A-induced TNF-alpha production.	Acetylcysteine	34-37	tumor necrosis factor	Mus musculus	65-74
19063961-6	2009	TNFalpha plus PY treatment elevated 3-nitrotyrosine adduct formation and induced NOS2 in the liver; 1400W and NAC blocked these changes.	Acetylcysteine	110-113	tumor necrosis factor	Mus musculus	0-8
19071156-6	2009	IFN-gamma treatment increased ROS production, and an antioxidant, N-acetylcysteine, inhibited IFN-gamma-induced cellular senescence.	Acetylcysteine	66-82	interferon gamma	Homo sapiens	94-103
19011150-7	2009	MEASUREMENTS AND MAIN RESULTS: Oxidants evoked the release of CXCL8 from monocytes/macrophages; this was abrogated by pretreatment with N-acetylcysteine or binding antibodies to TLR2 and was associated with the rapid phosphorylation of IL-1 receptor-associated kinase 1.	Acetylcysteine	136-152	C-X-C motif chemokine ligand 8	Homo sapiens	62-67
19234179-5	2009	Pretreatment of KB cells with antioxidants vitamin C and N-acetylcysteine or the pharmacological inhibitor PD168393 specific for the epidermal growth factor receptor all inhibited UVB-induced ROS as well as PAF-R agonists, yet had no effect on fMLP-mediated PAF-R agonist production.	Acetylcysteine	57-73	formyl peptide receptor 1	Homo sapiens	244-248
19063961-13	2009	NF-kappaB activation products such as Bcl-2, Bcl-X(L), cFLIP(S), cFLIP(L), and Mn-SOD were reduced by TNFalpha plus PY and restored by 1400W or NAC.	Acetylcysteine	144-147	tumor necrosis factor	Mus musculus	102-110
19033392-9	2009	A significant inhibition of the expression of hmox1 and nqo1 mRNAs and CD86 expression was found in 1-chloro 2,4-dinitrobenzene-treated THP-1 cells preincubated with N-acetyl cysteine, a glutathione precursor.	Acetylcysteine	166-183	NAD(P)H quinone dehydrogenase 1	Homo sapiens	56-60
19014919-7	2009	N-acetyl-l-cysteine pre-treatment rescued cells from MSt-2-induced ROS formation, mitochondrial membrane potential (Delta psi(m)) loss, Fas expression, caspase-8 and -3 activation and DNA fragmentation.	Acetylcysteine	0-19	serine/threonine kinase 3	Homo sapiens	53-58
18952368-7	2009	Pre-treatment with N-acetyl-l-cysteine significantly attenuated the combined treatment-induced ROS generation and caspase-3-dependent apoptosis, implying the involvement of ROS in this type of cell death.	Acetylcysteine	19-38	caspase 3	Homo sapiens	114-123
19111613-7	2009	The high Il-6 plasma levels found during AP, both in NAC-treated and non-treated rats, pointed out cytokines as activating factors of chemokine expression in non-acinar cells.	Acetylcysteine	53-56	interleukin 6	Rattus norvegicus	9-13
19202317-9	2009	We also confirmed that PDGF-induced JNK and Akt activations were inhibited by antioxidants, N-acetylcysteine and diphenyleneiodonium chloride, in RASMCs.	Acetylcysteine	92-108	AKT serine/threonine kinase 1	Rattus norvegicus	44-47
19033392-9	2009	A significant inhibition of the expression of hmox1 and nqo1 mRNAs and CD86 expression was found in 1-chloro 2,4-dinitrobenzene-treated THP-1 cells preincubated with N-acetyl cysteine, a glutathione precursor.	Acetylcysteine	166-183	GLI family zinc finger 2	Homo sapiens	136-141
19017541-4	2009	In this work, we hypothesize that cadmium exposure induces oxidative stress which leads to decreased RUNX2 mRNA expression and increased apoptotic death, and predict that the antioxidant NAC mitigates the damaging effects of cadmium.	Acetylcysteine	187-190	RUNX family transcription factor 2	Homo sapiens	101-106
19017541-8	2009	Pretreatment with the antioxidant NAC (1mM) prevented cadmium-induced decrease in RUNX2 mRNA and protected cells from apoptotic death.	Acetylcysteine	34-37	RUNX family transcription factor 2	Homo sapiens	82-87
18805632-5	2009	ROS activated almost immediately in a time- and concentration-dependent manner the MAPK pathways p38, ERK and JNK (their activation was abrogated by the antioxidant N-acetylcysteine).	Acetylcysteine	165-181	mitogen-activated protein kinase 1	Homo sapiens	83-87
19272177-7	2009	RESULTS: Exposure of human umbilical vein endothelial cells (HUVECs) to laminar shear stress (12 dyne/cm2) induced Nrf2 nuclear translocation, which was inhibited by a phosphatidylinositol 3-kinase (PI3K) inhibitor, a protein kinase C (PKC) inhibitor, and an antioxidant agent N-acetyl cysteine (NAC), but not by other protein kinase inhibitors.	Acetylcysteine	279-294	NFE2 like bZIP transcription factor 2	Homo sapiens	115-119
19272177-7	2009	RESULTS: Exposure of human umbilical vein endothelial cells (HUVECs) to laminar shear stress (12 dyne/cm2) induced Nrf2 nuclear translocation, which was inhibited by a phosphatidylinositol 3-kinase (PI3K) inhibitor, a protein kinase C (PKC) inhibitor, and an antioxidant agent N-acetyl cysteine (NAC), but not by other protein kinase inhibitors.	Acetylcysteine	296-299	NFE2 like bZIP transcription factor 2	Homo sapiens	115-119
18805632-5	2009	ROS activated almost immediately in a time- and concentration-dependent manner the MAPK pathways p38, ERK and JNK (their activation was abrogated by the antioxidant N-acetylcysteine).	Acetylcysteine	165-181	mitogen-activated protein kinase 14	Homo sapiens	97-100
18805632-5	2009	ROS activated almost immediately in a time- and concentration-dependent manner the MAPK pathways p38, ERK and JNK (their activation was abrogated by the antioxidant N-acetylcysteine).	Acetylcysteine	165-181	mitogen-activated protein kinase 1	Homo sapiens	102-105
18805632-5	2009	ROS activated almost immediately in a time- and concentration-dependent manner the MAPK pathways p38, ERK and JNK (their activation was abrogated by the antioxidant N-acetylcysteine).	Acetylcysteine	165-181	mitogen-activated protein kinase 8	Homo sapiens	110-113
19372642-10	2009	Moreover, the enhanced expression of HSP72 induced by PDF exposure was also reversed by NAC.	Acetylcysteine	88-91	heat shock protein family A (Hsp70) member 1A	Homo sapiens	37-42
20140304-0	2009	Upregulation of liver inducible nitric oxide synthase following thyroid hormone preconditioning: suppression by N-acetylcysteine.	Acetylcysteine	112-128	nitric oxide synthase 2	Rattus norvegicus	22-53
18617679-5	2009	Pretreatment with N-acetylcysteine (NAC) or EUK-134, in a dose-dependent manner, attenuated PM-induced ROS production, COX-2 expression, and IL-6 release.	Acetylcysteine	18-34	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	119-124
18617679-5	2009	Pretreatment with N-acetylcysteine (NAC) or EUK-134, in a dose-dependent manner, attenuated PM-induced ROS production, COX-2 expression, and IL-6 release.	Acetylcysteine	18-34	interleukin 6	Homo sapiens	141-145
18617679-5	2009	Pretreatment with N-acetylcysteine (NAC) or EUK-134, in a dose-dependent manner, attenuated PM-induced ROS production, COX-2 expression, and IL-6 release.	Acetylcysteine	36-39	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	119-124
18617679-5	2009	Pretreatment with N-acetylcysteine (NAC) or EUK-134, in a dose-dependent manner, attenuated PM-induced ROS production, COX-2 expression, and IL-6 release.	Acetylcysteine	36-39	interleukin 6	Homo sapiens	141-145
18617679-8	2009	Furthermore, NAC or EUK-134 attenuated PM-induced activation of NF-kappaB; however, NAC or EUK-134 had no effect on phosphorylation of C/EBPbeta.	Acetylcysteine	13-16	nuclear factor kappa B subunit 1	Homo sapiens	64-73
18635816-10	2009	The reducing agent N-acetyl-cysteine decreases IL8 message and promoter H4 acetylation to non-CF levels, suggesting that oxidative stress contributes to IL8 expression in these models.	Acetylcysteine	19-36	C-X-C motif chemokine ligand 8	Homo sapiens	47-50
18635816-10	2009	The reducing agent N-acetyl-cysteine decreases IL8 message and promoter H4 acetylation to non-CF levels, suggesting that oxidative stress contributes to IL8 expression in these models.	Acetylcysteine	19-36	C-X-C motif chemokine ligand 8	Homo sapiens	153-156
19330623-5	2009	We observed that the vitamin C and chemical oxidant scavenger N-acetyl-cysteine have an inhibitory effect on the generation of ROS, the activation of MAP kinase pathways, and the MIP-2 gene expression in DNFB-treated RAW 264.7 cells.	Acetylcysteine	62-79	chemokine (C-X-C motif) ligand 2	Mus musculus	179-184
19106626-10	2009	Of note, co-incubation with agents that block reactive oxygen species (ROS) production (e.g., N-acetylcysteine) dramatically enhanced the ability of metformin to decrease HER2 expression.	Acetylcysteine	94-110	erb-b2 receptor tyrosine kinase 2	Homo sapiens	171-175
19118006-9	2009	In addition, TP53INP1 deficiency results in an antioxidant (N-acetylcysteine)-sensitive acceleration of cell proliferation.	Acetylcysteine	60-76	tumor protein p53 inducible nuclear protein 1	Homo sapiens	13-21
19050604-10	2009	Dx, administered before or after AP, and NAC reduced the leukocytosis induced by AP and blocked the ability of circulating monocytes to produce tumor necrosis factor-alpha and monocyte chemoattractant protein-1; however none of them significantly reduced the overexpression of intercellular cell adhesion molecule-1 found in monocytes 6 hrs after inducing AP.	Acetylcysteine	41-44	tumor necrosis factor	Rattus norvegicus	144-171
19127075-5	2009	Analysis of the signaling pathways responsible for RANTES production by Langerhans cells was performed by ELISA using N-acetyl-L-cysteine, SP600125, SB203580 and PD98059, which are specific inhibitors of NF-kappaB activation, JNK, p38 MAPK and ERK, respectively, and was finally confirmed by Western blot analysis.	Acetylcysteine	118-137	chemokine (C-C motif) ligand 5	Mus musculus	51-57
18849615-8	2009	Treatment with N-acetylcysteine reversed the augmented Gadd45a mRNA response and caused the suppressed IFN-gamma mRNA response to recover.	Acetylcysteine	15-31	interferon gamma	Homo sapiens	103-112
19127075-7	2009	Treatment with N-acetyl-L-cysteine inhibited all TLR agonist-induced RANTES production.	Acetylcysteine	15-34	chemokine (C-C motif) ligand 5	Mus musculus	69-75
19202565-6	2009	Scavenging of DADS-induced ROS by N-acetyl cysteine or reduced glutathione inhibited cell cycle arrest, apoptosis and p53 activation by DADS.	Acetylcysteine	34-51	tumor protein p53	Homo sapiens	118-121
18956976-4	2008	This effect was dependent on Cyp2e1 expression and alcohol-metabolized oxidative stress (OS), because the antioxidant N-acetylcysteine blocked this effect.	Acetylcysteine	118-134	cytochrome P450 family 2 subfamily E member 1	Homo sapiens	29-35
19009558-4	2009	N-Acetylcysteine (ROS scavenger) and BAPTA-AM (Ca(2+) chelator) abrogated p38 MAPK activation and upregulation of Fas and FasL expression, but restored phosphorylation of ERK.	Acetylcysteine	0-16	mitogen-activated protein kinase 14	Homo sapiens	74-77
19009558-4	2009	N-Acetylcysteine (ROS scavenger) and BAPTA-AM (Ca(2+) chelator) abrogated p38 MAPK activation and upregulation of Fas and FasL expression, but restored phosphorylation of ERK.	Acetylcysteine	0-16	mitogen-activated protein kinase 1	Homo sapiens	78-82
19009558-4	2009	N-Acetylcysteine (ROS scavenger) and BAPTA-AM (Ca(2+) chelator) abrogated p38 MAPK activation and upregulation of Fas and FasL expression, but restored phosphorylation of ERK.	Acetylcysteine	0-16	mitogen-activated protein kinase 1	Homo sapiens	171-174
19610261-10	2009	H2O2-triggered PS externalization and cleavage of caspase-3 were markedly inhibited by pretreatment with the mitochondrial ROS scavenger N-acetyl-L-cysteine.	Acetylcysteine	137-156	caspase 3	Homo sapiens	50-59
19012744-4	2009	Cytochrome c release, caspase 3 activation, and apoptosis induction were all inhibited by the antioxidant N-acetylcysteine.	Acetylcysteine	106-122	cytochrome c, somatic	Homo sapiens	0-12
19012744-4	2009	Cytochrome c release, caspase 3 activation, and apoptosis induction were all inhibited by the antioxidant N-acetylcysteine.	Acetylcysteine	106-122	caspase 3	Homo sapiens	22-31
19093729-7	2009	NAC significantly elevated the level of GSH (+33%), EPO (+26%), Hb (+9%) and Hct (+9%) compared with C(NAC).	Acetylcysteine	0-3	erythropoietin	Homo sapiens	52-55
18976633-6	2008	The radical scavenger N-acetyl-l-cysteine profoundly inhibited pkr induction via the reduction of IFN-gamma expression.	Acetylcysteine	22-41	interferon gamma	Homo sapiens	98-107
18840412-6	2008	Pretreatment with antioxidant N-acetyl-l-cysteine (NAC) prevented glibenclamide-induced JNK activation, apoptosis and cellular viability decline.	Acetylcysteine	30-49	mitogen-activated protein kinase 8	Homo sapiens	88-91
19548360-5	2008	The increases in reactive species and HO-1 protein are inhibited by agonists of glucocorticoid receptors (GR), such as RU28362, prednisolone, and dexamethasone, as well as by N-acetyl-L-cysteine and SB203580 (a p38 inhibitor), suggesting a role of GR in NF-induced increases in reactive species and HO-1.	Acetylcysteine	175-194	mitogen-activated protein kinase 14	Homo sapiens	211-214
18713279-6	2008	RESULTS: N-acetylcysteine treatment significantly improved liver function parameters including the plasma levels of aspartate aminotransferase, alkaline phosphatase, gamma-glutamyl transpeptidase and bilirubin.	Acetylcysteine	9-25	glutamic-oxaloacetic transaminase 2	Rattus norvegicus	116-142
19087113-11	2008	In Unverricht-Lundborg PME, new cohorts with genotyped cystatin B mutations have led to the chronic use of antioxidant N-acetylcysteine and combination valproate clobazam or clonazepam plus antimyoclonic drugs topiramate, zonisamide, piracetam, levetiracetam, or brivaracetam.	Acetylcysteine	119-135	cystatin B	Homo sapiens	55-65
18790835-4	2008	The presence of the antioxidant N-acetylcysteine reduced I/R-induced homodimerization of Bnip3.	Acetylcysteine	32-48	BCL2 interacting protein 3	Homo sapiens	89-94
19008713-8	2008	The specific extracellular signal-regulated kinase (ERK) inhibitor PD98059, antioxidant N-acetylcysteine, and ERK siRNA attenuated the induction of resistin protein by hypoxia.	Acetylcysteine	88-104	resistin	Rattus norvegicus	148-156
19008713-9	2008	It increased the phosphorylated ERK protein expression (3.2-fold, P &lt; 0.001), whereas pretreatment with PD98059 and N-acetylcysteine significantly blocked the increase of phosphorylated ERK by hypoxia.	Acetylcysteine	119-135	Eph receptor B1	Rattus norvegicus	32-35
19008713-9	2008	It increased the phosphorylated ERK protein expression (3.2-fold, P &lt; 0.001), whereas pretreatment with PD98059 and N-acetylcysteine significantly blocked the increase of phosphorylated ERK by hypoxia.	Acetylcysteine	119-135	Eph receptor B1	Rattus norvegicus	189-192
19008713-12	2008	Pretreatment with PD98059 and N-acetylcysteine significantly attenuated the resistin promoter activity induced by hypoxia.	Acetylcysteine	30-46	resistin	Rattus norvegicus	76-84
18954524-7	2008	The ability of both N-acetylcysteine and apocynin (1-[4-hydroxy-3-methoxyphenyl]ethanone, a NADPH oxidase inhibitor) to inhibit uric acid-induced ET-1 secretion and cell proliferation suggested the involvement of intracellular redox pathways.	Acetylcysteine	20-36	endothelin 1	Homo sapiens	146-150
19059111-9	2008	By the use of NAC, VE-cadherin expression remained comparable with control, according to both immunocytochemistry and western blot analysis.	Acetylcysteine	14-17	cadherin 5	Homo sapiens	19-30
18690414-8	2008	Cotreatment with gamma-GCS inhibitor, buthionine sulfoximine (BSO), accelerated, whereas GSH precursor, N-acetylcysteine (NAC), attenuated leptin-induced changes in gamma-GCS, SOD, and GPx.	Acetylcysteine	122-125	glutamate-cysteine ligase, catalytic subunit	Rattus norvegicus	165-174
18313257-5	2008	The quenching of ROS generation with antioxidant N-acetyl-L-cysteine conferred significant protection against sulforaphane-elicited ROS generation, disruption of the MMP, caspase-3 activation and apoptosis.	Acetylcysteine	49-68	caspase 3	Homo sapiens	171-180
18980980-8	2008	The quenching of ROS generation with antioxidant N-acetyl-L-cysteine conferred significant protection against sulforaphane-induced ROS generation, mitochondrial membrane potential disruption, caspase-3 activation, and apoptosis.	Acetylcysteine	49-68	caspase 3	Homo sapiens	192-201
19010165-0	2008	Effect of N-acetylcysteine administration on intraoperative plasma levels of interleukin-4 and interleukin-10 in liver transplant recipients.	Acetylcysteine	10-26	interleukin 4	Homo sapiens	77-90
18928848-3	2008	In addition, treatment with N-acetylcysteine, indomethacin, and heme oxygenase-1 inhibitors blocked reactive oxygen species production, antioxidant response element (ARE) gene expression, and Nrf2 accumulation that occurred in response to mechanical stress.	Acetylcysteine	28-44	NFE2 like bZIP transcription factor 2	Homo sapiens	192-196
18941206-9	2008	NAC blocked the activation of JNK and down-regulation of ERK, but both z-VAD-fmk (N-benzyloxycarbonyl-Val-Ala-Asp-fluoromethylketone) and ZB4 did not inhibit JNK activation of B7-H1 stimulation.	Acetylcysteine	0-3	mitogen-activated protein kinase 1	Mus musculus	57-60
18941206-9	2008	NAC blocked the activation of JNK and down-regulation of ERK, but both z-VAD-fmk (N-benzyloxycarbonyl-Val-Ala-Asp-fluoromethylketone) and ZB4 did not inhibit JNK activation of B7-H1 stimulation.	Acetylcysteine	0-3	CD274 antigen	Mus musculus	176-181
19047834-6	2008	The quenching of ROS generation by N-acetyl-L-cysteine administration, a scavenger of ROS, reversed the streptochlorin-induced apoptosis effects via inhibition of ROS production, MMP collapse, and the subsequent activation of caspase-3.	Acetylcysteine	35-54	caspase 3	Homo sapiens	226-235
18568337-8	2008	We report here that the increase of DCFH oxidation might be due to the increase in the release of cytochrome C caused by warfarin, as cytosolic cytochrome C content was significantly elevated in the warfarin-treated cells compared with control cells, and because cotreatment with antioxidants N- acetylcysteine or 4,5-dihydroxy-1,3-benzene-disulfonic acid (Tiron) was unable to prevent cytochrome C release and DCFH oxidation induced by the drug.	Acetylcysteine	293-310	cytochrome c, somatic	Homo sapiens	98-110
18568337-8	2008	We report here that the increase of DCFH oxidation might be due to the increase in the release of cytochrome C caused by warfarin, as cytosolic cytochrome C content was significantly elevated in the warfarin-treated cells compared with control cells, and because cotreatment with antioxidants N- acetylcysteine or 4,5-dihydroxy-1,3-benzene-disulfonic acid (Tiron) was unable to prevent cytochrome C release and DCFH oxidation induced by the drug.	Acetylcysteine	293-310	cytochrome c, somatic	Homo sapiens	144-156
18568337-8	2008	We report here that the increase of DCFH oxidation might be due to the increase in the release of cytochrome C caused by warfarin, as cytosolic cytochrome C content was significantly elevated in the warfarin-treated cells compared with control cells, and because cotreatment with antioxidants N- acetylcysteine or 4,5-dihydroxy-1,3-benzene-disulfonic acid (Tiron) was unable to prevent cytochrome C release and DCFH oxidation induced by the drug.	Acetylcysteine	293-310	cytochrome c, somatic	Homo sapiens	144-156
19010165-6	2008	Plasma IL-4 levels were significantly higher among the NAC-treated group than the placebo group at I-3 (P = .046) and I-4 (P = .041).	Acetylcysteine	55-58	interleukin 4	Homo sapiens	7-11
19010165-8	2008	We concluded that intraoperative NAC administration during the anhepatic phase of liver transplantation significantly increased recipient IL-4 plasma levels before and after reperfusion, and IL-10 plasma values before reperfusion (I-3).	Acetylcysteine	33-36	interleukin 4	Homo sapiens	138-142
18847491-12	2008	Moreover, NAC or U0126 pretreatment significantly attenuated Triphala-induced p53 transcriptional activity.	Acetylcysteine	10-13	tumor protein p53	Homo sapiens	78-81
18718914-8	2008	Pretreatment with antioxidant N-acetylcysteine prevented the p53 accumulation, the phosphorylations of JNK and p38 MAPK, the inhibition of NF-kappaB activity, as well as the apoptosis induced by 15d-PGJ(2).	Acetylcysteine	30-46	tumor protein p53	Homo sapiens	61-64
18718914-8	2008	Pretreatment with antioxidant N-acetylcysteine prevented the p53 accumulation, the phosphorylations of JNK and p38 MAPK, the inhibition of NF-kappaB activity, as well as the apoptosis induced by 15d-PGJ(2).	Acetylcysteine	30-46	mitogen-activated protein kinase 8	Homo sapiens	103-106
18718914-8	2008	Pretreatment with antioxidant N-acetylcysteine prevented the p53 accumulation, the phosphorylations of JNK and p38 MAPK, the inhibition of NF-kappaB activity, as well as the apoptosis induced by 15d-PGJ(2).	Acetylcysteine	30-46	mitogen-activated protein kinase 14	Homo sapiens	111-114
18772130-5	2008	The antioxidant agents, including catalase and N-acetyl-L-cysteine, could inhibit cardiomyocyte hypertrophy induced by insulin, suggesting that ROS is necessary for insulin to induce hypertrophy.	Acetylcysteine	47-66	insulin	Homo sapiens	119-126
18772130-5	2008	The antioxidant agents, including catalase and N-acetyl-L-cysteine, could inhibit cardiomyocyte hypertrophy induced by insulin, suggesting that ROS is necessary for insulin to induce hypertrophy.	Acetylcysteine	47-66	insulin	Homo sapiens	165-172
18625331-6	2008	Meanwhile more primary CD34(+)CD38(-) cells were obtained when cultivation was performed under hypoxia or with N-acetyl cysteine (the precursor of GSH) under normoxia.	Acetylcysteine	111-128	CD34 molecule	Homo sapiens	23-27
18599801-11	2008	Pretreatment with the nonspecific antioxidant N-acetylcysteine and the Rho kinase inhibitors (Fasudil and Y-27632) prevented MLC and MYPT-1 phosphorylation by UFP suggesting a O(2)(.-)-mediated mechanism for PM(2.5) and UFP effects.	Acetylcysteine	46-62	modulator of VRAC current 1	Homo sapiens	125-128
18542053-3	2008	Both N-acetylcysteine and glutathione (GSH) supplementation ablated the DNA lesions and DNA damage-response pathways in Nrf2(-/-) cells; however only GSH could rescue the impaired colocalization of mitosis-promoting factors and the growth arrest.	Acetylcysteine	5-21	NFE2 like bZIP transcription factor 2	Homo sapiens	120-124
18829485-8	2008	The induction of many of these genes with SOD2 knockdown, such as VEGFA and FKBP5, is reversible with the antioxidant N-acetylcysteine, suggesting that this mechanism is directly linked to ROS.	Acetylcysteine	118-134	vascular endothelial growth factor A	Homo sapiens	66-71
18829485-8	2008	The induction of many of these genes with SOD2 knockdown, such as VEGFA and FKBP5, is reversible with the antioxidant N-acetylcysteine, suggesting that this mechanism is directly linked to ROS.	Acetylcysteine	118-134	FKBP prolyl isomerase 5	Homo sapiens	76-81
18806095-7	2008	NAC attenuated increased hepatic oxidative stress (TBARS; P &lt;/= 0.05) and prevented increases in cytochrome P450 2E1 apoprotein and mRNA and in tumor necrosis factor-alpha (TNFalpha) mRNA.	Acetylcysteine	0-3	tumor necrosis factor	Rattus norvegicus	147-174
18599524-8	2008	The antioxidant N-acetylcysteine significantly inhibited ROS generation, Akt/protein kinase B, and tuberin phosphorylation and resulted in deceased 8-oxodG accumulation and upregulation of OGG1 protein expression.	Acetylcysteine	16-32	AKT serine/threonine kinase 1	Rattus norvegicus	73-76
18802057-9	2008	In contrast to Nrf2(+/+) DCs, coincubation of Nrf2(-/-) DCs with PM and the antioxidant N-acetyl cysteine attenuated PM-induced up-regulation of CD80 and CD86.	Acetylcysteine	88-105	NFE2 like bZIP transcription factor 2	Homo sapiens	46-50
18806095-7	2008	NAC attenuated increased hepatic oxidative stress (TBARS; P &lt;/= 0.05) and prevented increases in cytochrome P450 2E1 apoprotein and mRNA and in tumor necrosis factor-alpha (TNFalpha) mRNA.	Acetylcysteine	0-3	tumor necrosis factor	Rattus norvegicus	176-184
18806095-11	2008	Using NAC in a TEN model of NASH, we have demonstrated that NAC prevents many aspects of NASH progression by decreasing development of oxidative stress and subsequent increases in TNFalpha but does not block development of steatosis.	Acetylcysteine	60-63	tumor necrosis factor	Rattus norvegicus	180-188
18710947-7	2008	SPC recruitment and protein changes were inhibited by siRNA specific to lactate dehydrogenase, TrxR, or HIF-1 and by oxamate, apocynin, U0126, N-acetylcysteine, dithioerythritol, and antibodies to VEGF or SDF-1.	Acetylcysteine	143-159	sparse coat	Mus musculus	0-3
18671962-6	2008	Urotensin II-increased cell proliferation and intracellular reactive oxygen species levels which were inhibited by antioxidants N-acetylcysteine, and the flavin inhibitor diphenyleneiodonium.	Acetylcysteine	128-144	urotensin 2	Rattus norvegicus	0-12
18657320-7	2008	Moreover, both the DNA-binding activity and phosphorylation induced by NAC were reduced by the overexpression of a dominant negative Akt in HeLa cells.	Acetylcysteine	71-74	AKT serine/threonine kinase 1	Homo sapiens	133-136
18512759-1	2008	Although previous studies have indicated that the neuroprotective effect of N-acetylcysteine (NAC) required activation of the Ras-extracellular-signal-regulated kinase (ERK) pathway, the detailed mechanisms and signal cascades leading to activation ERK are not clear.	Acetylcysteine	76-92	mitogen-activated protein kinase 1	Homo sapiens	126-167
18512759-1	2008	Although previous studies have indicated that the neuroprotective effect of N-acetylcysteine (NAC) required activation of the Ras-extracellular-signal-regulated kinase (ERK) pathway, the detailed mechanisms and signal cascades leading to activation ERK are not clear.	Acetylcysteine	76-92	mitogen-activated protein kinase 1	Homo sapiens	169-172
18512759-1	2008	Although previous studies have indicated that the neuroprotective effect of N-acetylcysteine (NAC) required activation of the Ras-extracellular-signal-regulated kinase (ERK) pathway, the detailed mechanisms and signal cascades leading to activation ERK are not clear.	Acetylcysteine	76-92	mitogen-activated protein kinase 1	Homo sapiens	249-252
18512759-1	2008	Although previous studies have indicated that the neuroprotective effect of N-acetylcysteine (NAC) required activation of the Ras-extracellular-signal-regulated kinase (ERK) pathway, the detailed mechanisms and signal cascades leading to activation ERK are not clear.	Acetylcysteine	94-97	mitogen-activated protein kinase 1	Homo sapiens	126-167
18512759-1	2008	Although previous studies have indicated that the neuroprotective effect of N-acetylcysteine (NAC) required activation of the Ras-extracellular-signal-regulated kinase (ERK) pathway, the detailed mechanisms and signal cascades leading to activation ERK are not clear.	Acetylcysteine	94-97	mitogen-activated protein kinase 1	Homo sapiens	169-172
18512759-1	2008	Although previous studies have indicated that the neuroprotective effect of N-acetylcysteine (NAC) required activation of the Ras-extracellular-signal-regulated kinase (ERK) pathway, the detailed mechanisms and signal cascades leading to activation ERK are not clear.	Acetylcysteine	94-97	mitogen-activated protein kinase 1	Homo sapiens	249-252
18512759-2	2008	In the present study, we investigated the effect of NAC on A beta(25-35)-induced neuronal death.	Acetylcysteine	52-55	amyloid beta precursor protein	Homo sapiens	59-65
18512759-7	2008	A beta(25-35) caused a significant decrease in the level of p35, with a concomitant increase in p25, which was completely prevented by NAC.	Acetylcysteine	135-138	amyloid beta precursor protein	Homo sapiens	0-6
18512759-10	2008	A beta(25-35) treatment decreased phosphorylated levels of ERK, which could be reversed by NAC.	Acetylcysteine	91-94	amyloid beta precursor protein	Homo sapiens	0-6
18512759-10	2008	A beta(25-35) treatment decreased phosphorylated levels of ERK, which could be reversed by NAC.	Acetylcysteine	91-94	mitogen-activated protein kinase 1	Homo sapiens	59-62
18512759-12	2008	NAC reversed the A beta(25-35)-induced decrease in the expression of Bcl-2, which could be blocked by the MAPK kinase (MEK) inhibitor or Cdk5 inhibitors.	Acetylcysteine	0-3	amyloid beta precursor protein	Homo sapiens	17-23
18512759-12	2008	NAC reversed the A beta(25-35)-induced decrease in the expression of Bcl-2, which could be blocked by the MAPK kinase (MEK) inhibitor or Cdk5 inhibitors.	Acetylcysteine	0-3	BCL2 apoptosis regulator	Homo sapiens	69-74
18512759-12	2008	NAC reversed the A beta(25-35)-induced decrease in the expression of Bcl-2, which could be blocked by the MAPK kinase (MEK) inhibitor or Cdk5 inhibitors.	Acetylcysteine	0-3	mitogen-activated protein kinase kinase 7	Homo sapiens	119-122
18512759-13	2008	These results suggest that NAC-mediated neuroprotection against A beta toxicity is likely mediated by the p35/Cdk5-ERKs-Bcl-2 signal pathway.	Acetylcysteine	27-30	amyloid beta precursor protein	Homo sapiens	64-70
18512759-13	2008	These results suggest that NAC-mediated neuroprotection against A beta toxicity is likely mediated by the p35/Cdk5-ERKs-Bcl-2 signal pathway.	Acetylcysteine	27-30	mitogen-activated protein kinase 1	Homo sapiens	115-119
18512759-13	2008	These results suggest that NAC-mediated neuroprotection against A beta toxicity is likely mediated by the p35/Cdk5-ERKs-Bcl-2 signal pathway.	Acetylcysteine	27-30	BCL2 apoptosis regulator	Homo sapiens	120-125
18541003-10	2008	PDTC and NAC inhibited NF-kappaB activation during monocyte interaction with collagen I.	Acetylcysteine	9-12	nuclear factor kappa B subunit 1	Homo sapiens	23-32
18590811-6	2008	Furthermore, comicroinjection of either NAC or PDTC with LPS was also able to suppress LPS-stimulated expression of CD11b in striatum in vivo.	Acetylcysteine	40-43	integrin alpha M	Mus musculus	116-121
18546268-7	2008	However, it elicited N-acetyl-L-cysteine-inhibitable phosphorylation of p38-MAPK and AMPK, and apoptosis was attenuated by pharmacologic inhibitors against these kinases.	Acetylcysteine	21-40	mitogen-activated protein kinase 14	Homo sapiens	72-75
19160131-8	2008	TNF-alpha and IL-6 levels were significantly elevated in the control group and decreased in the NAC and beta GLU groups.	Acetylcysteine	96-99	tumor necrosis factor	Rattus norvegicus	0-9
19160131-8	2008	TNF-alpha and IL-6 levels were significantly elevated in the control group and decreased in the NAC and beta GLU groups.	Acetylcysteine	96-99	interleukin 6	Rattus norvegicus	14-18
19160131-10	2008	Superoxide dismutase and catalase levels in the liver tissue were significantly increased in the NAC and beta GLU groups, whereas superoxide dismutase levels were higher in the beta GLU pretreatment group than the NAC pretreatment group (p &lt; 0.05).	Acetylcysteine	97-100	catalase	Rattus norvegicus	25-33
18657320-0	2008	DNA-binding activity of NF-kappaB and phosphorylation of p65 are induced by N-acetylcysteine through phosphatidylinositol (PI) 3-kinase.	Acetylcysteine	76-92	nuclear factor kappa B subunit 1	Homo sapiens	24-33
18657320-1	2008	N-Acetylcysteine (NAC) has been widely used as an antioxidant in research, however, it has also been found to reduce the binding of TNF to its receptor independent of its antioxidative role.	Acetylcysteine	0-16	tumor necrosis factor	Homo sapiens	132-135
18657320-1	2008	N-Acetylcysteine (NAC) has been widely used as an antioxidant in research, however, it has also been found to reduce the binding of TNF to its receptor independent of its antioxidative role.	Acetylcysteine	18-21	tumor necrosis factor	Homo sapiens	132-135
18657320-2	2008	In this study, we investigated the effect of NAC on NF-kappaB activation.	Acetylcysteine	45-48	nuclear factor kappa B subunit 1	Homo sapiens	52-61
18657320-3	2008	In HeLa cells, Hep3B cells, and A549 cells, DNA-binding activity of NF-kappaB was induced by NAC without any other stimulation but not by tetramethylthiourea (TMTU) or vitamin C, suggesting that ROS is not involved in the effect of NAC.	Acetylcysteine	93-96	nuclear factor kappa B subunit 1	Homo sapiens	68-77
18657320-3	2008	In HeLa cells, Hep3B cells, and A549 cells, DNA-binding activity of NF-kappaB was induced by NAC without any other stimulation but not by tetramethylthiourea (TMTU) or vitamin C, suggesting that ROS is not involved in the effect of NAC.	Acetylcysteine	232-235	nuclear factor kappa B subunit 1	Homo sapiens	68-77
18657320-5	2008	The phosphorylation of p65 at serine 536 was induced by NAC, which is known to contribute to the enhancement of DNA-binding activity of NF-kappaB, however, NAC did not directly phosphorylate p65.	Acetylcysteine	56-59	nuclear factor kappa B subunit 1	Homo sapiens	136-145
18657320-5	2008	The phosphorylation of p65 at serine 536 was induced by NAC, which is known to contribute to the enhancement of DNA-binding activity of NF-kappaB, however, NAC did not directly phosphorylate p65.	Acetylcysteine	156-159	nuclear factor kappa B subunit 1	Homo sapiens	136-145
18657320-6	2008	The NAC-induced DNA-binding activity of NF-kappaB and phosphorylation of p65 were sensitive to a phosphatidylinositol (PI) 3-kinase inhibitor, partially sensitive to an IkappaB kinase (IKK) inhibitor, but not sensitive to a Bruton"s tyrosine kinase (Btk) inhibitor.	Acetylcysteine	4-7	nuclear factor kappa B subunit 1	Homo sapiens	40-49
18657320-8	2008	These results suggest that NAC activates mainly PI3K to phosphorylate p65 and subsequently induces DNA-binding activity of NF-kappaB, independent of its antioxidative function.	Acetylcysteine	27-30	nuclear factor kappa B subunit 1	Homo sapiens	123-132
18463198-7	2008	Subsequent experiments demonstrated that preincubation of 3-OHCBZ with human liver microsomes or recombinant CYP3A4 led to decreased CYP3A4 activity, which was both preincubation time- and concentration-dependent, but not inhibited by inclusion of glutathione or N-acetylcysteine.	Acetylcysteine	263-279	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	109-115
18684975-5	2008	Mechanistically, CNI cause a rapid activation of latent TGFbeta, which is prevented in the presence of the antioxidant N-acetyl cysteine.	Acetylcysteine	119-136	transforming growth factor, beta 1	Rattus norvegicus	56-63
18676857-6	2008	Incubation of cells with a reactive oxygen species (ROS) scavenger, N-acetyl cysteine, partially restored kinase activity and also partially prevented BRAF(V600E) degradation due to 17-DMAG treatment.	Acetylcysteine	68-85	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	151-156
18275839-7	2008	N-Acetylcysteine and alpha-lipoic acid inhibited TNFalpha-induced oxidant increase but did not affect NF-kappaB activation.	Acetylcysteine	0-16	tumor necrosis factor	Homo sapiens	49-57
18463198-7	2008	Subsequent experiments demonstrated that preincubation of 3-OHCBZ with human liver microsomes or recombinant CYP3A4 led to decreased CYP3A4 activity, which was both preincubation time- and concentration-dependent, but not inhibited by inclusion of glutathione or N-acetylcysteine.	Acetylcysteine	263-279	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	133-139
18155508-6	2008	The effects of cyclosporine A and N-acetyl cysteine suggest the involvement of mPTP and intracellular GSH level in the cytotoxicity.	Acetylcysteine	34-51	protein tyrosine phosphatase, receptor type, U	Mus musculus	79-83
18687213-2	2008	METHODS: The levels of reactive oxygen species (ROS) in cord blood CD34(+) cells were reduced by superoxide dismutase (SOD), catalase (CAT) or N-acetylcysteine (NAC) in ex vivo expansion.	Acetylcysteine	143-159	CD34 molecule	Homo sapiens	67-71
18719315-3	2008	Moreover, the ROS activated the p38 kinase, which in turn promoted the activation of p53, as verified by evidence showing that the ROS scavenger N-acetyl-cysteine (NAC) not only blocked the phosphorylation of p38 but also partially inhibited the activation of p53, and the p38 inhibitor SB203580 reduced the activation of p53 as well.	Acetylcysteine	145-162	mitogen-activated protein kinase 14	Homo sapiens	32-35
18719315-3	2008	Moreover, the ROS activated the p38 kinase, which in turn promoted the activation of p53, as verified by evidence showing that the ROS scavenger N-acetyl-cysteine (NAC) not only blocked the phosphorylation of p38 but also partially inhibited the activation of p53, and the p38 inhibitor SB203580 reduced the activation of p53 as well.	Acetylcysteine	145-162	tumor protein p53	Homo sapiens	85-88
18719315-3	2008	Moreover, the ROS activated the p38 kinase, which in turn promoted the activation of p53, as verified by evidence showing that the ROS scavenger N-acetyl-cysteine (NAC) not only blocked the phosphorylation of p38 but also partially inhibited the activation of p53, and the p38 inhibitor SB203580 reduced the activation of p53 as well.	Acetylcysteine	145-162	mitogen-activated protein kinase 14	Homo sapiens	209-212
18719315-3	2008	Moreover, the ROS activated the p38 kinase, which in turn promoted the activation of p53, as verified by evidence showing that the ROS scavenger N-acetyl-cysteine (NAC) not only blocked the phosphorylation of p38 but also partially inhibited the activation of p53, and the p38 inhibitor SB203580 reduced the activation of p53 as well.	Acetylcysteine	145-162	tumor protein p53	Homo sapiens	260-263
18719315-3	2008	Moreover, the ROS activated the p38 kinase, which in turn promoted the activation of p53, as verified by evidence showing that the ROS scavenger N-acetyl-cysteine (NAC) not only blocked the phosphorylation of p38 but also partially inhibited the activation of p53, and the p38 inhibitor SB203580 reduced the activation of p53 as well.	Acetylcysteine	145-162	mitogen-activated protein kinase 14	Homo sapiens	209-212
18719315-3	2008	Moreover, the ROS activated the p38 kinase, which in turn promoted the activation of p53, as verified by evidence showing that the ROS scavenger N-acetyl-cysteine (NAC) not only blocked the phosphorylation of p38 but also partially inhibited the activation of p53, and the p38 inhibitor SB203580 reduced the activation of p53 as well.	Acetylcysteine	145-162	tumor protein p53	Homo sapiens	260-263
18719315-3	2008	Moreover, the ROS activated the p38 kinase, which in turn promoted the activation of p53, as verified by evidence showing that the ROS scavenger N-acetyl-cysteine (NAC) not only blocked the phosphorylation of p38 but also partially inhibited the activation of p53, and the p38 inhibitor SB203580 reduced the activation of p53 as well.	Acetylcysteine	164-167	mitogen-activated protein kinase 14	Homo sapiens	32-35
18719315-3	2008	Moreover, the ROS activated the p38 kinase, which in turn promoted the activation of p53, as verified by evidence showing that the ROS scavenger N-acetyl-cysteine (NAC) not only blocked the phosphorylation of p38 but also partially inhibited the activation of p53, and the p38 inhibitor SB203580 reduced the activation of p53 as well.	Acetylcysteine	164-167	tumor protein p53	Homo sapiens	85-88
18719315-3	2008	Moreover, the ROS activated the p38 kinase, which in turn promoted the activation of p53, as verified by evidence showing that the ROS scavenger N-acetyl-cysteine (NAC) not only blocked the phosphorylation of p38 but also partially inhibited the activation of p53, and the p38 inhibitor SB203580 reduced the activation of p53 as well.	Acetylcysteine	164-167	mitogen-activated protein kinase 14	Homo sapiens	209-212
18719315-3	2008	Moreover, the ROS activated the p38 kinase, which in turn promoted the activation of p53, as verified by evidence showing that the ROS scavenger N-acetyl-cysteine (NAC) not only blocked the phosphorylation of p38 but also partially inhibited the activation of p53, and the p38 inhibitor SB203580 reduced the activation of p53 as well.	Acetylcysteine	164-167	tumor protein p53	Homo sapiens	260-263
18719315-3	2008	Moreover, the ROS activated the p38 kinase, which in turn promoted the activation of p53, as verified by evidence showing that the ROS scavenger N-acetyl-cysteine (NAC) not only blocked the phosphorylation of p38 but also partially inhibited the activation of p53, and the p38 inhibitor SB203580 reduced the activation of p53 as well.	Acetylcysteine	164-167	mitogen-activated protein kinase 14	Homo sapiens	209-212
18719315-3	2008	Moreover, the ROS activated the p38 kinase, which in turn promoted the activation of p53, as verified by evidence showing that the ROS scavenger N-acetyl-cysteine (NAC) not only blocked the phosphorylation of p38 but also partially inhibited the activation of p53, and the p38 inhibitor SB203580 reduced the activation of p53 as well.	Acetylcysteine	164-167	tumor protein p53	Homo sapiens	260-263
18719315-5	2008	This study showed that oridonin stimulated mitochondrial transmembrane permeabilization in a ROS-dependent manner because NAC almost thoroughly reversed the drop of mitochondrial transmembrane potential (Deltapsim) and the release of cytochrome c from the mitochondrial inter-membrane space into cytosol.	Acetylcysteine	122-125	cytochrome c, somatic	Homo sapiens	234-246
18480072-8	2008	Both NAC and Bay 117085 prevented the enhancement in COX-2 expression and PGE2 secretion by the cotreatment of E(2) and OHE(2) in BEAS-2B cells.	Acetylcysteine	5-8	prostaglandin-endoperoxide synthase 2	Homo sapiens	53-58
18687213-2	2008	METHODS: The levels of reactive oxygen species (ROS) in cord blood CD34(+) cells were reduced by superoxide dismutase (SOD), catalase (CAT) or N-acetylcysteine (NAC) in ex vivo expansion.	Acetylcysteine	161-164	CD34 molecule	Homo sapiens	67-71
18486599-5	2008	TNFalpha production induced by LPS stimulation was greatly suppressed by N-acetyl-L-cysteine.	Acetylcysteine	73-92	tumor necrosis factor	Mus musculus	0-8
18547707-11	2008	The antioxidant N-acetyl-cysteine (NAC) could prevent Bax mRNA increase and caspase 3 activation, confirming that Cr (VI)-induced apoptosis involves oxidative stress generation.	Acetylcysteine	16-33	BCL2 associated X, apoptosis regulator	Homo sapiens	54-57
18547707-11	2008	The antioxidant N-acetyl-cysteine (NAC) could prevent Bax mRNA increase and caspase 3 activation, confirming that Cr (VI)-induced apoptosis involves oxidative stress generation.	Acetylcysteine	16-33	caspase 3	Homo sapiens	76-85
18547707-11	2008	The antioxidant N-acetyl-cysteine (NAC) could prevent Bax mRNA increase and caspase 3 activation, confirming that Cr (VI)-induced apoptosis involves oxidative stress generation.	Acetylcysteine	35-38	BCL2 associated X, apoptosis regulator	Homo sapiens	54-57
18547707-11	2008	The antioxidant N-acetyl-cysteine (NAC) could prevent Bax mRNA increase and caspase 3 activation, confirming that Cr (VI)-induced apoptosis involves oxidative stress generation.	Acetylcysteine	35-38	caspase 3	Homo sapiens	76-85
18555989-0	2008	Blockade of sensory abnormalities and kinin B(1) receptor expression by N-acetyl-L-cysteine and ramipril in a rat model of insulin resistance.	Acetylcysteine	72-91	bradykinin receptor B1	Rattus norvegicus	38-57
18558410-9	2008	The induction of PlGF protein by HBO was significantly blocked by the addition of N-acetylcysteine, while wortmannin, PD98059, SP600125 and SB203580 had no effect on PlGF protein expression.	Acetylcysteine	82-98	placental growth factor	Homo sapiens	17-21
18579320-7	2008	oxLDL (35 microg/ml) significantly enhanced ERK phosphorylation, ROS generation, AP-1 activity, mRNA expression, secretion and promoter activity of ET-1 in HUVECs, all of which were abrogated by alpha-ZAL and the antioxidant N-acetyl-l-cysteine.	Acetylcysteine	225-244	endothelin 1	Homo sapiens	148-152
18535259-5	2008	The induction of GCLM and NQO1 was attenuated by reduction of electrophilic groups with sodium borohydrate, as well as treatment with thiol antioxidant N-acetylcysteine, suggesting that the thiol reactivity of oxPAPC is largely mediating its effect on Nrf2-responsive genes.	Acetylcysteine	152-168	nuclear factor, erythroid derived 2, like 2	Mus musculus	252-256
18652771-4	2008	Administration of C1-INH + factor XIII and NAC + TM both resulted in reduced leucocyte adherence and reduced levels of interleukin-1beta (IL-1beta).	Acetylcysteine	43-46	interleukin 1 beta	Rattus norvegicus	119-136
18443432-4	2008	Kaempferol treatment was shown to profoundly induce the generation of fluorescent DCF in the MCF-7 cells, and treatment with N-acetyl cysteine suppressed kaempferol-induced PARP cleavage.	Acetylcysteine	125-142	poly(ADP-ribose) polymerase 1	Homo sapiens	173-177
18270969-5	2008	Interestingly, post-TPA-treatment with N-acetylcysteine (NAC) stimulated a marked and a rapid dephosphorylation of Erk1/2, suggesting a regeneration of Erk1/2-directed phospahatase activity by NAC.	Acetylcysteine	39-55	mitogen-activated protein kinase 3	Homo sapiens	115-121
18270969-5	2008	Interestingly, post-TPA-treatment with N-acetylcysteine (NAC) stimulated a marked and a rapid dephosphorylation of Erk1/2, suggesting a regeneration of Erk1/2-directed phospahatase activity by NAC.	Acetylcysteine	39-55	mitogen-activated protein kinase 3	Homo sapiens	152-158
18270969-5	2008	Interestingly, post-TPA-treatment with N-acetylcysteine (NAC) stimulated a marked and a rapid dephosphorylation of Erk1/2, suggesting a regeneration of Erk1/2-directed phospahatase activity by NAC.	Acetylcysteine	57-60	mitogen-activated protein kinase 3	Homo sapiens	115-121
18270969-5	2008	Interestingly, post-TPA-treatment with N-acetylcysteine (NAC) stimulated a marked and a rapid dephosphorylation of Erk1/2, suggesting a regeneration of Erk1/2-directed phospahatase activity by NAC.	Acetylcysteine	57-60	mitogen-activated protein kinase 3	Homo sapiens	152-158
18270969-5	2008	Interestingly, post-TPA-treatment with N-acetylcysteine (NAC) stimulated a marked and a rapid dephosphorylation of Erk1/2, suggesting a regeneration of Erk1/2-directed phospahatase activity by NAC.	Acetylcysteine	193-196	mitogen-activated protein kinase 3	Homo sapiens	115-121
18270969-5	2008	Interestingly, post-TPA-treatment with N-acetylcysteine (NAC) stimulated a marked and a rapid dephosphorylation of Erk1/2, suggesting a regeneration of Erk1/2-directed phospahatase activity by NAC.	Acetylcysteine	193-196	mitogen-activated protein kinase 3	Homo sapiens	152-158
18652771-4	2008	Administration of C1-INH + factor XIII and NAC + TM both resulted in reduced leucocyte adherence and reduced levels of interleukin-1beta (IL-1beta).	Acetylcysteine	43-46	interleukin 1 beta	Rattus norvegicus	138-146
18652771-7	2008	In conclusion, the administration of C1-INH + factor XIII and NAC + TM reduced endothelial leucocyte adherence and IL-1beta plasma levels, but increased IL-6 levels.	Acetylcysteine	62-65	interleukin 1 beta	Rattus norvegicus	115-123
18652771-7	2008	In conclusion, the administration of C1-INH + factor XIII and NAC + TM reduced endothelial leucocyte adherence and IL-1beta plasma levels, but increased IL-6 levels.	Acetylcysteine	62-65	interleukin 6	Rattus norvegicus	153-157
18645026-7	2008	Pretreatment with an antioxidant (N-acetylcysteine) or a c-Jun NH(2)-terminal kinase inhibitor (SP600125) effectively prevented Andro-induced p53 activation and DR4 up-regulation and eventually blocked the Andro-induced sensitization on TRAIL-induced apoptosis.	Acetylcysteine	34-50	tumor protein p53	Homo sapiens	142-145
18419763-6	2008	Inhibition of reactive oxygen species (ROS) by N-acetyl-cysteine or diphenylene iodonium significantly suppressed the expression of MMP-3, MMP-9, NO and TNF-alpha in LPS-stimulated microglia, suggesting that ROS is an early signaling inducer in LPS-stimulated microglial cells.	Acetylcysteine	47-64	tumor necrosis factor	Mus musculus	153-162
18645026-7	2008	Pretreatment with an antioxidant (N-acetylcysteine) or a c-Jun NH(2)-terminal kinase inhibitor (SP600125) effectively prevented Andro-induced p53 activation and DR4 up-regulation and eventually blocked the Andro-induced sensitization on TRAIL-induced apoptosis.	Acetylcysteine	34-50	TNF superfamily member 10	Homo sapiens	237-242
18533267-5	2008	The generation of interleukin-8 (CXCL8/IL-8) by human DCs conditioned with CSE was suppressed by the anti-oxidant n-acetyl cysteine (NAC), implying the involvement of oxidant sensitive pathways as a primary mechanism involved in the enhanced CXCL8/IL-8 generation.	Acetylcysteine	114-131	C-X-C motif chemokine ligand 8	Homo sapiens	18-31
18533267-5	2008	The generation of interleukin-8 (CXCL8/IL-8) by human DCs conditioned with CSE was suppressed by the anti-oxidant n-acetyl cysteine (NAC), implying the involvement of oxidant sensitive pathways as a primary mechanism involved in the enhanced CXCL8/IL-8 generation.	Acetylcysteine	114-131	C-X-C motif chemokine ligand 8	Homo sapiens	33-38
18533267-5	2008	The generation of interleukin-8 (CXCL8/IL-8) by human DCs conditioned with CSE was suppressed by the anti-oxidant n-acetyl cysteine (NAC), implying the involvement of oxidant sensitive pathways as a primary mechanism involved in the enhanced CXCL8/IL-8 generation.	Acetylcysteine	114-131	C-X-C motif chemokine ligand 8	Homo sapiens	39-43
18533267-5	2008	The generation of interleukin-8 (CXCL8/IL-8) by human DCs conditioned with CSE was suppressed by the anti-oxidant n-acetyl cysteine (NAC), implying the involvement of oxidant sensitive pathways as a primary mechanism involved in the enhanced CXCL8/IL-8 generation.	Acetylcysteine	114-131	C-X-C motif chemokine ligand 8	Homo sapiens	242-247
18533267-5	2008	The generation of interleukin-8 (CXCL8/IL-8) by human DCs conditioned with CSE was suppressed by the anti-oxidant n-acetyl cysteine (NAC), implying the involvement of oxidant sensitive pathways as a primary mechanism involved in the enhanced CXCL8/IL-8 generation.	Acetylcysteine	114-131	C-X-C motif chemokine ligand 8	Homo sapiens	248-252
18533267-5	2008	The generation of interleukin-8 (CXCL8/IL-8) by human DCs conditioned with CSE was suppressed by the anti-oxidant n-acetyl cysteine (NAC), implying the involvement of oxidant sensitive pathways as a primary mechanism involved in the enhanced CXCL8/IL-8 generation.	Acetylcysteine	133-136	C-X-C motif chemokine ligand 8	Homo sapiens	18-31
18385389-5	2008	CDDP-triggered NF-kappaB translocation into the nucleus and TNF-alpha mRNA increase in the kidney were also inhibited in NAC-treated rats.	Acetylcysteine	121-124	tumor necrosis factor	Rattus norvegicus	60-69
18533267-5	2008	The generation of interleukin-8 (CXCL8/IL-8) by human DCs conditioned with CSE was suppressed by the anti-oxidant n-acetyl cysteine (NAC), implying the involvement of oxidant sensitive pathways as a primary mechanism involved in the enhanced CXCL8/IL-8 generation.	Acetylcysteine	133-136	C-X-C motif chemokine ligand 8	Homo sapiens	33-38
18533267-5	2008	The generation of interleukin-8 (CXCL8/IL-8) by human DCs conditioned with CSE was suppressed by the anti-oxidant n-acetyl cysteine (NAC), implying the involvement of oxidant sensitive pathways as a primary mechanism involved in the enhanced CXCL8/IL-8 generation.	Acetylcysteine	133-136	C-X-C motif chemokine ligand 8	Homo sapiens	39-43
18533267-5	2008	The generation of interleukin-8 (CXCL8/IL-8) by human DCs conditioned with CSE was suppressed by the anti-oxidant n-acetyl cysteine (NAC), implying the involvement of oxidant sensitive pathways as a primary mechanism involved in the enhanced CXCL8/IL-8 generation.	Acetylcysteine	133-136	C-X-C motif chemokine ligand 8	Homo sapiens	242-247
18533267-5	2008	The generation of interleukin-8 (CXCL8/IL-8) by human DCs conditioned with CSE was suppressed by the anti-oxidant n-acetyl cysteine (NAC), implying the involvement of oxidant sensitive pathways as a primary mechanism involved in the enhanced CXCL8/IL-8 generation.	Acetylcysteine	133-136	C-X-C motif chemokine ligand 8	Homo sapiens	248-252
18533267-7	2008	Whereas NAC suppressed production of CXCL8 by CSE-conditioned DCs, it augmented production of PGE2 and cellular COX-2 levels in maturing DCs.	Acetylcysteine	8-11	C-X-C motif chemokine ligand 8	Homo sapiens	37-42
18441204-8	2008	The HNP-induced COX-2 and ET-1 production was attenuated by the treatment with the oxygen free radical scavenger N-acetyl-L-cysteine and the inhibitors of p38 MAPK and NF-kappaB, respectively.	Acetylcysteine	113-132	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	16-21
18417716-11	2008	In fact, incubation of retinal EC or aortic rings from bcl-2-/- mice with the antioxidant N-acetylcysteine rescued their capillary morphogenesis and sprouting defects.	Acetylcysteine	90-106	B cell leukemia/lymphoma 2	Mus musculus	55-60
18407833-7	2008	Crucially, both ROS formation and PIMT induction by PAO were inhibited by antioxidant N-acetyl-L-cysteine and NADPH oxidase inhibitor diphenyleneiodonium chloride.	Acetylcysteine	86-105	protein-L-isoaspartate (D-aspartate) O-methyltransferase	Homo sapiens	34-38
18441204-8	2008	The HNP-induced COX-2 and ET-1 production was attenuated by the treatment with the oxygen free radical scavenger N-acetyl-L-cysteine and the inhibitors of p38 MAPK and NF-kappaB, respectively.	Acetylcysteine	113-132	endothelin 1	Homo sapiens	26-30
18275980-7	2008	Berberine-induced apoptosis was blocked in the presence of antioxidant, N-acetylcysteine, through the prevention of disruption of mitochondrial membrane potential and subsequently release of cytochrome c and Smac/DIABLO.	Acetylcysteine	72-88	cytochrome c, somatic	Homo sapiens	191-203
18569013-6	2008	N-acetylcysteine, superoxide dismutase and catalase can block the ROS generation and alleviate the insulin resistance induced by Cr(VI) treatment.	Acetylcysteine	0-16	insulin	Homo sapiens	99-106
18569013-7	2008	In addition, Cr(VI) treatment induced endoplasmic reticulum (ER) stress and JNK activation and these effects were diminished by N-acetylcysteine.	Acetylcysteine	128-144	mitogen-activated protein kinase 8	Homo sapiens	76-79
18323457-9	2008	However, the antioxidant N-acetylcysteine opposed MSFTZ-mediated mitochondrial dysfunction, caspase activation, Bcl-2/Bax modulation, and apoptosis, supporting the role of ROS in the apoptotic process.	Acetylcysteine	25-41	BCL2 apoptosis regulator	Homo sapiens	112-117
18323457-9	2008	However, the antioxidant N-acetylcysteine opposed MSFTZ-mediated mitochondrial dysfunction, caspase activation, Bcl-2/Bax modulation, and apoptosis, supporting the role of ROS in the apoptotic process.	Acetylcysteine	25-41	BCL2 associated X, apoptosis regulator	Homo sapiens	118-121
18496137-8	2008	Treatment with NAC inhibited superoxide radical generation and decreased plasma malondialdehyde to a comparable level to that in Postcon, concomitant with an inhibition of NF-kappa B expression (42% +/- 8%*) and reduction of release of TNF-alpha (231 +/- 72* pg/mL).	Acetylcysteine	15-18	tumor necrosis factor	Rattus norvegicus	236-245
18483248-5	2008	Treatment with the antioxidant N-acetyl-l-cysteine relieved hydroquinone-induced suppression of colony formation by Wt hematopoietic cells, suggesting that the decreased oxidative damage to Fhit-deficient cells, relative to Wt hematopoietic cells, accounts for the survival advantage of Fhit-deficient bone marrow.	Acetylcysteine	31-50	fragile histidine triad gene	Mus musculus	190-194
17936662-11	2008	The anti-oxidant, N-acetyl cysteine, inhibited TNF-alpha-induced PAPP-A expression without altering the induction in VCAM, ICAM, and MCP-1.	Acetylcysteine	18-35	tumor necrosis factor	Homo sapiens	47-56
18628592-6	2008	Treatment with N-acetyl-L-cysteine also inhibited expression of apoptotic proteins such as Bax and Smac and abrogated caspase-8 activation.	Acetylcysteine	15-34	BCL2 associated X, apoptosis regulator	Homo sapiens	91-94
18628592-7	2008	Moreover, treatment with N-acetyl-L-cysteine prior to induction with TRAIL increased expression of the anti-apoptotic Bcl-2 protein.	Acetylcysteine	25-44	TNF superfamily member 10	Homo sapiens	69-74
18628592-7	2008	Moreover, treatment with N-acetyl-L-cysteine prior to induction with TRAIL increased expression of the anti-apoptotic Bcl-2 protein.	Acetylcysteine	25-44	BCL2 apoptosis regulator	Homo sapiens	118-123
18325346-6	2008	In addition, rotenone induced production of reactive oxygen species (ROS), and pretreatment with N-acetylcysteine abrogated ferritin H mRNA induction by rotenone, suggesting that this response is oxidative stress-mediated.	Acetylcysteine	97-113	ferritin mitochondrial	Mus musculus	124-134
18353872-7	2008	High glucose increased the generation of ROS, whereas both alpha-lipoic acid and N-acetylcysteine scavenged the ROS and decreased high glucose-induced tyrosine phosphorylation of IkappaBalpha, nuclear translocation of p65, and NF-kappaB DNA binding activity.	Acetylcysteine	81-97	NFKB inhibitor alpha	Homo sapiens	179-191
18353872-7	2008	High glucose increased the generation of ROS, whereas both alpha-lipoic acid and N-acetylcysteine scavenged the ROS and decreased high glucose-induced tyrosine phosphorylation of IkappaBalpha, nuclear translocation of p65, and NF-kappaB DNA binding activity.	Acetylcysteine	81-97	nuclear factor kappa B subunit 1	Homo sapiens	227-236
18199003-7	2008	LPS-induced HIF-1 activation was blocked by treatment with antioxidant (N-acetylcysteine or thioredoxin-1), NADPH oxidase inhibitor (diphenyleneiodonium), indicating that reactive oxygen species generated in response to LPS are essential in this process.	Acetylcysteine	72-88	hypoxia inducible factor 1 subunit alpha	Homo sapiens	12-17
18281048-8	2008	Estrogen increased Id3 phosphorylation which was reduced by catalase and N-acetylcysteine treatments.	Acetylcysteine	73-89	inhibitor of DNA binding 3, HLH protein	Homo sapiens	19-22
18176610-8	2008	Increase and recovery of ALT and AST were the same in patients randomized to NAC or controls.	Acetylcysteine	77-80	solute carrier family 17 member 5	Homo sapiens	33-36
18728404-8	2008	Moreover, NAC effectively blocked apoptosis and decreased the levels of phosphorylated JNK induced by selenite.	Acetylcysteine	10-13	mitogen-activated protein kinase 8	Homo sapiens	87-90
18456507-5	2008	N-acetylcysteine (NAC), a thiol reducing agent, but not reactive oxygen species scavengers, prevented 15d-PGJ(2)-induced COX-2 up-regulation.	Acetylcysteine	0-16	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	121-126
18064629-5	2008	Antioxidant N-acetyl-L-cysteine or NAC blocks UV-induced MEK/ERK activation and down-regulation of AQP3.	Acetylcysteine	12-31	mitogen-activated protein kinase kinase 7	Homo sapiens	57-60
18064629-5	2008	Antioxidant N-acetyl-L-cysteine or NAC blocks UV-induced MEK/ERK activation and down-regulation of AQP3.	Acetylcysteine	12-31	mitogen-activated protein kinase 1	Homo sapiens	61-64
18398338-4	2008	RESULTS: oxLDL (35 microg/ml) significantly enhanced reactive oxygen species (ROS), mRNA expression, secretion and promoter activity of ET-1 in human umbilical vein endothelial cells (HUVECs), all of which were nullified by the antioxidant N-acetyl cysteine (NAC).	Acetylcysteine	240-257	endothelin 1	Homo sapiens	136-140
18398338-4	2008	RESULTS: oxLDL (35 microg/ml) significantly enhanced reactive oxygen species (ROS), mRNA expression, secretion and promoter activity of ET-1 in human umbilical vein endothelial cells (HUVECs), all of which were nullified by the antioxidant N-acetyl cysteine (NAC).	Acetylcysteine	259-262	endothelin 1	Homo sapiens	136-140
18398338-5	2008	oxLDL stimulated the extracellular signal-regulated kinase (ERK) phosphorylation in HUVECs, which was blocked by NAC and the mitogen-activated protein/extracellular signal-regulated kinase (MEK) inhibitor PD98059.	Acetylcysteine	113-116	mitogen-activated protein kinase 1	Homo sapiens	21-58
18398338-5	2008	oxLDL stimulated the extracellular signal-regulated kinase (ERK) phosphorylation in HUVECs, which was blocked by NAC and the mitogen-activated protein/extracellular signal-regulated kinase (MEK) inhibitor PD98059.	Acetylcysteine	113-116	mitogen-activated protein kinase 1	Homo sapiens	60-63
18398338-6	2008	NAC and PD98059 stopped oxLDL-elicited increase in mRNA expression, secretion and promoter activity of ET-1.	Acetylcysteine	0-3	endothelin 1	Homo sapiens	103-107
18205750-0	2008	Modulation of peroxisome proliferator-activated receptor-alpha activity by N-acetyl cysteine attenuates inhibition of oligodendrocyte development in lipopolysaccharide stimulated mixed glial cultures.	Acetylcysteine	75-92	peroxisome proliferator activated receptor alpha	Mus musculus	14-62
18205750-7	2008	Similar to WY14643, NAC attenuated LCM-induced inhibition of PPAR-alpha activity in developing OLs.	Acetylcysteine	20-23	peroxisome proliferator activated receptor alpha	Mus musculus	61-71
18205750-10	2008	Collectively, these data provide evidence that the modulation of PPAR-alpha activity, thus peroxisomal function by NAC attenuates LPS-induced glial factors-mediated inhibition of OL development suggesting new therapeutic interventions to prevent the devastating effects of maternal infections.	Acetylcysteine	115-118	peroxisome proliferator activated receptor alpha	Mus musculus	65-75
18252805-7	2008	The antioxidant compound N-acetylcysteine blocked the curcumin-induced increased reactive oxygen species (ROS), sustained activation of ERK1/2, and decreased survival after IR in HeLa cells, implicating a ROS-dependent mechanism for curcumin radiosensitivity.	Acetylcysteine	25-41	mitogen-activated protein kinase 3	Homo sapiens	136-142
18504181-0	2008	[Effect of N-acetylcysteine on HMGB1 and RAGE expression in the lungs of asthmatic mice].	Acetylcysteine	11-27	MOK protein kinase	Mus musculus	41-45
18504181-5	2008	After NAC treatment, both of HMGB1 and RAGE mRNA levels (0.98-/+0.05 and 1.58-/+0.21) were significantly higher than those in the other two groups (P&lt;0.05).	Acetylcysteine	6-9	MOK protein kinase	Mus musculus	39-43
18404532-7	2008	NAC decreased IKK and IkB-a phosphorylation, and Rel-A/p65 and NF-kB binding, though the last two were affected with less intensity compared to the NF-kB inhibitor.	Acetylcysteine	0-3	synaptotagmin 1	Rattus norvegicus	55-58
18206249-4	2008	Consistent with previous reports in other cell types, blockade of TNFalpha-induced ROS by treatment with N-acetylcysteine, diphenylene iodonium or NADPH oxidase 4 (NOX4) siRNA suppressed TNFalpha-induced ICAM-1 expression and subsequent monocytic adhesion, indicating that TNFalpha mediates pro-inflammatory signals via NOX4-dependent ROS generation in human endothelial cells.	Acetylcysteine	105-121	tumor necrosis factor	Homo sapiens	66-74
18206249-4	2008	Consistent with previous reports in other cell types, blockade of TNFalpha-induced ROS by treatment with N-acetylcysteine, diphenylene iodonium or NADPH oxidase 4 (NOX4) siRNA suppressed TNFalpha-induced ICAM-1 expression and subsequent monocytic adhesion, indicating that TNFalpha mediates pro-inflammatory signals via NOX4-dependent ROS generation in human endothelial cells.	Acetylcysteine	105-121	tumor necrosis factor	Homo sapiens	187-195
18206249-4	2008	Consistent with previous reports in other cell types, blockade of TNFalpha-induced ROS by treatment with N-acetylcysteine, diphenylene iodonium or NADPH oxidase 4 (NOX4) siRNA suppressed TNFalpha-induced ICAM-1 expression and subsequent monocytic adhesion, indicating that TNFalpha mediates pro-inflammatory signals via NOX4-dependent ROS generation in human endothelial cells.	Acetylcysteine	105-121	tumor necrosis factor	Homo sapiens	187-195
18218673-8	2008	Moreover, TNF-alpha-induced cytosolic ROS production was inhibited by Rac1 inhibition, diphenyleneiodonium (DPI, an inhibitor of NADPH oxidase), and NAC.	Acetylcysteine	149-152	tumor necrosis factor	Homo sapiens	10-19
18630824-5	2008	AST/ALT levels are measured on admission, 12 hours after, and according to outcome every 12-24 h. N-acetylcysteine (NAC) administration within 8-10 hours protects against acetaminophen-induced hepatotoxicity.	Acetylcysteine	98-114	solute carrier family 17 member 5	Homo sapiens	0-3
18630824-5	2008	AST/ALT levels are measured on admission, 12 hours after, and according to outcome every 12-24 h. N-acetylcysteine (NAC) administration within 8-10 hours protects against acetaminophen-induced hepatotoxicity.	Acetylcysteine	116-119	solute carrier family 17 member 5	Homo sapiens	0-3
18219322-6	2008	TNF-induced SENP1 nuclear translocation is specifically blocked by antioxidants such as N-acetyl-cysteine, suggesting that TNF-induced translocation of SENP1 is ROS dependent.	Acetylcysteine	88-105	tumor necrosis factor	Mus musculus	0-3
18219322-6	2008	TNF-induced SENP1 nuclear translocation is specifically blocked by antioxidants such as N-acetyl-cysteine, suggesting that TNF-induced translocation of SENP1 is ROS dependent.	Acetylcysteine	88-105	tumor necrosis factor	Mus musculus	123-126
18059323-12	2008	However, the effects of cigarette smoke extract on LPS-induced nitrite formation were mimicked by hydrogen peroxide and reversed by the anti-oxidants N-acetyl cysteine and glutathione.	Acetylcysteine	150-167	toll-like receptor 4	Mus musculus	51-54
18325696-4	2008	Caspase-3 activation and DNA fragmentation were considerably inhibited by N-acetyl-cysteine (NAC).	Acetylcysteine	74-91	caspase 3	Homo sapiens	0-9
18325696-4	2008	Caspase-3 activation and DNA fragmentation were considerably inhibited by N-acetyl-cysteine (NAC).	Acetylcysteine	93-96	caspase 3	Homo sapiens	0-9
18507034-9	2008	Furthermore, rosiglitazone stimulates formation of superoxide anions, whereas induction of caveolin-1 expression by rosiglitazone is attenuated by the antioxidant N-acetyl-cysteine.	Acetylcysteine	163-180	caveolin 1	Homo sapiens	91-101
18630691-0	2008	[Effect of N-acetylcysteine on lipopolysaccharide stimulating IL-8 expression of human uterine smooth cell].	Acetylcysteine	11-27	C-X-C motif chemokine ligand 8	Homo sapiens	62-66
18630691-1	2008	OBJECTIVE: To investigate the effects of N-acetylcysteine (NAC)on the expression of IL-8 and the activity of NF-kappaB, which are induced by lipopolysaccharide (LPS) in human uterine smooth cell.	Acetylcysteine	41-57	C-X-C motif chemokine ligand 8	Homo sapiens	84-88
18630691-1	2008	OBJECTIVE: To investigate the effects of N-acetylcysteine (NAC)on the expression of IL-8 and the activity of NF-kappaB, which are induced by lipopolysaccharide (LPS) in human uterine smooth cell.	Acetylcysteine	41-57	nuclear factor kappa B subunit 1	Homo sapiens	109-118
17941088-8	2008	The thiol antioxidant, N-acetyl cysteine (NAC), completely inhibited stretch- and Ang II-induced apoptosis.	Acetylcysteine	23-40	angiotensinogen	Homo sapiens	82-88
17941088-8	2008	The thiol antioxidant, N-acetyl cysteine (NAC), completely inhibited stretch- and Ang II-induced apoptosis.	Acetylcysteine	42-45	angiotensinogen	Homo sapiens	82-88
18258657-7	2008	Immunoblotting showed that NAC treatment decreased the nuclear protein expression of NF-kappaB, a transcription factor involved in pro-inflammatory cytokine expression.	Acetylcysteine	27-30	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	85-94
18258657-8	2008	Finally, we show that NAC treatment reduced caveolin-3 protein levels and increased the sarcolemmal expression of beta-dystroglycan and the dystrophin homologue, utrophin.	Acetylcysteine	22-25	dystrophin, muscular dystrophy	Mus musculus	140-150
18258657-8	2008	Finally, we show that NAC treatment reduced caveolin-3 protein levels and increased the sarcolemmal expression of beta-dystroglycan and the dystrophin homologue, utrophin.	Acetylcysteine	22-25	utrophin	Mus musculus	162-170
18182160-7	2008	Diphenyleneiodonium, an inhibitor of NADPH oxidase, and N-acetylcysteine, a potent antioxidant, also inhibited TNF-alpha-induced activation of Mst1 and caspase 3, as well as apoptosis.	Acetylcysteine	56-72	tumor necrosis factor	Homo sapiens	111-120
18182160-7	2008	Diphenyleneiodonium, an inhibitor of NADPH oxidase, and N-acetylcysteine, a potent antioxidant, also inhibited TNF-alpha-induced activation of Mst1 and caspase 3, as well as apoptosis.	Acetylcysteine	56-72	caspase 3	Homo sapiens	152-161
17920721-5	2008	The activity of SOD was down-regulated, but the activity of catalase was up-regulated by pyrogallol at 72 h. ROS scavengers, including Tempol, Tiron, Trimetazidine, and N-acetylcysteine (NAC), did not reduce the levels of the intracellular O2*-.	Acetylcysteine	169-185	catalase	Homo sapiens	60-68
17920721-5	2008	The activity of SOD was down-regulated, but the activity of catalase was up-regulated by pyrogallol at 72 h. ROS scavengers, including Tempol, Tiron, Trimetazidine, and N-acetylcysteine (NAC), did not reduce the levels of the intracellular O2*-.	Acetylcysteine	187-190	catalase	Homo sapiens	60-68
18082636-2	2008	In the present study we tested a novel thiol compound, N-acetylcysteine amide (AD4), the amide form of N-acetyl cysteine (NAC) for its antioxidant effects.	Acetylcysteine	103-120	presenilin 2	Homo sapiens	79-82
18082636-2	2008	In the present study we tested a novel thiol compound, N-acetylcysteine amide (AD4), the amide form of N-acetyl cysteine (NAC) for its antioxidant effects.	Acetylcysteine	122-125	presenilin 2	Homo sapiens	79-82
17786977-7	2008	Pre-treatment with the free radical scavenger N-acetyl cysteine (NAC) and the superoxide dismutase mimetic EUK-8 abolished caspase-3 and PARP-1 induction, suggesting that apoptosis in oral mucosa cancer cells is initated by ROS generation in response to DC electrical field treatment.	Acetylcysteine	46-63	caspase 3	Homo sapiens	123-132
18031542-7	2008	The UVB-induced HSP27 phosphorylation was inhibited when melanocytes were treated with the antioxidant N-acetyl cysteine or inhibitor of p38 MAP kinase prior to UVB exposure, suggesting that UVB induced HSP27 phosphorylation through reactive oxygen species/p38 MAP kinase pathway.	Acetylcysteine	103-120	mitogen-activated protein kinase 14	Homo sapiens	257-260
17728093-9	2008	Pretreatment with N-acetyl cysteine (NAC), a GSH precursor, prevented enzymatic changes in CAT, Se-dependent GSH-Px, GR, SOD1 activities, and significantly decreased SOD2 activity following exposure to thiram.	Acetylcysteine	18-35	superoxide dismutase [Cu-Zn]	Cricetulus griseus	121-125
17728093-9	2008	Pretreatment with N-acetyl cysteine (NAC), a GSH precursor, prevented enzymatic changes in CAT, Se-dependent GSH-Px, GR, SOD1 activities, and significantly decreased SOD2 activity following exposure to thiram.	Acetylcysteine	37-40	superoxide dismutase [Cu-Zn]	Cricetulus griseus	121-125
17991881-8	2008	In support of this mechanism, a chemical antioxidant, N-acetyl-cysteine, is sufficient to block the hyperoxia-mediated increase in PDE5 expression and activity and rescue cGMP responsiveness to exogenous NO.	Acetylcysteine	54-71	phosphodiesterase 5A	Homo sapiens	131-135
18314480-10	2008	N-acetyl-l-cysteine additionally reversed the salvicine-induced activation of ERK and p38 MAPK, thereby maintaining functional beta(1) integrin activity and restoring cell adhesion and spreading.	Acetylcysteine	0-19	mitogen-activated protein kinase 1	Homo sapiens	78-81
17980396-9	2008	Pretreatment with cell-permeable catalase, N-acetyl-L-cysteine or GSH-monoethyl ester markedly reduced expression of NQO-1 and GCLC under HOCl challenge conditions, suggesting intracellular ROS-scavenging capacity affects HOCl-induced Nrf2 activation.	Acetylcysteine	43-62	NAD(P)H quinone dehydrogenase 1	Homo sapiens	117-122
17980396-9	2008	Pretreatment with cell-permeable catalase, N-acetyl-L-cysteine or GSH-monoethyl ester markedly reduced expression of NQO-1 and GCLC under HOCl challenge conditions, suggesting intracellular ROS-scavenging capacity affects HOCl-induced Nrf2 activation.	Acetylcysteine	43-62	NFE2 like bZIP transcription factor 2	Homo sapiens	235-239
17967787-5	2008	Inhibiting hemin-induced ERK-1/2 activation by U0126 (MAPK-inhibitor), the antioxidant N-acetyl cysteine, the NADPH oxidase inhibitors apocynin and diphenyleneiodonium chloride, the superoxide scavenger tiron, or tricarbonyldichlororuthenium(II)-dimer (carbon-monoxide donor; CORM-2) blocked hemin-induced Egr-1 expression.	Acetylcysteine	87-104	mitogen-activated protein kinase 3	Homo sapiens	25-32
17965279-5	2008	Here we demonstrate that the antioxidant N-acetylcysteine reduced nerve-stimulated norepinephrine and increased NPY overflow in the mesenteric arterial bed taken from the SHR.	Acetylcysteine	41-57	neuropeptide Y	Rattus norvegicus	112-115
18032526-8	2008	AGE-induced phosphorylation of FKHRL1 led to a 70% downregulation of MnSOD, an effect partially blocked by a phosphatidylinositol 3-kinase inhibitor (LY-294002) and strongly inhibited by an antioxidant (N-acetylcysteine).	Acetylcysteine	203-219	forkhead box O3	Homo sapiens	31-37
17786977-7	2008	Pre-treatment with the free radical scavenger N-acetyl cysteine (NAC) and the superoxide dismutase mimetic EUK-8 abolished caspase-3 and PARP-1 induction, suggesting that apoptosis in oral mucosa cancer cells is initated by ROS generation in response to DC electrical field treatment.	Acetylcysteine	46-63	poly(ADP-ribose) polymerase 1	Homo sapiens	137-143
17786977-7	2008	Pre-treatment with the free radical scavenger N-acetyl cysteine (NAC) and the superoxide dismutase mimetic EUK-8 abolished caspase-3 and PARP-1 induction, suggesting that apoptosis in oral mucosa cancer cells is initated by ROS generation in response to DC electrical field treatment.	Acetylcysteine	65-68	caspase 3	Homo sapiens	123-132
17786977-7	2008	Pre-treatment with the free radical scavenger N-acetyl cysteine (NAC) and the superoxide dismutase mimetic EUK-8 abolished caspase-3 and PARP-1 induction, suggesting that apoptosis in oral mucosa cancer cells is initated by ROS generation in response to DC electrical field treatment.	Acetylcysteine	65-68	poly(ADP-ribose) polymerase 1	Homo sapiens	137-143
18006470-9	2008	Moreover, pretreating myocytes with exogenous GSH or the GSH precursor N-acetylcysteine also prevented myocyte contractile impairment and abnormal Ca2+ transients elicited by TGF-beta1.	Acetylcysteine	71-87	transforming growth factor, beta 1	Rattus norvegicus	175-184
18047631-14	2008	Moreover, we observed that N-acetylcysteine inhibited collagen type I expression induced by AngII as did the PPAR-gamma agonists.	Acetylcysteine	27-43	angiotensinogen	Rattus norvegicus	92-97
17461432-3	2008	The aim of this study was to investigate the effects of N-acetylcysteine (NAC) treatment on CsA-induced hepatic damage by both analysing superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), aspartate aminotransferase (AST) and alanine transaminase (ALT) activities with malondialdehyde (MDA) and nitric oxide (NO) levels, and using an histological approach.	Acetylcysteine	56-72	glutamic-oxaloacetic transaminase 2	Rattus norvegicus	198-224
18990976-9	2008	NAC increased CF transport by MRP1 in a concentration-dependent manner.	Acetylcysteine	0-3	ATP binding cassette subfamily C member 1	Homo sapiens	30-34
18990976-10	2008	CONCLUSIONS: Our data suggest that, besides their positive effects on respiratory symptoms, budesonide, formoterol, ipratropium bromide, and NAC modulate MRP1 activity in bronchial epithelial cells.	Acetylcysteine	141-144	ATP binding cassette subfamily C member 1	Homo sapiens	154-158
18226399-4	2008	N-acetylcysteine (NAC) is a thiol molecule that has direct and indirect antioxidant effects which decrease reactive oxidant species and increase the bioavailability of the DDAH enzyme.	Acetylcysteine	0-16	dimethylarginine dimethylaminohydrolase 1	Homo sapiens	172-176
18226399-4	2008	N-acetylcysteine (NAC) is a thiol molecule that has direct and indirect antioxidant effects which decrease reactive oxidant species and increase the bioavailability of the DDAH enzyme.	Acetylcysteine	18-21	dimethylarginine dimethylaminohydrolase 1	Homo sapiens	172-176
18306112-4	2008	The potency of both NAC and PDTC corresponded to their ability to inhibit NF-kappaB activation.	Acetylcysteine	20-23	nuclear factor kappa B subunit 1	Homo sapiens	74-83
17461432-3	2008	The aim of this study was to investigate the effects of N-acetylcysteine (NAC) treatment on CsA-induced hepatic damage by both analysing superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), aspartate aminotransferase (AST) and alanine transaminase (ALT) activities with malondialdehyde (MDA) and nitric oxide (NO) levels, and using an histological approach.	Acetylcysteine	56-72	glutamic-oxaloacetic transaminase 2	Rattus norvegicus	226-229
17461432-3	2008	The aim of this study was to investigate the effects of N-acetylcysteine (NAC) treatment on CsA-induced hepatic damage by both analysing superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), aspartate aminotransferase (AST) and alanine transaminase (ALT) activities with malondialdehyde (MDA) and nitric oxide (NO) levels, and using an histological approach.	Acetylcysteine	74-77	glutathione peroxidase 1	Rattus norvegicus	189-195
17461432-3	2008	The aim of this study was to investigate the effects of N-acetylcysteine (NAC) treatment on CsA-induced hepatic damage by both analysing superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), aspartate aminotransferase (AST) and alanine transaminase (ALT) activities with malondialdehyde (MDA) and nitric oxide (NO) levels, and using an histological approach.	Acetylcysteine	74-77	glutamic-oxaloacetic transaminase 2	Rattus norvegicus	198-224
17461432-3	2008	The aim of this study was to investigate the effects of N-acetylcysteine (NAC) treatment on CsA-induced hepatic damage by both analysing superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), aspartate aminotransferase (AST) and alanine transaminase (ALT) activities with malondialdehyde (MDA) and nitric oxide (NO) levels, and using an histological approach.	Acetylcysteine	74-77	glutamic-oxaloacetic transaminase 2	Rattus norvegicus	226-229
17461432-6	2008	A significant elevation in serum AST and ALT activities was observed in the CsA group, and when NAC and CsA were co-administered, the activities of AST and ALT were close to the control levels.	Acetylcysteine	96-99	glutamic-oxaloacetic transaminase 2	Rattus norvegicus	33-36
17461432-6	2008	A significant elevation in serum AST and ALT activities was observed in the CsA group, and when NAC and CsA were co-administered, the activities of AST and ALT were close to the control levels.	Acetylcysteine	96-99	glutamic-oxaloacetic transaminase 2	Rattus norvegicus	148-151
18322419-8	2008	As paclitaxel treatment produced reactive oxygen species (ROS), VEGF expression was increased by H2O2 treatment and reduced by various ROS scavengers such as N-acetyl-L-cysteine, pyrrolidine dithiocarbamate and diphenylene iodonium.	Acetylcysteine	158-177	vascular endothelial growth factor A	Homo sapiens	64-68
18755394-6	2008	Treatment with N-acetyl-l-cysteine (NAC) did not significantly increase intracellular content of GSH but significantly reduced the secretion of TNF-alpha.	Acetylcysteine	15-34	tumor necrosis factor	Homo sapiens	144-153
18755394-6	2008	Treatment with N-acetyl-l-cysteine (NAC) did not significantly increase intracellular content of GSH but significantly reduced the secretion of TNF-alpha.	Acetylcysteine	36-39	tumor necrosis factor	Homo sapiens	144-153
18231637-7	2008	Oxidative stress caused by emodin, an ROS producer, in combination with arsenic trioxide (ATO) led to RhoA inactivation that triggered structural disruption of focal adhesion complex and eventually resulted in anoikis, and these effects could be partially reversed by antioxidant N-acetylcysteine (NAC).	Acetylcysteine	280-296	ras homolog family member A	Homo sapiens	102-106
18231637-7	2008	Oxidative stress caused by emodin, an ROS producer, in combination with arsenic trioxide (ATO) led to RhoA inactivation that triggered structural disruption of focal adhesion complex and eventually resulted in anoikis, and these effects could be partially reversed by antioxidant N-acetylcysteine (NAC).	Acetylcysteine	298-301	ras homolog family member A	Homo sapiens	102-106
18483565-4	2008	In this work, we investigated the effect of NAC administration on cortical expressions of nuclear factor kappa B (NF-kappaB) and inflammatory proteins such as interleukin-1beta (IL-1beta), tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6), and intercellular adhesion molecule-1 (ICAM-1) after TBI.	Acetylcysteine	44-47	interleukin 1 beta	Rattus norvegicus	159-176
18483565-4	2008	In this work, we investigated the effect of NAC administration on cortical expressions of nuclear factor kappa B (NF-kappaB) and inflammatory proteins such as interleukin-1beta (IL-1beta), tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6), and intercellular adhesion molecule-1 (ICAM-1) after TBI.	Acetylcysteine	44-47	tumor necrosis factor	Rattus norvegicus	218-227
18483565-4	2008	In this work, we investigated the effect of NAC administration on cortical expressions of nuclear factor kappa B (NF-kappaB) and inflammatory proteins such as interleukin-1beta (IL-1beta), tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6), and intercellular adhesion molecule-1 (ICAM-1) after TBI.	Acetylcysteine	44-47	interleukin 6	Rattus norvegicus	230-243
18483565-4	2008	In this work, we investigated the effect of NAC administration on cortical expressions of nuclear factor kappa B (NF-kappaB) and inflammatory proteins such as interleukin-1beta (IL-1beta), tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6), and intercellular adhesion molecule-1 (ICAM-1) after TBI.	Acetylcysteine	44-47	interleukin 6	Rattus norvegicus	245-249
18483565-6	2008	In animals given NAC post-TBI, NF-kappaB, IL-1beta, TNF-alpha, and ICAM-1 were decreased in comparison to vehicle-treated animals.	Acetylcysteine	17-20	interleukin 1 beta	Rattus norvegicus	42-50
18483565-6	2008	In animals given NAC post-TBI, NF-kappaB, IL-1beta, TNF-alpha, and ICAM-1 were decreased in comparison to vehicle-treated animals.	Acetylcysteine	17-20	tumor necrosis factor	Rattus norvegicus	52-61
18062818-0	2007	N-acetylcysteine prevents HIV gp 120-related damage of human cultured astrocytes: correlation with glutamine synthase dysfunction.	Acetylcysteine	0-16	glutamate-ammonia ligase	Homo sapiens	99-117
17913704-5	2007	Treatment with either neutralizing anti-TNFR1 antibodies or the glutathione precursor, N-acetylcysteine (NAC), favored the emergence of TNFR2 signaling that mediated a positive effect of TNFalpha on [Ca(2+)] transient and cell fractional shortening.	Acetylcysteine	87-103	tumor necrosis factor	Rattus norvegicus	187-195
17913704-5	2007	Treatment with either neutralizing anti-TNFR1 antibodies or the glutathione precursor, N-acetylcysteine (NAC), favored the emergence of TNFR2 signaling that mediated a positive effect of TNFalpha on [Ca(2+)] transient and cell fractional shortening.	Acetylcysteine	105-108	tumor necrosis factor	Rattus norvegicus	187-195
17913704-10	2007	In vivo NAC treatment proved to be a unique tool to selectively neutralize TNFR1-mediated effects of TNFalpha while releasing TNFR2 pathways.	Acetylcysteine	8-11	tumor necrosis factor	Rattus norvegicus	101-109
17964282-3	2007	Valsartan, a selective Ang II type 1 (AT1) receptor blocker, and N-acetylcysteine, an antioxidant, inhibited both of these modifications, indicating the contribution of AT1 receptor and reactive oxygen species to oxidation of Prx2 and phosphorylation of GRP58 by Ang II.	Acetylcysteine	65-81	peroxiredoxin 2	Homo sapiens	226-230
17964282-3	2007	Valsartan, a selective Ang II type 1 (AT1) receptor blocker, and N-acetylcysteine, an antioxidant, inhibited both of these modifications, indicating the contribution of AT1 receptor and reactive oxygen species to oxidation of Prx2 and phosphorylation of GRP58 by Ang II.	Acetylcysteine	65-81	protein disulfide isomerase family A member 3	Homo sapiens	254-259
17964282-3	2007	Valsartan, a selective Ang II type 1 (AT1) receptor blocker, and N-acetylcysteine, an antioxidant, inhibited both of these modifications, indicating the contribution of AT1 receptor and reactive oxygen species to oxidation of Prx2 and phosphorylation of GRP58 by Ang II.	Acetylcysteine	65-81	angiotensinogen	Homo sapiens	263-269
17848102-6	2007	Moreover, ERp57 conjugates are blocked by N-acetylcysteine and glutathione, suggesting that they represent oxidized forms of protein.	Acetylcysteine	42-58	protein disulfide isomerase family A member 3	Homo sapiens	10-15
17436097-9	2007	Aspartate aminotransferase (AST) and alkaline phosphatase levels in the BDL+NAC group were lower than the BDL group and were higher than the control groups (all P&lt; .001).	Acetylcysteine	76-79	glutamic-oxaloacetic transaminase 2	Rattus norvegicus	0-26
18077580-7	2007	In the mitochondrial pathway, NAC attenuated arsenite-induced elevation in Bcl-2 level and cytosolic cytochrome c, as well as arsenite-induced reduction in procaspase-3 levels.	Acetylcysteine	30-33	BCL2 apoptosis regulator	Homo sapiens	75-80
18077580-7	2007	In the mitochondrial pathway, NAC attenuated arsenite-induced elevation in Bcl-2 level and cytosolic cytochrome c, as well as arsenite-induced reduction in procaspase-3 levels.	Acetylcysteine	30-33	cytochrome c, somatic	Homo sapiens	101-113
18077580-8	2007	In the ER pathway, NAC suppressed arsenite-induced increases in activating transcription factor 6 and C/EBP homologous protein in the nuclear fraction.	Acetylcysteine	19-22	transcription factor A, mitochondrial	Homo sapiens	75-97
18077580-8	2007	In the ER pathway, NAC suppressed arsenite-induced increases in activating transcription factor 6 and C/EBP homologous protein in the nuclear fraction.	Acetylcysteine	19-22	CCAAT enhancer binding protein alpha	Homo sapiens	102-107
18077580-9	2007	Furthermore, arsenite-induced reductions in procaspase-12 and elevation in BIP and caspase-12, an ER-specific enzyme, were prevented after NAC incubation.	Acetylcysteine	139-142	heat shock protein family A (Hsp70) member 5	Homo sapiens	75-78
17706954-9	2007	Antioxidant, N-acetyl-l-cysteine or superoxide dismutase attenuated Ang II- or Aldo-induced VSMC senescence and Ki-ras2A expression.	Acetylcysteine	13-32	angiotensinogen	Rattus norvegicus	68-74
17979524-6	2007	Prior exposure of cells to N-acetyl-L -cysteine blocked not only the ROS production but also the nuclear translocation of Nrf2 and its ARE binding, as well as HO-1 induction by capsaicin.	Acetylcysteine	27-47	NFE2 like bZIP transcription factor 2	Homo sapiens	122-126
17436097-14	2007	NAC improved some biochemical parameters (AST, alkaline phosphatase) and oxidative stress parameters (malondialdehyde, luminol, glutathione) in the BDL model.	Acetylcysteine	0-3	glutamic-oxaloacetic transaminase 2	Rattus norvegicus	42-45
17660951-7	2007	The ability of NAC to block MG-impairment of PI3K activity and IRS-1 phosphorylation further confirmed the role of MG in the development of insulin resistance.	Acetylcysteine	15-18	insulin receptor substrate 1	Rattus norvegicus	63-68
18096486-6	2007	RESULTS: NAC administered prior to hilar clamping led to a significant decrease in macrophages and lymphocytes and interleukin (IL)-1 beta levels after ischemia.	Acetylcysteine	9-12	interleukin 1 beta	Mus musculus	115-138
18096486-7	2007	NAC also resulted in significantly fewer macrophages, lymphocytes and neutrophils as well as IL-1 beta, keratinocyte cytokine (KC), monocyte chemoattractant protein (MCP)-1 and IL-6 levels in BAL taken after reperfusion.	Acetylcysteine	0-3	interleukin 1 beta	Mus musculus	93-102
18096486-7	2007	NAC also resulted in significantly fewer macrophages, lymphocytes and neutrophils as well as IL-1 beta, keratinocyte cytokine (KC), monocyte chemoattractant protein (MCP)-1 and IL-6 levels in BAL taken after reperfusion.	Acetylcysteine	0-3	interleukin 6	Mus musculus	177-181
18170962-1	2007	The present study was designed to determine whether N-acetylcysteine (NAC), a potent antioxidant, modulates nitric oxide (NO) production stimulated by lipopolysaccharide (LPS) and tumor necrosis factor-alpha (TNF-alpha) in adipocytes.	Acetylcysteine	52-68	tumor necrosis factor	Mus musculus	180-207
18170962-1	2007	The present study was designed to determine whether N-acetylcysteine (NAC), a potent antioxidant, modulates nitric oxide (NO) production stimulated by lipopolysaccharide (LPS) and tumor necrosis factor-alpha (TNF-alpha) in adipocytes.	Acetylcysteine	52-68	tumor necrosis factor	Mus musculus	209-218
18170962-1	2007	The present study was designed to determine whether N-acetylcysteine (NAC), a potent antioxidant, modulates nitric oxide (NO) production stimulated by lipopolysaccharide (LPS) and tumor necrosis factor-alpha (TNF-alpha) in adipocytes.	Acetylcysteine	70-73	tumor necrosis factor	Mus musculus	180-207
18170962-1	2007	The present study was designed to determine whether N-acetylcysteine (NAC), a potent antioxidant, modulates nitric oxide (NO) production stimulated by lipopolysaccharide (LPS) and tumor necrosis factor-alpha (TNF-alpha) in adipocytes.	Acetylcysteine	70-73	tumor necrosis factor	Mus musculus	209-218
18170962-5	2007	The decrease in NO production by NAC was accompanied by a decrease in inducible nitric oxide synthase (iNOS) protein, detected by immunoblot analysis, and iNOS mRNA, determined by real-time reverse-transcriptase coupled polymerase chain reaction analysis.	Acetylcysteine	33-36	nitric oxide synthase 2, inducible	Mus musculus	70-101
18170962-5	2007	The decrease in NO production by NAC was accompanied by a decrease in inducible nitric oxide synthase (iNOS) protein, detected by immunoblot analysis, and iNOS mRNA, determined by real-time reverse-transcriptase coupled polymerase chain reaction analysis.	Acetylcysteine	33-36	nitric oxide synthase 2, inducible	Mus musculus	103-107
18170962-5	2007	The decrease in NO production by NAC was accompanied by a decrease in inducible nitric oxide synthase (iNOS) protein, detected by immunoblot analysis, and iNOS mRNA, determined by real-time reverse-transcriptase coupled polymerase chain reaction analysis.	Acetylcysteine	33-36	nitric oxide synthase 2, inducible	Mus musculus	155-159
18170962-11	2007	These results suggest that NAC regulates iNOS expression and NO production in adipocytes through the modulating activation of NF-kappa B.	Acetylcysteine	27-30	nitric oxide synthase 2, inducible	Mus musculus	41-45
18170962-11	2007	These results suggest that NAC regulates iNOS expression and NO production in adipocytes through the modulating activation of NF-kappa B.	Acetylcysteine	27-30	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	126-136
18356775-10	2007	NAC-treatment also reduced nitrotyrosine expression in uremic apoE-/- mice whereas the degree of macrophage infiltration was unchanged.	Acetylcysteine	0-3	apolipoprotein E	Mus musculus	62-66
17904098-7	2007	N-acetylcysteine (NAC), a well-known ROS scavenger, suppressed caspase-8 activation and the subsequent cleavage of caspase-9 and caspase-3, indicating the role of ROS in caspase-8-mediated apoptosis.	Acetylcysteine	0-16	caspase 3	Homo sapiens	129-138
17904098-7	2007	N-acetylcysteine (NAC), a well-known ROS scavenger, suppressed caspase-8 activation and the subsequent cleavage of caspase-9 and caspase-3, indicating the role of ROS in caspase-8-mediated apoptosis.	Acetylcysteine	18-21	caspase 3	Homo sapiens	129-138
17714694-9	2007	The capacity of NAC of counteracting the stimulatory activity of FP, supports the hypothesis that FP might induce the oxidative damage of specific G3PD binding sites in the membrane, causing the displacement of the enzyme into the cytosol and/or the release from its binding site and therefore its activation.	Acetylcysteine	16-19	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	147-151
17936186-6	2007	NAC inhibits HEMA-mediated toxicity through induction of differentiation in DPSCs, because the genes for dentin sialoprotein, osteopontin (OPN), osteocalcin, and alkaline phosphatase, which are induced during differentiation, are also induced by NAC.	Acetylcysteine	0-3	bone gamma-carboxyglutamate protein	Homo sapiens	145-156
17997855-11	2007	Treatment of G93A-SOD1 SH-SY5Y neuroblastoma cells with the antioxidant N-acetylcysteine reduced the toxicity of pneumolysin.	Acetylcysteine	72-88	superoxide dismutase 1	Homo sapiens	18-22
17600310-8	2007	CSE-evoked IL-8 release was remarkably (&gt; 80%) inhibited by N-acetyl-cysteine (0.1-3 mM) or glutathione monoethyl ester (1-3 mM).	Acetylcysteine	63-80	C-X-C motif chemokine ligand 8	Homo sapiens	11-15
17596533-6	2007	Moreover, NAC and taurine increased cyclin D1/cdk4 activation and suppressed p21(Waf1/Cip1) and p27(Kip1) expression in HG-treated cells.	Acetylcysteine	10-13	cyclin dependent kinase inhibitor 1A	Homo sapiens	77-80
18032928-5	2007	Pre-incubation with thiol antioxidants glutathione or N-acetyl-cysteine (NAC, precursor of intracellular glutathione) almost abolished the cytotoxicity of salvicine, which also could be attenuated by the H(2)O(2)-specific scavenger catalase.	Acetylcysteine	54-71	catalase	Homo sapiens	232-240
18032928-5	2007	Pre-incubation with thiol antioxidants glutathione or N-acetyl-cysteine (NAC, precursor of intracellular glutathione) almost abolished the cytotoxicity of salvicine, which also could be attenuated by the H(2)O(2)-specific scavenger catalase.	Acetylcysteine	73-76	catalase	Homo sapiens	232-240
18032928-8	2007	Furthermore, pretreatment of K562/A02 cells with NAC eliminated P-gp downregulation, JNK phosphorylation and c-Jun activation induced by salvicine.	Acetylcysteine	49-52	ATP binding cassette subfamily B member 1	Homo sapiens	64-68
18032928-8	2007	Furthermore, pretreatment of K562/A02 cells with NAC eliminated P-gp downregulation, JNK phosphorylation and c-Jun activation induced by salvicine.	Acetylcysteine	49-52	mitogen-activated protein kinase 8	Homo sapiens	85-88
18097876-8	2007	NAC significantly prevented caspase-3 activation in pneumocytes (p = .001 vs Placebo).	Acetylcysteine	0-3	caspase 3	Sus scrofa	28-37
17919343-5	2007	N-acetylcysteine (NAC), a H2O2 scavenger, inhibited both insulin-stimulated H2O2 release and insulin-stimulated autophosphorylation of insulin receptor.	Acetylcysteine	0-16	insulin	Homo sapiens	57-64
17919343-5	2007	N-acetylcysteine (NAC), a H2O2 scavenger, inhibited both insulin-stimulated H2O2 release and insulin-stimulated autophosphorylation of insulin receptor.	Acetylcysteine	0-16	insulin	Homo sapiens	93-100
17919343-5	2007	N-acetylcysteine (NAC), a H2O2 scavenger, inhibited both insulin-stimulated H2O2 release and insulin-stimulated autophosphorylation of insulin receptor.	Acetylcysteine	0-16	insulin	Homo sapiens	93-100
17919343-5	2007	N-acetylcysteine (NAC), a H2O2 scavenger, inhibited both insulin-stimulated H2O2 release and insulin-stimulated autophosphorylation of insulin receptor.	Acetylcysteine	18-21	insulin	Homo sapiens	57-64
17919343-5	2007	N-acetylcysteine (NAC), a H2O2 scavenger, inhibited both insulin-stimulated H2O2 release and insulin-stimulated autophosphorylation of insulin receptor.	Acetylcysteine	18-21	insulin	Homo sapiens	93-100
17919343-5	2007	N-acetylcysteine (NAC), a H2O2 scavenger, inhibited both insulin-stimulated H2O2 release and insulin-stimulated autophosphorylation of insulin receptor.	Acetylcysteine	18-21	insulin	Homo sapiens	93-100
17893047-6	2007	Pretreatment with MAPK inhibitors SB203580 and U0126, or addition of the exogenous thiol N-acetylcysteine, abrogated both p38(MAPK) and ERK2 activation as well as downstream effects on gene expression.	Acetylcysteine	89-105	mitogen-activated protein kinase 1	Mus musculus	136-140
17693623-7	2007	Vice versa, increased GSH content in hepatocytes from aged animals by treatment with N-acetylcysteine inhibits NSMase activity and restores normal IL-1beta response.	Acetylcysteine	85-101	interleukin 1 beta	Rattus norvegicus	147-155
18067231-12	2007	In contrast, the expressions of IRS-1, IRS-2, Glut-2 in NAC group increased by 40.2%, 30.2% and 19.1%, respectively than those in HF group.	Acetylcysteine	56-59	insulin receptor substrate 1	Rattus norvegicus	32-37
18067231-12	2007	In contrast, the expressions of IRS-1, IRS-2, Glut-2 in NAC group increased by 40.2%, 30.2% and 19.1%, respectively than those in HF group.	Acetylcysteine	56-59	insulin receptor substrate 2	Rattus norvegicus	39-44
17596533-9	2007	However, NAC or taurine markedly inhibited the stimulation by HG of fibronectin and type IV collagen protein levels.	Acetylcysteine	9-12	fibronectin 1	Homo sapiens	68-79
17596533-10	2007	It is concluded that both NAC and taurine significantly attenuated HG-induced activation of the Raf-1/MAPK and the JAK2-STAT1/STAT3 signaling pathways and hypertrophic growth in renal tubular epithelial cells.	Acetylcysteine	26-29	signal transducer and activator of transcription 3	Homo sapiens	126-131
17652361-6	2007	ANG II increased retinal leukostasis from 0.3 +/- 0.5 to 3.7 +/- 0.4 leukocytes/ mm(2) (P &lt; 0.01), and these changes were markedly decreased by treatment with tempol + NAC or apocynin, and also by a blocking antibody against vascular endothelial growth factor given intravitreally (P &lt; 0.01).	Acetylcysteine	171-174	angiotensinogen	Rattus norvegicus	0-6
17596533-6	2007	Moreover, NAC and taurine increased cyclin D1/cdk4 activation and suppressed p21(Waf1/Cip1) and p27(Kip1) expression in HG-treated cells.	Acetylcysteine	10-13	cyclin dependent kinase inhibitor 1A	Homo sapiens	81-85
17596533-6	2007	Moreover, NAC and taurine increased cyclin D1/cdk4 activation and suppressed p21(Waf1/Cip1) and p27(Kip1) expression in HG-treated cells.	Acetylcysteine	10-13	cyclin dependent kinase inhibitor 1A	Homo sapiens	86-90
18038907-7	2007	In addition, NAC prevented LPS-induced activation of p38 MAPK and JNK but not phosphorylation and subsequent degradation of IkB.	Acetylcysteine	13-16	mitogen-activated protein kinase 14	Homo sapiens	53-56
18038907-7	2007	In addition, NAC prevented LPS-induced activation of p38 MAPK and JNK but not phosphorylation and subsequent degradation of IkB.	Acetylcysteine	13-16	mitogen-activated protein kinase 8	Homo sapiens	66-69
18038907-8	2007	These results indicate that NAC exerts anti-inflammatory effects in LPS-stimulated gingival fibroblasts, functioning at least in part via down-regulation of JNK and p38 MAPK activation.	Acetylcysteine	28-31	mitogen-activated protein kinase 8	Homo sapiens	157-160
18038907-8	2007	These results indicate that NAC exerts anti-inflammatory effects in LPS-stimulated gingival fibroblasts, functioning at least in part via down-regulation of JNK and p38 MAPK activation.	Acetylcysteine	28-31	mitogen-activated protein kinase 14	Homo sapiens	165-168
17503468-6	2007	In addition, endosulfan has been shown to generate transient reactive oxygen species (ROS), and blocking this oxidative stress by N-acetyl cysteine (NAC) strongly prevented both persistent nuclear ERK1/2 phosphorylation and cell growth decrease.	Acetylcysteine	130-147	mitogen-activated protein kinase 3	Homo sapiens	197-203
17765224-7	2007	ROS scavengers, pyrrolidinedithiocarbamate (PDTC) and N-acetyl-cysteine (NAC), reduced the levels of ROS induced by TNF-alpha, IL-1 beta and IFN-gamma (P&lt;0.05).	Acetylcysteine	54-71	tumor necrosis factor	Homo sapiens	116-125
17765224-7	2007	ROS scavengers, pyrrolidinedithiocarbamate (PDTC) and N-acetyl-cysteine (NAC), reduced the levels of ROS induced by TNF-alpha, IL-1 beta and IFN-gamma (P&lt;0.05).	Acetylcysteine	54-71	interleukin 1 beta	Homo sapiens	127-136
17765224-7	2007	ROS scavengers, pyrrolidinedithiocarbamate (PDTC) and N-acetyl-cysteine (NAC), reduced the levels of ROS induced by TNF-alpha, IL-1 beta and IFN-gamma (P&lt;0.05).	Acetylcysteine	54-71	interferon gamma	Homo sapiens	141-150
17765224-7	2007	ROS scavengers, pyrrolidinedithiocarbamate (PDTC) and N-acetyl-cysteine (NAC), reduced the levels of ROS induced by TNF-alpha, IL-1 beta and IFN-gamma (P&lt;0.05).	Acetylcysteine	73-76	tumor necrosis factor	Homo sapiens	116-125
17765224-7	2007	ROS scavengers, pyrrolidinedithiocarbamate (PDTC) and N-acetyl-cysteine (NAC), reduced the levels of ROS induced by TNF-alpha, IL-1 beta and IFN-gamma (P&lt;0.05).	Acetylcysteine	73-76	interleukin 1 beta	Homo sapiens	127-136
17765224-7	2007	ROS scavengers, pyrrolidinedithiocarbamate (PDTC) and N-acetyl-cysteine (NAC), reduced the levels of ROS induced by TNF-alpha, IL-1 beta and IFN-gamma (P&lt;0.05).	Acetylcysteine	73-76	interferon gamma	Homo sapiens	141-150
17503468-6	2007	In addition, endosulfan has been shown to generate transient reactive oxygen species (ROS), and blocking this oxidative stress by N-acetyl cysteine (NAC) strongly prevented both persistent nuclear ERK1/2 phosphorylation and cell growth decrease.	Acetylcysteine	149-152	mitogen-activated protein kinase 3	Homo sapiens	197-203
17597576-9	2007	Additionally, N-acetylcysteine (an antioxidant) attenuated high glucose-induced growth arrest and p15(INK4b) protein expression.	Acetylcysteine	14-30	cyclin dependent kinase inhibitor 2B	Homo sapiens	98-101
17889685-5	2007	Furthermore, the eugenol-modulated COX-2 expression was inhibited by an NF-kappaB inhibitor, N-acetylcysteine.	Acetylcysteine	93-109	prostaglandin-endoperoxide synthase 2	Homo sapiens	35-40
17889685-5	2007	Furthermore, the eugenol-modulated COX-2 expression was inhibited by an NF-kappaB inhibitor, N-acetylcysteine.	Acetylcysteine	93-109	nuclear factor kappa B subunit 1	Homo sapiens	72-81
17597576-9	2007	Additionally, N-acetylcysteine (an antioxidant) attenuated high glucose-induced growth arrest and p15(INK4b) protein expression.	Acetylcysteine	14-30	cyclin dependent kinase inhibitor 2B	Homo sapiens	102-107
17542780-6	2007	The antioxidant NAC (N-acetylcysteine) also showed the same effects as morphine on DOX-induced ROS generation, caspase-3 activation and cytochrome c release and changes in Bax (Bcl-2-associated X protein) and Bcl-2 protein expression.	Acetylcysteine	16-19	caspase 3	Homo sapiens	111-120
17958324-8	2007	Pretreatment of ESMC with N-acetylcysteine, a ROS scavenger, also attenuated the ET-1-induced ERK1/2 activation.	Acetylcysteine	26-42	endothelin 1	Homo sapiens	81-85
17958324-8	2007	Pretreatment of ESMC with N-acetylcysteine, a ROS scavenger, also attenuated the ET-1-induced ERK1/2 activation.	Acetylcysteine	26-42	mitogen-activated protein kinase 3	Homo sapiens	94-100
17542780-6	2007	The antioxidant NAC (N-acetylcysteine) also showed the same effects as morphine on DOX-induced ROS generation, caspase-3 activation and cytochrome c release and changes in Bax (Bcl-2-associated X protein) and Bcl-2 protein expression.	Acetylcysteine	16-19	cytochrome c, somatic	Homo sapiens	136-148
17542780-6	2007	The antioxidant NAC (N-acetylcysteine) also showed the same effects as morphine on DOX-induced ROS generation, caspase-3 activation and cytochrome c release and changes in Bax (Bcl-2-associated X protein) and Bcl-2 protein expression.	Acetylcysteine	16-19	BCL2 associated X, apoptosis regulator	Homo sapiens	172-175
17542780-6	2007	The antioxidant NAC (N-acetylcysteine) also showed the same effects as morphine on DOX-induced ROS generation, caspase-3 activation and cytochrome c release and changes in Bax (Bcl-2-associated X protein) and Bcl-2 protein expression.	Acetylcysteine	16-19	BCL2 associated X, apoptosis regulator	Homo sapiens	177-204
17542780-6	2007	The antioxidant NAC (N-acetylcysteine) also showed the same effects as morphine on DOX-induced ROS generation, caspase-3 activation and cytochrome c release and changes in Bax (Bcl-2-associated X protein) and Bcl-2 protein expression.	Acetylcysteine	16-19	BCL2 apoptosis regulator	Homo sapiens	177-182
17542780-6	2007	The antioxidant NAC (N-acetylcysteine) also showed the same effects as morphine on DOX-induced ROS generation, caspase-3 activation and cytochrome c release and changes in Bax (Bcl-2-associated X protein) and Bcl-2 protein expression.	Acetylcysteine	21-37	caspase 3	Homo sapiens	111-120
17542780-6	2007	The antioxidant NAC (N-acetylcysteine) also showed the same effects as morphine on DOX-induced ROS generation, caspase-3 activation and cytochrome c release and changes in Bax (Bcl-2-associated X protein) and Bcl-2 protein expression.	Acetylcysteine	21-37	cytochrome c, somatic	Homo sapiens	136-148
17542780-6	2007	The antioxidant NAC (N-acetylcysteine) also showed the same effects as morphine on DOX-induced ROS generation, caspase-3 activation and cytochrome c release and changes in Bax (Bcl-2-associated X protein) and Bcl-2 protein expression.	Acetylcysteine	21-37	BCL2 associated X, apoptosis regulator	Homo sapiens	172-175
17542780-6	2007	The antioxidant NAC (N-acetylcysteine) also showed the same effects as morphine on DOX-induced ROS generation, caspase-3 activation and cytochrome c release and changes in Bax (Bcl-2-associated X protein) and Bcl-2 protein expression.	Acetylcysteine	21-37	BCL2 associated X, apoptosis regulator	Homo sapiens	177-204
17542780-6	2007	The antioxidant NAC (N-acetylcysteine) also showed the same effects as morphine on DOX-induced ROS generation, caspase-3 activation and cytochrome c release and changes in Bax (Bcl-2-associated X protein) and Bcl-2 protein expression.	Acetylcysteine	21-37	BCL2 apoptosis regulator	Homo sapiens	177-182
17687726-7	2007	Pretreatment of cells with NAC or R6G also inhibited silica-induced production of interleukin (IL)-1beta and tumor necrosis factor (TNF)-alpha, but the inhibition of these cytokines with agents known to block their secretion did not protect cells from silica-induced apoptosis.	Acetylcysteine	27-30	interleukin 1 beta	Rattus norvegicus	82-104
17785204-4	2007	Ectopic expression of an oxygen-independent, stabilized HIF-1 mutant rescued lymphoma xenografts from inhibition by two antioxidants: N-acetylcysteine and vitamin C.	Acetylcysteine	134-150	hypoxia inducible factor 1 subunit alpha	Homo sapiens	56-61
17707397-6	2007	Attenuation of oxidative stress, downregulation of the pro-inflammatory cytokine tumor necrosis factor-alpha (TNF-alpha) and its TNF-R1 receptor were significant after 1-month NAC treatment.	Acetylcysteine	176-179	tumor necrosis factor	Rattus norvegicus	81-108
17707397-6	2007	Attenuation of oxidative stress, downregulation of the pro-inflammatory cytokine tumor necrosis factor-alpha (TNF-alpha) and its TNF-R1 receptor were significant after 1-month NAC treatment.	Acetylcysteine	176-179	tumor necrosis factor	Rattus norvegicus	110-119
17632094-11	2007	CONCLUSION: Acrolein inactivates paraoxonase 1 in HDL, a process that is inhibited by N-acetylcysteine.	Acetylcysteine	86-102	paraoxonase 1	Homo sapiens	33-46
17917164-1	2007	In this study, we evaluated the effect of lipoic acid (LA) and N-acetyl cysteine (NAC) on oxidative [4-hydroxy-2-nonenal, N(epsilon)-(carboxymethyl)lysine and heme oxygenase-1] and apoptotic (caspase 9 and Bax) markers in fibroblasts from patients with Alzheimer disease (AD) and age-matched and young controls.	Acetylcysteine	82-85	BCL2 associated X, apoptosis regulator	Homo sapiens	206-209
17687726-9	2007	The secretion of IL-1beta and TNF-alpha by silica-exposed AM was markedly inhibited by NAC and R6G, suggesting that the production of these cytokines is also ROS dependent.	Acetylcysteine	87-90	tumor necrosis factor	Rattus norvegicus	30-39
17687726-7	2007	Pretreatment of cells with NAC or R6G also inhibited silica-induced production of interleukin (IL)-1beta and tumor necrosis factor (TNF)-alpha, but the inhibition of these cytokines with agents known to block their secretion did not protect cells from silica-induced apoptosis.	Acetylcysteine	27-30	tumor necrosis factor	Rattus norvegicus	109-142
17687726-9	2007	The secretion of IL-1beta and TNF-alpha by silica-exposed AM was markedly inhibited by NAC and R6G, suggesting that the production of these cytokines is also ROS dependent.	Acetylcysteine	87-90	interleukin 1 beta	Rattus norvegicus	17-25
17665043-7	2007	Further, we found that the expression of Snail, an important transcription factor in EMT, was increased in this process, which is inhibited by the nuclear factor kappa B (NFkappaB) inhibitor aspirin while not affected by the reactive oxygen species (ROS) scavenger N-acetyl cysteine.	Acetylcysteine	265-282	snail family transcriptional repressor 1	Homo sapiens	41-46
17846503-7	2007	Pretreatment of cells with N-acetylcysteine (NAC) reduced ROS generation and cell growth inhibition, and pretreatment with NAC or a caspase 8 inhibitor (Z-IETD-FMK) inhibited the acacetin-induced loss of mitochondrial membrane potential and release of cytochrome c and AIF.	Acetylcysteine	27-43	cytochrome c, somatic	Homo sapiens	252-264
17846503-7	2007	Pretreatment of cells with N-acetylcysteine (NAC) reduced ROS generation and cell growth inhibition, and pretreatment with NAC or a caspase 8 inhibitor (Z-IETD-FMK) inhibited the acacetin-induced loss of mitochondrial membrane potential and release of cytochrome c and AIF.	Acetylcysteine	45-48	cytochrome c, somatic	Homo sapiens	252-264
17846503-7	2007	Pretreatment of cells with N-acetylcysteine (NAC) reduced ROS generation and cell growth inhibition, and pretreatment with NAC or a caspase 8 inhibitor (Z-IETD-FMK) inhibited the acacetin-induced loss of mitochondrial membrane potential and release of cytochrome c and AIF.	Acetylcysteine	123-126	cytochrome c, somatic	Homo sapiens	252-264
17718901-6	2007	The ability of resveratrol to sensitize TRAIL-resistant LNCaP cells was inhibited by dominant negative FADD, caspase-8 siRNA or N-acetyl cysteine.	Acetylcysteine	128-145	TNF superfamily member 10	Homo sapiens	40-45
17602961-9	2007	The 8-isoprostane production levels at P15 were suppressed in both the gliclazide group (-20%, P&lt;0.05) and the N-acetylcysteine-treated group (-31%, P&lt;0.01).	Acetylcysteine	114-130	cyclin dependent kinase inhibitor 2B	Mus musculus	39-42
17568325-9	2007	Lipopolysaccharide increased body temperature and plasma concentrations of tumor necrosis factor-alpha, which was mitigated during N-acetylcysteine infusions.	Acetylcysteine	131-147	tumor necrosis factor	Homo sapiens	75-102
17521393-0	2007	Mycobacterium tuberculosis H37Rv induces monocytic release of interleukin-6 via activation of mitogen-activated protein kinases: inhibition by N-acetyl-L-cysteine.	Acetylcysteine	143-162	interleukin 6	Homo sapiens	62-75
17521393-3	2007	The aim of this study was to investigate the role of mitogen-activated protein kinases in the secretion of interleukin-6 in THP-1 cells and human primary monocytes that were infected with Mycobacterium tuberculosis H37Rv, and its regulation by N-acetyl-L-cysteine, a potential antimycobacterial agent.	Acetylcysteine	244-263	interleukin 6	Homo sapiens	107-120
17521393-6	2007	Pretreatment with N-acetyl-L-cysteine reduced, in a dose-dependent manner, M. tuberculosis H37Rv-induced activation of mitogen-activated protein kinase kinase 3/6 and interleukin-6 production in THP-1 cells.	Acetylcysteine	18-37	interleukin 6	Homo sapiens	167-180
17521393-6	2007	Pretreatment with N-acetyl-L-cysteine reduced, in a dose-dependent manner, M. tuberculosis H37Rv-induced activation of mitogen-activated protein kinase kinase 3/6 and interleukin-6 production in THP-1 cells.	Acetylcysteine	18-37	GLI family zinc finger 2	Homo sapiens	195-200
17385713-7	2007	Pretreatment with the antioxidant, N-acetyl-L-cysteine, completely suppressed the effect of parthenolide on JAK1 and STAT3.	Acetylcysteine	35-54	Janus kinase 1	Homo sapiens	108-112
17533199-8	2007	Further, there was reduced insulin induced Akt activation and increased tumor necrosis factor-alpha levels in vascular smooth muscle cells from Ren2 and Sprague-Dawley rats treated with angiotensin II, abnormalities that were abrogated by angiotensin type 1 receptor blockade with valsartan or antioxidant N-acetylcysteine.	Acetylcysteine	306-322	angiotensinogen	Rattus norvegicus	186-200
17385713-7	2007	Pretreatment with the antioxidant, N-acetyl-L-cysteine, completely suppressed the effect of parthenolide on JAK1 and STAT3.	Acetylcysteine	35-54	signal transducer and activator of transcription 3	Homo sapiens	117-122
17884964-8	2007	NAC and vitamin E significantly reduced the increases in the local production of TNF-alpha and VEGF, and perivascular MPO activity.	Acetylcysteine	0-3	tumor necrosis factor	Rattus norvegicus	81-90
17692765-5	2007	Reports of AST/ALT &gt; 1000, a major effect, and death were 1301 (2.9%), 2957 (6.6%), and 232 (0.5%), respectively, for patients receiving NAC plus AC, vs. 5273 (12%), 4534 (10.3%), and 369 (0.8%), respectively, for patients receiving NAC alone (p &lt; 0.01).	Acetylcysteine	140-143	solute carrier family 17 member 5	Homo sapiens	11-14
17522181-3	2007	This mechanism was redox-sensitive; N-acetylcysteine totally abrogated the down-regulation of SphK1 activity and strongly inhibited Abeta-induced cell death.	Acetylcysteine	36-52	amyloid beta precursor protein	Homo sapiens	132-137
17566772-5	2007	Unlike aortic rings with endothelium from controls, those from angiotensin II-infused rats exhibited persistent hyporesponsiveness to phenylephrine after pre-exposure to GSNO, as well as relaxation upon addition of N-acetylcysteine (NAC, which can displace NO from cysteine-NO residues) or HgCl(2) (which cleaves S-NO bonds).	Acetylcysteine	215-231	angiotensinogen	Rattus norvegicus	63-77
17566772-5	2007	Unlike aortic rings with endothelium from controls, those from angiotensin II-infused rats exhibited persistent hyporesponsiveness to phenylephrine after pre-exposure to GSNO, as well as relaxation upon addition of N-acetylcysteine (NAC, which can displace NO from cysteine-NO residues) or HgCl(2) (which cleaves S-NO bonds).	Acetylcysteine	233-236	angiotensinogen	Rattus norvegicus	63-77
17526490-6	2007	Pretreatment with the antioxidant N-acetylcysteine (NAC) and expression of MT1 in the Ikkbeta(-)(/)(-) cells prevented JNK activation; moreover, NAC pretreatment, MT1 expression, MKK4 ablation, and JNK inhibition all protected cells from death induced by arsenic.	Acetylcysteine	34-50	metallothionein 1	Mus musculus	163-166
17526490-6	2007	Pretreatment with the antioxidant N-acetylcysteine (NAC) and expression of MT1 in the Ikkbeta(-)(/)(-) cells prevented JNK activation; moreover, NAC pretreatment, MT1 expression, MKK4 ablation, and JNK inhibition all protected cells from death induced by arsenic.	Acetylcysteine	145-148	metallothionein 1	Mus musculus	75-78
17526490-6	2007	Pretreatment with the antioxidant N-acetylcysteine (NAC) and expression of MT1 in the Ikkbeta(-)(/)(-) cells prevented JNK activation; moreover, NAC pretreatment, MT1 expression, MKK4 ablation, and JNK inhibition all protected cells from death induced by arsenic.	Acetylcysteine	145-148	metallothionein 1	Mus musculus	163-166
17616699-0	2007	Superoxide signaling mediates N-acetyl-L-cysteine-induced G1 arrest: regulatory role of cyclin D1 and manganese superoxide dismutase.	Acetylcysteine	30-49	superoxide dismutase 2, mitochondrial	Mus musculus	102-132
17616699-2	2007	We investigated the hypothesis that NAC-induced reactive oxygen species (ROS) signaling perturbs cellular proliferation by regulating the cell cycle regulatory protein cyclin D1 and the ROS scavenging enzyme Mn-superoxide dismutase (MnSOD).	Acetylcysteine	36-39	superoxide dismutase 2, mitochondrial	Mus musculus	208-231
17616699-2	2007	We investigated the hypothesis that NAC-induced reactive oxygen species (ROS) signaling perturbs cellular proliferation by regulating the cell cycle regulatory protein cyclin D1 and the ROS scavenging enzyme Mn-superoxide dismutase (MnSOD).	Acetylcysteine	36-39	superoxide dismutase 2, mitochondrial	Mus musculus	233-238
17616699-5	2007	A delayed response to NAC exposure was an increase in both MnSOD protein and activity.	Acetylcysteine	22-25	superoxide dismutase 2, mitochondrial	Mus musculus	59-64
17616699-6	2007	NAC-induced G(1) arrest is exacerbated in MnSOD heterozygous fibroblasts.	Acetylcysteine	0-3	superoxide dismutase 2, mitochondrial	Mus musculus	42-47
17561100-6	2007	Activation of p38 MAPK and HIF-1alpha accumulation were attenuated by N-acetyl-L-cysteine (antioxidant), catalase (hydrogen peroxide scavenger), or a selective p38 MAPK inhibitor (SB203580).	Acetylcysteine	70-89	hypoxia inducible factor 1 subunit alpha	Homo sapiens	27-37
17481858-11	2007	Among various antioxidants used in this study, only thiol-containing antioxidants such as NAC or GSH inhibited both JNK and p38 MAPK activation and apoptosis, indicating the unique protective capacity of thiol compounds.	Acetylcysteine	90-93	mitogen-activated protein kinase 8	Homo sapiens	116-119
17481858-11	2007	Among various antioxidants used in this study, only thiol-containing antioxidants such as NAC or GSH inhibited both JNK and p38 MAPK activation and apoptosis, indicating the unique protective capacity of thiol compounds.	Acetylcysteine	90-93	mitogen-activated protein kinase 14	Homo sapiens	124-127
17376491-11	2007	In contrast, we found that addition of N-acetylcysteine or vitamin C enhanced transcription of MCP-1 by B[a]P. In conclusion, our studies revealed potent vascular pro-inflammatory effects of B[a]P, as evidenced by AhR-mediated induction of MCP-1.	Acetylcysteine	39-55	aryl-hydrocarbon receptor	Mus musculus	214-217
17693979-8	2007	It is suggested that CFS patients should be treated with antioxidants, which inhibit the production of NFkappabeta, such as curcumin, N-Acetyl-Cysteine, quercitin, silimarin, lipoic acid and omega-3 fatty acids.	Acetylcysteine	134-151	nuclear factor kappa B subunit 1	Homo sapiens	103-114
17487501-7	2007	Pretreatment with the ROS scavenger N-acetylcysteine (NAC), the p38 MAPK inhibitor SB203580 or the caspase-3 inhibitor Ac-DEVD-CHO was found to effectively prevent UVA-induced apoptosis, indicating that ROS, p38 MAPK and caspase-3 play important roles in apoptosis.	Acetylcysteine	36-52	mitogen-activated protein kinase 14	Homo sapiens	208-211
17487501-7	2007	Pretreatment with the ROS scavenger N-acetylcysteine (NAC), the p38 MAPK inhibitor SB203580 or the caspase-3 inhibitor Ac-DEVD-CHO was found to effectively prevent UVA-induced apoptosis, indicating that ROS, p38 MAPK and caspase-3 play important roles in apoptosis.	Acetylcysteine	36-52	caspase 3	Homo sapiens	221-230
17487501-7	2007	Pretreatment with the ROS scavenger N-acetylcysteine (NAC), the p38 MAPK inhibitor SB203580 or the caspase-3 inhibitor Ac-DEVD-CHO was found to effectively prevent UVA-induced apoptosis, indicating that ROS, p38 MAPK and caspase-3 play important roles in apoptosis.	Acetylcysteine	54-57	mitogen-activated protein kinase 14	Homo sapiens	208-211
17487501-7	2007	Pretreatment with the ROS scavenger N-acetylcysteine (NAC), the p38 MAPK inhibitor SB203580 or the caspase-3 inhibitor Ac-DEVD-CHO was found to effectively prevent UVA-induced apoptosis, indicating that ROS, p38 MAPK and caspase-3 play important roles in apoptosis.	Acetylcysteine	54-57	caspase 3	Homo sapiens	221-230
17532486-3	2007	The addition of the ERK inhibitor, PD98059, (but not the p38 inhibitor, SB203580, or the JNK inhibitor, SP600125) and the chemical antioxidant, N-acetyl cysteine (NAC), significantly reduced BE-induced HO-1 protein expression by respectively blocking ERK protein phosphorylation and intracellular peroxide production.	Acetylcysteine	144-161	heme oxygenase 1	Mus musculus	202-206
17532486-3	2007	The addition of the ERK inhibitor, PD98059, (but not the p38 inhibitor, SB203580, or the JNK inhibitor, SP600125) and the chemical antioxidant, N-acetyl cysteine (NAC), significantly reduced BE-induced HO-1 protein expression by respectively blocking ERK protein phosphorylation and intracellular peroxide production.	Acetylcysteine	144-161	mitogen-activated protein kinase 1	Mus musculus	251-254
17616699-9	2007	These results show that an O(2)(*-) signaling pathway regulates NAC-induced G(1) arrest by decreasing cyclin D1 protein levels and increasing MnSOD activity.	Acetylcysteine	64-67	superoxide dismutase 2, mitochondrial	Mus musculus	142-147
17697525-6	2007	Telmisartan and the antioxidant, N-acetylcysteine, completely inhibited AGEs-induced MCP-1 overproduction by mesangial cells.	Acetylcysteine	33-49	mast cell protease 1	Mus musculus	85-90
17760840-5	2007	Both apocynin and NAC abolished the PC ability of Ang II.	Acetylcysteine	18-21	angiotensinogen	Rattus norvegicus	50-56
17760840-6	2007	In Ang II treated heart, there was a decreased association of p38MAPKbeta &amp; extracellular-signal regulated kinase (ERK) 1/ 2 (anti-death signalling component) with caveolin while there was an increased association of p38MAPKalpha &amp; Jun N-terminal kinase (JNK) (death signalling component) indicating reduced amount of death signal components and increased amount of anti-death signalling components being available to the Ang II treated heart to generate a survival signal, which was reversed with NAC or apocynin.	Acetylcysteine	506-509	angiotensinogen	Rattus norvegicus	3-9
17760840-7	2007	The survival signal was also demonstrated by increased phosphorylation of serine/threonine-protein kinase B (AKT) and enhanced induction of expression of Bcl-2 during Ang II PC and its reversal with NAC &amp; apocynin treated heart.	Acetylcysteine	199-202	AKT serine/threonine kinase 1	Homo sapiens	109-112
17760840-7	2007	The survival signal was also demonstrated by increased phosphorylation of serine/threonine-protein kinase B (AKT) and enhanced induction of expression of Bcl-2 during Ang II PC and its reversal with NAC &amp; apocynin treated heart.	Acetylcysteine	199-202	BCL2 apoptosis regulator	Homo sapiens	154-159
17760840-7	2007	The survival signal was also demonstrated by increased phosphorylation of serine/threonine-protein kinase B (AKT) and enhanced induction of expression of Bcl-2 during Ang II PC and its reversal with NAC &amp; apocynin treated heart.	Acetylcysteine	199-202	angiotensinogen	Rattus norvegicus	167-173
17549348-9	2007	This sensitization was inhibited with N-acetyl-L-cysteine (NAC) treatment by abrogating the ROS which was generated by the combined treatment of CCCP and TRAIL.	Acetylcysteine	38-57	TNF superfamily member 10	Homo sapiens	154-159
17549348-9	2007	This sensitization was inhibited with N-acetyl-L-cysteine (NAC) treatment by abrogating the ROS which was generated by the combined treatment of CCCP and TRAIL.	Acetylcysteine	59-62	TNF superfamily member 10	Homo sapiens	154-159
17549348-10	2007	Of interest, NAC also inhibited reduction of the Delta Psi m and Bax translocation after CCCP pretreatment which suggest that the generation of ROS may precede the loss in MTP.	Acetylcysteine	13-16	BCL2 associated X, apoptosis regulator	Homo sapiens	65-68
17553538-5	2007	Pre-incubation with N-acetylcysteine (NAC) reduced the increased ROS and caspase 3 activity as well as phosphatidyl serine exposure.	Acetylcysteine	20-36	caspase 3	Homo sapiens	73-82
17574387-6	2007	The pre-intake of NAC, SEC, SMC, and SPC significantly attenuated MPTP-induced glutathione loss, retained the activity of GPX and SOD, diminished oxidative stress, and suppressed MPTP-induced elevation of IL-6 and TNF-alpha (P < 0.05).	Acetylcysteine	18-21	interleukin 6	Mus musculus	205-209
17574387-6	2007	The pre-intake of NAC, SEC, SMC, and SPC significantly attenuated MPTP-induced glutathione loss, retained the activity of GPX and SOD, diminished oxidative stress, and suppressed MPTP-induced elevation of IL-6 and TNF-alpha (P < 0.05).	Acetylcysteine	18-21	tumor necrosis factor	Mus musculus	214-223
17574387-8	2007	Compared with MPTP treatment alone, the pre-intake of NAC, SEC, SMC, and SPC significantly elevated GPX mRNA expression and diminished TNF-alpha mRNA expression (P < 0.05), in which SPC showed the greatest suppressive effect against MPTP-induced TNF-alpha mRNA expression (P < 0.05).	Acetylcysteine	54-57	tumor necrosis factor	Mus musculus	135-144
17574387-8	2007	Compared with MPTP treatment alone, the pre-intake of NAC, SEC, SMC, and SPC significantly elevated GPX mRNA expression and diminished TNF-alpha mRNA expression (P < 0.05), in which SPC showed the greatest suppressive effect against MPTP-induced TNF-alpha mRNA expression (P < 0.05).	Acetylcysteine	54-57	tumor necrosis factor	Mus musculus	246-255
17553538-5	2007	Pre-incubation with N-acetylcysteine (NAC) reduced the increased ROS and caspase 3 activity as well as phosphatidyl serine exposure.	Acetylcysteine	38-41	caspase 3	Homo sapiens	73-82
17512465-5	2007	Incubation of WI38 cells with N-acetylcysteine (NAC) replenishes intracellular GSH, abrogates the increased production of ROS, ameliorates Erk and p38 MAPK activation, and attenuates senescence induction by BU.	Acetylcysteine	30-46	mitogen-activated protein kinase 1	Homo sapiens	139-142
17468103-1	2007	In murine embryonic fibroblasts, N-acetyl-L-cysteine (NAC), a GSH generating agent, enhances hypoxic apoptosis by blocking the NFkappaB survival pathway (Qanungo, S., Wang, M., and Nieminen, A. L. (2004) J. Biol.	Acetylcysteine	33-52	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	127-135
17475277-3	2007	Moreover, LPS/D-GalN-induced apoptosis was associated with increased inducible nitric oxide synthase (iNOS) and nitric oxide (NO) production, as well as elevated reactive oxygen species (ROS) production, which were all strongly inhibited by treatment with the antioxidant N-acetyl-L-cysteine (NAC) and an iNOS/NO inhibitor, L-NMMA.	Acetylcysteine	272-291	galanin and GMAP prepropeptide	Mus musculus	16-20
17475277-3	2007	Moreover, LPS/D-GalN-induced apoptosis was associated with increased inducible nitric oxide synthase (iNOS) and nitric oxide (NO) production, as well as elevated reactive oxygen species (ROS) production, which were all strongly inhibited by treatment with the antioxidant N-acetyl-L-cysteine (NAC) and an iNOS/NO inhibitor, L-NMMA.	Acetylcysteine	293-296	galanin and GMAP prepropeptide	Mus musculus	16-20
17631703-5	2007	The level of TNF-alpha in portal vein and plasma ALT increased continually in I/R group at 1 hour and 3 hours after reperfusion compared with SH group, however, they were significantly lowered in the group pretreated by NAC (P&lt;0.05 or P&lt;0.01).	Acetylcysteine	220-223	tumor necrosis factor	Mus musculus	13-22
17631703-7	2007	NAC can inhibit the activation of TLR2/4 and the induction of TNF-alpha resulted from I/R injury via modulating the state of redox process; thus it might mitigate liver and lung injury following partial hepatic I/R in mice.	Acetylcysteine	0-3	tumor necrosis factor	Mus musculus	62-71
17536822-9	2007	N-acetylcysteine (NAC) and catalase prevented up-regulation of GADD153 expression caused by 5-OH-HxMF.	Acetylcysteine	0-16	DNA damage inducible transcript 3	Homo sapiens	63-70
17536822-9	2007	N-acetylcysteine (NAC) and catalase prevented up-regulation of GADD153 expression caused by 5-OH-HxMF.	Acetylcysteine	18-21	DNA damage inducible transcript 3	Homo sapiens	63-70
17477906-2	2007	In this report, we showed that p21(Cip1) was degraded at an early phase after low dose H(2)O(2) treatment of a variety of cell types and that preincubation of cells with the antioxidant, N-acetylcysteine, prolonged p21(Cip1) half-life.	Acetylcysteine	187-203	cyclin dependent kinase inhibitor 1A	Homo sapiens	35-39
17475277-6	2007	In STAT1-deficient mice, nuclear factor kappaB (NF-kappaB) activation by TNF-alpha/IFN-gamma was attenuated and strongly inhibited by both NAC and L-NMMA.	Acetylcysteine	139-142	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	48-57
17475277-6	2007	In STAT1-deficient mice, nuclear factor kappaB (NF-kappaB) activation by TNF-alpha/IFN-gamma was attenuated and strongly inhibited by both NAC and L-NMMA.	Acetylcysteine	139-142	tumor necrosis factor	Mus musculus	73-82
17475277-6	2007	In STAT1-deficient mice, nuclear factor kappaB (NF-kappaB) activation by TNF-alpha/IFN-gamma was attenuated and strongly inhibited by both NAC and L-NMMA.	Acetylcysteine	139-142	interferon gamma	Mus musculus	83-92
17512465-5	2007	Incubation of WI38 cells with N-acetylcysteine (NAC) replenishes intracellular GSH, abrogates the increased production of ROS, ameliorates Erk and p38 MAPK activation, and attenuates senescence induction by BU.	Acetylcysteine	30-46	mitogen-activated protein kinase 14	Homo sapiens	147-150
17512465-5	2007	Incubation of WI38 cells with N-acetylcysteine (NAC) replenishes intracellular GSH, abrogates the increased production of ROS, ameliorates Erk and p38 MAPK activation, and attenuates senescence induction by BU.	Acetylcysteine	30-46	mitogen-activated protein kinase 1	Homo sapiens	151-155
17512465-5	2007	Incubation of WI38 cells with N-acetylcysteine (NAC) replenishes intracellular GSH, abrogates the increased production of ROS, ameliorates Erk and p38 MAPK activation, and attenuates senescence induction by BU.	Acetylcysteine	48-51	mitogen-activated protein kinase 1	Homo sapiens	139-142
17512465-5	2007	Incubation of WI38 cells with N-acetylcysteine (NAC) replenishes intracellular GSH, abrogates the increased production of ROS, ameliorates Erk and p38 MAPK activation, and attenuates senescence induction by BU.	Acetylcysteine	48-51	mitogen-activated protein kinase 14	Homo sapiens	147-150
17512465-5	2007	Incubation of WI38 cells with N-acetylcysteine (NAC) replenishes intracellular GSH, abrogates the increased production of ROS, ameliorates Erk and p38 MAPK activation, and attenuates senescence induction by BU.	Acetylcysteine	48-51	mitogen-activated protein kinase 1	Homo sapiens	151-155
17414623-4	2007	Thiol compounds such as N-acetyl cysteine, glutathione and dithiothreitol protected the cells against chloroacetaldehyde-induced cell death, although other nonthiol compounds and the antioxidative enzymes superoxide dismutase and catalase did not, suggesting that reactive oxygen species might not mediate cell death.	Acetylcysteine	24-41	catalase	Homo sapiens	230-238
17540521-5	2007	Furthermore, when cells were pretreated with N-acetyl cysteine (NAC), a scavenger of reactive oxygen species (ROS), DM-induced Nrf2 signaling was suppressed.	Acetylcysteine	45-62	NFE2 like bZIP transcription factor 2	Rattus norvegicus	127-131
17540521-5	2007	Furthermore, when cells were pretreated with N-acetyl cysteine (NAC), a scavenger of reactive oxygen species (ROS), DM-induced Nrf2 signaling was suppressed.	Acetylcysteine	64-67	NFE2 like bZIP transcription factor 2	Rattus norvegicus	127-131
17462539-7	2007	NAC also lowers Akt activity, extracellular signal-regulated kinase 1/2, and the redox-sensitive transcription factor NF-kappaB, all of which are ROS related and seem to be in close connection with cell proliferation.	Acetylcysteine	0-3	AKT serine/threonine kinase 1	Rattus norvegicus	16-19
17448897-8	2007	We observed that BzATP stimulates MAP kinase (ERK1/ERK2, p38, and JNK1/JNK2) phosphorylation and that the antioxidants N-acetylcysteine and ascorbic acid strongly attenuate BzATP-mediated JNK1/JNK2 and p38 phosphorylation but only slightly reduce BzATP-induced ERK1/ERK2 phosphorylation.	Acetylcysteine	119-135	mitogen-activated protein kinase 9	Mus musculus	193-197
17171638-3	2007	Curcumin-induced GADD153 gene upregulation was attenuated by reduced glutathione (GSH) or N-acetylcysteine (NAC) and potentiated by the glutathione synthesis inhibitor, L-buthionine-(S,R)-sulfoximine (BSO).	Acetylcysteine	90-106	DNA damage inducible transcript 3	Homo sapiens	17-24
17171638-3	2007	Curcumin-induced GADD153 gene upregulation was attenuated by reduced glutathione (GSH) or N-acetylcysteine (NAC) and potentiated by the glutathione synthesis inhibitor, L-buthionine-(S,R)-sulfoximine (BSO).	Acetylcysteine	108-111	DNA damage inducible transcript 3	Homo sapiens	17-24
17526765-6	2007	Since NAC treatment reduced neutrophil infiltration in the pancreas, we conclude that CD11b/CD18 over-expression is required for leukocyte recruitment; however, other adhesion molecules in addition to ICAM-1 seem to contribute to leukocyte homing during BPDO-induced AP.	Acetylcysteine	6-9	integrin subunit beta 2	Homo sapiens	92-96
17548252-0	2007	N-acetylcysteine inhibits activation of toll-like receptor 2 and 4 gene expression in the liver and lung after partial hepatic ischemia-reperfusion injury in mice.	Acetylcysteine	0-16	toll-like receptor 4	Mus musculus	40-66
17548252-7	2007	The levels of portal vein TNF-alpha and plasma ALT increased continuously in the I/R group at 1 and 3 hours of reperfusion compared with the SH group; however, they declined significantly in the group pretreated with NAC (P&lt;0.05).	Acetylcysteine	217-220	tumor necrosis factor	Mus musculus	26-35
17548252-10	2007	NAC inhibited the activation of TLR2/4 and the induction of TNF-alpha resulting from I/R injury via modulating the redox state, thus it may mitigate liver and lung injury following partial hepatic I/R in mice.	Acetylcysteine	0-3	tumor necrosis factor	Mus musculus	60-69
17448897-8	2007	We observed that BzATP stimulates MAP kinase (ERK1/ERK2, p38, and JNK1/JNK2) phosphorylation and that the antioxidants N-acetylcysteine and ascorbic acid strongly attenuate BzATP-mediated JNK1/JNK2 and p38 phosphorylation but only slightly reduce BzATP-induced ERK1/ERK2 phosphorylation.	Acetylcysteine	119-135	mitogen-activated protein kinase 1	Mus musculus	266-270
17531120-11	2007	Preincubation with N-acetylcysteine or ginkgo biloba extract increased GSH level, suppressed AGEs-induced oxidative stress and TGF-beta1, CTGF and Fn mRNA overexpression.	Acetylcysteine	19-35	transforming growth factor, beta 1	Rattus norvegicus	127-136
17428624-8	2007	MNNG-induced DNA damage (measured by the comet assay) and thymocyte death (measured by propidium iodide uptake) was prevented by the PARP inhibitor PJ-34 and by glutathione (GSH) or N-acetylcysteine (NAC).	Acetylcysteine	200-203	poly(ADP-ribose) polymerase 1	Homo sapiens	133-137
17289842-9	2007	In EDCs treated with a recombinant adenovirus expressing superoxide dismutase or N-acetyl-cysteine (but not catalase), the p53-Bax pathway activated by oxLDL was blocked, and apoptosis was prevented.	Acetylcysteine	81-98	tumor protein p53	Homo sapiens	123-126
17363366-9	2007	Treatment of BAEC with EGCG generated intracellular H(2)O(2) (assessed with H(2)O(2)-specific fluorescent dye CM-H(2)DCF-DA), whereas treatment with N-acetylcysteine inhibited EGCG-stimulated phosphorylation of Fyn, Akt, and eNOS.	Acetylcysteine	149-165	AKT serine/threonine kinase 1	Rattus norvegicus	216-219
17289842-9	2007	In EDCs treated with a recombinant adenovirus expressing superoxide dismutase or N-acetyl-cysteine (but not catalase), the p53-Bax pathway activated by oxLDL was blocked, and apoptosis was prevented.	Acetylcysteine	81-98	BCL2 associated X, apoptosis regulator	Homo sapiens	127-130
17216608-10	2007	Erdosteine, NAC and vitamin E significantly reduced the increases in the local production of TNF-alpha and heart MPO activity.	Acetylcysteine	12-15	tumor necrosis factor	Rattus norvegicus	93-102
17331500-10	2007	Induced VEGF expression was completely abrogated by inhibitors of protein kinase C (PKC) (Ro318220), nuclear factor-kappaB (NF-kappaB) [caffeic acid phenethyl ester (CAPE)], and reactive oxygen species (ROS) [N-acetyl-cysteine (Nac) and diphenyleneiodonium (DPI)].	Acetylcysteine	209-226	vascular endothelial growth factor A	Homo sapiens	8-12
17331500-10	2007	Induced VEGF expression was completely abrogated by inhibitors of protein kinase C (PKC) (Ro318220), nuclear factor-kappaB (NF-kappaB) [caffeic acid phenethyl ester (CAPE)], and reactive oxygen species (ROS) [N-acetyl-cysteine (Nac) and diphenyleneiodonium (DPI)].	Acetylcysteine	209-226	nuclear factor kappa B subunit 1	Homo sapiens	101-122
17331500-10	2007	Induced VEGF expression was completely abrogated by inhibitors of protein kinase C (PKC) (Ro318220), nuclear factor-kappaB (NF-kappaB) [caffeic acid phenethyl ester (CAPE)], and reactive oxygen species (ROS) [N-acetyl-cysteine (Nac) and diphenyleneiodonium (DPI)].	Acetylcysteine	209-226	nuclear factor kappa B subunit 1	Homo sapiens	124-133
17331500-10	2007	Induced VEGF expression was completely abrogated by inhibitors of protein kinase C (PKC) (Ro318220), nuclear factor-kappaB (NF-kappaB) [caffeic acid phenethyl ester (CAPE)], and reactive oxygen species (ROS) [N-acetyl-cysteine (Nac) and diphenyleneiodonium (DPI)].	Acetylcysteine	228-231	vascular endothelial growth factor A	Homo sapiens	8-12
17331500-10	2007	Induced VEGF expression was completely abrogated by inhibitors of protein kinase C (PKC) (Ro318220), nuclear factor-kappaB (NF-kappaB) [caffeic acid phenethyl ester (CAPE)], and reactive oxygen species (ROS) [N-acetyl-cysteine (Nac) and diphenyleneiodonium (DPI)].	Acetylcysteine	228-231	nuclear factor kappa B subunit 1	Homo sapiens	101-122
17331500-10	2007	Induced VEGF expression was completely abrogated by inhibitors of protein kinase C (PKC) (Ro318220), nuclear factor-kappaB (NF-kappaB) [caffeic acid phenethyl ester (CAPE)], and reactive oxygen species (ROS) [N-acetyl-cysteine (Nac) and diphenyleneiodonium (DPI)].	Acetylcysteine	228-231	nuclear factor kappa B subunit 1	Homo sapiens	124-133
17131361-6	2007	Pretreatment of the cells with N-acetylcysteine, an antioxidant, completely prevented the SPC-induced ROS generation, apoptosis, and ERK activation, whereas the ROS generation was not abrogated by treatment with U0126.	Acetylcysteine	31-47	mitogen-activated protein kinase 1	Homo sapiens	133-136
17296806-7	2007	It is noteworthy that suppression of ROS accumulation by ROS scavengers butylated hydroxyanisole, and N-acetyl-L-cysteine prevented the luteolin-induced suppression of NF-kappaB and potentiation of JNK and significantly suppressed the synergistic cytotoxicity seen with cotreatment of luteolin and TNF.	Acetylcysteine	102-121	nuclear factor kappa B subunit 1	Homo sapiens	168-177
17296806-7	2007	It is noteworthy that suppression of ROS accumulation by ROS scavengers butylated hydroxyanisole, and N-acetyl-L-cysteine prevented the luteolin-induced suppression of NF-kappaB and potentiation of JNK and significantly suppressed the synergistic cytotoxicity seen with cotreatment of luteolin and TNF.	Acetylcysteine	102-121	mitogen-activated protein kinase 8	Homo sapiens	198-201
17296806-7	2007	It is noteworthy that suppression of ROS accumulation by ROS scavengers butylated hydroxyanisole, and N-acetyl-L-cysteine prevented the luteolin-induced suppression of NF-kappaB and potentiation of JNK and significantly suppressed the synergistic cytotoxicity seen with cotreatment of luteolin and TNF.	Acetylcysteine	102-121	tumor necrosis factor	Homo sapiens	298-301
17633826-12	2007	CONCLUSION: NAC may have the effect of retarding pathological change of the liver, which may associate with the decrease of NO and GSH in serum and hepatic tissue and iNOS activity in the tissue.	Acetylcysteine	12-15	nitric oxide synthase 2, inducible	Mus musculus	167-171
17309078-7	2007	Inhibition of ROS production by N-acetyl-L-cysteine and catalase prevented necrosis and switched the cell death mode to apoptosis that depends on mitochondrial death pathway involving caspase-9 and caspase-3 activation, indicating a critical role of ROS in determination of GD-induced cell death mode.	Acetylcysteine	32-51	caspase 3	Homo sapiens	198-207
17440103-8	2007	Finally, N-acetylcysteine, an inhibitor of ROS, inhibits sanguinarine-induced generation of ROS, up-regulation of DR5, Bax conformational changes, activation of caspase-3, and down-regulation of IAPs.	Acetylcysteine	9-25	BCL2 associated X, apoptosis regulator	Homo sapiens	119-122
17108007-4	2007	In this study, we found that antioxidant enzyme catalase and antioxidants N-acetyl-l-cysteine, alpha-phenyl-N-tert-butylnitrone, and lipoic acid prevent ANG II from activating NFAT3 promoter-luciferase.	Acetylcysteine	74-93	angiotensinogen	Homo sapiens	153-159
17440103-8	2007	Finally, N-acetylcysteine, an inhibitor of ROS, inhibits sanguinarine-induced generation of ROS, up-regulation of DR5, Bax conformational changes, activation of caspase-3, and down-regulation of IAPs.	Acetylcysteine	9-25	caspase 3	Homo sapiens	161-170
17108007-4	2007	In this study, we found that antioxidant enzyme catalase and antioxidants N-acetyl-l-cysteine, alpha-phenyl-N-tert-butylnitrone, and lipoic acid prevent ANG II from activating NFAT3 promoter-luciferase.	Acetylcysteine	74-93	nuclear factor of activated T cells 3	Homo sapiens	176-181
16996755-6	2007	The antioxidant N-acetyl-cysteine avoided ROS increase, prevented the NO-induced caspase 3 activation, and reduced the NO apoptotic effect.	Acetylcysteine	16-33	caspase 3	Homo sapiens	81-90
17135302-9	2007	In addition, IL-1beta could induce the production of reactive oxygen species (ROS), and N-acetyl-L-cysteine, a scavenger of ROS, reversed the decreased level of ABCA1 induced by IL-1beta.	Acetylcysteine	88-107	interleukin 1 beta	Homo sapiens	178-186
17245372-11	2007	This process is mediated by an increase in cytochrome c release and caspase 3 activation and is prevented by N-acetylcysteine or the superoxide dismutase mimetic, MnTBAP.	Acetylcysteine	109-125	cytochrome c, somatic	Homo sapiens	43-55
17245372-11	2007	This process is mediated by an increase in cytochrome c release and caspase 3 activation and is prevented by N-acetylcysteine or the superoxide dismutase mimetic, MnTBAP.	Acetylcysteine	109-125	caspase 3	Homo sapiens	68-77
17122189-8	2007	Subsequently, the levels of cardiac free 15-F(2t)-isoprostane, HO-1, Cu-Zn-SOD, total SOD, IL-6, and COX-2 in diabetic rats were decreased by NAC.	Acetylcysteine	142-145	superoxide dismutase 1	Rattus norvegicus	69-78
17122189-8	2007	Subsequently, the levels of cardiac free 15-F(2t)-isoprostane, HO-1, Cu-Zn-SOD, total SOD, IL-6, and COX-2 in diabetic rats were decreased by NAC.	Acetylcysteine	142-145	interleukin 6	Rattus norvegicus	91-95
17334646-11	2007	With the aid of NAC and H2O2, it was determined that reactive oxygen species (ROS) is an upstream signaling molecule for activating the NF-kappaB induced by H. pylori.	Acetylcysteine	16-19	nuclear factor kappa B subunit 1	Homo sapiens	136-145
17287397-5	2007	The oye2Delta phenotype can be completely suppressed by removing the potential for formation of the actin C285-C374 disulfide bond, the likely substrate of the Oye2p enzyme or by treating the cells with the clinically important reductant N-acetylcysteine.	Acetylcysteine	238-254	actin	Saccharomyces cerevisiae S288C	100-105
17010595-11	2007	Inhaled NAC induced the overexpression of Mn superoxide dismutase (MnSOD) mRNA and protein, but did not alter the expressions of other antioxidant enzymes, including CuZnSOD, extracellular SOD, and glutathione peroxydase 1.	Acetylcysteine	8-11	superoxide dismutase 2, mitochondrial	Mus musculus	42-65
17010595-11	2007	Inhaled NAC induced the overexpression of Mn superoxide dismutase (MnSOD) mRNA and protein, but did not alter the expressions of other antioxidant enzymes, including CuZnSOD, extracellular SOD, and glutathione peroxydase 1.	Acetylcysteine	8-11	superoxide dismutase 2, mitochondrial	Mus musculus	67-72
17010595-11	2007	Inhaled NAC induced the overexpression of Mn superoxide dismutase (MnSOD) mRNA and protein, but did not alter the expressions of other antioxidant enzymes, including CuZnSOD, extracellular SOD, and glutathione peroxydase 1.	Acetylcysteine	8-11	superoxide dismutase 1, soluble	Mus musculus	69-72
17010595-12	2007	CONCLUSION: These findings suggest that the antioxidant properties of NAC in hyperoxic lung injury involve a decrease in mitochondrial ROS in association with the induction of MnSOD, in addition to its role as a precursor of GSH.	Acetylcysteine	70-73	superoxide dismutase 2, mitochondrial	Mus musculus	176-181
17270171-6	2007	N-acetylcysteine treatment attenuated the increased oxidative stress, plasma and renal lipids, urine protein excretion rate, mesangial matrix expansion index, and protein expression of renal CTGF, but did not affect plasma adiponectin levels, renal protein expression of adiponectin receptor 1, phosphorylation of AMPK-alpha (Thr172) and renal protein expression of phospho-ACC (Ser79) in diabetic rats.	Acetylcysteine	0-16	adiponectin receptor 1	Rattus norvegicus	271-293
17266944-1	2007	OBJECTIVES: The aim of this study was to investigate the effect of the antioxidants pyrrolidine dithiocarbamate (PDTC) and N-acetylcysteine (NAC) on the ionizing radiation (IR)- and tumor necrosis factor-alpha (TNF-alpha) induced tissue factor (TF) expression and its release from human umbilical vein endothelial cells (HUVECs).	Acetylcysteine	123-139	tumor necrosis factor	Homo sapiens	182-209
17266944-1	2007	OBJECTIVES: The aim of this study was to investigate the effect of the antioxidants pyrrolidine dithiocarbamate (PDTC) and N-acetylcysteine (NAC) on the ionizing radiation (IR)- and tumor necrosis factor-alpha (TNF-alpha) induced tissue factor (TF) expression and its release from human umbilical vein endothelial cells (HUVECs).	Acetylcysteine	123-139	tumor necrosis factor	Homo sapiens	211-220
17266944-1	2007	OBJECTIVES: The aim of this study was to investigate the effect of the antioxidants pyrrolidine dithiocarbamate (PDTC) and N-acetylcysteine (NAC) on the ionizing radiation (IR)- and tumor necrosis factor-alpha (TNF-alpha) induced tissue factor (TF) expression and its release from human umbilical vein endothelial cells (HUVECs).	Acetylcysteine	141-144	tumor necrosis factor	Homo sapiens	182-209
17266944-1	2007	OBJECTIVES: The aim of this study was to investigate the effect of the antioxidants pyrrolidine dithiocarbamate (PDTC) and N-acetylcysteine (NAC) on the ionizing radiation (IR)- and tumor necrosis factor-alpha (TNF-alpha) induced tissue factor (TF) expression and its release from human umbilical vein endothelial cells (HUVECs).	Acetylcysteine	141-144	tumor necrosis factor	Homo sapiens	211-220
17334226-8	2007	Inhibition of Tat-induced ROS generation by N-acetyl cysteine, vitamin C and diphenyl iodonium suppressed Tat-induced NF-kappaB activation, ICAM-1 and VCAM-1 expression, and monocyte adhesion in CRT-MG.	Acetylcysteine	44-61	vascular cell adhesion molecule 1	Homo sapiens	151-157
17188792-10	2007	We analyzed the formation of APAP-NAC metabolite in the presence of human recombinant NQO1.	Acetylcysteine	34-37	NAD(P)H quinone dehydrogenase 1	Homo sapiens	86-90
17283157-9	2007	SP600125, an inhibitor of JNK, or antioxidant N-acetyl-L-cysteine inhibited the enhancement of chemosensitivity against CDDP by galectin-7 transfection.	Acetylcysteine	46-65	galectin 7	Homo sapiens	128-138
17189831-6	2007	Incubation with the thiol antioxidant N-acetylcysteine strongly inhibited both the Nrf2 accumulation and the expression of Nrf2-regulated genes such as HO-1, GCLM, and SQSTM1.	Acetylcysteine	38-54	NFE2 like bZIP transcription factor 2	Homo sapiens	83-87
17237434-2	2007	Administration of anti-inflammatory drugs, i.e., N-acetylcysteine (NAC) or mitoquinone-Q (mito-Q) in low concentrations in the human pulmonary aortic endothelial cells offered protection against depletion of reduced glutathione and oxidative stress mediated by TNF-alpha.	Acetylcysteine	49-65	tumor necrosis factor	Homo sapiens	261-270
17237434-2	2007	Administration of anti-inflammatory drugs, i.e., N-acetylcysteine (NAC) or mitoquinone-Q (mito-Q) in low concentrations in the human pulmonary aortic endothelial cells offered protection against depletion of reduced glutathione and oxidative stress mediated by TNF-alpha.	Acetylcysteine	67-70	tumor necrosis factor	Homo sapiens	261-270
17237434-5	2007	Of the two catalytic subunits of IKK (IKKalpha and IKKbeta), low concentrations of NAC and mito-Q activated IKKalpha activity, thereby inhibiting the downstream NF-kappaB and ICAM-1 induction by TNF-alpha.	Acetylcysteine	83-86	tumor necrosis factor	Homo sapiens	195-204
17237434-6	2007	High concentrations of NAC and mito-Q instead caused glutathionylation of IKKalpha, thereby inhibiting its activity that in turn enhanced the downstream NF-kappaB activation and ICAM-1 expression by TNF-alpha.	Acetylcysteine	23-26	tumor necrosis factor	Homo sapiens	199-208
17149372-7	2007	Hcy increased p38-MAPK activity (fivefold), with maximal effect at 50 microM and 20 min; p38-MAPK activation was attenuated by N-acetylcysteine (Nac) and catalase (Cat), further indicating that the effect was via oxidative stress.	Acetylcysteine	127-143	mitogen-activated protein kinase 14	Homo sapiens	89-92
17149372-7	2007	Hcy increased p38-MAPK activity (fivefold), with maximal effect at 50 microM and 20 min; p38-MAPK activation was attenuated by N-acetylcysteine (Nac) and catalase (Cat), further indicating that the effect was via oxidative stress.	Acetylcysteine	145-148	mitogen-activated protein kinase 14	Homo sapiens	89-92
17149372-9	2007	In addition, Hcy-induced apoptosis as determined by TUNEL and ssDNA assay was abrogated by Nac, Cat, and SB203580 (p38-MAPK inhibitor).	Acetylcysteine	91-94	mitogen-activated protein kinase 14	Homo sapiens	115-123
17082565-9	2007	Upregulation of NF-kappaB and COX-2 expression by AcQ treatment was suppressed by the antioxidant N-acetylcysteine (NAC).	Acetylcysteine	98-114	nuclear factor kappa B subunit 1	Homo sapiens	16-25
17082565-9	2007	Upregulation of NF-kappaB and COX-2 expression by AcQ treatment was suppressed by the antioxidant N-acetylcysteine (NAC).	Acetylcysteine	98-114	prostaglandin-endoperoxide synthase 2	Homo sapiens	30-35
17082565-9	2007	Upregulation of NF-kappaB and COX-2 expression by AcQ treatment was suppressed by the antioxidant N-acetylcysteine (NAC).	Acetylcysteine	116-119	nuclear factor kappa B subunit 1	Homo sapiens	16-25
17082565-9	2007	Upregulation of NF-kappaB and COX-2 expression by AcQ treatment was suppressed by the antioxidant N-acetylcysteine (NAC).	Acetylcysteine	116-119	prostaglandin-endoperoxide synthase 2	Homo sapiens	30-35
17222881-3	2007	N-Acetyl-l-cysteine (20 mM), dimethyl thiourea (20 mM) and catalase (5 microM) significantly inhibited TNF release by primed AMs incubated with CAPs.	Acetylcysteine	0-19	tumor necrosis factor	Homo sapiens	103-106
17189831-6	2007	Incubation with the thiol antioxidant N-acetylcysteine strongly inhibited both the Nrf2 accumulation and the expression of Nrf2-regulated genes such as HO-1, GCLM, and SQSTM1.	Acetylcysteine	38-54	NFE2 like bZIP transcription factor 2	Homo sapiens	123-127
17189831-6	2007	Incubation with the thiol antioxidant N-acetylcysteine strongly inhibited both the Nrf2 accumulation and the expression of Nrf2-regulated genes such as HO-1, GCLM, and SQSTM1.	Acetylcysteine	38-54	glutamate-cysteine ligase modifier subunit	Homo sapiens	158-162
17295135-8	2007	NAC inhibited LPS-induced intracameral elevation of TNF-alpha, IL-6, and nitrite.	Acetylcysteine	0-3	tumor necrosis factor	Rattus norvegicus	52-61
17613008-5	2007	The increased level of LP and activities of superoxide dismutase and catalase in hyperoxaluric rats were restored after NAC treatment.	Acetylcysteine	120-123	catalase	Rattus norvegicus	69-77
17295135-8	2007	NAC inhibited LPS-induced intracameral elevation of TNF-alpha, IL-6, and nitrite.	Acetylcysteine	0-3	interleukin 6	Rattus norvegicus	63-67
17094942-5	2006	The reactive oxygen species (ROS) scavenger N-acetylcysteine and the NADPH oxidase inhibitor diphenyleneiodonium also inhibited the LPS-induced expression of TNF-alpha.	Acetylcysteine	44-60	tumor necrosis factor	Rattus norvegicus	158-167
17237268-4	2007	N-acetyl-l-cysteine, a thiol-containing antioxidant, completely blocked Bax relocalization, PARP-1 activation, and cytochrome c release.	Acetylcysteine	0-19	BCL2 associated X, apoptosis regulator	Homo sapiens	72-75
17237268-4	2007	N-acetyl-l-cysteine, a thiol-containing antioxidant, completely blocked Bax relocalization, PARP-1 activation, and cytochrome c release.	Acetylcysteine	0-19	poly(ADP-ribose) polymerase 1	Homo sapiens	92-98
17237268-4	2007	N-acetyl-l-cysteine, a thiol-containing antioxidant, completely blocked Bax relocalization, PARP-1 activation, and cytochrome c release.	Acetylcysteine	0-19	cytochrome c, somatic	Homo sapiens	115-127
17237268-8	2007	In addition, antioxidant N-acetyl-l-cysteine completely blocked p38 MAPK activation.	Acetylcysteine	25-44	mitogen-activated protein kinase 14	Homo sapiens	64-67
17349145-15	2007	Compared with the LPS group, the levels of ALT, NO and iNOS mRNA of NAC group were lower at the time points 6 h and 12 h (P &lt; 0.01).	Acetylcysteine	68-71	nitric oxide synthase 2, inducible	Mus musculus	55-59
16868182-6	2007	In contrast, N-acetyl-cysteine dramatically blocked GA/LPS-induced ROS production, simultaneously decreasing caspase-3 activity and the presence of apoptotic nuclei.	Acetylcysteine	13-30	caspase 3	Homo sapiens	109-118
17260537-8	2007	Further, in the younger age rats the NAC treatment resulted in the decrease of lipid peroxidation in both the regions that was accompanied by the increase catalase activity in cerebral cortex region along with increase in GSH content and SOD in cerebellum regions.	Acetylcysteine	37-40	catalase	Rattus norvegicus	155-163
17284935-7	2007	In vitro, PEDF or an antioxidant N-acetylcysteine blocked the AGE-induced RAGE gene induction in microvascular endothelial cells.	Acetylcysteine	33-49	advanced glycosylation end product-specific receptor	Rattus norvegicus	74-78
17046137-10	2006	Posttreatment with erdosteine and NAC significantly reduced the increases in the local production of TNF-alpha and VEGF, and epithelial MPO activity.	Acetylcysteine	34-37	tumor necrosis factor	Rattus norvegicus	101-110
17046137-11	2006	The effects of NAC on apoptosis, the increases in the local production of TNF-alpha and VEGF, were weaker than the effects of erdosteine.	Acetylcysteine	15-18	tumor necrosis factor	Rattus norvegicus	74-83
16973888-2	2006	Addition of antioxidants such as N-acetyl-l-cysteine or catalase attenuates G-Rh2-induced ROS generation, JNK1 activation, and apoptosis.	Acetylcysteine	33-52	mitogen-activated protein kinase 8	Homo sapiens	106-110
16990553-6	2006	NAC treatment prevented H2O2-induced PTP inhibition, and reduced H2O2- and ligand-induced PDGF beta-receptor phosphorylation, PDGF-induced proliferation, and chemotaxis of VSMCs.	Acetylcysteine	0-3	protein tyrosine phosphatase, non-receptor type 1	Rattus norvegicus	37-40
17142801-7	2006	Attenuating reactive oxygen species (ROS) in reoxygenation using the antioxidant N-acetyl cysteine results in inhibition of Nrf-2 activation.	Acetylcysteine	81-98	NFE2 like bZIP transcription factor 2	Homo sapiens	124-129
16563723-8	2006	PEITC and NAC-PEITC also increased the mRNA levels of tissue inhibitors of matrix metalloproteinase (TIMPs) 1 and 2.	Acetylcysteine	10-13	TIMP metallopeptidase inhibitor 1	Homo sapiens	54-115
16950408-7	2006	Moreover, an enhanced iNOS expression was also observed in the cells treated directly with MG which was significantly inhibited when co-application with N-acetyl-l-cysteine.	Acetylcysteine	153-172	nitric oxide synthase 2	Homo sapiens	22-26
16860347-12	2006	We conclude that post-treatment with NAC suppresses the release of plasma TNF-alpha, IL-6, and IL-10 in endotoxin shock, and decreases the markers of organ injury.	Acetylcysteine	37-40	tumor necrosis factor	Rattus norvegicus	74-83
17026986-0	2006	N-acetylcysteine attenuates TNF-alpha-induced human vascular endothelial cell apoptosis and restores eNOS expression.	Acetylcysteine	0-16	tumor necrosis factor	Homo sapiens	28-37
17026986-0	2006	N-acetylcysteine attenuates TNF-alpha-induced human vascular endothelial cell apoptosis and restores eNOS expression.	Acetylcysteine	0-16	nitric oxide synthase 3	Homo sapiens	101-105
17026986-3	2006	We investigated the effects of the antioxidant N-acetylcysteine on TNF-alpha-induced apoptosis in human vascular endothelial cell (cell line ECV304) apoptosis, NO production and lipid peroxidation.	Acetylcysteine	47-63	tumor necrosis factor	Homo sapiens	67-76
17026986-11	2006	N-acetylcysteine attenuation of TNF-alpha-induced human vascular endothelial cell apoptosis is associated with the restoration of eNOS expression.	Acetylcysteine	0-16	tumor necrosis factor	Homo sapiens	32-41
17026986-11	2006	N-acetylcysteine attenuation of TNF-alpha-induced human vascular endothelial cell apoptosis is associated with the restoration of eNOS expression.	Acetylcysteine	0-16	nitric oxide synthase 3	Homo sapiens	130-134
17030433-0	2006	Antioxidant N-acetylcysteine inhibits the activation of JNK3 mediated by the GluR6-PSD95-MLK3 signaling module during cerebral ischemia in rat hippocampus.	Acetylcysteine	12-28	mitogen-activated protein kinase kinase kinase 11	Rattus norvegicus	89-93
17030433-8	2006	Results indicate that NAC distinctly inhibited the association of PSD95 with GluR6 and MLK3, the autophosphorylation of MLK3, the combination of MLK3 with JNK3 and JNK3 activation.	Acetylcysteine	22-25	mitogen-activated protein kinase kinase kinase 11	Rattus norvegicus	87-91
17030433-8	2006	Results indicate that NAC distinctly inhibited the association of PSD95 with GluR6 and MLK3, the autophosphorylation of MLK3, the combination of MLK3 with JNK3 and JNK3 activation.	Acetylcysteine	22-25	mitogen-activated protein kinase kinase kinase 11	Rattus norvegicus	120-124
17030433-8	2006	Results indicate that NAC distinctly inhibited the association of PSD95 with GluR6 and MLK3, the autophosphorylation of MLK3, the combination of MLK3 with JNK3 and JNK3 activation.	Acetylcysteine	22-25	mitogen-activated protein kinase kinase kinase 11	Rattus norvegicus	120-124
17023264-0	2006	Evidence that N-acetylcysteine inhibits TNF-alpha-induced cerebrovascular endothelin-1 upregulation via inhibition of mitogen- and stress-activated protein kinase.	Acetylcysteine	14-30	tumor necrosis factor	Homo sapiens	40-49
17023264-0	2006	Evidence that N-acetylcysteine inhibits TNF-alpha-induced cerebrovascular endothelin-1 upregulation via inhibition of mitogen- and stress-activated protein kinase.	Acetylcysteine	14-30	endothelin 1	Homo sapiens	74-86
17023264-3	2006	Gene expression of endothelin-1 (ET-1), which contributes to cerebral blood flow decline in acute brain injury, is partially regulated by reactive oxygen species, and thus a potential target of NAC.	Acetylcysteine	194-197	endothelin 1	Homo sapiens	19-31
17023264-3	2006	Gene expression of endothelin-1 (ET-1), which contributes to cerebral blood flow decline in acute brain injury, is partially regulated by reactive oxygen species, and thus a potential target of NAC.	Acetylcysteine	194-197	endothelin 1	Homo sapiens	33-37
17023264-4	2006	We therefore examined the effect of NAC on tumor necrosis factor (TNF)-alpha-induced ET-1 production in cerebrovascular endothelial cells.	Acetylcysteine	36-39	tumor necrosis factor	Homo sapiens	43-76
17023264-4	2006	We therefore examined the effect of NAC on tumor necrosis factor (TNF)-alpha-induced ET-1 production in cerebrovascular endothelial cells.	Acetylcysteine	36-39	endothelin 1	Homo sapiens	85-89
17023264-5	2006	NAC dose dependently inhibited TNF-alpha-induced preproET-1 mRNA upregulation and ET-1 protein secretion, while upregulation of inducible nitric oxide synthase (iNOS) was unaffected.	Acetylcysteine	0-3	tumor necrosis factor	Homo sapiens	31-40
17023264-5	2006	NAC dose dependently inhibited TNF-alpha-induced preproET-1 mRNA upregulation and ET-1 protein secretion, while upregulation of inducible nitric oxide synthase (iNOS) was unaffected.	Acetylcysteine	0-3	endothelin 1	Homo sapiens	55-59
17023264-5	2006	NAC dose dependently inhibited TNF-alpha-induced preproET-1 mRNA upregulation and ET-1 protein secretion, while upregulation of inducible nitric oxide synthase (iNOS) was unaffected.	Acetylcysteine	0-3	nitric oxide synthase 2	Homo sapiens	161-165
17023264-7	2006	However, transient inhibition of NF-kappaB DNA binding suggested that NAC may inhibit ET-1 upregulation by inhibiting (a) parallel pathway(s) necessary for full transcriptional activation of NF-kappaB-mediated ET-1 gene expression.	Acetylcysteine	70-73	nuclear factor kappa B subunit 1	Homo sapiens	33-42
17023264-7	2006	However, transient inhibition of NF-kappaB DNA binding suggested that NAC may inhibit ET-1 upregulation by inhibiting (a) parallel pathway(s) necessary for full transcriptional activation of NF-kappaB-mediated ET-1 gene expression.	Acetylcysteine	70-73	endothelin 1	Homo sapiens	86-90
17023264-7	2006	However, transient inhibition of NF-kappaB DNA binding suggested that NAC may inhibit ET-1 upregulation by inhibiting (a) parallel pathway(s) necessary for full transcriptional activation of NF-kappaB-mediated ET-1 gene expression.	Acetylcysteine	70-73	nuclear factor kappa B subunit 1	Homo sapiens	191-200
17023264-7	2006	However, transient inhibition of NF-kappaB DNA binding suggested that NAC may inhibit ET-1 upregulation by inhibiting (a) parallel pathway(s) necessary for full transcriptional activation of NF-kappaB-mediated ET-1 gene expression.	Acetylcysteine	70-73	endothelin 1	Homo sapiens	210-214
16952378-0	2006	N-acetylcysteine attenuates TNF-alpha induced changes in secretion of interleukin-6, plasminogen activator inhibitor-1 and adiponectin from 3T3-L1 adipocytes.	Acetylcysteine	0-16	tumor necrosis factor	Mus musculus	28-37
16952378-0	2006	N-acetylcysteine attenuates TNF-alpha induced changes in secretion of interleukin-6, plasminogen activator inhibitor-1 and adiponectin from 3T3-L1 adipocytes.	Acetylcysteine	0-16	interleukin 6	Mus musculus	70-83
16952378-2	2006	This study was designed to determine whether N-acetylcysteine (NAC), an antioxidant, prevents the activation of nuclear factor-kappaB (NF-kappaB) by exogenously administered TNF-alpha in adipocytes, and whether such change affects the production of adipocytokines.	Acetylcysteine	45-61	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	112-133
16952378-2	2006	This study was designed to determine whether N-acetylcysteine (NAC), an antioxidant, prevents the activation of nuclear factor-kappaB (NF-kappaB) by exogenously administered TNF-alpha in adipocytes, and whether such change affects the production of adipocytokines.	Acetylcysteine	45-61	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	135-144
16952378-2	2006	This study was designed to determine whether N-acetylcysteine (NAC), an antioxidant, prevents the activation of nuclear factor-kappaB (NF-kappaB) by exogenously administered TNF-alpha in adipocytes, and whether such change affects the production of adipocytokines.	Acetylcysteine	45-61	tumor necrosis factor	Mus musculus	174-183
16952378-2	2006	This study was designed to determine whether N-acetylcysteine (NAC), an antioxidant, prevents the activation of nuclear factor-kappaB (NF-kappaB) by exogenously administered TNF-alpha in adipocytes, and whether such change affects the production of adipocytokines.	Acetylcysteine	63-66	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	112-133
16952378-2	2006	This study was designed to determine whether N-acetylcysteine (NAC), an antioxidant, prevents the activation of nuclear factor-kappaB (NF-kappaB) by exogenously administered TNF-alpha in adipocytes, and whether such change affects the production of adipocytokines.	Acetylcysteine	63-66	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	135-144
16952378-2	2006	This study was designed to determine whether N-acetylcysteine (NAC), an antioxidant, prevents the activation of nuclear factor-kappaB (NF-kappaB) by exogenously administered TNF-alpha in adipocytes, and whether such change affects the production of adipocytokines.	Acetylcysteine	63-66	tumor necrosis factor	Mus musculus	174-183
16952378-5	2006	The activation of NF-kappaB was significantly prevented by the pretreatment with 20 mM of NAC.	Acetylcysteine	90-93	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	18-27
16952378-7	2006	NAC (5-20 mM) attenuated the TNF-alpha-induced changes in these adipocytokine secretions in a dose-dependent manner.	Acetylcysteine	0-3	tumor necrosis factor	Mus musculus	29-38
16952378-9	2006	The present study revealed that NAC inhibited the TNF-alpha-mediated activation of NF-kappaB and improved the adverse changes in the levels of IL-6, PAI-1 and adiponectin in 3T3-L1 adipocytes.	Acetylcysteine	32-35	tumor necrosis factor	Mus musculus	50-59
16952378-9	2006	The present study revealed that NAC inhibited the TNF-alpha-mediated activation of NF-kappaB and improved the adverse changes in the levels of IL-6, PAI-1 and adiponectin in 3T3-L1 adipocytes.	Acetylcysteine	32-35	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	83-92
16952378-9	2006	The present study revealed that NAC inhibited the TNF-alpha-mediated activation of NF-kappaB and improved the adverse changes in the levels of IL-6, PAI-1 and adiponectin in 3T3-L1 adipocytes.	Acetylcysteine	32-35	interleukin 6	Mus musculus	143-147
16952378-10	2006	NAC may have the potential to improve the obesity-related abnormal adipocytokine metabolism by attenuating the TNF-alpha-induced oxidant-antioxidant imbalance in adipocytes.	Acetylcysteine	0-3	tumor necrosis factor	Mus musculus	111-120
17108112-7	2006	Addition of NAC to the culture medium prolonged the life span of cells treated with 4-OHT and prevented the up-regulation of Foxo3a protein levels caused by PKB activation.	Acetylcysteine	12-15	thymoma viral proto-oncogene 1	Mus musculus	157-160
17023264-8	2006	Similar to NAC, the MEK1/2 inhibitor U0126, the p38 inhibitor SB203580, and the protein kinase inhibitor H-89 selectively inhibited ET-1 upregulation without affecting nuclear p65 translocation, suggesting that NAC inhibits ET-1 upregulation via inhibition of mitogen- and stress-activated protein kinase (MSK).	Acetylcysteine	211-214	endothelin 1	Homo sapiens	132-136
17023264-9	2006	Supporting this notion, cotreatment with NAC inhibited the TNF-alpha-induced rise in MSK1 and MSK2 kinase activity, while siRNA knock-down experiments showed that MSK2 is the predominant isoform involved in TNF-alpha-induced ET-1 upregulation.	Acetylcysteine	41-44	tumor necrosis factor	Homo sapiens	59-68
17023264-9	2006	Supporting this notion, cotreatment with NAC inhibited the TNF-alpha-induced rise in MSK1 and MSK2 kinase activity, while siRNA knock-down experiments showed that MSK2 is the predominant isoform involved in TNF-alpha-induced ET-1 upregulation.	Acetylcysteine	41-44	tumor necrosis factor	Homo sapiens	207-216
17023264-9	2006	Supporting this notion, cotreatment with NAC inhibited the TNF-alpha-induced rise in MSK1 and MSK2 kinase activity, while siRNA knock-down experiments showed that MSK2 is the predominant isoform involved in TNF-alpha-induced ET-1 upregulation.	Acetylcysteine	41-44	endothelin 1	Homo sapiens	225-229
17095404-14	2006	Administration of LA and NAC can improve the antioxidant capacity and activity of LPL and reduce blood lipid significantly.	Acetylcysteine	25-28	lipoprotein lipase	Rattus norvegicus	82-85
16860347-2	2006	In a previous study, we found that pretreatment with NAC attenuated organ dysfunction and damage, reduced the production of free radicals, tumor necrosis factor-alpha (TNF-alpha) and interleukin-1beta (IL-1beta) following endotoxemia elicited by administration of lipopolysaccharide (LPS).	Acetylcysteine	53-56	tumor necrosis factor	Rattus norvegicus	139-166
16860347-2	2006	In a previous study, we found that pretreatment with NAC attenuated organ dysfunction and damage, reduced the production of free radicals, tumor necrosis factor-alpha (TNF-alpha) and interleukin-1beta (IL-1beta) following endotoxemia elicited by administration of lipopolysaccharide (LPS).	Acetylcysteine	53-56	tumor necrosis factor	Rattus norvegicus	168-177
16860347-2	2006	In a previous study, we found that pretreatment with NAC attenuated organ dysfunction and damage, reduced the production of free radicals, tumor necrosis factor-alpha (TNF-alpha) and interleukin-1beta (IL-1beta) following endotoxemia elicited by administration of lipopolysaccharide (LPS).	Acetylcysteine	53-56	interleukin 1 beta	Rattus norvegicus	183-200
16860347-2	2006	In a previous study, we found that pretreatment with NAC attenuated organ dysfunction and damage, reduced the production of free radicals, tumor necrosis factor-alpha (TNF-alpha) and interleukin-1beta (IL-1beta) following endotoxemia elicited by administration of lipopolysaccharide (LPS).	Acetylcysteine	53-56	interleukin 1 beta	Rattus norvegicus	202-210
16860347-11	2006	Post-treatment with NAC diminished the decrease in MAP, increased the HR, and decreased the markers of organ injury (BUN, Cre, LDH, CPK, GOT, GPT) and inflammatory biomarkers (TNF-alpha, IL-6, IL-10) after LPS.	Acetylcysteine	20-23	tumor necrosis factor	Rattus norvegicus	176-185
16860347-11	2006	Post-treatment with NAC diminished the decrease in MAP, increased the HR, and decreased the markers of organ injury (BUN, Cre, LDH, CPK, GOT, GPT) and inflammatory biomarkers (TNF-alpha, IL-6, IL-10) after LPS.	Acetylcysteine	20-23	interleukin 6	Rattus norvegicus	187-191
16860347-12	2006	We conclude that post-treatment with NAC suppresses the release of plasma TNF-alpha, IL-6, and IL-10 in endotoxin shock, and decreases the markers of organ injury.	Acetylcysteine	37-40	interleukin 6	Rattus norvegicus	85-89
16987006-6	2006	The antioxidant N-acetylcysteine abolished Ang II- and AA-induced Akt/PKB activation and fibronectin expression.	Acetylcysteine	16-32	AKT serine/threonine kinase 1	Homo sapiens	70-73
16968467-11	2006	Treatment with N-acetylcysteine and doxazosin partially decreased myostatin mRNA and protein expression as compared with the shunt group.	Acetylcysteine	15-31	myostatin	Rattus norvegicus	66-75
16886168-5	2006	N-Acetylcysteine treatment delayed and reduced the down-regulation of CD45 expression induced by AP and prevented acinar cells from producing TNF-alpha.	Acetylcysteine	0-16	tumor necrosis factor	Homo sapiens	142-151
17000238-6	2006	RESULTS: After maternal lipopolysaccharide administration, fetal blood interleukin-6 markedly increased (3 +/- 2 to 1265 +/- 574 pg/mL); N-acetylcysteine that was given before or before and after lipopolysaccharide administration reduced fetal interleukin-6 response to control levels.	Acetylcysteine	137-153	interleukin 6	Rattus norvegicus	71-84
17000238-6	2006	RESULTS: After maternal lipopolysaccharide administration, fetal blood interleukin-6 markedly increased (3 +/- 2 to 1265 +/- 574 pg/mL); N-acetylcysteine that was given before or before and after lipopolysaccharide administration reduced fetal interleukin-6 response to control levels.	Acetylcysteine	137-153	interleukin 6	Rattus norvegicus	244-257
17670639-2	2006	As both myocardial ischemia and reperfusion (by reactive oxygen intermediates) can activate NFkappaB, we investigated the impact of the antioxidant N-acetylcysteine (NAC) on NFkappaB-regulation in patients subjected to cardioplegic arrest (CA) on cardiopulmonary bypass (CPB).	Acetylcysteine	166-169	nuclear factor kappa B subunit 1	Homo sapiens	174-182
17670639-9	2006	Antioxidative treatment with NAC decreases NFkappaB-activity following I/R in endothelial cells.	Acetylcysteine	29-32	nuclear factor kappa B subunit 1	Homo sapiens	43-51
16987006-6	2006	The antioxidant N-acetylcysteine abolished Ang II- and AA-induced Akt/PKB activation and fibronectin expression.	Acetylcysteine	16-32	fibronectin 1	Homo sapiens	89-100
16616762-8	2006	RESULTS: Relative to CONTROL, depletion of PMNs or NAC treatment reduced levels of plasma TNFalpha (567 +/- 130* and 231 +/- 72* versus 1994 +/- 447 pg/ml) and IL-6 (791 +/- 473* and 666 +/- 300* versus 3724 +/- 1233, pg/ml), accompanying a reduction in PMN accumulation (12 +/- 1* and 13 +/- 0.6* versus 20 +/- 1 mm2 myocardium) in ischemic myocardium.	Acetylcysteine	51-54	tumor necrosis factor	Rattus norvegicus	90-98
17072061-4	2006	In this study we evaluated the influence of N-acetylcysteine (NAC) (0.01 mM-30 mM) on the cytokine-induced (TNF-alpha/IL-1 beta) expression of the ICAM-1 adhesion molecule and on IL-8 release in endothelial (ECV-304) and bronchial epithelial (H292) cell lines.	Acetylcysteine	44-60	tumor necrosis factor	Homo sapiens	108-117
17072061-4	2006	In this study we evaluated the influence of N-acetylcysteine (NAC) (0.01 mM-30 mM) on the cytokine-induced (TNF-alpha/IL-1 beta) expression of the ICAM-1 adhesion molecule and on IL-8 release in endothelial (ECV-304) and bronchial epithelial (H292) cell lines.	Acetylcysteine	44-60	interleukin 1 beta	Homo sapiens	118-127
16616762-8	2006	RESULTS: Relative to CONTROL, depletion of PMNs or NAC treatment reduced levels of plasma TNFalpha (567 +/- 130* and 231 +/- 72* versus 1994 +/- 447 pg/ml) and IL-6 (791 +/- 473* and 666 +/- 300* versus 3724 +/- 1233, pg/ml), accompanying a reduction in PMN accumulation (12 +/- 1* and 13 +/- 0.6* versus 20 +/- 1 mm2 myocardium) in ischemic myocardium.	Acetylcysteine	51-54	interleukin 6	Rattus norvegicus	160-164
17072061-4	2006	In this study we evaluated the influence of N-acetylcysteine (NAC) (0.01 mM-30 mM) on the cytokine-induced (TNF-alpha/IL-1 beta) expression of the ICAM-1 adhesion molecule and on IL-8 release in endothelial (ECV-304) and bronchial epithelial (H292) cell lines.	Acetylcysteine	62-65	tumor necrosis factor	Homo sapiens	108-117
17072061-4	2006	In this study we evaluated the influence of N-acetylcysteine (NAC) (0.01 mM-30 mM) on the cytokine-induced (TNF-alpha/IL-1 beta) expression of the ICAM-1 adhesion molecule and on IL-8 release in endothelial (ECV-304) and bronchial epithelial (H292) cell lines.	Acetylcysteine	62-65	interleukin 1 beta	Homo sapiens	118-127
16616762-13	2006	CONCLUSION: These data suggest that the oxidants generated from activated PMNs after ischemia/reperfusion trigger myocardial apoptosis, which is further supported by an anti-oxidant therapy with NAC, potentially mediated by enhanced NFkappaB-TNFalpha signaling pathway, activated caspase-3 and down-regulated Bcl-2.	Acetylcysteine	195-198	tumor necrosis factor	Rattus norvegicus	242-250
17072061-4	2006	In this study we evaluated the influence of N-acetylcysteine (NAC) (0.01 mM-30 mM) on the cytokine-induced (TNF-alpha/IL-1 beta) expression of the ICAM-1 adhesion molecule and on IL-8 release in endothelial (ECV-304) and bronchial epithelial (H292) cell lines.	Acetylcysteine	62-65	C-X-C motif chemokine ligand 8	Homo sapiens	179-183
17072061-6	2006	NAC inhibited the TNF-alpha/IL-1 beta-stimulated ICAM-1 expression and IL-8 release from both cell lines in a concentration dependent manner.	Acetylcysteine	0-3	tumor necrosis factor	Homo sapiens	18-27
16616762-13	2006	CONCLUSION: These data suggest that the oxidants generated from activated PMNs after ischemia/reperfusion trigger myocardial apoptosis, which is further supported by an anti-oxidant therapy with NAC, potentially mediated by enhanced NFkappaB-TNFalpha signaling pathway, activated caspase-3 and down-regulated Bcl-2.	Acetylcysteine	195-198	BCL2, apoptosis regulator	Rattus norvegicus	309-314
17072061-6	2006	NAC inhibited the TNF-alpha/IL-1 beta-stimulated ICAM-1 expression and IL-8 release from both cell lines in a concentration dependent manner.	Acetylcysteine	0-3	interleukin 1 beta	Homo sapiens	28-37
17072061-6	2006	NAC inhibited the TNF-alpha/IL-1 beta-stimulated ICAM-1 expression and IL-8 release from both cell lines in a concentration dependent manner.	Acetylcysteine	0-3	C-X-C motif chemokine ligand 8	Homo sapiens	71-75
16616945-9	2006	Ciglitazone treatment increased Bax expression and caused a loss of mitochondrial membrane potential, and its effect was prevented by N-acetylcysteine, PD98059, and SB203580.	Acetylcysteine	134-150	BCL2 associated X, apoptosis regulator	Homo sapiens	32-35
17072061-8	2006	We conclude that NAC is an effective inhibitor of TNF-alpha/IL-1 beta- stimulated ICAM-1 and IL-8 release in endothelial and epithelial cells.	Acetylcysteine	17-20	tumor necrosis factor	Homo sapiens	50-59
17072061-8	2006	We conclude that NAC is an effective inhibitor of TNF-alpha/IL-1 beta- stimulated ICAM-1 and IL-8 release in endothelial and epithelial cells.	Acetylcysteine	17-20	interleukin 1 beta	Homo sapiens	60-69
17072061-8	2006	We conclude that NAC is an effective inhibitor of TNF-alpha/IL-1 beta- stimulated ICAM-1 and IL-8 release in endothelial and epithelial cells.	Acetylcysteine	17-20	C-X-C motif chemokine ligand 8	Homo sapiens	93-97
16863997-6	2006	Importantly, reduction of hydrogen peroxide by administration of the antioxidant N-acetylcysteine to Atm(-/-) mice attenuates the elevation of Nrf-2, c-Myc, and DNA synthesis in their thymocytes, suggesting that ATM may control c-Myc and DNA synthesis during postnatal thymocyte development by preventing accumulation of reactive oxygen species.	Acetylcysteine	81-97	nuclear factor, erythroid derived 2, like 2	Mus musculus	143-148
16859669-8	2006	N-acetylcysteine abolished the compensatory increase in myocardial Cu/Zn-SOD.	Acetylcysteine	0-16	superoxide dismutase 1	Rattus norvegicus	67-76
16928829-5	2006	Pretreatment with N-acetylcysteine, a GSH precursor, blocked the down-regulation of AR mRNA and protein expression by selenite and restored AR ligand binding and prostate-specific antigen expression to control levels.	Acetylcysteine	18-34	androgen receptor	Homo sapiens	84-86
16737972-11	2006	Interestingly, the antioxidants vitamin E and N-acetylcysteine abolished both the alcohol-mediated down-regulation of C/EBPalpha binding activity and hepcidin expression in the liver and the up-regulation of duodenal divalent metal transporter 1.	Acetylcysteine	46-62	CCAAT enhancer binding protein alpha	Homo sapiens	118-128
16697003-9	2006	NAC, PD 098059 and SP600125, but not SB202190, also abolished the cardioprotective effect of Ang II preconditioning.	Acetylcysteine	0-3	angiotensinogen	Rattus norvegicus	93-99
16872365-5	2006	Because the tumour suppressor p53 (tumour protein p53) is known to induce transcription of genes associated with cell response to oxidative stress, we have compared the intensity of constitutive H2AX phosphorylation, and the effect of N-acetyl-L-cysteine on it, in cells with different tumour protein p53 status.	Acetylcysteine	235-254	tumor protein p53	Homo sapiens	30-33
16803874-3	2006	Using the oxidant pervanadate to mimic B cell receptor activation and thiol antioxidants such as N-acetylcysteine (NAC) and glutathione (GSH) we show that CD21 shedding is a redox-regulated process inducible by oxidation presumably through activation of a tyrosine kinase-mediated signal pathway involving protein kinase C (PKC), and by reducing agents that either directly activate the metalloprotease and/or modify intramolecular disulfide bridges within CD21 and thereby facilitate access to the cleavage site.	Acetylcysteine	97-113	complement C3d receptor 2	Homo sapiens	155-159
16803874-3	2006	Using the oxidant pervanadate to mimic B cell receptor activation and thiol antioxidants such as N-acetylcysteine (NAC) and glutathione (GSH) we show that CD21 shedding is a redox-regulated process inducible by oxidation presumably through activation of a tyrosine kinase-mediated signal pathway involving protein kinase C (PKC), and by reducing agents that either directly activate the metalloprotease and/or modify intramolecular disulfide bridges within CD21 and thereby facilitate access to the cleavage site.	Acetylcysteine	115-118	complement C3d receptor 2	Homo sapiens	155-159
16757516-5	2006	The thiol N-acetyl-L-cysteine, the micronutrient selenite as well as selenoprotein P and the lipid peroxidation inhibitors alpha-tocopherol and butylated hydroxytoluene significantly lower both the number of TGFbeta1-initiated myofibroblasts and the secretion of HGF, VEGF and IL-6, correlating with a diminished invasive capacity of tumor cells.	Acetylcysteine	10-29	transforming growth factor beta 1	Homo sapiens	208-216
16387404-5	2006	However, pretreatment of the cells with LY294002 and SB203580, inhibitors of PI3K and p38, respectively, BAPTA-AM, an intracellular Ca(2+) chelator, and antioxidants such as N-acetylcysteine (NAC) and Trolox had no effect on the alpha-chaconine-induced cell death.	Acetylcysteine	174-190	mitogen-activated protein kinase 1	Homo sapiens	86-89
16632470-9	2006	In contrast, treatment of HEL cells with the antioxidant N-acetylcysteine decreased cell growth or expression of cyclin D2 and increased expression of p27(Kip).	Acetylcysteine	57-73	cyclin D2	Homo sapiens	113-122
16754540-9	2006	Silica induced AM production of IL-1 and TNF-alpha, which may be inhibited by ex vivo treatment of cells with N-acetylcysteine (NAC) or microtubule modifiers such as tetrandrine and taxol.	Acetylcysteine	110-126	tumor necrosis factor	Rattus norvegicus	41-50
16754540-9	2006	Silica induced AM production of IL-1 and TNF-alpha, which may be inhibited by ex vivo treatment of cells with N-acetylcysteine (NAC) or microtubule modifiers such as tetrandrine and taxol.	Acetylcysteine	128-131	tumor necrosis factor	Rattus norvegicus	41-50
16754540-10	2006	NAC was shown to prevent intracellular GSH depletion and silica-induced production of IL-1beta and TNF-alpha but not apoptosis in AM from silica-exposed rats.	Acetylcysteine	0-3	interleukin 1 beta	Rattus norvegicus	86-94
16754540-10	2006	NAC was shown to prevent intracellular GSH depletion and silica-induced production of IL-1beta and TNF-alpha but not apoptosis in AM from silica-exposed rats.	Acetylcysteine	0-3	tumor necrosis factor	Rattus norvegicus	99-108
16731823-5	2006	Antioxidant N-acetyl-l-cysteine (NAC) prevented mercury-induced insulin secretion inhibition and Akt phosphorylation but not increased PI3K activity.	Acetylcysteine	12-31	thymoma viral proto-oncogene 1	Mus musculus	97-100
16731823-5	2006	Antioxidant N-acetyl-l-cysteine (NAC) prevented mercury-induced insulin secretion inhibition and Akt phosphorylation but not increased PI3K activity.	Acetylcysteine	33-36	thymoma viral proto-oncogene 1	Mus musculus	97-100
16387404-5	2006	However, pretreatment of the cells with LY294002 and SB203580, inhibitors of PI3K and p38, respectively, BAPTA-AM, an intracellular Ca(2+) chelator, and antioxidants such as N-acetylcysteine (NAC) and Trolox had no effect on the alpha-chaconine-induced cell death.	Acetylcysteine	192-195	mitogen-activated protein kinase 1	Homo sapiens	86-89
16728380-8	2006	NAC inhibited cadmium-induced activation of mitogen-activated protein kinases, the c-Jun NH2-terminal protein kinase (JNK) and extracellular signal-regulated kinase (ERK).	Acetylcysteine	0-3	mitogen-activated protein kinase 1	Mus musculus	127-164
16728380-8	2006	NAC inhibited cadmium-induced activation of mitogen-activated protein kinases, the c-Jun NH2-terminal protein kinase (JNK) and extracellular signal-regulated kinase (ERK).	Acetylcysteine	0-3	mitogen-activated protein kinase 1	Mus musculus	166-169
16543392-13	2006	The antioxidant N-acetyl l-cysteine, however, opposed LY83583-mediated mitochondrial dysfunction, ERK1/2 inactivation, COX-2 down-regulation, and apoptosis.	Acetylcysteine	16-35	mitogen-activated protein kinase 3	Homo sapiens	98-104
16543392-13	2006	The antioxidant N-acetyl l-cysteine, however, opposed LY83583-mediated mitochondrial dysfunction, ERK1/2 inactivation, COX-2 down-regulation, and apoptosis.	Acetylcysteine	16-35	prostaglandin-endoperoxide synthase 2	Homo sapiens	119-124
16321413-9	2006	NAC exacerbated the SMD-induced suppression of IL-12 and the SMD-induced enhancement of IL-10 in the serum.	Acetylcysteine	0-3	interleukin 10	Mus musculus	88-93
16672365-12	2006	In conclusion, heterozygosity for FHIT affects susceptibility of mice to spontaneous alopecia areata and B[a]P-induced preneoplastic lesions of the uterus and does not alter responsiveness to budesonide and NAC.	Acetylcysteine	207-210	fragile histidine triad gene	Mus musculus	34-38
16861097-5	2006	Immediate administration of continuous IV N-acetylcysteine 150 mg/kg for the first 90 minutes and then 50 mg/kg q4h for the next 3 days was followed by clinical improvement and a rapid decrease in AST and ALT.	Acetylcysteine	42-58	solute carrier family 17 member 5	Homo sapiens	197-200
16338951-2	2006	Intergastric treatment with NAC or SMC five times a week resulted in decreased numbers and areas of preneoplastic, glutathione S-transferase placental form (GST-P) positive foci of the liver in a dose-dependent manner.	Acetylcysteine	28-31	glutathione S-transferase pi 1	Rattus norvegicus	115-162
16338951-4	2006	Insulin-like growth factor I (IGF-I) and inducible nitric oxide synthase (iNOS) mRNA expressions were found downregulated in the liver by NAC.	Acetylcysteine	138-141	nitric oxide synthase 2	Rattus norvegicus	41-72
16338951-4	2006	Insulin-like growth factor I (IGF-I) and inducible nitric oxide synthase (iNOS) mRNA expressions were found downregulated in the liver by NAC.	Acetylcysteine	138-141	nitric oxide synthase 2	Rattus norvegicus	74-78
16338951-5	2006	The studies indicate that NAC can serve as a chemopreventive agent for rat hepatocarcinogenesis induced by MeIQx by reducing cell proliferation, which may involve IGF-I and iNOS downregulation.	Acetylcysteine	26-29	nitric oxide synthase 2	Rattus norvegicus	173-177
16543237-10	2006	Finally, epidermal growth factor induced H2O2 production, PLCgamma1 activation, and [Ca2+]i increases, which were attenuated by N-acetylcysteine and diphenyleneiodonium and by the overexpression of peroxiredoxin type II.	Acetylcysteine	128-144	phospholipase C, gamma 1	Rattus norvegicus	58-67
16632117-9	2006	The cisplatin-induced renal injury and the increase in TNF-alpha content were reversed by NAC or beraprost.	Acetylcysteine	90-93	tumor necrosis factor	Rattus norvegicus	55-64
16672770-0	2006	Association of anti-obesity activity of N-acetylcysteine with metallothionein-II down-regulation.	Acetylcysteine	40-56	metallothionein 2	Mus musculus	62-80
16214328-8	2006	Moreover, NAC supplementation in PM mice restored the expression of IkappaBalpha, IL-1beta and TNF-alpha and infiltration of neutrophils to levels observed in control animals.	Acetylcysteine	10-13	nuclear factor of kappa light polypeptide gene enhancer in B cells inhibitor, alpha	Mus musculus	68-80
16214328-8	2006	Moreover, NAC supplementation in PM mice restored the expression of IkappaBalpha, IL-1beta and TNF-alpha and infiltration of neutrophils to levels observed in control animals.	Acetylcysteine	10-13	interleukin 1 beta	Mus musculus	82-90
16214328-8	2006	Moreover, NAC supplementation in PM mice restored the expression of IkappaBalpha, IL-1beta and TNF-alpha and infiltration of neutrophils to levels observed in control animals.	Acetylcysteine	10-13	tumor necrosis factor	Mus musculus	95-104
16948472-5	2006	Ang II significantly stimulated DNA synthesis in MOLT-3 T cells, which was inhibited by PEDF, olmesartan, an Ang II type I receptor blocker, an anti-oxidant N-acetylcysteine (NAC), or antibodies directed against IL-2.	Acetylcysteine	157-173	angiotensinogen	Homo sapiens	0-6
16948472-5	2006	Ang II significantly stimulated DNA synthesis in MOLT-3 T cells, which was inhibited by PEDF, olmesartan, an Ang II type I receptor blocker, an anti-oxidant N-acetylcysteine (NAC), or antibodies directed against IL-2.	Acetylcysteine	175-178	angiotensinogen	Homo sapiens	0-6
16948472-6	2006	PEDF or NAC suppressed gene expression of interleukin-2 (IL-2) in Ang II-exposed MOLT-3 T cells.	Acetylcysteine	8-11	interleukin 2	Homo sapiens	42-55
16948472-6	2006	PEDF or NAC suppressed gene expression of interleukin-2 (IL-2) in Ang II-exposed MOLT-3 T cells.	Acetylcysteine	8-11	interleukin 2	Homo sapiens	57-61
16948472-6	2006	PEDF or NAC suppressed gene expression of interleukin-2 (IL-2) in Ang II-exposed MOLT-3 T cells.	Acetylcysteine	8-11	angiotensinogen	Homo sapiens	66-72
16672770-4	2006	The study demonstrates that MT-II may play an important role in adipocyte differentiation of 3T3L1 preadipocytes, and that N-acetylcysteine (NAC) inhibits the adipocyte differentiation of 3T3L1 cells by repressing MT-II in a time- and dose-dependent manner.	Acetylcysteine	123-139	metallothionein 2	Mus musculus	214-219
16672770-4	2006	The study demonstrates that MT-II may play an important role in adipocyte differentiation of 3T3L1 preadipocytes, and that N-acetylcysteine (NAC) inhibits the adipocyte differentiation of 3T3L1 cells by repressing MT-II in a time- and dose-dependent manner.	Acetylcysteine	141-144	metallothionein 2	Mus musculus	214-219
16169029-8	2006	NAC treatment also completely blocked the Cd-induced intracellular ROS generation, MMP collapse and Cyt c release, indicating that Cd-induced mitochondrial dysfunction may be regulated indirectly by ROS-mediated signaling pathway.	Acetylcysteine	0-3	cytochrome c, somatic	Homo sapiens	100-105
16648577-8	2006	Whereas the antioxidant N-acetyl-l-cysteine blocked the generation of reactive oxygen species and activation of JNK and AMPK, it did not block immunotoxin-induced apoptosis.	Acetylcysteine	24-43	mitogen-activated protein kinase 8	Homo sapiens	112-115
16680064-4	2006	Control and STZ diabetic rats were treated orally for 9 weeks with N-acetylcysteine (NAC), an antioxidant and inhibitor of iNOS.	Acetylcysteine	67-83	nitric oxide synthase 2	Rattus norvegicus	123-127
16680064-4	2006	Control and STZ diabetic rats were treated orally for 9 weeks with N-acetylcysteine (NAC), an antioxidant and inhibitor of iNOS.	Acetylcysteine	85-88	nitric oxide synthase 2	Rattus norvegicus	123-127
16680064-10	2006	N-acetylcysteine treatment of diabetic rats not only restored the antioxidant capacity but also reduced the expression of iNOS and nitrotyrosine and normalized the expression of eNOS to that of control rats in heart and superior mesenteric arteries.	Acetylcysteine	0-16	nitric oxide synthase 2	Rattus norvegicus	122-126
16585223-8	2006	The oral administration of N-acetylcysteine attenuated the ECS-related loss of Fhit, whereas oltipraz, 5,6-benzoflavone, phenethyl isothiocyanate, and indole 3-carbinol, and their combinations had no significant effect.	Acetylcysteine	27-43	fragile histidine triad gene	Mus musculus	79-83
16515547-7	2006	Furthermore, suppression of the 6-OHDA-generated reactive oxygen species (ROS) by pre-incubation of cells with N-acetyl-L-cysteine effectively inhibited the 6-OHDA-induced activation of ASK1, p38 and JNK, and protected the cells from apoptosis.	Acetylcysteine	111-130	mitogen-activated protein kinase 14	Homo sapiens	192-195
16515547-7	2006	Furthermore, suppression of the 6-OHDA-generated reactive oxygen species (ROS) by pre-incubation of cells with N-acetyl-L-cysteine effectively inhibited the 6-OHDA-induced activation of ASK1, p38 and JNK, and protected the cells from apoptosis.	Acetylcysteine	111-130	mitogen-activated protein kinase 8	Homo sapiens	200-203
16391241-10	2006	SHP-2 was transiently oxidized during ET-1 treatment, and this transient oxidization could be repressed by DPI or NAC treatment.	Acetylcysteine	114-117	protein tyrosine phosphatase, non-receptor type 11	Rattus norvegicus	0-5
16391241-10	2006	SHP-2 was transiently oxidized during ET-1 treatment, and this transient oxidization could be repressed by DPI or NAC treatment.	Acetylcysteine	114-117	endothelin 1	Rattus norvegicus	38-42
16391241-11	2006	In SHP-2 knockdown cells, ET-1-induced phosphorylation of EGFR was dramatically elevated and is not influenced by NAC and DPI.	Acetylcysteine	114-117	endothelin 1	Rattus norvegicus	26-30
16261333-4	2006	Both NAD(P)H oxidase inhibitor, diphenyliodonium (DPI) and ROS scavenger N-acetylcysteine (NAC), inhibited EGFR transactivation and extracellular signal-regulated kinase (ERK) phosphorylation caused by ET-1.	Acetylcysteine	73-89	Eph receptor B1	Rattus norvegicus	132-169
16261333-4	2006	Both NAD(P)H oxidase inhibitor, diphenyliodonium (DPI) and ROS scavenger N-acetylcysteine (NAC), inhibited EGFR transactivation and extracellular signal-regulated kinase (ERK) phosphorylation caused by ET-1.	Acetylcysteine	73-89	Eph receptor B1	Rattus norvegicus	171-174
16261333-4	2006	Both NAD(P)H oxidase inhibitor, diphenyliodonium (DPI) and ROS scavenger N-acetylcysteine (NAC), inhibited EGFR transactivation and extracellular signal-regulated kinase (ERK) phosphorylation caused by ET-1.	Acetylcysteine	73-89	endothelin 1	Rattus norvegicus	202-206
16261333-4	2006	Both NAD(P)H oxidase inhibitor, diphenyliodonium (DPI) and ROS scavenger N-acetylcysteine (NAC), inhibited EGFR transactivation and extracellular signal-regulated kinase (ERK) phosphorylation caused by ET-1.	Acetylcysteine	91-94	Eph receptor B1	Rattus norvegicus	132-169
16261333-4	2006	Both NAD(P)H oxidase inhibitor, diphenyliodonium (DPI) and ROS scavenger N-acetylcysteine (NAC), inhibited EGFR transactivation and extracellular signal-regulated kinase (ERK) phosphorylation caused by ET-1.	Acetylcysteine	91-94	Eph receptor B1	Rattus norvegicus	171-174
16261333-4	2006	Both NAD(P)H oxidase inhibitor, diphenyliodonium (DPI) and ROS scavenger N-acetylcysteine (NAC), inhibited EGFR transactivation and extracellular signal-regulated kinase (ERK) phosphorylation caused by ET-1.	Acetylcysteine	91-94	endothelin 1	Rattus norvegicus	202-206
16497268-7	2006	Antioxidants such as trolox and N-acetylcysteine increased GRP78 and GRP94 levels in the E47 cells, suggesting that CYP2E1- derived oxidant stress was responsible for down regulation of these GRPs in the E47 cells.	Acetylcysteine	32-48	heat shock protein family A (Hsp70) member 5	Homo sapiens	59-64
16553950-11	2006	More interestingly, CysLT1-R stimulation increased the production of ROS and N-acetylcysteine (NAC) abolished LTD4-induced EGF-R phosphorylation and thymidine incorporation.	Acetylcysteine	77-93	cysteinyl leukotriene receptor 1	Homo sapiens	20-26
16553950-11	2006	More interestingly, CysLT1-R stimulation increased the production of ROS and N-acetylcysteine (NAC) abolished LTD4-induced EGF-R phosphorylation and thymidine incorporation.	Acetylcysteine	77-93	epidermal growth factor receptor	Homo sapiens	123-128
16553950-11	2006	More interestingly, CysLT1-R stimulation increased the production of ROS and N-acetylcysteine (NAC) abolished LTD4-induced EGF-R phosphorylation and thymidine incorporation.	Acetylcysteine	95-98	cysteinyl leukotriene receptor 1	Homo sapiens	20-26
16553950-11	2006	More interestingly, CysLT1-R stimulation increased the production of ROS and N-acetylcysteine (NAC) abolished LTD4-induced EGF-R phosphorylation and thymidine incorporation.	Acetylcysteine	95-98	epidermal growth factor receptor	Homo sapiens	123-128
16497268-7	2006	Antioxidants such as trolox and N-acetylcysteine increased GRP78 and GRP94 levels in the E47 cells, suggesting that CYP2E1- derived oxidant stress was responsible for down regulation of these GRPs in the E47 cells.	Acetylcysteine	32-48	cytochrome P450 family 2 subfamily E member 1	Homo sapiens	116-122
16505371-9	2006	Detoxification by NAC greatly attenuates CHOP induction in arylating quinone-treated cells, suggesting that ER stress is a cellular mechanism for arylating quinone cytotoxicity.	Acetylcysteine	18-21	DNA damage inducible transcript 3	Homo sapiens	41-45
16234311-10	2006	The stimulatory effect of high glucose on ROS production, ERK1/2, and Akt/PKB activation was prevented by the antioxidants catalase, diphenylene iodonium, and N-acetylcysteine.	Acetylcysteine	159-175	mitogen-activated protein kinase 3	Homo sapiens	58-64
16234311-10	2006	The stimulatory effect of high glucose on ROS production, ERK1/2, and Akt/PKB activation was prevented by the antioxidants catalase, diphenylene iodonium, and N-acetylcysteine.	Acetylcysteine	159-175	AKT serine/threonine kinase 1	Homo sapiens	70-77
16251475-7	2006	ERK activation was attenuated by preincubation with N-acetylcysteine (NAC) and SOD, suggesting the role of oxidation in Hcy-induced ERK activation.	Acetylcysteine	52-68	mitogen-activated protein kinase 1	Homo sapiens	0-3
16282349-11	2006	The antioxidant N-acetyl-L-cysteine diminished G-CSF-induced ROS production and cell proliferation by inhibiting Akt activation.	Acetylcysteine	16-35	AKT serine/threonine kinase 1	Homo sapiens	113-116
16251475-7	2006	ERK activation was attenuated by preincubation with N-acetylcysteine (NAC) and SOD, suggesting the role of oxidation in Hcy-induced ERK activation.	Acetylcysteine	52-68	mitogen-activated protein kinase 1	Homo sapiens	132-135
16251475-7	2006	ERK activation was attenuated by preincubation with N-acetylcysteine (NAC) and SOD, suggesting the role of oxidation in Hcy-induced ERK activation.	Acetylcysteine	70-73	mitogen-activated protein kinase 1	Homo sapiens	0-3
16251475-7	2006	ERK activation was attenuated by preincubation with N-acetylcysteine (NAC) and SOD, suggesting the role of oxidation in Hcy-induced ERK activation.	Acetylcysteine	70-73	mitogen-activated protein kinase 1	Homo sapiens	132-135
16410725-5	2006	Quenching of ROS with N-acetyl-L-cysteine prevented cytochrome c release by manumycin.	Acetylcysteine	22-41	cytochrome c, somatic	Homo sapiens	52-64
16439183-11	2006	Correspondingly, pretreatment with NAC significantly attenuated acute ethanol-induced lipid peroxidation and GSH depletion and inhibited hepatic TNF-alpha mRNA expression.	Acetylcysteine	35-38	tumor necrosis factor	Mus musculus	145-154
16298169-4	2006	T(3) elicits an 80-fold increase in the serum levels of tumor necrosis factor-alpha (TNF-alpha), which is abolished by pretreatment with the antioxidants alpha-tocopherol and N-acetylcysteine, the Kupffer-cell inactivator GdCl(3), or an antisense oligonucleotide against TNF-alpha.	Acetylcysteine	175-191	tumor necrosis factor	Homo sapiens	56-83
16298169-4	2006	T(3) elicits an 80-fold increase in the serum levels of tumor necrosis factor-alpha (TNF-alpha), which is abolished by pretreatment with the antioxidants alpha-tocopherol and N-acetylcysteine, the Kupffer-cell inactivator GdCl(3), or an antisense oligonucleotide against TNF-alpha.	Acetylcysteine	175-191	tumor necrosis factor	Homo sapiens	85-94
16520234-8	2006	The long-term exposure to oxidized LDL also significantly enhanced tumor necrosis factor-alpha (TNF-alpha)-stimulated ROS production and endothelial adhesiveness of MMCs, which could be completely abolished by the short-term existence of pyrrolidine dithiocarbamate (PDTC), an antioxidant and NF-kappaB blocker and by long-term coincubation with N-acetylcysteine, a nonspecific antioxidant.	Acetylcysteine	346-362	tumor necrosis factor	Homo sapiens	67-94
16520234-8	2006	The long-term exposure to oxidized LDL also significantly enhanced tumor necrosis factor-alpha (TNF-alpha)-stimulated ROS production and endothelial adhesiveness of MMCs, which could be completely abolished by the short-term existence of pyrrolidine dithiocarbamate (PDTC), an antioxidant and NF-kappaB blocker and by long-term coincubation with N-acetylcysteine, a nonspecific antioxidant.	Acetylcysteine	346-362	tumor necrosis factor	Homo sapiens	96-105
15982852-6	2006	Moreover, NAC treatment reduced the expression levels of c-Myc, Cyclin D2, and Cyclin E, and induced expression of p27, thus inhibiting the G1 to S phase transition of cells cultured with IL-3.	Acetylcysteine	10-13	interleukin 3	Mus musculus	188-192
16343695-7	2006	Pretreatment with the sulfhydryl antioxidant N-acetylcysteine or the quinone reductase inducer dimethyl fumarate prevents the ETC inhibition and cytochrome c release following BH4 exposure, suggesting the involvement of quinone products.	Acetylcysteine	45-61	cytochrome c, somatic	Homo sapiens	145-157
16081117-8	2006	Pretreatment of mice with the antioxidant, N-acetylcysteine (NAC) prevented APAP-induced depletion of glutathione and CuZnSOD, as well as hepatotoxicity.	Acetylcysteine	43-59	superoxide dismutase 1, soluble	Mus musculus	118-125
16081117-8	2006	Pretreatment of mice with the antioxidant, N-acetylcysteine (NAC) prevented APAP-induced depletion of glutathione and CuZnSOD, as well as hepatotoxicity.	Acetylcysteine	61-64	superoxide dismutase 1, soluble	Mus musculus	118-125
16081117-9	2006	NAC also abrogated APAP-induced increases in TNFalpha, KC/gro, and IL-10, but augmented expression of the anti-inflammatory cytokines interleukin-4 (IL-4) and transforming growth factor-beta (TGFbeta).	Acetylcysteine	0-3	tumor necrosis factor	Mus musculus	45-53
16081117-9	2006	NAC also abrogated APAP-induced increases in TNFalpha, KC/gro, and IL-10, but augmented expression of the anti-inflammatory cytokines interleukin-4 (IL-4) and transforming growth factor-beta (TGFbeta).	Acetylcysteine	0-3	chemokine (C-X-C motif) ligand 1	Mus musculus	55-61
16081117-9	2006	NAC also abrogated APAP-induced increases in TNFalpha, KC/gro, and IL-10, but augmented expression of the anti-inflammatory cytokines interleukin-4 (IL-4) and transforming growth factor-beta (TGFbeta).	Acetylcysteine	0-3	interleukin 10	Mus musculus	67-72
16081117-12	2006	As observed with NAC pretreatment, the loss of NF-kappaB p50 was associated with decreased ability of APAP to upregulate TNFalpha, KC/gro, and IL-10 expression and increased expression of IL-4 and TGFbeta.	Acetylcysteine	17-20	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	47-60
16081117-12	2006	As observed with NAC pretreatment, the loss of NF-kappaB p50 was associated with decreased ability of APAP to upregulate TNFalpha, KC/gro, and IL-10 expression and increased expression of IL-4 and TGFbeta.	Acetylcysteine	17-20	tumor necrosis factor	Mus musculus	121-129
16081117-12	2006	As observed with NAC pretreatment, the loss of NF-kappaB p50 was associated with decreased ability of APAP to upregulate TNFalpha, KC/gro, and IL-10 expression and increased expression of IL-4 and TGFbeta.	Acetylcysteine	17-20	chemokine (C-X-C motif) ligand 1	Mus musculus	131-137
16081117-12	2006	As observed with NAC pretreatment, the loss of NF-kappaB p50 was associated with decreased ability of APAP to upregulate TNFalpha, KC/gro, and IL-10 expression and increased expression of IL-4 and TGFbeta.	Acetylcysteine	17-20	interleukin 10	Mus musculus	143-148
15982852-4	2006	The antioxidant N-acetyl-L-cysteine (NAC) inhibited IL-3-induced tyrosine phosphorylation of Jak2, IL-3 receptor betac subunit (IL-3Rbetac), and STAT5 as well as activation-specific phosphorylation of Akt, MEK, and ERK, while treatment of cells with H2O2 activated these signaling events.	Acetylcysteine	16-35	interleukin 3	Mus musculus	52-56
15982852-4	2006	The antioxidant N-acetyl-L-cysteine (NAC) inhibited IL-3-induced tyrosine phosphorylation of Jak2, IL-3 receptor betac subunit (IL-3Rbetac), and STAT5 as well as activation-specific phosphorylation of Akt, MEK, and ERK, while treatment of cells with H2O2 activated these signaling events.	Acetylcysteine	16-35	interleukin 3	Mus musculus	99-103
15982852-4	2006	The antioxidant N-acetyl-L-cysteine (NAC) inhibited IL-3-induced tyrosine phosphorylation of Jak2, IL-3 receptor betac subunit (IL-3Rbetac), and STAT5 as well as activation-specific phosphorylation of Akt, MEK, and ERK, while treatment of cells with H2O2 activated these signaling events.	Acetylcysteine	16-35	thymoma viral proto-oncogene 1	Mus musculus	201-204
15982852-4	2006	The antioxidant N-acetyl-L-cysteine (NAC) inhibited IL-3-induced tyrosine phosphorylation of Jak2, IL-3 receptor betac subunit (IL-3Rbetac), and STAT5 as well as activation-specific phosphorylation of Akt, MEK, and ERK, while treatment of cells with H2O2 activated these signaling events.	Acetylcysteine	37-40	interleukin 3	Mus musculus	52-56
15982852-4	2006	The antioxidant N-acetyl-L-cysteine (NAC) inhibited IL-3-induced tyrosine phosphorylation of Jak2, IL-3 receptor betac subunit (IL-3Rbetac), and STAT5 as well as activation-specific phosphorylation of Akt, MEK, and ERK, while treatment of cells with H2O2 activated these signaling events.	Acetylcysteine	37-40	interleukin 3	Mus musculus	99-103
15982852-4	2006	The antioxidant N-acetyl-L-cysteine (NAC) inhibited IL-3-induced tyrosine phosphorylation of Jak2, IL-3 receptor betac subunit (IL-3Rbetac), and STAT5 as well as activation-specific phosphorylation of Akt, MEK, and ERK, while treatment of cells with H2O2 activated these signaling events.	Acetylcysteine	37-40	thymoma viral proto-oncogene 1	Mus musculus	201-204
16384711-6	2006	RESULTS: PMA and fMLP-induced neutrophil respiratory burst and chemotaxis were lower after 14 days of NAC intake but not after 2 h. In vitro incubation with NAC inhibited release of elastase (p &lt; 0.05), IL-8 (p &lt; 0.05), respiratory burst and NFkappaB activation at 10 mM but not at lower concentrations.	Acetylcysteine	102-105	formyl peptide receptor 1	Homo sapiens	17-21
16384711-6	2006	RESULTS: PMA and fMLP-induced neutrophil respiratory burst and chemotaxis were lower after 14 days of NAC intake but not after 2 h. In vitro incubation with NAC inhibited release of elastase (p &lt; 0.05), IL-8 (p &lt; 0.05), respiratory burst and NFkappaB activation at 10 mM but not at lower concentrations.	Acetylcysteine	102-105	C-X-C motif chemokine ligand 8	Homo sapiens	206-210
16384711-6	2006	RESULTS: PMA and fMLP-induced neutrophil respiratory burst and chemotaxis were lower after 14 days of NAC intake but not after 2 h. In vitro incubation with NAC inhibited release of elastase (p &lt; 0.05), IL-8 (p &lt; 0.05), respiratory burst and NFkappaB activation at 10 mM but not at lower concentrations.	Acetylcysteine	102-105	nuclear factor kappa B subunit 1	Homo sapiens	248-256
16384711-6	2006	RESULTS: PMA and fMLP-induced neutrophil respiratory burst and chemotaxis were lower after 14 days of NAC intake but not after 2 h. In vitro incubation with NAC inhibited release of elastase (p &lt; 0.05), IL-8 (p &lt; 0.05), respiratory burst and NFkappaB activation at 10 mM but not at lower concentrations.	Acetylcysteine	157-160	formyl peptide receptor 1	Homo sapiens	17-21
16384711-6	2006	RESULTS: PMA and fMLP-induced neutrophil respiratory burst and chemotaxis were lower after 14 days of NAC intake but not after 2 h. In vitro incubation with NAC inhibited release of elastase (p &lt; 0.05), IL-8 (p &lt; 0.05), respiratory burst and NFkappaB activation at 10 mM but not at lower concentrations.	Acetylcysteine	157-160	C-X-C motif chemokine ligand 8	Homo sapiens	206-210
16384711-6	2006	RESULTS: PMA and fMLP-induced neutrophil respiratory burst and chemotaxis were lower after 14 days of NAC intake but not after 2 h. In vitro incubation with NAC inhibited release of elastase (p &lt; 0.05), IL-8 (p &lt; 0.05), respiratory burst and NFkappaB activation at 10 mM but not at lower concentrations.	Acetylcysteine	157-160	nuclear factor kappa B subunit 1	Homo sapiens	248-256
16487852-1	2006	OBJECTIVES: The objective was to determine the effects of antioxidant N-acetylcysteine (NAC) on reversal and attenuation of established interstitial fibrosis in the cardiac troponin T (cTnT) mouse model of human hypertrophic cardiomyopathy (HCM) mutation.	Acetylcysteine	70-86	troponin T2, cardiac	Mus musculus	185-189
16487852-1	2006	OBJECTIVES: The objective was to determine the effects of antioxidant N-acetylcysteine (NAC) on reversal and attenuation of established interstitial fibrosis in the cardiac troponin T (cTnT) mouse model of human hypertrophic cardiomyopathy (HCM) mutation.	Acetylcysteine	88-91	troponin T2, cardiac	Mus musculus	165-183
16377052-10	2006	Erdosteine, NAC, and vitamin E significantly reduced the increases in TNF-alpha staining and lung MPO activity.	Acetylcysteine	12-15	tumor necrosis factor	Rattus norvegicus	70-79
16195541-9	2006	Akt phosphorylation and cell proliferation were also blocked by the antioxidants, N-acetyl-l-cysteine, Ginko biloba 501, and tiron, the reduced nicotinamide adenine dinucleotide phosphate oxidase inhibitor, diphenyleneiodonium, and the 5-HT2 receptor antagonists ketanserin and mianserin, but not by the 5-HT serotonin transporter or 5-HT 1B/1D receptor antagonists.	Acetylcysteine	82-101	AKT serine/threonine kinase 1	Homo sapiens	0-3
16195541-9	2006	Akt phosphorylation and cell proliferation were also blocked by the antioxidants, N-acetyl-l-cysteine, Ginko biloba 501, and tiron, the reduced nicotinamide adenine dinucleotide phosphate oxidase inhibitor, diphenyleneiodonium, and the 5-HT2 receptor antagonists ketanserin and mianserin, but not by the 5-HT serotonin transporter or 5-HT 1B/1D receptor antagonists.	Acetylcysteine	82-101	5-hydroxytryptamine receptor 2A	Homo sapiens	236-250
16195541-9	2006	Akt phosphorylation and cell proliferation were also blocked by the antioxidants, N-acetyl-l-cysteine, Ginko biloba 501, and tiron, the reduced nicotinamide adenine dinucleotide phosphate oxidase inhibitor, diphenyleneiodonium, and the 5-HT2 receptor antagonists ketanserin and mianserin, but not by the 5-HT serotonin transporter or 5-HT 1B/1D receptor antagonists.	Acetylcysteine	82-101	solute carrier family 6 member 4	Homo sapiens	309-330
16195541-9	2006	Akt phosphorylation and cell proliferation were also blocked by the antioxidants, N-acetyl-l-cysteine, Ginko biloba 501, and tiron, the reduced nicotinamide adenine dinucleotide phosphate oxidase inhibitor, diphenyleneiodonium, and the 5-HT2 receptor antagonists ketanserin and mianserin, but not by the 5-HT serotonin transporter or 5-HT 1B/1D receptor antagonists.	Acetylcysteine	82-101	5-hydroxytryptamine receptor 1B	Homo sapiens	334-341
15979845-4	2006	ERK activation by TGF-beta1 was significantly attenuated by treatment with N-acetyl-l-cysteine or catalase, indicating that reactive oxygen species (ROS) generated by TGF-beta1, mainly H2O2, stimulates ERK signaling pathway to induce the p21WAF1/Cip1 expression.	Acetylcysteine	75-94	mitogen-activated protein kinase 1	Homo sapiens	0-3
15979845-4	2006	ERK activation by TGF-beta1 was significantly attenuated by treatment with N-acetyl-l-cysteine or catalase, indicating that reactive oxygen species (ROS) generated by TGF-beta1, mainly H2O2, stimulates ERK signaling pathway to induce the p21WAF1/Cip1 expression.	Acetylcysteine	75-94	transforming growth factor beta 1	Homo sapiens	18-27
15979845-4	2006	ERK activation by TGF-beta1 was significantly attenuated by treatment with N-acetyl-l-cysteine or catalase, indicating that reactive oxygen species (ROS) generated by TGF-beta1, mainly H2O2, stimulates ERK signaling pathway to induce the p21WAF1/Cip1 expression.	Acetylcysteine	75-94	transforming growth factor beta 1	Homo sapiens	167-176
15979845-4	2006	ERK activation by TGF-beta1 was significantly attenuated by treatment with N-acetyl-l-cysteine or catalase, indicating that reactive oxygen species (ROS) generated by TGF-beta1, mainly H2O2, stimulates ERK signaling pathway to induce the p21WAF1/Cip1 expression.	Acetylcysteine	75-94	mitogen-activated protein kinase 1	Homo sapiens	202-205
15979845-4	2006	ERK activation by TGF-beta1 was significantly attenuated by treatment with N-acetyl-l-cysteine or catalase, indicating that reactive oxygen species (ROS) generated by TGF-beta1, mainly H2O2, stimulates ERK signaling pathway to induce the p21WAF1/Cip1 expression.	Acetylcysteine	75-94	cyclin dependent kinase inhibitor 1A	Homo sapiens	246-250
16263740-12	2006	Phosphorylated extracellular signal-regulated kinase (ERK) was found in podocytes incubated with CML and was prevented by N-acetyl-l-cysteine or 7"-amino 4 [trifluoromethyl].	Acetylcysteine	122-141	mitogen-activated protein kinase 1	Mus musculus	15-52
16354720-5	2006	Treatment with the anti-oxidant N-acetylcysteine inhibited KGFR endocytosis, suggesting that the receptor internalization is mediated by the intracellular production of ROS.	Acetylcysteine	32-48	fibroblast growth factor 7	Homo sapiens	59-63
16187297-5	2006	The addition of antioxidant N-acetylcysteine (NAC; 20 mM) 30 min prior to stimulation with LPS attenuated the inhibition of BSP mRNA levels.	Acetylcysteine	28-44	integrin-binding sialoprotein	Rattus norvegicus	124-127
16187297-5	2006	The addition of antioxidant N-acetylcysteine (NAC; 20 mM) 30 min prior to stimulation with LPS attenuated the inhibition of BSP mRNA levels.	Acetylcysteine	46-49	integrin-binding sialoprotein	Rattus norvegicus	124-127
16263740-12	2006	Phosphorylated extracellular signal-regulated kinase (ERK) was found in podocytes incubated with CML and was prevented by N-acetyl-l-cysteine or 7"-amino 4 [trifluoromethyl].	Acetylcysteine	122-141	mitogen-activated protein kinase 1	Mus musculus	54-57
16201965-5	2006	TNF (tumour necrosis factor)-a, which decreases the levels of endogenous GSH, increased the generation of C16-cer in response to C6-cer, and this was blocked by exogenous GSH or NAC, or by the overexpression of TPx I (thioredoxin peroxidase I), an enzyme that reduces the generation of intracellular ROS (reactive oxygen species).	Acetylcysteine	178-181	tumor necrosis factor	Homo sapiens	0-3
16429300-7	2006	Catalase (CAT) activity was decreased in the IR group in comparison with control and IR + erdosteine groups (P&lt;0.05), whereas it was higher in the IR + erdosteine group than in the IR + NAC group (P&lt;0.05).	Acetylcysteine	189-192	catalase	Rattus norvegicus	0-8
16429300-7	2006	Catalase (CAT) activity was decreased in the IR group in comparison with control and IR + erdosteine groups (P&lt;0.05), whereas it was higher in the IR + erdosteine group than in the IR + NAC group (P&lt;0.05).	Acetylcysteine	189-192	catalase	Rattus norvegicus	10-13
16201965-5	2006	TNF (tumour necrosis factor)-a, which decreases the levels of endogenous GSH, increased the generation of C16-cer in response to C6-cer, and this was blocked by exogenous GSH or NAC, or by the overexpression of TPx I (thioredoxin peroxidase I), an enzyme that reduces the generation of intracellular ROS (reactive oxygen species).	Acetylcysteine	178-181	tumor necrosis factor	Homo sapiens	5-27
16174550-9	2006	Administration of antioxidant N-acetylcysteine (NAC) can obviously affected the level of MLK3, JNK3 and Akt1 binding to JIP-1 and JNK3 activation in the hippocampus at 15min ischemia.	Acetylcysteine	30-46	mitogen-activated protein kinase kinase kinase 11	Rattus norvegicus	89-93
16424008-3	2006	Furthermore, in three human cell lines derived from human oral squamous cell carcinoma, the accumulation of HIF-1alpha was prevented either by inhibition of NOS activity with the nonspecific NOS inhibitor N(G)-monomethyl-L-arginine or by the antioxidants N-acetyl-L-cysteine and ascorbic acid.	Acetylcysteine	255-274	hypoxia inducible factor 1 subunit alpha	Homo sapiens	108-118
16482627-18	2006	Additionally, L(+)-ascorbic acid + N-acetyl cysteine significantly increased pancreatic GPx (P = 0.002) and hepatic CAT and GPx activities (P = 0.001, P = 0.007, respectively).	Acetylcysteine	35-52	catalase	Rattus norvegicus	116-119
16482631-7	2006	Partial protection was observed with NAC against RMP-induced changes in liver, which was evidenced from the prevention of increase in lipid peroxidation and the reduction in SOD and catalase enzyme levels.	Acetylcysteine	37-40	catalase	Rattus norvegicus	182-190
16174550-9	2006	Administration of antioxidant N-acetylcysteine (NAC) can obviously affected the level of MLK3, JNK3 and Akt1 binding to JIP-1 and JNK3 activation in the hippocampus at 15min ischemia.	Acetylcysteine	30-46	AKT serine/threonine kinase 1	Rattus norvegicus	104-108
16174550-9	2006	Administration of antioxidant N-acetylcysteine (NAC) can obviously affected the level of MLK3, JNK3 and Akt1 binding to JIP-1 and JNK3 activation in the hippocampus at 15min ischemia.	Acetylcysteine	48-51	mitogen-activated protein kinase kinase kinase 11	Rattus norvegicus	89-93
16174550-9	2006	Administration of antioxidant N-acetylcysteine (NAC) can obviously affected the level of MLK3, JNK3 and Akt1 binding to JIP-1 and JNK3 activation in the hippocampus at 15min ischemia.	Acetylcysteine	48-51	AKT serine/threonine kinase 1	Rattus norvegicus	104-108
15907373-3	2006	Rapamycin, the mammalian target of rapamycin (FRAP/mTOR) inhibitor, prevents the effect of NAC on H2O2-induced eIF4F complex formation inhibition.	Acetylcysteine	91-94	mechanistic target of rapamycin kinase	Homo sapiens	15-44
16389042-6	2006	Pretreatment and/or posttreatment with NAC attenuated IL-6 in the maternal serum and amniotic fluid and IL-10 in the amniotic fluid.	Acetylcysteine	39-42	interleukin 6	Rattus norvegicus	54-58
16389042-7	2006	LPS also induced placental IL-6 messenger RNA that was inhibited by treatment with NAC before and after LPS.	Acetylcysteine	83-86	interleukin 6	Rattus norvegicus	27-31
16614485-7	2006	Although NAC and CYS attenuated CCl4-induced pulmonary inflammation and fibrosis, the order of preventive potency was SAC &gt; NAC &gt; CYS according to their applied doses.	Acetylcysteine	9-12	C-C motif chemokine ligand 4	Rattus norvegicus	32-36
15907373-3	2006	Rapamycin, the mammalian target of rapamycin (FRAP/mTOR) inhibitor, prevents the effect of NAC on H2O2-induced eIF4F complex formation inhibition.	Acetylcysteine	91-94	mechanistic target of rapamycin kinase	Homo sapiens	46-50
15907373-3	2006	Rapamycin, the mammalian target of rapamycin (FRAP/mTOR) inhibitor, prevents the effect of NAC on H2O2-induced eIF4F complex formation inhibition.	Acetylcysteine	91-94	mechanistic target of rapamycin kinase	Homo sapiens	51-55
16445696-25	2006	In addition, NAC diminished the LPS-induced increases in nitrate/nitrite, MG, TNF-a and IL-1b.	Acetylcysteine	13-16	tumor necrosis factor	Rattus norvegicus	78-83
16293568-8	2006	N-acetylcysteine blocked angiotensin II-induced NF-kappaB activity and integrin beta3 expression.	Acetylcysteine	0-16	angiotensinogen	Homo sapiens	25-39
16293568-8	2006	N-acetylcysteine blocked angiotensin II-induced NF-kappaB activity and integrin beta3 expression.	Acetylcysteine	0-16	nuclear factor kappa B subunit 1	Homo sapiens	48-57
16293568-8	2006	N-acetylcysteine blocked angiotensin II-induced NF-kappaB activity and integrin beta3 expression.	Acetylcysteine	0-16	integrin subunit beta 3	Homo sapiens	71-85
16440148-7	2006	Tumor necrosis factor-alpha levels increased in the control group but, in contrast, a significant decrease was detected in the NAC group (P &lt; 0.01).	Acetylcysteine	127-130	tumor necrosis factor	Homo sapiens	0-27
16456238-6	2006	Both apocynin and NAC almost abolished the preconditioning ability of Ang II.	Acetylcysteine	18-21	angiotensinogen	Rattus norvegicus	70-76
16456238-7	2006	Ang II resulted in increase in ROS activity in the heart, which was reduced by either NAC or apocynin.	Acetylcysteine	86-89	angiotensinogen	Rattus norvegicus	0-6
16456238-8	2006	Ang II also increased both the NADPH oxidase subunits gp91 phox and p22phox mRNA expression, which was abolished with apocynin and NAC.	Acetylcysteine	131-134	angiotensinogen	Rattus norvegicus	0-6
16456238-10	2006	Both NAC and apocynin reduced ROS activities simultaneously abolishing preconditioning ability of Ang II, suggesting that Ang II preconditioning occurs through redox cycling.	Acetylcysteine	5-8	angiotensinogen	Rattus norvegicus	98-104
16456238-10	2006	Both NAC and apocynin reduced ROS activities simultaneously abolishing preconditioning ability of Ang II, suggesting that Ang II preconditioning occurs through redox cycling.	Acetylcysteine	5-8	angiotensinogen	Rattus norvegicus	122-128
16456238-11	2006	That both NAC and apocynin reduced ROS activities and abolished Ang II-mediated increase in p22phox and gp91phox activity further suggest that such redox cycling occurs via both NADPH oxidase-dependent and -independent pathways.	Acetylcysteine	10-13	angiotensinogen	Rattus norvegicus	64-70
16563228-12	2006	Our results suggest that TGF-beta signalling and subsequent expression of fibrogenesis related proteins in Dupuytren"s disease is abrogated by NAC thus providing a basis for a therapeutic strategy in Dupuytren"s disease and other fibroproliferative disorders.	Acetylcysteine	143-146	transforming growth factor, beta 1	Rattus norvegicus	25-33
17338280-6	2006	Following 3 months of Following NAC supplementation, GSH, GST, and CAT levels were found to be similar to the levels before treatment.	Acetylcysteine	32-35	catalase	Homo sapiens	67-70
16563228-0	2006	N-acetyl-L-cysteine abrogates fibrogenic properties of fibroblasts isolated from Dupuytren"s disease by blunting TGF-beta signalling.	Acetylcysteine	0-19	transforming growth factor, beta 1	Rattus norvegicus	113-121
16374848-7	2006	Increases in Nrf2 protein and mRNA are blocked by inhibitors of CYP2E1 activity and a reactive oxygen species (ROS) scavenger, N-acetylcysteine, which decrease ROS levels as well as Nrf2 mRNA induction.	Acetylcysteine	127-143	NFE2 like bZIP transcription factor 2	Homo sapiens	13-17
16374848-7	2006	Increases in Nrf2 protein and mRNA are blocked by inhibitors of CYP2E1 activity and a reactive oxygen species (ROS) scavenger, N-acetylcysteine, which decrease ROS levels as well as Nrf2 mRNA induction.	Acetylcysteine	127-143	NFE2 like bZIP transcription factor 2	Homo sapiens	182-186
16424790-8	2006	However, there were some significant differences among Captopril (30 mg/kg or 45 mg/kg), enalapril (20 mg/kg), and N-acetylcysteine particular in the activity of PON1 and ACE.	Acetylcysteine	115-131	angiotensin I converting enzyme	Rattus norvegicus	171-174
16479148-6	2006	The inductive properties of angiotensin II on extracellular signal-regulated kinase (ERK) phosphorylation were found reversed with isosteviol and antioxidants such as N-acetylcysteine.	Acetylcysteine	167-183	angiotensinogen	Rattus norvegicus	28-42
16409471-6	2006	The HCy effect on p38 MAPK phosphorylation was prevented by N-acetyl-L-cysteine and iloprost and was partially inhibited by nordihydroguaiaretic acid.	Acetylcysteine	60-79	mitogen-activated protein kinase 14	Homo sapiens	18-26
16479148-6	2006	The inductive properties of angiotensin II on extracellular signal-regulated kinase (ERK) phosphorylation were found reversed with isosteviol and antioxidants such as N-acetylcysteine.	Acetylcysteine	167-183	Eph receptor B1	Rattus norvegicus	46-83
16479148-6	2006	The inductive properties of angiotensin II on extracellular signal-regulated kinase (ERK) phosphorylation were found reversed with isosteviol and antioxidants such as N-acetylcysteine.	Acetylcysteine	167-183	Eph receptor B1	Rattus norvegicus	85-88
16489261-1	2005	The aim of the present study was to evaluate the effects of N-acetylcysteine (NAC) and L-carnitine (LCAR) supplementations on polymorphonuclear leukocytes myeloperoxidase (MPO) and Cu/Zn-superoxide dismutase (Cu/Zn-SOD) and plasma malondialdehyde (MDA) in acetic acid (AA)-induced ulcerative colitis model.	Acetylcysteine	60-76	superoxide dismutase 1	Rattus norvegicus	181-207
16154687-0	2005	N-Acetylcysteine inhibit the translocation of mixed lineage kinase-3 from cytosol to plasma membrane during transient brain ischemia in rat hippocampus.	Acetylcysteine	0-16	mitogen-activated protein kinase kinase kinase 11	Rattus norvegicus	46-68
16154687-5	2005	The antioxidant N-acetylcysteine (NAC) could inhibit the translocation of MLK3 from cytosolic fraction to the membrane fraction and decrease the interactions of MLK3 and PSD-95 in the membrane fraction.	Acetylcysteine	16-32	mitogen-activated protein kinase kinase kinase 11	Rattus norvegicus	74-78
16154687-5	2005	The antioxidant N-acetylcysteine (NAC) could inhibit the translocation of MLK3 from cytosolic fraction to the membrane fraction and decrease the interactions of MLK3 and PSD-95 in the membrane fraction.	Acetylcysteine	16-32	mitogen-activated protein kinase kinase kinase 11	Rattus norvegicus	161-165
16154687-5	2005	The antioxidant N-acetylcysteine (NAC) could inhibit the translocation of MLK3 from cytosolic fraction to the membrane fraction and decrease the interactions of MLK3 and PSD-95 in the membrane fraction.	Acetylcysteine	34-37	mitogen-activated protein kinase kinase kinase 11	Rattus norvegicus	74-78
16154687-5	2005	The antioxidant N-acetylcysteine (NAC) could inhibit the translocation of MLK3 from cytosolic fraction to the membrane fraction and decrease the interactions of MLK3 and PSD-95 in the membrane fraction.	Acetylcysteine	34-37	mitogen-activated protein kinase kinase kinase 11	Rattus norvegicus	161-165
16298690-4	2005	Pretreatment with the antioxidants, 2(3)-t-butyl-4-hydroxyanisole or N-acetyl-l-cysteine enhanced the amount of DNA-PKcs phosphorylated at threonine 2609 (DNA-PK(pThr2609)) at the DNA dsbs and DNA-PK activity.	Acetylcysteine	69-88	protein kinase, DNA-activated, catalytic subunit	Homo sapiens	112-120
16298690-4	2005	Pretreatment with the antioxidants, 2(3)-t-butyl-4-hydroxyanisole or N-acetyl-l-cysteine enhanced the amount of DNA-PKcs phosphorylated at threonine 2609 (DNA-PK(pThr2609)) at the DNA dsbs and DNA-PK activity.	Acetylcysteine	69-88	protein kinase, DNA-activated, catalytic subunit	Homo sapiens	112-118
16298690-4	2005	Pretreatment with the antioxidants, 2(3)-t-butyl-4-hydroxyanisole or N-acetyl-l-cysteine enhanced the amount of DNA-PKcs phosphorylated at threonine 2609 (DNA-PK(pThr2609)) at the DNA dsbs and DNA-PK activity.	Acetylcysteine	69-88	protein kinase, DNA-activated, catalytic subunit	Homo sapiens	155-161
16489261-3	2005	Both NAC and LCAR pretreatment markedly decreased MPO and Cu/Zn-SOD activity compared to colitis group.	Acetylcysteine	5-8	superoxide dismutase 1	Rattus norvegicus	58-67
16984740-3	2006	In this report, we try to determine the effects of antioxidants (catalase or N-acetylcysteine [NAC]) on the regulation of intrinsic MDR1 overexpression in HepG2 cells.	Acetylcysteine	77-93	ATP binding cassette subfamily B member 1	Homo sapiens	132-136
16984740-3	2006	In this report, we try to determine the effects of antioxidants (catalase or N-acetylcysteine [NAC]) on the regulation of intrinsic MDR1 overexpression in HepG2 cells.	Acetylcysteine	95-98	ATP binding cassette subfamily B member 1	Homo sapiens	132-136
16984740-4	2006	Adding catalase or N-acetylcysteine to the HepG2 culture led to a significant increase of MDR1 mRNA and P-glycoprotein drug transporter activity.	Acetylcysteine	19-35	ATP binding cassette subfamily B member 1	Homo sapiens	90-94
16298685-4	2005	These effects of Ang-II were suppressed by the Ang-II receptor type I (AT1) inhibitor CV-11974 as well as by the antioxidants diphenylene iodonium (DPI) and N-acetyl-L-cysteine (NAC), but not by AT2 antagonist PD 122319.	Acetylcysteine	157-176	angiotensinogen	Rattus norvegicus	17-23
16298685-4	2005	These effects of Ang-II were suppressed by the Ang-II receptor type I (AT1) inhibitor CV-11974 as well as by the antioxidants diphenylene iodonium (DPI) and N-acetyl-L-cysteine (NAC), but not by AT2 antagonist PD 122319.	Acetylcysteine	178-181	angiotensinogen	Rattus norvegicus	17-23
16298685-5	2005	Furthermore, Ang-II induced a two- to threefold increase in protein synthesis and cell size during 12-24 h, which could be inhibited by CV-11974 as well as by DPI and NAC.	Acetylcysteine	167-170	angiotensinogen	Rattus norvegicus	13-19
16489261-1	2005	The aim of the present study was to evaluate the effects of N-acetylcysteine (NAC) and L-carnitine (LCAR) supplementations on polymorphonuclear leukocytes myeloperoxidase (MPO) and Cu/Zn-superoxide dismutase (Cu/Zn-SOD) and plasma malondialdehyde (MDA) in acetic acid (AA)-induced ulcerative colitis model.	Acetylcysteine	78-81	superoxide dismutase 1	Rattus norvegicus	181-207
16489261-1	2005	The aim of the present study was to evaluate the effects of N-acetylcysteine (NAC) and L-carnitine (LCAR) supplementations on polymorphonuclear leukocytes myeloperoxidase (MPO) and Cu/Zn-superoxide dismutase (Cu/Zn-SOD) and plasma malondialdehyde (MDA) in acetic acid (AA)-induced ulcerative colitis model.	Acetylcysteine	78-81	superoxide dismutase 1	Rattus norvegicus	209-218
16099896-10	2005	Catalase activity increased after NAC treatment in both age groups.	Acetylcysteine	34-37	catalase	Rattus norvegicus	0-8
16166164-6	2005	Treatment of THP-1 with various test compounds such as dietary supplements (alpha-tocopherol, N-acetylcysteine, catechin and epigallocatechin gallate) as well as pharmacologic agents (statins, peroxisome proliferator-activated receptor-gamma agonists, and an angiotensin II receptor blocker) significantly inhibited LPS-stimulated TNF-alpha release.	Acetylcysteine	94-110	GLI family zinc finger 2	Homo sapiens	13-18
16162852-13	2005	Correspondingly, pretreatment with NAC significantly attenuated LPS-induced elevation in TNF-alpha concentration in maternal serum and amniotic fluid and lipid peroxidation in maternal and fetal livers.	Acetylcysteine	35-38	tumor necrosis factor	Mus musculus	89-98
16277400-8	2005	NAC prevented up-regulation of GADD153 mRNA expression caused by HMDB.	Acetylcysteine	0-3	DNA damage inducible transcript 3	Homo sapiens	31-38
16316327-3	2005	We evaluated the effect of CsA and the antioxidant N-acetylcysteine (NAC) on inducible nitric oxide synthase (iNOS) mRNA expression and nitric oxide synthesis, in rat renal artery vascular smooth muscle cells (rVSMCs) primary culture.	Acetylcysteine	51-67	nitric oxide synthase 2	Rattus norvegicus	110-114
16316327-3	2005	We evaluated the effect of CsA and the antioxidant N-acetylcysteine (NAC) on inducible nitric oxide synthase (iNOS) mRNA expression and nitric oxide synthesis, in rat renal artery vascular smooth muscle cells (rVSMCs) primary culture.	Acetylcysteine	69-72	nitric oxide synthase 2	Rattus norvegicus	110-114
16140340-9	2005	RESULTS: The administration of NAC resulted in lower levels of aspartate aminotransferase, alanine aminotransferase, and alpha-glutathione S-transferase, decreased platelet aggregation, and increased levels of ischemic tissue cAMP at all time points after reperfusion.	Acetylcysteine	31-34	glutamic-oxaloacetic transaminase 2	Rattus norvegicus	63-89
16280646-4	2005	The suppression of oxidative stress by a potent antioxidant, N-acetyl-l-cysteine or probucol, led to the recovery of insulin biosynthesis and PDX-1 expression in nuclei and improved glucose tolerance in animal models for type 2 diabetes.	Acetylcysteine	61-80	insulin	Homo sapiens	117-124
16098950-0	2005	N-acetyl-L-cysteine suppresses TGF-beta signaling at distinct molecular steps: the biochemical and biological efficacy of a multifunctional, antifibrotic drug.	Acetylcysteine	0-19	transforming growth factor beta 1	Homo sapiens	31-39
15958730-5	2005	Pretreatment with antioxidants catalase completely, whereas the other tested superoxide dismutase, N-acetyl-l-cysteine and sodium formate partially attenuated H(2)O(2)-induced CAV1 phosphorylation in a concentration-dependent manner.	Acetylcysteine	99-118	caveolin 1	Homo sapiens	176-180
16151024-7	2005	Pretreatment of rat VSMCs with the NOX inhibitor diphenylene iodonium or the antioxidants N-acetylcysteine or ebselen significantly inhibited Ang II-induced cAbl phosphorylation.	Acetylcysteine	90-106	angiotensinogen	Rattus norvegicus	142-148
16098950-2	2005	This prompted us to investigate the influence of the antioxidant N-acetyl-L-cysteine on TGF-beta signaling in culture-activated hepatic stellate cells, the most relevant pro-fibrogenic cell type in liver.	Acetylcysteine	65-84	transforming growth factor beta 1	Homo sapiens	88-96
16098950-3	2005	Dissection of the molecular steps involved in TGF-beta signaling revealed that N-acetyl-L-cysteine dose-dependently abrogated the induction of the TGF-beta1 signaling reporter gene activation, the phosphorylation of Smad2 and Smad3, and the up-regulation of Smad7 mRNA.	Acetylcysteine	79-98	transforming growth factor beta 1	Homo sapiens	46-54
16098950-3	2005	Dissection of the molecular steps involved in TGF-beta signaling revealed that N-acetyl-L-cysteine dose-dependently abrogated the induction of the TGF-beta1 signaling reporter gene activation, the phosphorylation of Smad2 and Smad3, and the up-regulation of Smad7 mRNA.	Acetylcysteine	79-98	transforming growth factor beta 1	Homo sapiens	147-156
16098950-3	2005	Dissection of the molecular steps involved in TGF-beta signaling revealed that N-acetyl-L-cysteine dose-dependently abrogated the induction of the TGF-beta1 signaling reporter gene activation, the phosphorylation of Smad2 and Smad3, and the up-regulation of Smad7 mRNA.	Acetylcysteine	79-98	SMAD family member 7	Homo sapiens	258-263
16098950-5	2005	We conclude that N-acetyl-L-cysteine is a specific inhibitor of TGF-beta signaling targeting different components of the TGF-beta signaling machinery.	Acetylcysteine	17-36	transforming growth factor beta 1	Homo sapiens	64-72
16098950-5	2005	We conclude that N-acetyl-L-cysteine is a specific inhibitor of TGF-beta signaling targeting different components of the TGF-beta signaling machinery.	Acetylcysteine	17-36	transforming growth factor beta 1	Homo sapiens	121-129
16086031-7	2005	Reactive oxygen species (ROS) were also detected within 1 h after AF treatment, and the antioxidant N-acetyl-L-cysteine (NAC) effectively protected the cells from apoptosis by inhibiting the phosphorylation of p38 MAPK and the activation of caspases.	Acetylcysteine	100-119	mitogen-activated protein kinase 14	Homo sapiens	210-218
16382175-5	2005	In H9C2 cells, NAC pretreatment blocked cocaine-mediated increases in CRP, FAS, FAS ligand, and cytokine receptor-like factor1 (CRLF1) expression.	Acetylcysteine	15-18	C-reactive protein	Rattus norvegicus	70-73
16099944-4	2005	Oxidative stress-induced increases in T-cad were inhibited by the free radical-scavenging antioxidant, N-acetylcysteine, and the flavin-containing oxidase inhibitor, diphenyleneiodonium.	Acetylcysteine	103-119	cadherin 13	Homo sapiens	38-43
16192891-11	2005	Exogenous H2O2 enhanced IL-8 secretion and N-acetyl cysteine (NAC) prevented IL-1alpha-induced ROS production and IL-8 secretion.	Acetylcysteine	43-60	C-X-C motif chemokine ligand 8	Homo sapiens	114-118
15829913-9	2005	In addition, administration of N-acetylcysteine (NAC), a precursor of glutathione and a potent antioxidant, attenuated both Tat-induced ERK 1/2 activation and alterations in ZO-1 expression.	Acetylcysteine	49-52	mitogen-activated protein kinase 3	Homo sapiens	136-143
15829913-9	2005	In addition, administration of N-acetylcysteine (NAC), a precursor of glutathione and a potent antioxidant, attenuated both Tat-induced ERK 1/2 activation and alterations in ZO-1 expression.	Acetylcysteine	49-52	tight junction protein 1	Homo sapiens	174-178
15829913-9	2005	In addition, administration of N-acetylcysteine (NAC), a precursor of glutathione and a potent antioxidant, attenuated both Tat-induced ERK 1/2 activation and alterations in ZO-1 expression.	Acetylcysteine	31-47	mitogen-activated protein kinase 3	Homo sapiens	136-143
15829913-9	2005	In addition, administration of N-acetylcysteine (NAC), a precursor of glutathione and a potent antioxidant, attenuated both Tat-induced ERK 1/2 activation and alterations in ZO-1 expression.	Acetylcysteine	31-47	tight junction protein 1	Homo sapiens	174-178
16192891-11	2005	Exogenous H2O2 enhanced IL-8 secretion and N-acetyl cysteine (NAC) prevented IL-1alpha-induced ROS production and IL-8 secretion.	Acetylcysteine	62-65	C-X-C motif chemokine ligand 8	Homo sapiens	114-118
16148150-7	2005	The thiol antioxidant N-acetyl cysteine, extracellular catalase, and inducible NO synthase inhibitors inhibited ICAM-1 and IL-8 increases in response to both phenazines.	Acetylcysteine	22-39	C-X-C motif chemokine ligand 8	Homo sapiens	123-127
16109311-4	2005	Interestingly, both IL-1beta and TNF-alpha markedly inhibited the expression of MOG, CNPase, and PLP but not MBP, the effect that was blocked by antioxidants such as N-acetylcysteine (NAC) and pyrrolidine dithiocarbamate (PDTC).	Acetylcysteine	166-182	interleukin 1 beta	Homo sapiens	20-28
16109311-4	2005	Interestingly, both IL-1beta and TNF-alpha markedly inhibited the expression of MOG, CNPase, and PLP but not MBP, the effect that was blocked by antioxidants such as N-acetylcysteine (NAC) and pyrrolidine dithiocarbamate (PDTC).	Acetylcysteine	166-182	tumor necrosis factor	Homo sapiens	33-42
16109311-4	2005	Interestingly, both IL-1beta and TNF-alpha markedly inhibited the expression of MOG, CNPase, and PLP but not MBP, the effect that was blocked by antioxidants such as N-acetylcysteine (NAC) and pyrrolidine dithiocarbamate (PDTC).	Acetylcysteine	166-182	2',3'-cyclic nucleotide 3' phosphodiesterase	Homo sapiens	85-91
16109311-4	2005	Interestingly, both IL-1beta and TNF-alpha markedly inhibited the expression of MOG, CNPase, and PLP but not MBP, the effect that was blocked by antioxidants such as N-acetylcysteine (NAC) and pyrrolidine dithiocarbamate (PDTC).	Acetylcysteine	184-187	interleukin 1 beta	Homo sapiens	20-28
16109311-4	2005	Interestingly, both IL-1beta and TNF-alpha markedly inhibited the expression of MOG, CNPase, and PLP but not MBP, the effect that was blocked by antioxidants such as N-acetylcysteine (NAC) and pyrrolidine dithiocarbamate (PDTC).	Acetylcysteine	184-187	tumor necrosis factor	Homo sapiens	33-42
16024664-8	2005	On the other hand, when examining the impact of salvicine on DNA repair pathways, we unexpectedly observed that salvicine selectively down-regulated the catalytic subunit of DNA-dependent protein kinase (DNA-PK(CS)) protein levels and repressed DNA-PK kinase activity; both of these effects were attenuated by NAC pretreatment of MCF-7 cells.	Acetylcysteine	310-313	protein kinase, DNA-activated, catalytic subunit	Homo sapiens	204-214
16024664-8	2005	On the other hand, when examining the impact of salvicine on DNA repair pathways, we unexpectedly observed that salvicine selectively down-regulated the catalytic subunit of DNA-dependent protein kinase (DNA-PK(CS)) protein levels and repressed DNA-PK kinase activity; both of these effects were attenuated by NAC pretreatment of MCF-7 cells.	Acetylcysteine	310-313	protein kinase, DNA-activated, catalytic subunit	Homo sapiens	204-210
16231578-6	2005	Recently, in rat models of CHF, oral administration of the glutathione precursor, N-acetylcysteine (NAC), was shown to hinder pathways of TNF alpha harmful signalling and to rescue cardiac structure and function.	Acetylcysteine	82-98	tumor necrosis factor	Rattus norvegicus	138-147
16101137-6	2005	Furthermore, inhibition of SOD mRNAs expression by EUG was strongly potentiated by the addition of 5 mM N-acetyl cysteine (NAC) or glutathione (GSH), whereas NAC or GSH alone did not affect the expression of SOD mRNAs.	Acetylcysteine	104-121	superoxide dismutase 1	Homo sapiens	27-30
16101137-6	2005	Furthermore, inhibition of SOD mRNAs expression by EUG was strongly potentiated by the addition of 5 mM N-acetyl cysteine (NAC) or glutathione (GSH), whereas NAC or GSH alone did not affect the expression of SOD mRNAs.	Acetylcysteine	123-126	superoxide dismutase 1	Homo sapiens	27-30
16101137-6	2005	Furthermore, inhibition of SOD mRNAs expression by EUG was strongly potentiated by the addition of 5 mM N-acetyl cysteine (NAC) or glutathione (GSH), whereas NAC or GSH alone did not affect the expression of SOD mRNAs.	Acetylcysteine	123-126	superoxide dismutase 1	Homo sapiens	208-211
16101137-7	2005	The cytotoxicity of EUG was significantly enhanced by high concentrations of NAC or GSH, which may be attributed to the inhibition of SOD mRNAs expression by the synergistic action of EUG and GSH or NAC.	Acetylcysteine	77-80	superoxide dismutase 1	Homo sapiens	134-137
16115031-5	2005	AngII-induced MCP-1 protein expression in mProx at 6 h was largely blocked by ROS (N-acetylcysteine; 82 +/- 14%), Ras (N-acetyl-S-trans,trans-farnesyl-L-cysteine; 82 +/- 13%), and nuclear factor-kappaB (NF-kappaB) (parthenolide; 89 +/- 7.9%) inhibitors.	Acetylcysteine	83-99	angiotensinogen (serpin peptidase inhibitor, clade A, member 8)	Mus musculus	0-5
16231578-6	2005	Recently, in rat models of CHF, oral administration of the glutathione precursor, N-acetylcysteine (NAC), was shown to hinder pathways of TNF alpha harmful signalling and to rescue cardiac structure and function.	Acetylcysteine	100-103	tumor necrosis factor	Rattus norvegicus	138-147
16140881-10	2005	NAC inhibited the reductions in eNOS and iNOS transcription and protein levels.	Acetylcysteine	0-3	nitric oxide synthase 2	Rattus norvegicus	41-45
16204787-5	2005	NAC decreased sputum eosinophil cationic protein (318 +/-73 vs. 163 +/-30 ng/ml, P&lt;0.01) and sputum IL-8 (429 +/-80 vs. 347 +/-70 ng/ml, P&lt;0.05).	Acetylcysteine	0-3	C-X-C motif chemokine ligand 8	Homo sapiens	103-107
15962302-6	2005	Pretreatment of the cells with N-acetyl-L-cysteine (NAC) significantly prevented suppression of MMPs and uPA secretion, DNA binding activity of NF-kappaB, and in vitro invasion of HT1080 cells by As2O3, suggesting a role of reactive oxygen species (ROS) in this process.	Acetylcysteine	31-50	plasminogen activator, urokinase	Homo sapiens	105-108
16039951-5	2005	Both effects were inhibited by NAC which reduced the population with depolarized mitochondrial membranes to 24.1+/-1.2% and prevented PARP-cleavage indicating a central role oxidative stress in KP1019-induced apoptosis.	Acetylcysteine	31-34	poly(ADP-ribose) polymerase 1	Homo sapiens	134-138
15817678-4	2005	Application of N-acetylcysteine (NAC) or blocking the activity of Nox, a protein leading to the formation of ROS, with diphenylene iodonium (DPI) inhibits the responses of BMM cells to RANKL, including ROS production, activation of c-Jun N-terminal kinase (JNK), p38 mitogen-activated protein (MAP) kinase, and extracellular signal-regulated kinase (ERK), and osteoclast differentiation.	Acetylcysteine	15-31	mitogen-activated protein kinase 8	Homo sapiens	232-255
15817678-4	2005	Application of N-acetylcysteine (NAC) or blocking the activity of Nox, a protein leading to the formation of ROS, with diphenylene iodonium (DPI) inhibits the responses of BMM cells to RANKL, including ROS production, activation of c-Jun N-terminal kinase (JNK), p38 mitogen-activated protein (MAP) kinase, and extracellular signal-regulated kinase (ERK), and osteoclast differentiation.	Acetylcysteine	15-31	mitogen-activated protein kinase 8	Homo sapiens	257-260
15817678-4	2005	Application of N-acetylcysteine (NAC) or blocking the activity of Nox, a protein leading to the formation of ROS, with diphenylene iodonium (DPI) inhibits the responses of BMM cells to RANKL, including ROS production, activation of c-Jun N-terminal kinase (JNK), p38 mitogen-activated protein (MAP) kinase, and extracellular signal-regulated kinase (ERK), and osteoclast differentiation.	Acetylcysteine	15-31	mitogen-activated protein kinase 1	Homo sapiens	311-348
15817678-4	2005	Application of N-acetylcysteine (NAC) or blocking the activity of Nox, a protein leading to the formation of ROS, with diphenylene iodonium (DPI) inhibits the responses of BMM cells to RANKL, including ROS production, activation of c-Jun N-terminal kinase (JNK), p38 mitogen-activated protein (MAP) kinase, and extracellular signal-regulated kinase (ERK), and osteoclast differentiation.	Acetylcysteine	15-31	mitogen-activated protein kinase 1	Homo sapiens	350-353
16124875-3	2005	Both curcumin, a component of the spice turmeric, and N-acetylcysteine (NAC), an antioxidant, inhibit activation of NF-kappaB by inflammatory stimuli, albeit by different mechanisms.	Acetylcysteine	54-70	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	116-125
16124875-3	2005	Both curcumin, a component of the spice turmeric, and N-acetylcysteine (NAC), an antioxidant, inhibit activation of NF-kappaB by inflammatory stimuli, albeit by different mechanisms.	Acetylcysteine	72-75	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	116-125
16124875-4	2005	In the present study, we tested the hypothesis that dietary curcumin or NAC supplementation would inhibit unloading-induced NF-kappaB activity in skeletal muscle and thereby protect muscles against loss of mass and function caused by prolonged unloading.	Acetylcysteine	72-75	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	124-133
16124875-12	2005	In contrast, NAC prevented the increase in NF-kappaB activity induced by unloading but did not prevent losses of muscle mass or function.	Acetylcysteine	13-16	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	43-52
16124875-13	2005	CONCLUSION: In conclusion, neither dietary curcumin nor dietary NAC prevents unloading-induced skeletal muscle dysfunction and atrophy, although dietary NAC does prevent unloading induced NF-kappaB activation.	Acetylcysteine	153-156	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	188-197
15944340-0	2005	N-acetylcysteine decreases angiotensin II receptor binding in vascular smooth muscle cells.	Acetylcysteine	0-16	angiotensinogen	Homo sapiens	27-41
15944340-3	2005	Incubation of cultured vascular smooth muscle cells, which possess Ang II type 1a receptors, with the reducing agent n-acetylcysteine (NAC) for 1 h at 37 degrees C resulted in decreased Ang II radioligand binding in a concentration-dependent pattern.	Acetylcysteine	117-133	angiotensinogen	Homo sapiens	67-73
15944340-3	2005	Incubation of cultured vascular smooth muscle cells, which possess Ang II type 1a receptors, with the reducing agent n-acetylcysteine (NAC) for 1 h at 37 degrees C resulted in decreased Ang II radioligand binding in a concentration-dependent pattern.	Acetylcysteine	117-133	angiotensinogen	Homo sapiens	186-192
15944340-3	2005	Incubation of cultured vascular smooth muscle cells, which possess Ang II type 1a receptors, with the reducing agent n-acetylcysteine (NAC) for 1 h at 37 degrees C resulted in decreased Ang II radioligand binding in a concentration-dependent pattern.	Acetylcysteine	135-138	angiotensinogen	Homo sapiens	67-73
15944340-3	2005	Incubation of cultured vascular smooth muscle cells, which possess Ang II type 1a receptors, with the reducing agent n-acetylcysteine (NAC) for 1 h at 37 degrees C resulted in decreased Ang II radioligand binding in a concentration-dependent pattern.	Acetylcysteine	135-138	angiotensinogen	Homo sapiens	186-192
15944340-4	2005	NAC removal restored Ang II binding within 30 min.	Acetylcysteine	0-3	angiotensinogen	Homo sapiens	21-27
15944340-8	2005	NAC inhibited Ang II binding in cell membranes at 21 or 37 but not 4 degrees C. Dihydrolipoic acid (the reduced form of alpha-lipoic acid), which contains free sulfhydryl groups as NAC does, decreased Ang II receptor binding in cell membranes, whereas alpha-lipoic acid, which does not contain free sulfhydryl groups, did not.	Acetylcysteine	0-3	angiotensinogen	Homo sapiens	14-20
15944340-8	2005	NAC inhibited Ang II binding in cell membranes at 21 or 37 but not 4 degrees C. Dihydrolipoic acid (the reduced form of alpha-lipoic acid), which contains free sulfhydryl groups as NAC does, decreased Ang II receptor binding in cell membranes, whereas alpha-lipoic acid, which does not contain free sulfhydryl groups, did not.	Acetylcysteine	0-3	angiotensinogen	Homo sapiens	201-207
15944340-8	2005	NAC inhibited Ang II binding in cell membranes at 21 or 37 but not 4 degrees C. Dihydrolipoic acid (the reduced form of alpha-lipoic acid), which contains free sulfhydryl groups as NAC does, decreased Ang II receptor binding in cell membranes, whereas alpha-lipoic acid, which does not contain free sulfhydryl groups, did not.	Acetylcysteine	181-184	angiotensinogen	Homo sapiens	14-20
15944340-9	2005	Ang II-stimulated inositol phosphate formation was decreased by preincubation with NAC (1 h) or alpha-lipoic acid (24 h) but not vitamin E.	Acetylcysteine	83-86	angiotensinogen	Homo sapiens	0-6
15962302-6	2005	Pretreatment of the cells with N-acetyl-L-cysteine (NAC) significantly prevented suppression of MMPs and uPA secretion, DNA binding activity of NF-kappaB, and in vitro invasion of HT1080 cells by As2O3, suggesting a role of reactive oxygen species (ROS) in this process.	Acetylcysteine	52-55	plasminogen activator, urokinase	Homo sapiens	105-108
16042792-0	2005	Multidrug resistance-associated protein 1 (MRP1) mediated vincristine resistance: effects of N-acetylcysteine and Buthionine sulfoximine.	Acetylcysteine	93-109	ATP binding cassette subfamily C member 1	Homo sapiens	0-41
16184402-10	2005	This increase in superoxide production by ET-1 was significantly inhibited by trilinolein, diphenyleneiodonium, or N-acetylcysteine.	Acetylcysteine	115-131	endothelin 1	Rattus norvegicus	42-46
15888667-6	2005	Pre-treatment with the antioxidant molecule N-acetyl cysteine sharply decreased the level of phospho-ERK1/2 and had no effect on Raf and MEK1/2 activation, suggesting a Raf-independent mechanism.	Acetylcysteine	44-61	mitogen-activated protein kinase 3	Homo sapiens	101-107
15770640-4	2005	Following HDAC with NAC, AFP markedly decreased.	Acetylcysteine	20-23	alpha fetoprotein	Homo sapiens	25-28
15967733-5	2005	Pretreatment with NAC partially prevented tumor necrosis factor alpha (TNFalpha) production induced by the low concentration of LPS, while pretreatment with budesonide totally prevented the increased production of TNFalpha, interleukin (IL)-1beta, IL-6, and monocyte chemoattractive protein (MCP)-1 after LPS challenge at both low and high concentrations.	Acetylcysteine	18-21	tumor necrosis factor	Rattus norvegicus	42-69
15967733-5	2005	Pretreatment with NAC partially prevented tumor necrosis factor alpha (TNFalpha) production induced by the low concentration of LPS, while pretreatment with budesonide totally prevented the increased production of TNFalpha, interleukin (IL)-1beta, IL-6, and monocyte chemoattractive protein (MCP)-1 after LPS challenge at both low and high concentrations.	Acetylcysteine	18-21	tumor necrosis factor	Rattus norvegicus	71-79
16042792-0	2005	Multidrug resistance-associated protein 1 (MRP1) mediated vincristine resistance: effects of N-acetylcysteine and Buthionine sulfoximine.	Acetylcysteine	93-109	ATP binding cassette subfamily C member 1	Homo sapiens	43-47
16042792-5	2005	The aim of our study was to investigate the effect of NAC and BSO on MRP1-mediated vincristine resistance in Human Embryonic Kidney (HEK293) and its MRP1 transfected 293MRP cells.	Acetylcysteine	54-57	ATP binding cassette subfamily C member 1	Homo sapiens	69-73
16042792-10	2005	RESULTS: N-acetylcysteine increased the resistance of both cells against vincristine and BSO decreased NAC-enhanced MRP1-mediated vincristine resistance, indicating that induction of MRP1-mediated vincristine resistance depends on GSH.	Acetylcysteine	9-25	ATP binding cassette subfamily C member 1	Homo sapiens	183-187
16042792-10	2005	RESULTS: N-acetylcysteine increased the resistance of both cells against vincristine and BSO decreased NAC-enhanced MRP1-mediated vincristine resistance, indicating that induction of MRP1-mediated vincristine resistance depends on GSH.	Acetylcysteine	103-106	ATP binding cassette subfamily C member 1	Homo sapiens	116-120
16042792-10	2005	RESULTS: N-acetylcysteine increased the resistance of both cells against vincristine and BSO decreased NAC-enhanced MRP1-mediated vincristine resistance, indicating that induction of MRP1-mediated vincristine resistance depends on GSH.	Acetylcysteine	103-106	ATP binding cassette subfamily C member 1	Homo sapiens	183-187
16042792-13	2005	CONCLUSION: Our results demonstrate that NAC and BSO have opposite effects in MRP1 mediated vincristine resistance and BSO seems a promising chemotherapy improving agent in MRP1 overexpressing tumor cells.	Acetylcysteine	41-44	ATP binding cassette subfamily C member 1	Homo sapiens	78-82
16253189-15	2005	U0126, irbesartan, and NAC, as well as ACEUI, significantly inhibited the increased AP-1 DNA binding activity induced by Ang II.	Acetylcysteine	23-26	angiotensinogen	Rattus norvegicus	121-127
15941563-7	2005	Furthermore, the free radical scavenger ascorbic acid and N-acetylcysteine attenuated emodin-mediated ROS production, ERK and AKT inactivation, mitochondrial dysfunction, Bcl-2/Bax modulation, and apoptosis.	Acetylcysteine	58-74	mitogen-activated protein kinase 1	Homo sapiens	118-121
15941563-7	2005	Furthermore, the free radical scavenger ascorbic acid and N-acetylcysteine attenuated emodin-mediated ROS production, ERK and AKT inactivation, mitochondrial dysfunction, Bcl-2/Bax modulation, and apoptosis.	Acetylcysteine	58-74	AKT serine/threonine kinase 1	Homo sapiens	126-129
15941563-7	2005	Furthermore, the free radical scavenger ascorbic acid and N-acetylcysteine attenuated emodin-mediated ROS production, ERK and AKT inactivation, mitochondrial dysfunction, Bcl-2/Bax modulation, and apoptosis.	Acetylcysteine	58-74	BCL2 apoptosis regulator	Homo sapiens	171-176
15941563-7	2005	Furthermore, the free radical scavenger ascorbic acid and N-acetylcysteine attenuated emodin-mediated ROS production, ERK and AKT inactivation, mitochondrial dysfunction, Bcl-2/Bax modulation, and apoptosis.	Acetylcysteine	58-74	BCL2 associated X, apoptosis regulator	Homo sapiens	177-180
15882270-0	2005	The antioxidant N-acetylcysteine prevents accelerated atherosclerosis in uremic apolipoprotein E knockout mice.	Acetylcysteine	16-32	apolipoprotein E	Mus musculus	80-96
15764673-8	2005	NAC (20 mmol/l) or MnTMPyP (50 micromol/l) also abolished the cold-induced activation of RhoA in human cultured vascular smooth muscle cells and the cold-induced mobilization of alpha2C-ARs to the cell surface in human embryonic kidney 293 cells transfected with the receptor.	Acetylcysteine	0-3	ras homolog family member A	Homo sapiens	89-93
16026512-12	2005	Furthermore, pretreating cells with TMP or the anti-oxidant N-acetyl-cysteine decreased strain-induced increases in ET-1 secretion and ERK1/2 phosphorylation.	Acetylcysteine	60-77	endothelin 1	Homo sapiens	116-120
16026512-12	2005	Furthermore, pretreating cells with TMP or the anti-oxidant N-acetyl-cysteine decreased strain-induced increases in ET-1 secretion and ERK1/2 phosphorylation.	Acetylcysteine	60-77	mitogen-activated protein kinase 3	Homo sapiens	135-141
15817708-7	2005	The antioxidants (N-acetyl-L-cysteine and glutathione ethyl-ester) blunted IL-10 and IL-12 production, indicating a role for oxidative stress in the observed response differences between deficient and WT macrophages.	Acetylcysteine	18-37	interleukin 10	Mus musculus	75-80
15802620-6	2005	This phosphorylation was blocked by the Src inhibitor PP1 and by the antioxidants N-acetylcysteine and ebselen.	Acetylcysteine	82-98	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	40-43
15802620-6	2005	This phosphorylation was blocked by the Src inhibitor PP1 and by the antioxidants N-acetylcysteine and ebselen.	Acetylcysteine	82-98	neuropeptide Y receptor Y4	Homo sapiens	54-57
15998259-8	2005	Consistent with this idea, studies with antioxidants such as vitamin E, alpha-lipoic acid, and N-acetylcysteine indicate a beneficial impact on insulin sensitivity, and offer the possibility for new treatment approaches for insulin resistance.	Acetylcysteine	95-111	insulin	Homo sapiens	144-151
15998259-8	2005	Consistent with this idea, studies with antioxidants such as vitamin E, alpha-lipoic acid, and N-acetylcysteine indicate a beneficial impact on insulin sensitivity, and offer the possibility for new treatment approaches for insulin resistance.	Acetylcysteine	95-111	insulin	Homo sapiens	224-231
15788408-11	2005	In addition, the ability of a thiol antioxidant, N-acetylcysteine, to inhibit the effect of arsenite on VEGF expression coincided with its ability to inhibit phosphorylation of eIF2alpha and ATF4 protein expression.	Acetylcysteine	49-65	vascular endothelial growth factor A	Homo sapiens	104-108
15837587-5	2005	NF-kappa B activation and cybrid viability are enhanced by NAC.	Acetylcysteine	59-62	nuclear factor kappa B subunit 1	Homo sapiens	0-10
15965068-10	2005	N-acetylcysteine reduced the stimulatory effect of celecoxib on stress kinase activities, suggesting an involvement of JNK in HO-1 expression.	Acetylcysteine	0-16	mitogen-activated protein kinase 8	Homo sapiens	119-122
15878161-7	2005	The inductive properties of angiotensin II and H2O2 on ERK phosphorylation and activator protein-1-mediated reporter activity were found reversed with resveratrol and antioxidants such as N-acetyl-cysteine.	Acetylcysteine	188-205	angiotensinogen	Rattus norvegicus	28-42
15878161-7	2005	The inductive properties of angiotensin II and H2O2 on ERK phosphorylation and activator protein-1-mediated reporter activity were found reversed with resveratrol and antioxidants such as N-acetyl-cysteine.	Acetylcysteine	188-205	Eph receptor B1	Rattus norvegicus	55-58
15735709-6	2005	Bax activation by As(2)O(3) seemed to require stress-induced intracellular reactive oxygen species (ROS), since the ROS scavengers (N-acetyl-L-cysteine and lipoic acid) could completely block the conformational change and translocation of Bax from cytosol to mitochondria.	Acetylcysteine	132-151	BCL2 associated X, apoptosis regulator	Homo sapiens	0-3
15735709-6	2005	Bax activation by As(2)O(3) seemed to require stress-induced intracellular reactive oxygen species (ROS), since the ROS scavengers (N-acetyl-L-cysteine and lipoic acid) could completely block the conformational change and translocation of Bax from cytosol to mitochondria.	Acetylcysteine	132-151	BCL2 associated X, apoptosis regulator	Homo sapiens	239-242
15869713-1	2005	We report that N-acetyl-L-cysteine (NAC) treatment blocked induction of TNF-alpha, IL-1beta, IFN-gamma and iNOS in the CNS and attenuated clinical disease in the myelin basic protein induced model of experimental allergic encephalomyelitis (EAE) in Lewis rats.	Acetylcysteine	15-34	tumor necrosis factor	Rattus norvegicus	72-81
15869713-1	2005	We report that N-acetyl-L-cysteine (NAC) treatment blocked induction of TNF-alpha, IL-1beta, IFN-gamma and iNOS in the CNS and attenuated clinical disease in the myelin basic protein induced model of experimental allergic encephalomyelitis (EAE) in Lewis rats.	Acetylcysteine	15-34	interleukin 1 beta	Rattus norvegicus	83-91
15869713-1	2005	We report that N-acetyl-L-cysteine (NAC) treatment blocked induction of TNF-alpha, IL-1beta, IFN-gamma and iNOS in the CNS and attenuated clinical disease in the myelin basic protein induced model of experimental allergic encephalomyelitis (EAE) in Lewis rats.	Acetylcysteine	15-34	nitric oxide synthase 2	Rattus norvegicus	107-111
15869713-1	2005	We report that N-acetyl-L-cysteine (NAC) treatment blocked induction of TNF-alpha, IL-1beta, IFN-gamma and iNOS in the CNS and attenuated clinical disease in the myelin basic protein induced model of experimental allergic encephalomyelitis (EAE) in Lewis rats.	Acetylcysteine	36-39	tumor necrosis factor	Rattus norvegicus	72-81
15869713-1	2005	We report that N-acetyl-L-cysteine (NAC) treatment blocked induction of TNF-alpha, IL-1beta, IFN-gamma and iNOS in the CNS and attenuated clinical disease in the myelin basic protein induced model of experimental allergic encephalomyelitis (EAE) in Lewis rats.	Acetylcysteine	36-39	interleukin 1 beta	Rattus norvegicus	83-91
15869713-1	2005	We report that N-acetyl-L-cysteine (NAC) treatment blocked induction of TNF-alpha, IL-1beta, IFN-gamma and iNOS in the CNS and attenuated clinical disease in the myelin basic protein induced model of experimental allergic encephalomyelitis (EAE) in Lewis rats.	Acetylcysteine	36-39	nitric oxide synthase 2	Rattus norvegicus	107-111
15845704-7	2005	We also analyzed the effect of NAC on interleukin-8 (IL-8)-induced expression of CD11b in human whole blood.	Acetylcysteine	31-34	C-X-C motif chemokine ligand 8	Homo sapiens	38-51
15845704-7	2005	We also analyzed the effect of NAC on interleukin-8 (IL-8)-induced expression of CD11b in human whole blood.	Acetylcysteine	31-34	C-X-C motif chemokine ligand 8	Homo sapiens	53-57
15845704-8	2005	IL-8 (10 ng/mL) significantly upregulated the expression of CD11b, and the IL-8-induced upregulation was significantly attenuated by NAC (&gt;10 mM) in a dose-dependent manner.	Acetylcysteine	133-136	C-X-C motif chemokine ligand 8	Homo sapiens	0-4
15845704-8	2005	IL-8 (10 ng/mL) significantly upregulated the expression of CD11b, and the IL-8-induced upregulation was significantly attenuated by NAC (&gt;10 mM) in a dose-dependent manner.	Acetylcysteine	133-136	C-X-C motif chemokine ligand 8	Homo sapiens	75-79
15845704-9	2005	We conclude that NAC attenuates the increased expression of CD11b in either LPS or IL-8-stimulated human whole blood.	Acetylcysteine	17-20	C-X-C motif chemokine ligand 8	Homo sapiens	83-87
15965078-0	2005	Antioxidant N-acetylcysteine blocks nerve growth factor-induced H2O2/ERK signaling in PC12 cells.	Acetylcysteine	12-28	Eph receptor B1	Rattus norvegicus	69-72
15965078-5	2005	These findings demonstrate that NAC blocks the NGF-induced H2O2/ERK signaling in PC12 cells.	Acetylcysteine	32-35	Eph receptor B1	Rattus norvegicus	64-67
15718492-5	2005	Inhibition of nuclear factor-kappaB (NF-kappaB) activation by the p65-antisense, lactacystin, and N-acetyl-cysteine blocked the coculture-induced EC expression of proinflammatory genes, indicating that the NF-kappaB binding sites in the promoters of these genes play a significant role in their expression as a result of coculture with SMCs.	Acetylcysteine	98-115	nuclear factor kappa B subunit 1	Homo sapiens	14-35
15718492-5	2005	Inhibition of nuclear factor-kappaB (NF-kappaB) activation by the p65-antisense, lactacystin, and N-acetyl-cysteine blocked the coculture-induced EC expression of proinflammatory genes, indicating that the NF-kappaB binding sites in the promoters of these genes play a significant role in their expression as a result of coculture with SMCs.	Acetylcysteine	98-115	nuclear factor kappa B subunit 1	Homo sapiens	37-46
16088183-3	2005	The use of NAC inhibited the changes in urine output, pO(2), tissue activity of MPO and MDA in pancreas and lungs, and the serum activity of IL-6, ALT, and serum concentrations of urea and calcium.	Acetylcysteine	11-14	interleukin 6	Rattus norvegicus	141-145
15721278-8	2005	The binding of nucleolin to gadd45alpha mRNA could be prevented by the antioxidant, N-acetyl-cysteine.	Acetylcysteine	84-101	growth arrest and DNA-damage-inducible 45 alpha	Mus musculus	28-39
15829704-8	2005	Exogenously administered reactive oxygen species (ROS) were found to activate ERK1/ERK2 via the EGFR and src tyrosine kinase activity and pretreatment of cells with the antioxidant N-acetylcysteine (NAC) and the NADPH oxidase inhibitor DPI abrogated albumin-induced activation of ERK1/ERK2.	Acetylcysteine	181-197	mitogen-activated protein kinase 3	Homo sapiens	78-82
15829704-8	2005	Exogenously administered reactive oxygen species (ROS) were found to activate ERK1/ERK2 via the EGFR and src tyrosine kinase activity and pretreatment of cells with the antioxidant N-acetylcysteine (NAC) and the NADPH oxidase inhibitor DPI abrogated albumin-induced activation of ERK1/ERK2.	Acetylcysteine	181-197	mitogen-activated protein kinase 1	Homo sapiens	83-87
15829704-8	2005	Exogenously administered reactive oxygen species (ROS) were found to activate ERK1/ERK2 via the EGFR and src tyrosine kinase activity and pretreatment of cells with the antioxidant N-acetylcysteine (NAC) and the NADPH oxidase inhibitor DPI abrogated albumin-induced activation of ERK1/ERK2.	Acetylcysteine	181-197	epidermal growth factor receptor	Homo sapiens	96-100
15829704-8	2005	Exogenously administered reactive oxygen species (ROS) were found to activate ERK1/ERK2 via the EGFR and src tyrosine kinase activity and pretreatment of cells with the antioxidant N-acetylcysteine (NAC) and the NADPH oxidase inhibitor DPI abrogated albumin-induced activation of ERK1/ERK2.	Acetylcysteine	181-197	mitogen-activated protein kinase 3	Homo sapiens	280-284
15829704-8	2005	Exogenously administered reactive oxygen species (ROS) were found to activate ERK1/ERK2 via the EGFR and src tyrosine kinase activity and pretreatment of cells with the antioxidant N-acetylcysteine (NAC) and the NADPH oxidase inhibitor DPI abrogated albumin-induced activation of ERK1/ERK2.	Acetylcysteine	181-197	mitogen-activated protein kinase 1	Homo sapiens	285-289
15829704-10	2005	Finally, pretreatment with AG-1478, the MEK inhibitor UO126, and NAC prevented the albumin-induced increase in IL-8 expression.	Acetylcysteine	65-68	C-X-C motif chemokine ligand 8	Homo sapiens	111-115
15761843-4	2005	The role of oxygen free radicals as messengers of the mechanisms underlying acinar cell TNF-alpha production was assessed in BPDO rats treated with N-acetylcysteine (NAC).	Acetylcysteine	148-164	tumor necrosis factor	Rattus norvegicus	88-97
15761843-4	2005	The role of oxygen free radicals as messengers of the mechanisms underlying acinar cell TNF-alpha production was assessed in BPDO rats treated with N-acetylcysteine (NAC).	Acetylcysteine	166-169	tumor necrosis factor	Rattus norvegicus	88-97
15761843-9	2005	In addition, NAC delayed monocyte TNF-alpha production, thereby maintaining low TNF-alpha levels in plasma during BPDO.	Acetylcysteine	13-16	tumor necrosis factor	Rattus norvegicus	34-43
15761843-9	2005	In addition, NAC delayed monocyte TNF-alpha production, thereby maintaining low TNF-alpha levels in plasma during BPDO.	Acetylcysteine	13-16	tumor necrosis factor	Rattus norvegicus	80-89
15761843-11	2005	The blockade of oxidant-mediated signal transduction pathways induced by NAC treatment prevented acinar cell TNF-alpha production.	Acetylcysteine	73-76	tumor necrosis factor	Rattus norvegicus	109-118
15840023-11	2005	NAC effectively inhibited high glucose-induced, but not basal, PAI-1 expression.	Acetylcysteine	0-3	serpin family E member 1	Rattus norvegicus	63-68
15795323-5	2005	TNF-alpha induction was also inhibited by tempol, N-acetylcysteine, or 1,3-dimethyl-2-thiourea.	Acetylcysteine	50-66	tumor necrosis factor	Mus musculus	0-9
15699178-9	2005	Finally, by using a thiol antioxidant, N-acetyl cysteine, we found that the suppression of IFN-gamma production by DEP-treated T cells was mediated by oxidative stress.	Acetylcysteine	39-56	interferon gamma	Homo sapiens	91-100
15670787-3	2005	Both Cd-induced JNK and c-Jun phosphorylation and apoptosis were inhibited dramatically by N-acetyl-L-cysteine, a free radical scavenger.	Acetylcysteine	91-110	mitogen-activated protein kinase 8	Homo sapiens	16-19
15698597-12	2005	Conversely, L-cystathionine and N-acetyl-L-cysteine inhibited the translocation to membrane of p47(phox) and p67(phox) in a concentration-dependent manner.	Acetylcysteine	32-51	CD33 molecule	Homo sapiens	109-112
15698597-16	2005	L-cystathionine and N-acetyl-L-cysteine suppressed fMLP- and PMA-induced superoxide generation by the inhibition of translocation to membrane of p47(phox) and p67(phox).	Acetylcysteine	20-39	CD33 molecule	Homo sapiens	159-162
15733769-9	2005	TNF-alpha, IL-1beta, and reactive oxygen species (ROS) tended to be lower in the NAC-group (NS).	Acetylcysteine	81-84	tumor necrosis factor	Homo sapiens	0-9
15733769-9	2005	TNF-alpha, IL-1beta, and reactive oxygen species (ROS) tended to be lower in the NAC-group (NS).	Acetylcysteine	81-84	interleukin 1 beta	Homo sapiens	11-19
15819723-4	2005	NAC rescued cell growth that was suppressed by heat shock protein (Hsp) 90 inhibitors possibly by chemical modification of their quinone moiety.	Acetylcysteine	0-3	heat shock protein 90 alpha family class A member 1	Rattus norvegicus	47-74
15854525-14	2005	The increase of NF-kappaB activity induced by AngII could be inhibited by irbesartan, ACEI and NAC pretreatment and could not be inhibited by U0126 pretreatment.	Acetylcysteine	95-98	angiotensinogen	Rattus norvegicus	46-51
15854525-28	2005	The TNFalpha mRNA expression was significantly weaker in the irbesartan + AngII, NAC + AngII, and ACEI groups in comparison with the AngII group (all P &lt; 0.05).	Acetylcysteine	81-84	tumor necrosis factor	Rattus norvegicus	4-12
15496615-6	2005	Expression of tumor suppressor p53 and the cell cycle regulatory protein p21 was stimulated within 5 to 10 min by cisplatin in p53-positive LX-1 small cell lung carcinoma cells, and this effect was blocked by NAC.	Acetylcysteine	209-212	tumor protein p53	Homo sapiens	31-34
15664096-9	2005	Vitamins E and C and N-acetylcysteine blocked glucose- and fatty acid-induced NEP mRNA (p &lt; or = 0.05).	Acetylcysteine	21-37	membrane metalloendopeptidase	Homo sapiens	78-81
15496615-6	2005	Expression of tumor suppressor p53 and the cell cycle regulatory protein p21 was stimulated within 5 to 10 min by cisplatin in p53-positive LX-1 small cell lung carcinoma cells, and this effect was blocked by NAC.	Acetylcysteine	209-212	tumor protein p53	Homo sapiens	127-130
15496615-7	2005	In p53-negative SKOV3 cells, cisplatin toxicity and NAC chemoprotection remained effective, suggesting that chemoprotection may be mediated through both p53-dependent and -independent pathways.	Acetylcysteine	52-55	tumor protein p53	Homo sapiens	3-6
15895825-4	2005	Pre-treatment with L-mono-methyl-arginine and N-acetyl-cysteine in oxidized low-density lipoprotein (ox-LDL) exposed HA cells, inhibited not only nitrite but also superoxide production suggesting that O2(-) anion could partially derive from inducible NO synthase.	Acetylcysteine	46-63	nitric oxide synthase 2	Homo sapiens	241-262
15895830-9	2005	The ERK activation and cell death caused by H2O2 was inhibited by antioxidants (N-acetylcysteine and trolox), Ras inhibitor, and suramin.	Acetylcysteine	80-96	mitogen-activated protein kinase 1	Homo sapiens	4-7
15647642-0	2005	The administration of N-acetylcysteine causes a decrease in prothrombin time in patients with paracetamol overdose but without evidence of liver impairment.	Acetylcysteine	22-38	coagulation factor II, thrombin	Homo sapiens	60-71
15582350-7	2005	Furthermore, pretreatment of cells with N-acetyl cysteine gave a dose- and time-dependent reduction of caspase-3 cleavage, supporting the observations that caspase-3 cleavage is cell-redox-dependent.	Acetylcysteine	40-57	caspase 3	Homo sapiens	103-112
15582350-7	2005	Furthermore, pretreatment of cells with N-acetyl cysteine gave a dose- and time-dependent reduction of caspase-3 cleavage, supporting the observations that caspase-3 cleavage is cell-redox-dependent.	Acetylcysteine	40-57	caspase 3	Homo sapiens	156-165
15650392-3	2005	N-Acetyl-L-cysteine (20 mM) inhibited both H2O2- and TNFalpha-induced p38 phosphorylation (14 +/- 7 and 37 +/- 4% of control, respectively).	Acetylcysteine	0-19	tumor necrosis factor	Homo sapiens	53-61
15650392-3	2005	N-Acetyl-L-cysteine (20 mM) inhibited both H2O2- and TNFalpha-induced p38 phosphorylation (14 +/- 7 and 37 +/- 4% of control, respectively).	Acetylcysteine	0-19	mitogen-activated protein kinase 14	Homo sapiens	70-73
17532680-6	2005	RESULTS: Both NAC 600 and 1200 mg/day were associated with a significantly higher proportion of patients achieving normalised CRP levels compared with placebo (52% and 90% vs 19% of patients; p &lt;/= 0.01); however, NAC 1200 mg/day was superior to NAC 600 mg/day (p = 0.002).	Acetylcysteine	14-17	C-reactive protein	Homo sapiens	126-129
17532680-7	2005	Furthermore, treatment with NAC 1200 mg/day was more efficacious than NAC 600 mg/day in reducing IL-8 levels and difficulty of expectoration, while the two active regimens had similar beneficial effects on lung function and other clinical outcomes (cough intensity and frequency, and lung auscultation).	Acetylcysteine	28-31	C-X-C motif chemokine ligand 8	Homo sapiens	97-101
17532680-7	2005	Furthermore, treatment with NAC 1200 mg/day was more efficacious than NAC 600 mg/day in reducing IL-8 levels and difficulty of expectoration, while the two active regimens had similar beneficial effects on lung function and other clinical outcomes (cough intensity and frequency, and lung auscultation).	Acetylcysteine	70-73	C-X-C motif chemokine ligand 8	Homo sapiens	97-101
15588682-6	2005	Much like insulin, clove-mediated repression is reversed by PI3K inhibitors and N-acetylcysteine (NAC).	Acetylcysteine	80-96	insulin	Homo sapiens	10-17
15588682-6	2005	Much like insulin, clove-mediated repression is reversed by PI3K inhibitors and N-acetylcysteine (NAC).	Acetylcysteine	98-101	insulin	Homo sapiens	10-17
16400524-8	2005	NAC treatment also restored cell cycle progression inhibited by rk-2 and down-regulated p53 and nuclear p21(Waf1/Cip1) expression induced by rk-2.These data suggest that rk-2 induces the BCE cell cycle arrest at G(0)-G(1) phase through inhibition of the cyclin D1/CDK4 complex caused by increase of ROS generation and nuclear cyclin-dependent kinase inhibitors.	Acetylcysteine	0-3	tumor protein p53	Homo sapiens	88-91
16400524-8	2005	NAC treatment also restored cell cycle progression inhibited by rk-2 and down-regulated p53 and nuclear p21(Waf1/Cip1) expression induced by rk-2.These data suggest that rk-2 induces the BCE cell cycle arrest at G(0)-G(1) phase through inhibition of the cyclin D1/CDK4 complex caused by increase of ROS generation and nuclear cyclin-dependent kinase inhibitors.	Acetylcysteine	0-3	cyclin dependent kinase inhibitor 1A	Homo sapiens	104-107
16400524-8	2005	NAC treatment also restored cell cycle progression inhibited by rk-2 and down-regulated p53 and nuclear p21(Waf1/Cip1) expression induced by rk-2.These data suggest that rk-2 induces the BCE cell cycle arrest at G(0)-G(1) phase through inhibition of the cyclin D1/CDK4 complex caused by increase of ROS generation and nuclear cyclin-dependent kinase inhibitors.	Acetylcysteine	0-3	cyclin dependent kinase inhibitor 1A	Homo sapiens	108-112
16400524-8	2005	NAC treatment also restored cell cycle progression inhibited by rk-2 and down-regulated p53 and nuclear p21(Waf1/Cip1) expression induced by rk-2.These data suggest that rk-2 induces the BCE cell cycle arrest at G(0)-G(1) phase through inhibition of the cyclin D1/CDK4 complex caused by increase of ROS generation and nuclear cyclin-dependent kinase inhibitors.	Acetylcysteine	0-3	cyclin dependent kinase inhibitor 1A	Homo sapiens	113-117
15816534-6	2005	At a concentration that was cytotoxic to 50% of the cells (approximately 0.05 mM), HQ activated caspase-3; this effect was reduced in the presence of NAC.	Acetylcysteine	150-153	caspase 3	Homo sapiens	96-105
15816534-7	2005	Interestingly, higher concentrations of HQ (0.1-0.2 mM) caused direct cell death; however, when combined with 5 mM NAC, the activation of caspase-3 was strongly enhanced, suggesting the promotion of apoptosis.	Acetylcysteine	115-118	caspase 3	Homo sapiens	138-147
15816534-8	2005	The activation of caspase-3 by HQ/NAC combinations suggests that NAC, a precursor of intracellular glutathione synthesis, acts as a co-catalyst during HQ-induced apoptosis.	Acetylcysteine	34-37	caspase 3	Homo sapiens	18-27
15816534-8	2005	The activation of caspase-3 by HQ/NAC combinations suggests that NAC, a precursor of intracellular glutathione synthesis, acts as a co-catalyst during HQ-induced apoptosis.	Acetylcysteine	65-68	caspase 3	Homo sapiens	18-27
15759051-6	2005	Moreover, MG activated NF-kappaB p65, indicated by an increased immuno cytochemistry stain for NF-kappaB p65 located in the nucleus after the treatment of mesenteric artery SMCs with MG. MG-induced activation of NF-kappaB p65 was inhibited by NAC.	Acetylcysteine	243-246	synaptotagmin 1	Rattus norvegicus	33-36
15644661-12	2005	Acinar cell nuclear factor-kappaB was activated, but TNF-alpha production was not totally inhibited in presence of N-acetyl cysteine (30, 100 mM).	Acetylcysteine	115-132	tumor necrosis factor	Rattus norvegicus	53-62
15647642-1	2005	OBJECTIVE: To explore the effect of intravenous N-acetylcysteine (NAC) on the prothrombin time (PT) in patients with paracetamol overdose and persistent normal liver profile.	Acetylcysteine	48-64	coagulation factor II, thrombin	Homo sapiens	78-89
15647642-1	2005	OBJECTIVE: To explore the effect of intravenous N-acetylcysteine (NAC) on the prothrombin time (PT) in patients with paracetamol overdose and persistent normal liver profile.	Acetylcysteine	66-69	coagulation factor II, thrombin	Homo sapiens	78-89
15328380-10	2005	Furthermore, the ERK activation by H(2)O(2) was blocked by pretreatment with either N-acetyl-cysteine, o-phenanthroline, or mannitol indicating that metal-catalyzed free radical formation may mediate the initiation of signal transduction by H(2)O(2).	Acetylcysteine	84-101	mitogen-activated protein kinase 1	Homo sapiens	17-20
15841722-5	2005	RESULTS: AP results in significant increases in plasma levels of IL-6 at 6 h and IL-10 at 3 and 6 h. Plasma levels of IL-6 were significantly decreased after administration of NAC.	Acetylcysteine	176-179	interleukin 6	Rattus norvegicus	65-69
16131811-8	2005	Calcium chelator, BAPTA-AM and anti-oxidants such as N-acetylcysteine and tiron suppressed CRP-induced NF-kappaB activation.	Acetylcysteine	53-69	C-reactive protein	Homo sapiens	91-94
15841722-5	2005	RESULTS: AP results in significant increases in plasma levels of IL-6 at 6 h and IL-10 at 3 and 6 h. Plasma levels of IL-6 were significantly decreased after administration of NAC.	Acetylcysteine	176-179	interleukin 6	Rattus norvegicus	118-122
15841722-6	2005	NAC pretreatment also increased the ratio of IL-10/IL-6.	Acetylcysteine	0-3	interleukin 6	Rattus norvegicus	51-55
15375156-0	2004	N-Acetyl-L-cysteine enhances apoptosis through inhibition of nuclear factor-kappaB in hypoxic murine embryonic fibroblasts.	Acetylcysteine	0-19	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	61-82
15489221-10	2004	In contrast, preincubation of cells with the hydroxyl radical scavenger, N-acetylcysteine, significantly attenuated the doxorubicin-mediated phosphorylation and accumulation of p53, p53-DNA binding, and the phosphorylation of H2AX, Nbs1, SMC1, Chk1, and Chk2, suggesting that hydroxyl radicals contribute to the doxorubicin-induced activation of ATM-dependent pathways.	Acetylcysteine	73-89	tumor protein p53	Homo sapiens	177-180
15489221-10	2004	In contrast, preincubation of cells with the hydroxyl radical scavenger, N-acetylcysteine, significantly attenuated the doxorubicin-mediated phosphorylation and accumulation of p53, p53-DNA binding, and the phosphorylation of H2AX, Nbs1, SMC1, Chk1, and Chk2, suggesting that hydroxyl radicals contribute to the doxorubicin-induced activation of ATM-dependent pathways.	Acetylcysteine	73-89	tumor protein p53	Homo sapiens	182-185
15489221-10	2004	In contrast, preincubation of cells with the hydroxyl radical scavenger, N-acetylcysteine, significantly attenuated the doxorubicin-mediated phosphorylation and accumulation of p53, p53-DNA binding, and the phosphorylation of H2AX, Nbs1, SMC1, Chk1, and Chk2, suggesting that hydroxyl radicals contribute to the doxorubicin-induced activation of ATM-dependent pathways.	Acetylcysteine	73-89	checkpoint kinase 1	Homo sapiens	244-248
15813983-10	2004	In the presence of the antioxidants glutathione and N-acetyl-L-cysteine, the PD- and HPD-induced release of ROS, TNF-alpha, and MIP-2 was significantly reduced.	Acetylcysteine	52-71	tumor necrosis factor	Rattus norvegicus	113-122
15564655-6	2004	Following NAC treatment, lead-induced lipid peroxidation decreased and antioxidant enzyme activities improved, with CAT showing enhancement in the cerebral region only and SOD showing enhancements in the cerebellar region.	Acetylcysteine	10-13	catalase	Rattus norvegicus	116-119
15513897-8	2004	The loss of EROD activity of P-450 1A1 with PMS was blocked by trapping agents such as glutathione, N-acetylcysteine, or dithiothreitol.	Acetylcysteine	100-116	solute carrier family 45 member 2	Homo sapiens	35-38
15788371-1	2005	Based on recent results that 1,2-dibromopropane (1,2-DBP) causes hepatotoxicity and immunotoxicity in female BALB/c mice as well as a reduction of hepatic glutathione levels, the possible formation of glutathione conjugates and mercapturic acids of 1,2-DBP was investigated in vivo in the present studies.	Acetylcysteine	228-245	D site albumin promoter binding protein	Mus musculus	53-56
15788371-6	2005	When female BALB/c mice were treated orally with 1,2-DBP at doses of 150, 300 and 600 mg kg(-1) once for 12 h, the production of glutathione conjugates and mercapturic acids in liver was apparently dose dependent, as were the concentrations of them in sera.	Acetylcysteine	156-173	D site albumin promoter binding protein	Mus musculus	53-56
15569303-11	2004	AGEs also were found to stimulate Ang II production in a time- and dose-dependent manner, which was completely prevented by an antioxidant, N-acetylcysteine (NAC).	Acetylcysteine	140-156	angiotensinogen	Rattus norvegicus	34-40
15569303-11	2004	AGEs also were found to stimulate Ang II production in a time- and dose-dependent manner, which was completely prevented by an antioxidant, N-acetylcysteine (NAC).	Acetylcysteine	158-161	angiotensinogen	Rattus norvegicus	34-40
15474610-5	2004	Western blot analysis demonstrated that cisplatin treatment induced time-dependent activation of ERK, which was inhibited by chemical inhibitors of the MEK signaling pathway (PD98059 and U0126) and N-acetylcysteine.	Acetylcysteine	198-214	mitogen-activated protein kinase 1	Homo sapiens	97-100
15474610-10	2004	Cisplatin-induced activation of caspase-3 was inhibited by N-acetylcysteine and PD98059.	Acetylcysteine	59-75	caspase 3	Homo sapiens	32-41
18969705-5	2004	Highly linear response is obtained for homocysteine, cysteine, glutathione, and N-acetylcysteine over the range of 5-50muM with detection limits of 0.75, 0.8, 2.9, and 3.3muM, respectively.	Acetylcysteine	80-96	latexin	Homo sapiens	119-122
15474995-4	2004	Overexpression of Txnip by infecting melanoma cells with adenovirus increased TEM 3-fold vs. control (P &lt; 0.001), and this increase was blocked by N-acetylcysteine, indicating a redox-sensitive mechanism.	Acetylcysteine	150-166	thioredoxin interacting protein	Homo sapiens	18-23
15389835-4	2004	Intraperitoneal pretreatment of pregnant female rats with NAC (50 mg/kg), 2 hr prior to administration of LPS at embryonic day 18 (E18), attenuated the LPS-induced expression of inflammatory cytokines such as tumor necrosis factor-alpha, interleukin-1beta, and inducible nitric oxide synthase in fetal rat brains.	Acetylcysteine	58-61	tumor necrosis factor	Rattus norvegicus	209-236
15621696-7	2004	The AHR-ligand-mediated decrease in cyp1a1 activity was reversed by the antioxidant N-acetylcysteine.	Acetylcysteine	84-100	aryl-hydrocarbon receptor	Mus musculus	4-7
15389835-4	2004	Intraperitoneal pretreatment of pregnant female rats with NAC (50 mg/kg), 2 hr prior to administration of LPS at embryonic day 18 (E18), attenuated the LPS-induced expression of inflammatory cytokines such as tumor necrosis factor-alpha, interleukin-1beta, and inducible nitric oxide synthase in fetal rat brains.	Acetylcysteine	58-61	interleukin 1 beta	Rattus norvegicus	238-255
15555443-0	2004	[NF-kappaB expression in lung tissue of acute lung injury rat model and the influence by antioxidant N-acetylcysteine].	Acetylcysteine	101-117	nuclear factor kappa B subunit 1	Homo sapiens	1-10
15378764-4	2004	The ovalbumin-induced degradation of annexin-1 was blocked by pretreatment of mice with the antioxidant N-acetylcysteine (NAC) or with sodium selenite, both of which have previously been shown to exert anti-inflammatory effects in this asthma model.	Acetylcysteine	104-120	serine (or cysteine) peptidase inhibitor, clade B, member 1, pseudogene	Mus musculus	4-13
15378764-4	2004	The ovalbumin-induced degradation of annexin-1 was blocked by pretreatment of mice with the antioxidant N-acetylcysteine (NAC) or with sodium selenite, both of which have previously been shown to exert anti-inflammatory effects in this asthma model.	Acetylcysteine	122-125	serine (or cysteine) peptidase inhibitor, clade B, member 1, pseudogene	Mus musculus	4-13
15378764-5	2004	Ovalbumin challenge also both increased the expression of cPLA(2) in lung tissue and reduced the extent of the interaction between cPLA(2) and annexin-1, and these effects were inhibited by NAC or selenite.	Acetylcysteine	190-193	serine (or cysteine) peptidase inhibitor, clade B, member 1, pseudogene	Mus musculus	0-9
15378764-6	2004	Moreover, the concentrations of cysteinyl leukotrienes in bronchoalveolar lavage fluid and of leukotriene B(4) in lung tissue were increased by ovalbumin challenge in a NAC- or selenite-sensitive manner.	Acetylcysteine	169-172	serine (or cysteine) peptidase inhibitor, clade B, member 1, pseudogene	Mus musculus	144-153
15378659-8	2004	Reactive oxygen species (ROS) scavengers (N-acetyl-cysteine [NAC] and trolox) reduced thrombin-induced CIS expression, and inhibitors of COX and LO reduced ROS produced by thrombin.	Acetylcysteine	42-59	coagulation factor II	Rattus norvegicus	86-94
15378659-8	2004	Reactive oxygen species (ROS) scavengers (N-acetyl-cysteine [NAC] and trolox) reduced thrombin-induced CIS expression, and inhibitors of COX and LO reduced ROS produced by thrombin.	Acetylcysteine	61-64	coagulation factor II	Rattus norvegicus	86-94
15555443-1	2004	AIM: To observe the NF-kappaB expression in the lung tissue of LPS-induced acute lung injury(ALI) rat model and the influence of N-acetylcysteine (NAC) on NF-kappaB expression.	Acetylcysteine	129-145	nuclear factor kappa B subunit 1	Homo sapiens	155-164
15555443-1	2004	AIM: To observe the NF-kappaB expression in the lung tissue of LPS-induced acute lung injury(ALI) rat model and the influence of N-acetylcysteine (NAC) on NF-kappaB expression.	Acetylcysteine	147-150	nuclear factor kappa B subunit 1	Homo sapiens	155-164
15555443-2	2004	METHODS: The expression of NF-kappaB in lung tissue in ALI rat model and the influence of NAC on NF-kappaB expression were detected by immunohistochemical (ABC) staining and Western blot.	Acetylcysteine	90-93	nuclear factor kappa B subunit 1	Homo sapiens	97-106
15555443-6	2004	The NF-kappaB expression-positive cells in NAC therapy group notably decreased compared with ALI group and control group(P&lt;0.01).	Acetylcysteine	43-46	nuclear factor kappa B subunit 1	Homo sapiens	4-13
15555443-10	2004	NAC could alleviate inflammation by inhibiting activation of NF-kappaB.	Acetylcysteine	0-3	nuclear factor kappa B subunit 1	Homo sapiens	61-70
15451068-4	2004	N-Acetyl-L-cysteine, an antioxidant, suppresses ROS generation, Akt inactivation, caspase-8 activation, and DNA fragmentation.	Acetylcysteine	0-19	AKT serine/threonine kinase 1	Homo sapiens	64-67
15483417-3	2004	We here describe the effects of N-acetylcysteine, deferoxamine, or both in the treatment of CCl4-induced hepatic failure.	Acetylcysteine	32-48	C-C motif chemokine ligand 4	Rattus norvegicus	92-96
15451797-0	2004	N-acetylcysteine treatment normalizes serum tumor necrosis factor-alpha level and hinders the progression of cardiac injury in hypertensive rats.	Acetylcysteine	0-16	tumor necrosis factor	Rattus norvegicus	44-71
15451797-1	2004	BACKGROUND: Studies in isolated cardiomyocytes showed that replenishment in cellular glutathione, achieved with the glutathione precursor N-acetylcysteine (NAC), abrogated deleterious effects of tumor necrosis factor-alpha (TNF-alpha).	Acetylcysteine	138-154	tumor necrosis factor	Rattus norvegicus	195-222
15451797-7	2004	NAC treatment, which replenished cardiac glutathione, had no effect on hypertension but reduced LV remodeling and dysfunction, normalized serum TNF-alpha level, and limited activation of matrix metalloproteinases -2 and -9 and collagen deposition in LV tissues.	Acetylcysteine	0-3	tumor necrosis factor	Rattus norvegicus	144-153
15483417-6	2004	SUBJECTS: Male Wistar rats, weighing 200-250 g. INTERVENTIONS: Rats exposed to CCl4 were treated with N-acetylcysteine and/or deferoxamine or vehicle.	Acetylcysteine	102-118	C-C motif chemokine ligand 4	Rattus norvegicus	79-83
15483417-7	2004	MEASUREMENTS AND MAIN RESULTS: N-acetylcysteine plus deferoxamine treatment significantly attenuated hepatic and central nervous system oxidative damage after acute hepatic failure induced by CCl4.	Acetylcysteine	31-47	C-C motif chemokine ligand 4	Rattus norvegicus	192-196
15483417-13	2004	CONCLUSIONS: Our data provide the first experimental demonstration that N-acetylcysteine plus deferoxamine reduces mortality rate, decreases oxidative stress, and limits inflammatory infiltration and hepatocyte necrosis induced by CCl4 in the rat.	Acetylcysteine	72-88	C-C motif chemokine ligand 4	Rattus norvegicus	231-235
15450387-7	2004	Treatment of amnion and choriodecidual tissues with SASP concentrations greater than 5 mM, 15 mM NAC, 30 microM 15d-PGJ(2) and 30 microM troglitazone significantly reduced the release of PTHrP (p &lt; 0.05).	Acetylcysteine	97-100	aspartic peptidase retroviral like 1	Homo sapiens	52-56
15502923-9	2004	Treatment with N-acetyl-cysteine accelerated the infiltration of mononuclear cells accompanied by CD8-positive cells into the intra-islet region of the recipient"s pancreas, and enhanced interferon-gamma mRNA expression in the pancreas.	Acetylcysteine	15-32	interferon gamma	Mus musculus	187-203
15502923-10	2004	In vitro, treatment with N-acetyl-cysteine enhanced interferon-gamma and interleukin-2 production by CD4-positive splenocytes of the diabetic donor mice.	Acetylcysteine	25-42	interferon gamma	Homo sapiens	52-68
15502923-10	2004	In vitro, treatment with N-acetyl-cysteine enhanced interferon-gamma and interleukin-2 production by CD4-positive splenocytes of the diabetic donor mice.	Acetylcysteine	25-42	interleukin 2	Homo sapiens	73-86
15502923-10	2004	In vitro, treatment with N-acetyl-cysteine enhanced interferon-gamma and interleukin-2 production by CD4-positive splenocytes of the diabetic donor mice.	Acetylcysteine	25-42	CD4 molecule	Homo sapiens	101-104
15518006-0	2004	[Effect of N-acetylcysteine on prothrombin index in patients with uncomplicated paracetamol poisoning].	Acetylcysteine	11-27	coagulation factor II, thrombin	Homo sapiens	31-42
15473893-0	2004	N-acetylcysteine enhances multidrug resistance-associated protein 1 mediated doxorubicin resistance.	Acetylcysteine	0-16	ATP binding cassette subfamily C member 1	Homo sapiens	26-67
15473893-5	2004	The aim of our study was to investigate the effect of NAC and BSO on MRP1-mediated doxorubicin resistance in human embryonic kidney (HEK293) and its MRP1-transfected 293MRP cells.	Acetylcysteine	54-57	ATP binding cassette subfamily C member 1	Homo sapiens	69-73
15473893-11	2004	DL-buthionine (S,R)-sulfoximine decreased NAC-enhanced MRP1-mediated doxorubicin resistance, indicating that induction of MRP1-mediated doxorubicin resistance depends on GSH synthesis.	Acetylcysteine	42-45	ATP binding cassette subfamily C member 1	Homo sapiens	55-59
15473893-11	2004	DL-buthionine (S,R)-sulfoximine decreased NAC-enhanced MRP1-mediated doxorubicin resistance, indicating that induction of MRP1-mediated doxorubicin resistance depends on GSH synthesis.	Acetylcysteine	42-45	ATP binding cassette subfamily C member 1	Homo sapiens	122-126
15473893-14	2004	CONCLUSION: Our results demonstrate that NAC enhances MRP1-mediated doxorubicin resistance and this effect depends on GSH synthesis.	Acetylcysteine	41-44	ATP binding cassette subfamily C member 1	Homo sapiens	54-58
15382121-5	2004	DCA activated the ERK1/2 pathway in HuH7 human hepatoma cells that was blocked by the incubation of cells with an ERBB1 inhibitor, NAC, TX, CsA, or BKA.	Acetylcysteine	131-134	mitogen-activated protein kinase 3	Homo sapiens	18-24
15281093-7	2004	NAC did not alter total cell mRNA and protein levels of alpha-epithelial Na(+) channel (EnaC) subunit, but reduced abundance of alpha-ENaC subunits in the apical cell membrane as quantified by biotinylation.	Acetylcysteine	0-3	sodium channel epithelial 1 subunit alpha	Homo sapiens	128-138
15350970-6	2004	Both 3-O-Me-SM and N-acetyl-L-cysteine, the selective and nonselective pharmacological inhibitors of nSMase, respectively, suppressed nSMase activation, ceramide production, and cytotoxic action induced by Abeta25-35 in CECs.	Acetylcysteine	19-38	sphingomyelin phosphodiesterase 2, neutral	Mus musculus	101-107
15350970-6	2004	Both 3-O-Me-SM and N-acetyl-L-cysteine, the selective and nonselective pharmacological inhibitors of nSMase, respectively, suppressed nSMase activation, ceramide production, and cytotoxic action induced by Abeta25-35 in CECs.	Acetylcysteine	19-38	sphingomyelin phosphodiesterase 2, neutral	Mus musculus	134-140
15130882-7	2004	Furthermore, the presence of E2 and antioxidants such as N-acetylcysteine and diphenylene iodonium were able to elicit a decrease in the level of strain-induced ET-1 secretion, ET-1 promoter activity, ET-1 mRNA, ERK phosphorylation, and activator protein-1 binding activity.	Acetylcysteine	57-73	endothelin 1	Homo sapiens	161-165
15130882-7	2004	Furthermore, the presence of E2 and antioxidants such as N-acetylcysteine and diphenylene iodonium were able to elicit a decrease in the level of strain-induced ET-1 secretion, ET-1 promoter activity, ET-1 mRNA, ERK phosphorylation, and activator protein-1 binding activity.	Acetylcysteine	57-73	endothelin 1	Homo sapiens	177-181
15130882-7	2004	Furthermore, the presence of E2 and antioxidants such as N-acetylcysteine and diphenylene iodonium were able to elicit a decrease in the level of strain-induced ET-1 secretion, ET-1 promoter activity, ET-1 mRNA, ERK phosphorylation, and activator protein-1 binding activity.	Acetylcysteine	57-73	endothelin 1	Homo sapiens	177-181
15130882-7	2004	Furthermore, the presence of E2 and antioxidants such as N-acetylcysteine and diphenylene iodonium were able to elicit a decrease in the level of strain-induced ET-1 secretion, ET-1 promoter activity, ET-1 mRNA, ERK phosphorylation, and activator protein-1 binding activity.	Acetylcysteine	57-73	mitogen-activated protein kinase 1	Homo sapiens	212-215
15130882-7	2004	Furthermore, the presence of E2 and antioxidants such as N-acetylcysteine and diphenylene iodonium were able to elicit a decrease in the level of strain-induced ET-1 secretion, ET-1 promoter activity, ET-1 mRNA, ERK phosphorylation, and activator protein-1 binding activity.	Acetylcysteine	57-73	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	237-256
15489055-6	2004	NAC supplementation enhanced GSH and PSH levels in the ileal but not in the colonic mucosa, GSH and RSNO in liver mitochondria, while GSH-Px and protein carbonyls were decreased everywhere.	Acetylcysteine	0-3	glutathione peroxidase 1	Rattus norvegicus	134-140
15367711-3	2004	N-acetylcysteine, a free radical scavenger, blocked induction of tumor necrosis factor-alpha by anticancer agents, supporting a role for reactive oxygen intermediates in activation of the CArG sequences.	Acetylcysteine	0-16	tumor necrosis factor	Homo sapiens	65-92
15276073-4	2004	Antioxidants, including N-acetylcysteine, inhibited the MG132-induced nuclear damage, loss in mitochondrial transmembrane potential, cytosolic accumulation of cytochrome c and caspase-3 activation.	Acetylcysteine	24-40	cytochrome c, somatic	Homo sapiens	159-171
15208668-8	2004	N-acetyl cysteine (NAC) prevented the IL-1beta-induced ROS production and IL-8 expression.	Acetylcysteine	0-17	interleukin 1 beta	Homo sapiens	38-46
15208668-8	2004	N-acetyl cysteine (NAC) prevented the IL-1beta-induced ROS production and IL-8 expression.	Acetylcysteine	0-17	C-X-C motif chemokine ligand 8	Homo sapiens	74-78
15208668-8	2004	N-acetyl cysteine (NAC) prevented the IL-1beta-induced ROS production and IL-8 expression.	Acetylcysteine	19-22	interleukin 1 beta	Homo sapiens	38-46
15208668-8	2004	N-acetyl cysteine (NAC) prevented the IL-1beta-induced ROS production and IL-8 expression.	Acetylcysteine	19-22	C-X-C motif chemokine ligand 8	Homo sapiens	74-78
15256225-4	2004	Pretreatment with NF-kappaB inhibitors Bay 11-7082 and N-acetyl cysteine (NAC) suppressed the upregulation of iNOS by blunting IkappaB degradation and NF-kappaB binding activity.	Acetylcysteine	55-72	nuclear factor kappa B subunit 1	Homo sapiens	18-27
15256225-4	2004	Pretreatment with NF-kappaB inhibitors Bay 11-7082 and N-acetyl cysteine (NAC) suppressed the upregulation of iNOS by blunting IkappaB degradation and NF-kappaB binding activity.	Acetylcysteine	55-72	nitric oxide synthase 2	Homo sapiens	110-114
15256225-4	2004	Pretreatment with NF-kappaB inhibitors Bay 11-7082 and N-acetyl cysteine (NAC) suppressed the upregulation of iNOS by blunting IkappaB degradation and NF-kappaB binding activity.	Acetylcysteine	55-72	nuclear factor kappa B subunit 1	Homo sapiens	151-160
15256225-4	2004	Pretreatment with NF-kappaB inhibitors Bay 11-7082 and N-acetyl cysteine (NAC) suppressed the upregulation of iNOS by blunting IkappaB degradation and NF-kappaB binding activity.	Acetylcysteine	74-77	nuclear factor kappa B subunit 1	Homo sapiens	18-27
15256225-4	2004	Pretreatment with NF-kappaB inhibitors Bay 11-7082 and N-acetyl cysteine (NAC) suppressed the upregulation of iNOS by blunting IkappaB degradation and NF-kappaB binding activity.	Acetylcysteine	74-77	nitric oxide synthase 2	Homo sapiens	110-114
15256225-4	2004	Pretreatment with NF-kappaB inhibitors Bay 11-7082 and N-acetyl cysteine (NAC) suppressed the upregulation of iNOS by blunting IkappaB degradation and NF-kappaB binding activity.	Acetylcysteine	74-77	nuclear factor kappa B subunit 1	Homo sapiens	151-160
15276073-4	2004	Antioxidants, including N-acetylcysteine, inhibited the MG132-induced nuclear damage, loss in mitochondrial transmembrane potential, cytosolic accumulation of cytochrome c and caspase-3 activation.	Acetylcysteine	24-40	caspase 3	Homo sapiens	176-185
15197348-5	2004	The reduction in cell growth and enhancement in cell killing by the combination of GST-MDA-7 and radiation were blocked by an ROS scavenger, N-acetyl cysteine (NAC), a JNK1/2/3 inhibitor SP600125, a pan-caspase inhibitor (zVAD) and by an inhibitor of caspase 9 (LEHD), but not by an inhibitor of caspase 8 (IETD).	Acetylcysteine	160-163	mitogen-activated protein kinase 8	Homo sapiens	168-176
15157676-5	2004	N-acetylcysteine (NAC), an antioxidant, completely inhibited the SMase-induced increase in sPLA2 activity, whereas NAC inhibited partially the activity stimulated with TNF-alpha alone.	Acetylcysteine	18-21	phospholipase A2 group X	Homo sapiens	91-96
15157676-5	2004	N-acetylcysteine (NAC), an antioxidant, completely inhibited the SMase-induced increase in sPLA2 activity, whereas NAC inhibited partially the activity stimulated with TNF-alpha alone.	Acetylcysteine	0-16	phospholipase A2 group X	Homo sapiens	91-96
15289320-10	2004	The antioxidant N-acetylcysteine significantly reversed the inhibition by 15d-PGJ(2) of AP-1 activity and COX-2 or VEGF transcriptional induction.	Acetylcysteine	16-32	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	106-111
15197348-9	2004	In contrast, incubation with NAC blocked JNK1/2/3 activation and cell killing, but not the increases in BAD and BAX expression.	Acetylcysteine	29-32	mitogen-activated protein kinase 8	Homo sapiens	41-49
15298726-4	2004	After treatment with these agents, the phosphorylation of protein kinase A, Bcl-2 (Thr56) and Bad (Ser155) was increased, especially in antioxidant (N-acetylcysteine and pyrrolidine dithiocarbamate)-pretreated control cells, but the phosphorylation levels were very low in the antisense-transfected cells.	Acetylcysteine	149-165	BCL2 apoptosis regulator	Homo sapiens	76-81
15157676-5	2004	N-acetylcysteine (NAC), an antioxidant, completely inhibited the SMase-induced increase in sPLA2 activity, whereas NAC inhibited partially the activity stimulated with TNF-alpha alone.	Acetylcysteine	115-118	tumor necrosis factor	Homo sapiens	168-177
15157676-6	2004	Under the conditions, NAC completely inhibited reactive oxygen species (ROS) production induced by SMase followed by TNF-alpha.	Acetylcysteine	22-25	tumor necrosis factor	Homo sapiens	117-126
15289320-10	2004	The antioxidant N-acetylcysteine significantly reversed the inhibition by 15d-PGJ(2) of AP-1 activity and COX-2 or VEGF transcriptional induction.	Acetylcysteine	16-32	vascular endothelial growth factor A	Homo sapiens	115-119
15203191-4	2004	In primary human and bovine chondrocytes, ROS scavenger and antioxidant N-acetylcysteine (NAC) inhibited TGF-beta1-induced TIMP-3 mRNA and protein increases.	Acetylcysteine	72-88	TIMP metallopeptidase inhibitor 3	Bos taurus	123-129
15276019-7	2004	PEDF or an antioxidant, N-acetylcysteine, significantly inhibited the TNF-alpha-induced NF-kappaB activation.	Acetylcysteine	24-40	tumor necrosis factor	Homo sapiens	70-79
15297771-0	2004	Antioxidant effects of stereoisomers of N-acetylcysteine (NAC), L-NAC and D-NAC, on angiotensin II-stimulated MAP kinase activation and vascular smooth muscle cell proliferation.	Acetylcysteine	40-56	angiotensinogen	Homo sapiens	84-98
15297771-0	2004	Antioxidant effects of stereoisomers of N-acetylcysteine (NAC), L-NAC and D-NAC, on angiotensin II-stimulated MAP kinase activation and vascular smooth muscle cell proliferation.	Acetylcysteine	58-61	angiotensinogen	Homo sapiens	84-98
15297771-0	2004	Antioxidant effects of stereoisomers of N-acetylcysteine (NAC), L-NAC and D-NAC, on angiotensin II-stimulated MAP kinase activation and vascular smooth muscle cell proliferation.	Acetylcysteine	64-69	angiotensinogen	Homo sapiens	84-98
15262850-4	2004	Although Ang II activated AMPK, this activation was significantly inhibited by catalase, N-acetylcysteine, and diphenyleneiodonium chloride, an NADPH oxidase inhibitor.	Acetylcysteine	89-105	angiotensinogen	Rattus norvegicus	9-15
15262850-4	2004	Although Ang II activated AMPK, this activation was significantly inhibited by catalase, N-acetylcysteine, and diphenyleneiodonium chloride, an NADPH oxidase inhibitor.	Acetylcysteine	89-105	protein kinase AMP-activated catalytic subunit alpha 2	Rattus norvegicus	26-30
15297771-3	2004	We found that L-NAC and D-NAC both inhibited Ang II-induced c-Jun N-terminal kinase and p38 mitogen-activated protein kinase activation and [(3)H]-thymidine incorporation in VSMC.	Acetylcysteine	14-19	angiotensinogen	Homo sapiens	45-51
15297771-3	2004	We found that L-NAC and D-NAC both inhibited Ang II-induced c-Jun N-terminal kinase and p38 mitogen-activated protein kinase activation and [(3)H]-thymidine incorporation in VSMC.	Acetylcysteine	14-19	mitogen-activated protein kinase 14	Homo sapiens	88-91
15249511-6	2004	In addition, Db-HAGE-LDL stimulated NF-kappaB activity significantly in ECV 304 and human umbilical vein endothelial cells (2.3-fold above baseline) in a manner inhibitable by a MEK inhibitor PD98059 (10 micromol/L), the antioxidant N-acetyl-l-cysteine, NAC (30 mmol/L), and the NADPH oxidase inhibitor DPI (20 micromol/L).	Acetylcysteine	233-252	mitogen-activated protein kinase kinase 7	Homo sapiens	178-181
15203192-9	2004	N-Acetylcysteine, a ROS scavenger, exhibited a response similar to that of DPI and inhibited ET-1-stimulated ERK1/2, PKB, and Pyk2 phosphorylation.	Acetylcysteine	0-16	endothelin 1	Homo sapiens	93-97
15203192-9	2004	N-Acetylcysteine, a ROS scavenger, exhibited a response similar to that of DPI and inhibited ET-1-stimulated ERK1/2, PKB, and Pyk2 phosphorylation.	Acetylcysteine	0-16	mitogen-activated protein kinase 3	Homo sapiens	109-115
15203191-4	2004	In primary human and bovine chondrocytes, ROS scavenger and antioxidant N-acetylcysteine (NAC) inhibited TGF-beta1-induced TIMP-3 mRNA and protein increases.	Acetylcysteine	90-93	TIMP metallopeptidase inhibitor 3	Bos taurus	123-129
15203191-6	2004	TGF-beta1 time-dependently induced ROS production that was suppressed by NAC.	Acetylcysteine	73-76	transforming growth factor beta 1	Homo sapiens	0-9
15203191-9	2004	TGF-beta1-stimulated Smad2 phosphorylation was inhibited by NAC.	Acetylcysteine	60-63	transforming growth factor beta 1	Homo sapiens	0-9
15203191-13	2004	TGF-beta-stimulated ERK and JNK phosphorylation was also inhibited by NAC.	Acetylcysteine	70-73	transforming growth factor beta 1	Homo sapiens	0-8
15203191-13	2004	TGF-beta-stimulated ERK and JNK phosphorylation was also inhibited by NAC.	Acetylcysteine	70-73	mitogen-activated protein kinase 1	Homo sapiens	20-23
15203191-13	2004	TGF-beta-stimulated ERK and JNK phosphorylation was also inhibited by NAC.	Acetylcysteine	70-73	mitogen-activated protein kinase 8	Homo sapiens	28-31
15178409-5	2004	Lowering the level of reactive oxygen species by antioxidants, such as the cell-permeable N-acetyl-L-cysteine, prevented TGF-beta1-mediated downregulation of intercellular communication between confluent fibroblasts.	Acetylcysteine	90-109	transforming growth factor beta 1	Homo sapiens	121-130
15070851-8	2004	AM also inhibited Ang II-induced up-regulation of Nox1, a critical membrane-bound component of reduced nicotinamide adenine dinucleotide phosphate oxidase in VSMCs, in the same degree as N-acetyl-l-cysteine.	Acetylcysteine	187-206	angiotensinogen	Rattus norvegicus	18-24
15175554-4	2004	Exposure of HUVECs to TNFalpha (200 U/ml) for 24 hours caused significant increases of both the PDGF-B expression and its promoter/enhancer activity, which were abolished by NAC (20 mmol/L).	Acetylcysteine	174-177	tumor necrosis factor	Homo sapiens	22-30
15175554-5	2004	Accordingly, a prolonged oxidative stress was induced by TNFalpha and that was prevented by pretreatment with NAC.	Acetylcysteine	110-113	tumor necrosis factor	Homo sapiens	57-65
15175554-7	2004	However, NAC only partially inhibited the TNFalpha-induced activation of NF-kappaB, but abolished the activation of SP-1.	Acetylcysteine	9-12	tumor necrosis factor	Homo sapiens	42-50
15027896-6	2004	The antioxidant N-acetylcysteine as well as the NAD(P)H oxidase inhibitors diphenylene iodonium and phenylarsine oxide abolished both Ang II- and AA-induced ERK1/ERK2 activation.	Acetylcysteine	16-32	angiotensinogen	Homo sapiens	134-140
15027896-6	2004	The antioxidant N-acetylcysteine as well as the NAD(P)H oxidase inhibitors diphenylene iodonium and phenylarsine oxide abolished both Ang II- and AA-induced ERK1/ERK2 activation.	Acetylcysteine	16-32	mitogen-activated protein kinase 3	Homo sapiens	157-161
15027896-6	2004	The antioxidant N-acetylcysteine as well as the NAD(P)H oxidase inhibitors diphenylene iodonium and phenylarsine oxide abolished both Ang II- and AA-induced ERK1/ERK2 activation.	Acetylcysteine	16-32	mitogen-activated protein kinase 1	Homo sapiens	162-166
15199099-8	2004	The results indicate that reducing conditions, achieved using N-propylgallate (nPG) or N-acetylcysteine (NAC), stabilize HIF-1alpha, facilitate its DNA binding, and increase its phosphorylation even under normal oxygen conditions.	Acetylcysteine	87-103	hypoxia-inducible factor 1-alpha	Oncorhynchus mykiss	121-131
15199099-8	2004	The results indicate that reducing conditions, achieved using N-propylgallate (nPG) or N-acetylcysteine (NAC), stabilize HIF-1alpha, facilitate its DNA binding, and increase its phosphorylation even under normal oxygen conditions.	Acetylcysteine	105-108	hypoxia-inducible factor 1-alpha	Oncorhynchus mykiss	121-131
15130276-5	2004	N-Acetyl-L-cysteine prevented growth inhibition by MnSOD.	Acetylcysteine	0-19	superoxide dismutase 2, mitochondrial	Mus musculus	51-56
15158123-6	2004	Pretreatment of the cells with an antioxidant, N-acetylcysteine (NAC), resulted in the inhibition of p38 MAPK phosphorylation and PKC- translocation during TGD.	Acetylcysteine	47-63	mitogen-activated protein kinase 14	Homo sapiens	101-104
15147565-9	2004	In contrast, a thiol antioxidant, N-acetyl-l-cysteine, completely blocked X-irradiation-induced up-regulation of CD80 expression in LPS-B cells, but not in A20-HL cells or in DCs.	Acetylcysteine	34-53	CD80 antigen	Mus musculus	113-117
15158123-6	2004	Pretreatment of the cells with an antioxidant, N-acetylcysteine (NAC), resulted in the inhibition of p38 MAPK phosphorylation and PKC- translocation during TGD.	Acetylcysteine	65-68	mitogen-activated protein kinase 14	Homo sapiens	101-104
15158123-7	2004	In addition, the induction of COX-2 and HO-1 expression by TGD was prevented by pretreatment with NAC or SB203580, a p38 MAPK inhibitor.	Acetylcysteine	98-101	prostaglandin-endoperoxide synthase 2	Homo sapiens	30-35
15158123-7	2004	In addition, the induction of COX-2 and HO-1 expression by TGD was prevented by pretreatment with NAC or SB203580, a p38 MAPK inhibitor.	Acetylcysteine	98-101	mitogen-activated protein kinase 14	Homo sapiens	117-120
15114624-11	2004	Immunohistochemical and quantitative real-time PCR studies demonstrated a reduction in the expression of proinflammatory cytokines such as tumor necrosis factor alpha (TNFalpha) and interleukin 1beta (IL-1beta) and inducible nitric oxide synthase (iNOS) in NAC compared to that in vehicle-treated animals.	Acetylcysteine	257-260	tumor necrosis factor	Rattus norvegicus	139-166
15469714-5	2004	Radical scavengers, azide, N-acetylcysteine, and catalase inhibited the oxidized catecholamine-mediated Cu,Zn-SOD aggregation.	Acetylcysteine	27-43	superoxide dismutase 1	Homo sapiens	110-113
15071361-7	2004	An inhibitor of AP-1, curcumin, or an anti-oxidant, N-acetylcysteine, also inhibited the TNF-alpha-induced IL-8 expression in HUVEC.	Acetylcysteine	52-68	tumor necrosis factor	Homo sapiens	89-98
15209356-0	2004	N-acetyl cysteine regulates TNF-alpha-inhibited differentiation in ROS 17/2.8 osteoblasts.	Acetylcysteine	0-17	tumor necrosis factor	Rattus norvegicus	28-37
15209356-5	2004	The addition of NAC (N-acetyl cysteine), free radical scavenger, completely prevented TNF-alpha-induced activation of NF-kappaB.	Acetylcysteine	16-19	tumor necrosis factor	Rattus norvegicus	86-95
15209356-5	2004	The addition of NAC (N-acetyl cysteine), free radical scavenger, completely prevented TNF-alpha-induced activation of NF-kappaB.	Acetylcysteine	21-38	tumor necrosis factor	Rattus norvegicus	86-95
15209356-9	2004	Here, we suggest that the degradations of IkappaB alpha and IkappaB beta and the following activation of NF-kappaB are the targets of NAC and that NF-kappaB transcription factor is a pivotal clue to regulation of differentiation in TNFalpha-exposed osteoblasts.	Acetylcysteine	134-137	NFKB inhibitor beta	Rattus norvegicus	60-72
15209356-9	2004	Here, we suggest that the degradations of IkappaB alpha and IkappaB beta and the following activation of NF-kappaB are the targets of NAC and that NF-kappaB transcription factor is a pivotal clue to regulation of differentiation in TNFalpha-exposed osteoblasts.	Acetylcysteine	134-137	tumor necrosis factor	Rattus norvegicus	232-240
15093752-6	2004	Lastly, the antioxidant N-acetyl-l-cysteine (LNAC) attenuated Bortezomib-mediated reactive oxygen species (ROS) generation, ERK inactivation, JNK activation, mitochondrial dysfunction, and apoptosis.	Acetylcysteine	24-43	mitogen-activated protein kinase 1	Homo sapiens	124-127
15093752-6	2004	Lastly, the antioxidant N-acetyl-l-cysteine (LNAC) attenuated Bortezomib-mediated reactive oxygen species (ROS) generation, ERK inactivation, JNK activation, mitochondrial dysfunction, and apoptosis.	Acetylcysteine	24-43	mitogen-activated protein kinase 8	Homo sapiens	142-145
15071361-7	2004	An inhibitor of AP-1, curcumin, or an anti-oxidant, N-acetylcysteine, also inhibited the TNF-alpha-induced IL-8 expression in HUVEC.	Acetylcysteine	52-68	C-X-C motif chemokine ligand 8	Homo sapiens	107-111
15039334-7	2004	LPS-stimulated IL-8 expression could be blocked by the antioxidants N-acetyl-L-cysteine and dimethyl sulfoxide at both the protein and mRNA levels.	Acetylcysteine	68-87	toll-like receptor 4	Mus musculus	0-3
15007512-2	2004	Diabetic patients show abnormally high ROS levels and a decrease in insulin reactivity which is ameliorated by antioxidants, such as N-acetylcysteine (NAC).	Acetylcysteine	133-149	insulin	Homo sapiens	68-75
15007512-2	2004	Diabetic patients show abnormally high ROS levels and a decrease in insulin reactivity which is ameliorated by antioxidants, such as N-acetylcysteine (NAC).	Acetylcysteine	151-154	insulin	Homo sapiens	68-75
14718647-7	2004	When cells were prelabeled with N-acetyl-cysteine (NAC), a substrate for glutathione synthesis, and catalase (CAT), the oxygen free radical scavenger, a significant reduction in cytogenetic damage was observed.	Acetylcysteine	51-54	catalase	Homo sapiens	100-108
14701705-7	2004	In addition, AR secretion was inhibited by the antioxidant N-acetyl cysteine, but not by a neutralizing anti-EGFR, suggesting an EGFR transactivation via oxidative stress.	Acetylcysteine	59-76	epidermal growth factor receptor	Homo sapiens	129-133
15023567-11	2004	In contrast to tempol and PEG-catalase, N-acetylcysteine (0.1-1 mM), which is able to release NO from intracellular stores, relaxed LPS-treated tissue, an effect that was abolished by long-term, but not by short-term, incubation with 1400 W. CONCLUSIONS: The present study provides direct evidence that exposure to LPS results in induction of iNOS and SOD associated with noradrenaline hyporeactivity, while increased NO is only measured when l-arginine is present.	Acetylcysteine	40-56	nitric oxide synthase 2	Rattus norvegicus	343-347
15007512-5	2004	In two double-blind trials involving a total of 140 non-diabetic subjects we found furthermore that NAC increased the HOMA-R index (derived from the fasting insulin and glucose concentrations) in smokers and obese patients, but not in nonobese non-smokers.	Acetylcysteine	100-103	insulin	Homo sapiens	157-164
14709335-6	2004	Antioxidants and activating protein-1 transcription factor inhibitors, nordihydroguaiaretic acid and N-acetyl-L-cysteine (NAC) suppressed MMP and ADAM-TS4 genes.	Acetylcysteine	101-120	ADAM metallopeptidase with thrombospondin type 1 motif 4	Bos taurus	146-154
14709335-6	2004	Antioxidants and activating protein-1 transcription factor inhibitors, nordihydroguaiaretic acid and N-acetyl-L-cysteine (NAC) suppressed MMP and ADAM-TS4 genes.	Acetylcysteine	122-125	ADAM metallopeptidase with thrombospondin type 1 motif 4	Bos taurus	146-154
14966365-9	2004	N-Acetylcysteine suppressed the release of TNF-alpha, IL-1 beta, and MG, but enhanced NO production.	Acetylcysteine	0-16	tumor necrosis factor	Rattus norvegicus	43-52
15044633-11	2004	NQO1 gene expression was not induced when mutant, inactive CYP1A1 was overexpressed or when the antioxidant N-acetyl cysteine (NAC) was added to Ad1A1.	Acetylcysteine	108-125	NAD(P)H quinone dehydrogenase 1	Homo sapiens	0-4
15044633-11	2004	NQO1 gene expression was not induced when mutant, inactive CYP1A1 was overexpressed or when the antioxidant N-acetyl cysteine (NAC) was added to Ad1A1.	Acetylcysteine	127-130	NAD(P)H quinone dehydrogenase 1	Homo sapiens	0-4
15044633-12	2004	Finally, either NAC or siRNA directed against CYP1A1 mRNA decreased the induction of NQO1 gene expression by TCDD.	Acetylcysteine	16-19	NAD(P)H quinone dehydrogenase 1	Homo sapiens	85-89
15093278-10	2004	For instance, in vitro SCE induction by styrene and by epoxide metabolites of 1,3-butadiene is modified by GSTM1 and GSTT1 genotypes--which also influence the excretion of specific mercapturic acids in humans exposed to butadiene and styrene.	Acetylcysteine	181-198	glutathione S-transferase mu 1	Homo sapiens	107-112
14769780-10	2004	The effects of CEES on the accumulation of ROS, the intracellular concentration of GSH, the mitochondrial membrane potential, and caspase-3 activity were all inhibited by pretreatment of cells with the GSH precursor N-acetyl cysteine or with GSH-ethyl ester.	Acetylcysteine	216-233	caspase 3	Homo sapiens	130-139
14966365-9	2004	N-Acetylcysteine suppressed the release of TNF-alpha, IL-1 beta, and MG, but enhanced NO production.	Acetylcysteine	0-16	interleukin 1 beta	Rattus norvegicus	54-63
14647418-7	2004	Lastly, antioxidants (e.g., L-N-acetylcysteine; L-NAC) opposed adaphostin-mediated mitochondrial dysfunction, Raf-1/MEK/ERK downregulation, JNK activation, and apoptosis.	Acetylcysteine	28-46	mitogen-activated protein kinase kinase 7	Homo sapiens	116-119
14726217-11	2004	The liver and renal tissue iNOS expression was increased in groups B, D, and F. After the administration of NAC (groups C-E) the liver and renal tissue iNOS expression were decreased.	Acetylcysteine	108-111	nitric oxide synthase 2	Rattus norvegicus	27-31
14726217-11	2004	The liver and renal tissue iNOS expression was increased in groups B, D, and F. After the administration of NAC (groups C-E) the liver and renal tissue iNOS expression were decreased.	Acetylcysteine	108-111	nitric oxide synthase 2	Rattus norvegicus	152-156
14726217-12	2004	Our results indicated that NAC prevented the deleterious effects of LPS in OJ by reducing iNOS expression via lipid peroxidation in liver and renal tissue; if it was administrated before LPS.	Acetylcysteine	27-30	nitric oxide synthase 2	Rattus norvegicus	90-94
14982601-6	2004	Stretch-induced IL-8 and IL-6 production were significantly inhibited when intracellular GSH was further increased by NAC or GSH-e (P &lt; 0.0001).	Acetylcysteine	118-121	C-X-C motif chemokine ligand 8	Homo sapiens	16-20
14982601-6	2004	Stretch-induced IL-8 and IL-6 production were significantly inhibited when intracellular GSH was further increased by NAC or GSH-e (P &lt; 0.0001).	Acetylcysteine	118-121	interleukin 6	Homo sapiens	25-29
14982601-8	2004	NAC blocked stretch-induced NF-kappa B and AP-1 binding and inhibited IL-8 mRNA expression.	Acetylcysteine	0-3	nuclear factor kappa B subunit 1	Homo sapiens	28-38
14982601-8	2004	NAC blocked stretch-induced NF-kappa B and AP-1 binding and inhibited IL-8 mRNA expression.	Acetylcysteine	0-3	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	43-47
14982601-8	2004	NAC blocked stretch-induced NF-kappa B and AP-1 binding and inhibited IL-8 mRNA expression.	Acetylcysteine	0-3	C-X-C motif chemokine ligand 8	Homo sapiens	70-74
14726217-0	2004	The effect of N-acetylcysteine (NAC) on liver and renal tissue inducible nitric oxide synthase (iNOS) and tissue lipid peroxidation in obstructive jaundice stimulated by lipopolysaccharide (LPS).	Acetylcysteine	32-35	nitric oxide synthase 2	Rattus norvegicus	63-94
14726217-4	2004	The aim of this study was to investigate the effects of NAC on liver and renal tissue iNOS, and liver tissue lipid peroxidation in lipopolysaccharide (LPS) induced obstructive jaundice.	Acetylcysteine	56-59	nitric oxide synthase 2	Rattus norvegicus	86-90
15036602-3	2004	Pretreatment with N-acetylcysteine, a free radical scavenger, effectively inhibited ERK5 activation in a dose-dependent manner.	Acetylcysteine	18-34	mitogen-activated protein kinase 7	Rattus norvegicus	84-88
14978478-9	2004	Serum starved human lens epithelial cells stimulated with different growth factors including EGF, b-FGF, PDGF, TGF-beta, and LPA demonstrated increased production of ROS, a response which was blocked by inhibitors of NADPH oxidase, such as DPI and the antioxidant-N-acetyl cysteine (NAC).	Acetylcysteine	264-281	fibroblast growth factor 2	Homo sapiens	98-103
14647418-7	2004	Lastly, antioxidants (e.g., L-N-acetylcysteine; L-NAC) opposed adaphostin-mediated mitochondrial dysfunction, Raf-1/MEK/ERK downregulation, JNK activation, and apoptosis.	Acetylcysteine	28-46	mitogen-activated protein kinase 1	Homo sapiens	120-123
14647418-7	2004	Lastly, antioxidants (e.g., L-N-acetylcysteine; L-NAC) opposed adaphostin-mediated mitochondrial dysfunction, Raf-1/MEK/ERK downregulation, JNK activation, and apoptosis.	Acetylcysteine	28-46	mitogen-activated protein kinase 8	Homo sapiens	140-143
14967008-8	2004	Moreover, exposure of PAECs to NAC alleviated the arsenite-induced JNK/AP-1 activation and apoptosis, whereas exposure of PAECs to BSO enhanced the arsenite-induced JNK/AP-1 activation and apoptosis.	Acetylcysteine	31-34	mitogen-activated protein kinase 8	Homo sapiens	67-70
14872485-10	2004	NF-kappaB inhibitors N-acetyl-L-cysteine and Bay 11-7085 and PI 3-kinase inhibitor LY294002 inhibited the enhancing effects of IL-18, but MAPK p38 inhibitor SB203580, ERK inhibitor PD98059, and JNK inhibitor SP600125 did not.	Acetylcysteine	21-40	nuclear factor kappa B subunit 1	Homo sapiens	0-9
14764725-6	2004	The decrease in cytoplasmic levels of IkappaBalpha produced by exposure of neutrophils to LPS was prevented by N-acetylcysteine or alpha-tocopherol.	Acetylcysteine	111-127	NFKB inhibitor alpha	Homo sapiens	38-50
15022809-10	2004	This effect was attenuated by treatment with N-acetylcysteine (MPO 43-9 microg/mL, BAL protein 605-198 microg/mL).	Acetylcysteine	45-61	myeloperoxidase	Homo sapiens	63-66
15009100-6	2004	Third, the structurally different antioxidants n-propyl gallate and N-acetylcysteine inhibited epidermal growth factor receptor phosphorylation induced by anthralin.	Acetylcysteine	68-84	epidermal growth factor receptor	Homo sapiens	95-127
14663554-7	2004	Furthermore, resveratrol, as well as the antioxidant N-acetyl-cysteine, decreased Ang II- or H2O2-increased protein synthesis, beta-MyHC promoter activity, and ERK phosphorylation.	Acetylcysteine	53-70	angiotensinogen	Rattus norvegicus	82-88
15036418-5	2004	N-acetylcysteine (NAC), an antioxidant, completely reverses the increased endogenous IL-6 promoter activity in the old mice determined by real-time bioluminescence imaging (BLI).	Acetylcysteine	0-16	interleukin 6	Mus musculus	85-89
15036418-5	2004	N-acetylcysteine (NAC), an antioxidant, completely reverses the increased endogenous IL-6 promoter activity in the old mice determined by real-time bioluminescence imaging (BLI).	Acetylcysteine	18-21	interleukin 6	Mus musculus	85-89
15106733-5	2004	As well, antioxidant-catalase, N-acetyl-cysteine or reduced glutathione-attenuated COX-2 expression in combined cytokines-treated cells.	Acetylcysteine	31-48	prostaglandin-endoperoxide synthase 2	Homo sapiens	83-88
14663554-7	2004	Furthermore, resveratrol, as well as the antioxidant N-acetyl-cysteine, decreased Ang II- or H2O2-increased protein synthesis, beta-MyHC promoter activity, and ERK phosphorylation.	Acetylcysteine	53-70	Eph receptor B1	Rattus norvegicus	160-163
15477121-8	2004	The MPO activity, MDA and 3-NT levels in lung homogenates were found to be increased in OA group and the administration of NAC significantly reduced tissue MPO, MDA and 3-NT levels (p = 0.0001) Lung histopathology was also affected by NAC in this OA-induced experimental lung injury model.	Acetylcysteine	123-126	myeloperoxidase	Homo sapiens	4-7
15470276-7	2004	Mononuclear cell adhesion to HAART-exposed HAECs was significantly enhanced following acute (24-h) exposure to the inflammatory cytokines, tumor necrosis factor (TNF)-alpha or interleukin (IL)-1beta and was suppressed by the antioxidants N-ace-tylcysteine and glutathione.	Acetylcysteine	238-255	interleukin 1 beta	Homo sapiens	176-198
14730205-7	2004	Both trilinolein and the antioxidant, N-acetyl-cysteine, decreased NE- and H(2)O(2)-induced protein synthesis, beta-MyHC promoter activity, and ERK phosphorylation.	Acetylcysteine	38-55	myosin heavy chain 13	Rattus norvegicus	116-120
14730205-7	2004	Both trilinolein and the antioxidant, N-acetyl-cysteine, decreased NE- and H(2)O(2)-induced protein synthesis, beta-MyHC promoter activity, and ERK phosphorylation.	Acetylcysteine	38-55	Eph receptor B1	Rattus norvegicus	144-147
14732751-0	2004	N-acetylcysteine prevents the deleterious effect of tumor necrosis factor-(alpha) on calcium transients and contraction in adult rat cardiomyocytes.	Acetylcysteine	0-16	tumor necrosis factor	Rattus norvegicus	52-80
14732751-6	2004	In cardiomyocytes obtained from NAC-treated rats, 25 ng/mL TNF-alpha had no effect on reactive oxygen species production or N-SMase activity but increased the amplitude of [Ca(2+)](i) transients and contraction in response to electrical stimulation by 40% to 50% over basal after 20 minutes.	Acetylcysteine	32-35	tumor necrosis factor	Rattus norvegicus	59-68
14729376-6	2004	Antioxidant N-acetylcysteine also decreased angiotensin II-increased protein synthesis and beta-myosin heavy chain promoter activity.	Acetylcysteine	12-28	angiotensinogen	Rattus norvegicus	44-58
14729376-7	2004	Furthermore, trilinolein and N-acetylcysteine decreased angiotensin II- or hydrogen peroxide (H2O2)-activated mitogen-activated protein kinases (MAPKs) phosphorylation, and activator protein-1 (AP-1)- [or nuclear factor-kappaB (NF-kappaB)]-reporter activities.	Acetylcysteine	29-45	angiotensinogen	Rattus norvegicus	56-70
14730207-11	2004	Furthermore, E(2) and antioxidants, such as N-acetyl cysteine and diphenylene iodonium, decreased Ang-II-induced cell proliferation, ET-1 promoter activity, ET-1 mRNA, ERK phosphorylation, and activator protein-1-mediated reporter activity.	Acetylcysteine	44-61	angiotensinogen	Rattus norvegicus	98-104
14730207-11	2004	Furthermore, E(2) and antioxidants, such as N-acetyl cysteine and diphenylene iodonium, decreased Ang-II-induced cell proliferation, ET-1 promoter activity, ET-1 mRNA, ERK phosphorylation, and activator protein-1-mediated reporter activity.	Acetylcysteine	44-61	endothelin 1	Rattus norvegicus	133-137
14730207-11	2004	Furthermore, E(2) and antioxidants, such as N-acetyl cysteine and diphenylene iodonium, decreased Ang-II-induced cell proliferation, ET-1 promoter activity, ET-1 mRNA, ERK phosphorylation, and activator protein-1-mediated reporter activity.	Acetylcysteine	44-61	endothelin 1	Rattus norvegicus	157-161
14730207-11	2004	Furthermore, E(2) and antioxidants, such as N-acetyl cysteine and diphenylene iodonium, decreased Ang-II-induced cell proliferation, ET-1 promoter activity, ET-1 mRNA, ERK phosphorylation, and activator protein-1-mediated reporter activity.	Acetylcysteine	44-61	Eph receptor B1	Rattus norvegicus	168-171
14734137-0	2004	N-acetylcysteine inhibits interleukin-17-induced interleukin-8 production from human airway smooth muscle cells: a possible role for anti-oxidative treatment in chronic lung rejection?	Acetylcysteine	0-16	C-X-C motif chemokine ligand 8	Homo sapiens	49-62
14734137-8	2004	N-acetylcysteine (NAC) was able to decrease IL-17-induced 8-isoprostane production, with a maximum decrease of 59.3 +/- 9% (p &lt; 0.001, n = 12) with 10 mmol/liter of N-acetylcysteine, which also decreased IL-17-induced IL-8 production in a concentration-dependent manner (with maximum inhibition of 86.3% when combined with NAC 10 mmol/liter as compared with IL-17 alone).	Acetylcysteine	0-16	C-X-C motif chemokine ligand 8	Homo sapiens	221-225
14734137-8	2004	N-acetylcysteine (NAC) was able to decrease IL-17-induced 8-isoprostane production, with a maximum decrease of 59.3 +/- 9% (p &lt; 0.001, n = 12) with 10 mmol/liter of N-acetylcysteine, which also decreased IL-17-induced IL-8 production in a concentration-dependent manner (with maximum inhibition of 86.3% when combined with NAC 10 mmol/liter as compared with IL-17 alone).	Acetylcysteine	18-21	C-X-C motif chemokine ligand 8	Homo sapiens	221-225
15477121-8	2004	The MPO activity, MDA and 3-NT levels in lung homogenates were found to be increased in OA group and the administration of NAC significantly reduced tissue MPO, MDA and 3-NT levels (p = 0.0001) Lung histopathology was also affected by NAC in this OA-induced experimental lung injury model.	Acetylcysteine	123-126	myeloperoxidase	Homo sapiens	156-159
14999536-7	2004	CONCLUSIONS: N-Acetylcysteine decreased pump-induced oxidoinflammatory response during CPB, suggesting that it could be a novel therapy for assisting in the prevention of CBP-induced oxidoinflammatory damage.	Acetylcysteine	13-29	CREB binding protein	Homo sapiens	171-174
14635187-8	2003	The effect of PEITC on GADD153 was attenuated by either actinomycin D or N-acetylcysteine, suggesting that PEITC-induced upregulation of GADD153 mRNA expression was partly at the level of transcriptional activation involving reactive oxygen species.	Acetylcysteine	73-89	DNA damage inducible transcript 3	Homo sapiens	23-30
14635187-8	2003	The effect of PEITC on GADD153 was attenuated by either actinomycin D or N-acetylcysteine, suggesting that PEITC-induced upregulation of GADD153 mRNA expression was partly at the level of transcriptional activation involving reactive oxygen species.	Acetylcysteine	73-89	DNA damage inducible transcript 3	Homo sapiens	137-144
14600028-2	2003	We explored the effects of the antioxidants alpha-lipoic acid and N-acetyl-l-cysteine on ERK activation in cultured mesangial cells and the role of ERK activation in the severity of glomerular injury in a rat model of anti-Thy 1 GN.	Acetylcysteine	66-85	Eph receptor B1	Rattus norvegicus	89-92
14690293-1	2003	Three different anti-inflammatory agents--diclofenac, dexamethasone, and N-acetylcysteine--were compared to evaluate their effectiveness in suppressing monocyte-macrophage cell culture activation and mediator release (tumor necrosis factor-alpha [TNF-alpha] and interleukin-1beta [IL-1beta]) in response to polymethylmethacrylate particulate debris.	Acetylcysteine	73-89	tumor necrosis factor	Homo sapiens	218-245
14623829-6	2003	Furthermore, pretreating cells with resveratrol or antioxidant N-acetyl-cysteine decreases strain-increased or hydrogen peroxide-increased ET-1 secretion, ET-1 promoter activity, and ET-1 mRNA and ERK1/2 phosphorylation.	Acetylcysteine	63-80	endothelin 1	Homo sapiens	139-143
14623829-6	2003	Furthermore, pretreating cells with resveratrol or antioxidant N-acetyl-cysteine decreases strain-increased or hydrogen peroxide-increased ET-1 secretion, ET-1 promoter activity, and ET-1 mRNA and ERK1/2 phosphorylation.	Acetylcysteine	63-80	endothelin 1	Homo sapiens	155-159
14623829-6	2003	Furthermore, pretreating cells with resveratrol or antioxidant N-acetyl-cysteine decreases strain-increased or hydrogen peroxide-increased ET-1 secretion, ET-1 promoter activity, and ET-1 mRNA and ERK1/2 phosphorylation.	Acetylcysteine	63-80	endothelin 1	Homo sapiens	155-159
14623829-6	2003	Furthermore, pretreating cells with resveratrol or antioxidant N-acetyl-cysteine decreases strain-increased or hydrogen peroxide-increased ET-1 secretion, ET-1 promoter activity, and ET-1 mRNA and ERK1/2 phosphorylation.	Acetylcysteine	63-80	mitogen-activated protein kinase 3	Homo sapiens	197-203
14690293-2	2003	N-acetylcysteine and diclofenac were most effective in suppressing TNF-alpha and IL-1beta expression by the monocyte-macrophages.	Acetylcysteine	0-16	tumor necrosis factor	Homo sapiens	67-76
14690293-2	2003	N-acetylcysteine and diclofenac were most effective in suppressing TNF-alpha and IL-1beta expression by the monocyte-macrophages.	Acetylcysteine	0-16	interleukin 1 beta	Homo sapiens	81-89
12966092-7	2003	Experiments with the Src inhibitor, PP2, and the antioxidant N-acetyl-L-cysteine revealed critical roles for Src and reactive oxygen species as upstream mediators of EGFR transactivation in response to PPAR ligands.	Acetylcysteine	61-80	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	109-112
12966092-7	2003	Experiments with the Src inhibitor, PP2, and the antioxidant N-acetyl-L-cysteine revealed critical roles for Src and reactive oxygen species as upstream mediators of EGFR transactivation in response to PPAR ligands.	Acetylcysteine	61-80	epidermal growth factor receptor	Homo sapiens	166-170
14605526-12	2003	Interleukin-8 decreased significantly only in those who received N-acetylcysteine (p =.0081).	Acetylcysteine	65-81	C-X-C motif chemokine ligand 8	Homo sapiens	0-13
14607909-5	2003	Augmenting intracellular soluble thiol pools ( approximately 2-fold) with 15 mM NAC blocked induction of IFN-gamma and increased production of IL-4 without causing significant changes in intracellular glutathione levels.	Acetylcysteine	80-83	interferon gamma	Homo sapiens	105-114
14607909-5	2003	Augmenting intracellular soluble thiol pools ( approximately 2-fold) with 15 mM NAC blocked induction of IFN-gamma and increased production of IL-4 without causing significant changes in intracellular glutathione levels.	Acetylcysteine	80-83	interleukin 4	Homo sapiens	143-147
14607909-6	2003	The effect of NAC on IL-4 production was not linked to an increase in STAT6 phosphorylation, as STAT6 levels were decreased, nor did the increase in IL-4 occur with purified CD4 cells.	Acetylcysteine	14-17	interleukin 4	Homo sapiens	21-25
14607909-7	2003	We found that NAC increased splenocyte IL-4 production via an effect on APCs.	Acetylcysteine	14-17	interleukin 4	Homo sapiens	39-43
14607909-8	2003	We also found that NAC increased two IL-4 relevant transcription factors (AP-1) and NFATc.	Acetylcysteine	19-22	interleukin 4	Homo sapiens	37-41
14633709-7	2003	The BPQ-induced EGFR activity and associated cell proliferation were attenuated by the EGFR inhibitor AG1478, as well as by the antioxidant N-acetyl cysteine.	Acetylcysteine	140-157	epidermal growth factor receptor	Homo sapiens	16-20
14599773-10	2003	Pre-treatment of A2780 cells with the glutathione (GSH) precursor, N-acetyl-L-cysteine prevented Cbl-induced increase in ROS, augmented the kinase activity of DNA-PKcs, decreased the levels of DNA dsbs and increased cell survival.	Acetylcysteine	67-86	protein kinase, DNA-activated, catalytic subunit	Homo sapiens	159-167
12969991-9	2003	LY294002, a PI3K inhibitor, and N-acetylcysteine, a scavenger of reactive oxygen species, inhibited the stretch activation of Akt.	Acetylcysteine	32-48	AKT serine/threonine kinase 1	Rattus norvegicus	126-129
14605526-14	2003	CONCLUSIONS: Administration of N-acetylcysteine results in decreased nuclear factor-kappa B activation in patients with sepsis, associated with decreases in interleukin-8 but not interleukin-6 or soluble intercellular adhesion molecule-1.	Acetylcysteine	31-47	C-X-C motif chemokine ligand 8	Homo sapiens	157-170
14605526-14	2003	CONCLUSIONS: Administration of N-acetylcysteine results in decreased nuclear factor-kappa B activation in patients with sepsis, associated with decreases in interleukin-8 but not interleukin-6 or soluble intercellular adhesion molecule-1.	Acetylcysteine	31-47	interleukin 6	Homo sapiens	179-192
14516795-8	2003	DNA binding activity of AP-1, downstream of ERK1/2, was also inhibited by catalase, N-acetyl-L-cysteine, and the MEK inhibitor PD98059, which significantly blocked arsenite activation of ERK1/2.	Acetylcysteine	84-103	mitogen-activated protein kinase 3	Homo sapiens	44-50
14573751-12	2003	In addition, antioxidant N-acetyl-cysteine was demonstrated to strongly inhibit VEGF-mediated Src activation, VE-cadherin tyrosine phosphorylation, and HUVEC tube formation.	Acetylcysteine	25-42	vascular endothelial growth factor A	Homo sapiens	80-84
14573751-12	2003	In addition, antioxidant N-acetyl-cysteine was demonstrated to strongly inhibit VEGF-mediated Src activation, VE-cadherin tyrosine phosphorylation, and HUVEC tube formation.	Acetylcysteine	25-42	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	94-97
14573751-12	2003	In addition, antioxidant N-acetyl-cysteine was demonstrated to strongly inhibit VEGF-mediated Src activation, VE-cadherin tyrosine phosphorylation, and HUVEC tube formation.	Acetylcysteine	25-42	cadherin 5	Homo sapiens	110-121
14516795-4	2003	Elimination of H(2)O(2) by catalase or N-acetyl-L-cysteine inhibited the arsenite-induced activation of p70(s6k) and ERK1/2, indicating the possible role of H(2)O(2) in the arsenite activation of the p70(s6k) and the ERK1/2 signaling pathways.	Acetylcysteine	39-58	mitogen-activated protein kinase 3	Homo sapiens	117-123
14708604-8	2003	Furthermore, the capacity of N-acetylcysteine to block the activation of p38 and ERK1/2 MAP kinases by 2,4,6-trinitrochlorobenzene was demonstrated.	Acetylcysteine	29-45	mitogen-activated protein kinase 1	Homo sapiens	73-76
14708604-8	2003	Furthermore, the capacity of N-acetylcysteine to block the activation of p38 and ERK1/2 MAP kinases by 2,4,6-trinitrochlorobenzene was demonstrated.	Acetylcysteine	29-45	mitogen-activated protein kinase 3	Homo sapiens	81-87
14644336-8	2003	The excretion of specific mercapturic acids (PHEMA) in workers exposed to styrene has clearly been shown to depend on GSTM1 genotype, and GSTT1 genotype seems to modulate the excretion of one PHEMA diastereoisomer.	Acetylcysteine	26-43	glutathione S-transferase mu 1	Homo sapiens	118-123
12907675-5	2003	Successive injections of LPS and dexamethasone or N-acetyl-cysteine prevented the induction of UCP2 in all three tissues, suggesting that oxygen free radical generation plays a role in UCP2 regulation.	Acetylcysteine	50-67	uncoupling protein 2 (mitochondrial, proton carrier)	Mus musculus	95-99
12907675-5	2003	Successive injections of LPS and dexamethasone or N-acetyl-cysteine prevented the induction of UCP2 in all three tissues, suggesting that oxygen free radical generation plays a role in UCP2 regulation.	Acetylcysteine	50-67	uncoupling protein 2 (mitochondrial, proton carrier)	Mus musculus	185-189
14516795-8	2003	DNA binding activity of AP-1, downstream of ERK1/2, was also inhibited by catalase, N-acetyl-L-cysteine, and the MEK inhibitor PD98059, which significantly blocked arsenite activation of ERK1/2.	Acetylcysteine	84-103	mitogen-activated protein kinase 3	Homo sapiens	187-193
13679067-5	2003	We further demonstrated that H(2)O(2) stimulates PAI-1 expression and suppresses plasmin activity and that N-acetylcysteine effectively reverses TGF-beta1- and H(2)O(2)-induced changes in PAI-1 expression and plasmin activity.	Acetylcysteine	107-123	transforming growth factor beta 1	Homo sapiens	145-154
14577570-5	2003	Additionally, B cell responses after long-term ligation of CD40, such as protein expression, nuclear transcription factor kappaB (NFkappaB) activation, and cell proliferation, were also affected when cells were treated with NAC.	Acetylcysteine	224-227	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	93-128
14511233-4	2003	In the present study, we examined the effects of the reducing agents, N-acetyl-l-cysteine (NAC) and reduced glutathione (GSH), on tumour necrosis factor-alpha (TNF-alpha)-induced phenotypic changes in murine DC.	Acetylcysteine	70-89	tumor necrosis factor	Mus musculus	160-169
14511233-4	2003	In the present study, we examined the effects of the reducing agents, N-acetyl-l-cysteine (NAC) and reduced glutathione (GSH), on tumour necrosis factor-alpha (TNF-alpha)-induced phenotypic changes in murine DC.	Acetylcysteine	91-94	tumor necrosis factor	Mus musculus	160-169
14511233-6	2003	Both NAC and GSH completely abolished the TNF-alpha-induced enhancement of CD40 expression, but had no considerable effect on the expression of CD80, CD86 and MHC.	Acetylcysteine	5-8	tumor necrosis factor	Mus musculus	42-51
14511233-9	2003	The inhibitory effect of NAC or GSH on TNF-alpha-induced CD40 expression was released by simply removing these agents from the culture.	Acetylcysteine	25-28	tumor necrosis factor	Mus musculus	39-48
14511233-10	2003	In contrast, culture of TNF-alpha-treated DC with NAC or GSH markedly decreased the expression of CD40 within 12 hr.	Acetylcysteine	50-53	tumor necrosis factor	Mus musculus	24-33
12942544-4	2003	Both GSE and NAC resulted in significant exacerbation of the LPS-stimulated increase in COX-2 gene and protein expression and prostaglandin release, and suppressed the LPS-induced decrease in COX-1.	Acetylcysteine	13-16	cytochrome c oxidase subunit II	Bos taurus	88-93
14577570-5	2003	Additionally, B cell responses after long-term ligation of CD40, such as protein expression, nuclear transcription factor kappaB (NFkappaB) activation, and cell proliferation, were also affected when cells were treated with NAC.	Acetylcysteine	224-227	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	130-138
12840032-6	2003	When the cells were pretreated with 10 mm N-acetyl-l-cysteine for 1 h, Erk1/2 activation was completely blocked.	Acetylcysteine	42-61	mitogen-activated protein kinase 3	Homo sapiens	71-77
12941301-7	2003	In addition, PP1 inhibitor tautomycin prevented both NAC-induced PP1 reactivation and eIF2 alpha P dephosphorylation in H(2)O(2)-treated cells.	Acetylcysteine	53-56	neuropeptide Y receptor Y4	Rattus norvegicus	13-16
12860993-5	2003	Ang II-induced Ser-65 phosphorylation was ROS-dependent as assessed by pretreatment with ebselen (3.6 +/- 0.2 versus 1.1 +/- 0.2), diphenylene iodonium (3.6 +/- 0.2 versus 1.0 +/- 0.1), and N-acetyl cysteine (3.6 +/- 0.2 versus 1.2 +/- 0.1), but Ang II-stimulated phosphorylation of Thr-70 was ROS-insensitive.	Acetylcysteine	190-207	angiotensinogen	Homo sapiens	0-6
12941301-4	2003	Thiol-antioxidant N-acetyl-cysteine (NAC) and reduced glutathione (GSH), when added in vitro to lysates from H(2)O(2)-treated cells, reversed PP1 inhibition.	Acetylcysteine	18-35	neuropeptide Y receptor Y4	Rattus norvegicus	142-145
12941301-6	2003	Interestingly, NAC pretreatment protected cells from H(2)O(2)-induced PP1 inactivation and, consequently, it abolished increased H(2)O(2)-induced eIF2 alpha phosphorylation and protein synthesis inhibition.	Acetylcysteine	15-18	neuropeptide Y receptor Y4	Rattus norvegicus	70-73
12941301-7	2003	In addition, PP1 inhibitor tautomycin prevented both NAC-induced PP1 reactivation and eIF2 alpha P dephosphorylation in H(2)O(2)-treated cells.	Acetylcysteine	53-56	neuropeptide Y receptor Y4	Rattus norvegicus	65-68
12941446-7	2003	The results illustrated that NAC preferably inhibited the MLK3 activation during the ischemia and the early reperfusion, whereas DNQX effectively attenuated the MLK3 activation of the late reperfusion.	Acetylcysteine	29-32	mitogen-activated protein kinase kinase kinase 11	Rattus norvegicus	58-62
14614324-7	2003	Lastly, the free radical scavenger L-N-acetylcysteine (LNAC) attenuated HDI-mediated ROS generation, JNK activation, and apoptosis.	Acetylcysteine	35-53	mitogen-activated protein kinase 8	Homo sapiens	101-104
14614324-7	2003	Lastly, the free radical scavenger L-N-acetylcysteine (LNAC) attenuated HDI-mediated ROS generation, JNK activation, and apoptosis.	Acetylcysteine	55-59	mitogen-activated protein kinase 8	Homo sapiens	101-104
13679868-4	2003	Treatment of MM cells with an antioxidant N-acetyl-L-cysteine blocks 2ME2, but not Dex-induced apoptosis as well as release of mitochondrial proteins cytochrome c (cyto c) and Smac.	Acetylcysteine	42-61	cytochrome c, somatic	Homo sapiens	150-162
13679868-4	2003	Treatment of MM cells with an antioxidant N-acetyl-L-cysteine blocks 2ME2, but not Dex-induced apoptosis as well as release of mitochondrial proteins cytochrome c (cyto c) and Smac.	Acetylcysteine	42-61	cytochrome c, somatic	Homo sapiens	164-170
12975476-10	2003	Expression of TNF-alpha, a target for NF-kappaB and a cytokine strongly implicated in estrogen-deficiency bone loss, was suppressed in osteoclasts by 17-beta estradiol and NAC.	Acetylcysteine	172-175	tumor necrosis factor	Homo sapiens	14-23
12819184-10	2003	EGCG-induced JNK activation was blocked by the antioxidants glutathione and N-acetyl-l-cysteine, suggesting that the cell death signaling was potentially triggered by oxidative stress.	Acetylcysteine	76-95	mitogen-activated protein kinase 8	Homo sapiens	13-16
12943989-8	2003	It was further shown that p38 MAPK and ERK activation was inhibited by the antioxidant, N-acetylcysteine (NAC), and that a treatment with haloperidol completely blocked the p38 and ERK activation induced by dopamine.	Acetylcysteine	88-104	Eph receptor B1	Rattus norvegicus	39-42
12943989-8	2003	It was further shown that p38 MAPK and ERK activation was inhibited by the antioxidant, N-acetylcysteine (NAC), and that a treatment with haloperidol completely blocked the p38 and ERK activation induced by dopamine.	Acetylcysteine	106-109	Eph receptor B1	Rattus norvegicus	39-42
12943989-8	2003	It was further shown that p38 MAPK and ERK activation was inhibited by the antioxidant, N-acetylcysteine (NAC), and that a treatment with haloperidol completely blocked the p38 and ERK activation induced by dopamine.	Acetylcysteine	106-109	Eph receptor B1	Rattus norvegicus	181-184
12898340-6	2003	Meanwhile, compared to that of the controls, our results showed decreased level of ROS, less JNK activity and lower expression of cleaved caspase-3 in pretreated NAC groups and in Rg1 pretreated groups.	Acetylcysteine	162-165	mitogen-activated protein kinase 8	Homo sapiens	93-96
12898340-6	2003	Meanwhile, compared to that of the controls, our results showed decreased level of ROS, less JNK activity and lower expression of cleaved caspase-3 in pretreated NAC groups and in Rg1 pretreated groups.	Acetylcysteine	162-165	caspase 3	Homo sapiens	138-147
12800192-6	2003	The antioxidants N-acetylcysteine, reduced glutathione, lipoic acid and ascorbic acid markedly reduced the enhancing effect of the hormone on TNFalpha-induced caspase activation.	Acetylcysteine	17-33	tumor necrosis factor	Homo sapiens	142-150
12800192-7	2003	N-acetylcysteine and reduced glutathione also decreased caspase-independent cytotoxicity in the presence or absence of calcitriol, indicating that reactive oxygen species (ROS) have a key role in the cross talk between TNFalpha and calcitriol.	Acetylcysteine	0-16	tumor necrosis factor	Homo sapiens	219-227
12930301-3	2003	Hydrogen peroxide (H2O2) treatment of HaCaT cells induced expression of COX-2 and pretreatment with the antioxidant N-acetylcysteine (NAC) partly inhibited the UVB-induced expression of COX-2 protein in HaCaT cells, suggesting that oxidative stress contributes to COX-2 induction.	Acetylcysteine	116-132	prostaglandin-endoperoxide synthase 2	Homo sapiens	72-77
12930301-3	2003	Hydrogen peroxide (H2O2) treatment of HaCaT cells induced expression of COX-2 and pretreatment with the antioxidant N-acetylcysteine (NAC) partly inhibited the UVB-induced expression of COX-2 protein in HaCaT cells, suggesting that oxidative stress contributes to COX-2 induction.	Acetylcysteine	116-132	prostaglandin-endoperoxide synthase 2	Homo sapiens	186-191
12930301-3	2003	Hydrogen peroxide (H2O2) treatment of HaCaT cells induced expression of COX-2 and pretreatment with the antioxidant N-acetylcysteine (NAC) partly inhibited the UVB-induced expression of COX-2 protein in HaCaT cells, suggesting that oxidative stress contributes to COX-2 induction.	Acetylcysteine	116-132	prostaglandin-endoperoxide synthase 2	Homo sapiens	186-191
12930301-3	2003	Hydrogen peroxide (H2O2) treatment of HaCaT cells induced expression of COX-2 and pretreatment with the antioxidant N-acetylcysteine (NAC) partly inhibited the UVB-induced expression of COX-2 protein in HaCaT cells, suggesting that oxidative stress contributes to COX-2 induction.	Acetylcysteine	134-137	prostaglandin-endoperoxide synthase 2	Homo sapiens	72-77
12930301-3	2003	Hydrogen peroxide (H2O2) treatment of HaCaT cells induced expression of COX-2 and pretreatment with the antioxidant N-acetylcysteine (NAC) partly inhibited the UVB-induced expression of COX-2 protein in HaCaT cells, suggesting that oxidative stress contributes to COX-2 induction.	Acetylcysteine	134-137	prostaglandin-endoperoxide synthase 2	Homo sapiens	186-191
12930301-3	2003	Hydrogen peroxide (H2O2) treatment of HaCaT cells induced expression of COX-2 and pretreatment with the antioxidant N-acetylcysteine (NAC) partly inhibited the UVB-induced expression of COX-2 protein in HaCaT cells, suggesting that oxidative stress contributes to COX-2 induction.	Acetylcysteine	134-137	prostaglandin-endoperoxide synthase 2	Homo sapiens	186-191
12860476-10	2003	Fraxetin (100 microM) and N-acetylcysteine (100 microM) not only reduced rotenone-induced reactive oxygen species formation, but also attenuated caspase-3 activity and poly(ADP-ribose) polymerase cleavage at 16 h against rotenone-induced apoptosis.	Acetylcysteine	26-42	caspase 3	Homo sapiens	145-154
12850239-8	2003	Moreover, lectin-II-induced activation of caspase-9 and 3-like protease and cleavage of poly(ADP-ribose) polymerase (PARP) were inhibited by pretreatment of cells with thiol antioxidants, GSH and NAC.	Acetylcysteine	196-199	poly(ADP-ribose) polymerase 1	Homo sapiens	88-115
12850239-8	2003	Moreover, lectin-II-induced activation of caspase-9 and 3-like protease and cleavage of poly(ADP-ribose) polymerase (PARP) were inhibited by pretreatment of cells with thiol antioxidants, GSH and NAC.	Acetylcysteine	196-199	poly(ADP-ribose) polymerase 1	Homo sapiens	117-121
12690112-5	2003	By contrast, bilirubin (1 microm) and the antioxidant N-acetyl-cysteine (1 mm) significantly reduced mitogen-induced cell proliferation, ROS production, and ERK1/2 phosphorylation.	Acetylcysteine	54-71	mitogen-activated protein kinase 3	Homo sapiens	157-163
12860476-10	2003	Fraxetin (100 microM) and N-acetylcysteine (100 microM) not only reduced rotenone-induced reactive oxygen species formation, but also attenuated caspase-3 activity and poly(ADP-ribose) polymerase cleavage at 16 h against rotenone-induced apoptosis.	Acetylcysteine	26-42	poly(ADP-ribose) polymerase 1	Homo sapiens	168-195
12934647-5	2003	The antioxidant, N-acetyl-cysteine, also reduced the glutathione or catalase- attenuated COX-2 expressions in IL-1beta and TNF-alpha-treated cells.	Acetylcysteine	17-34	interleukin 1 beta	Rattus norvegicus	110-118
12934647-5	2003	The antioxidant, N-acetyl-cysteine, also reduced the glutathione or catalase- attenuated COX-2 expressions in IL-1beta and TNF-alpha-treated cells.	Acetylcysteine	17-34	tumor necrosis factor	Rattus norvegicus	123-132
12832326-8	2003	N-acetylcysteine (NAC) prevented the IL-6 secretion in acetoacetate-treated U937 monocytes.	Acetylcysteine	0-16	interleukin 6	Homo sapiens	37-41
12807727-8	2003	Pre-treatment with N-acetyl-cysteine, markedly prevented dephosphorylation of Akt, and cytochrome c release, and cell death, suggesting a role for reactive oxygen species in this process.	Acetylcysteine	19-36	AKT serine/threonine kinase 1	Homo sapiens	78-81
12807727-8	2003	Pre-treatment with N-acetyl-cysteine, markedly prevented dephosphorylation of Akt, and cytochrome c release, and cell death, suggesting a role for reactive oxygen species in this process.	Acetylcysteine	19-36	cytochrome c, somatic	Homo sapiens	87-99
12810527-8	2003	N-acetylcysteine supplementation has been shown to reverse the metabolic abnormalities of the GGT-/- mice and in particular to restore the level of IGF-1 and sex steroids in these mice.	Acetylcysteine	0-16	gamma-glutamyltransferase 1	Mus musculus	94-100
12810527-9	2003	Consistent with these previous observations, N-acetylcysteine treatment of GGT-/- mice ameliorates their skeletal abnormalities by normalizing chondrocytes proliferation and osteoblastic function.	Acetylcysteine	45-61	gamma-glutamyltransferase 1	Mus musculus	75-81
12810527-10	2003	In contrast, resorbtion parameters are only partially normalized in GGT-/- N-acetylcysteine-treated mice, suggesting that GGT regulates osteoclast biology at least partly independently of these hormones.	Acetylcysteine	75-91	gamma-glutamyltransferase 1	Mus musculus	68-74
12810527-10	2003	In contrast, resorbtion parameters are only partially normalized in GGT-/- N-acetylcysteine-treated mice, suggesting that GGT regulates osteoclast biology at least partly independently of these hormones.	Acetylcysteine	75-91	gamma-glutamyltransferase 1	Mus musculus	68-71
12832326-8	2003	N-acetylcysteine (NAC) prevented the IL-6 secretion in acetoacetate-treated U937 monocytes.	Acetylcysteine	18-21	interleukin 6	Homo sapiens	37-41
12832326-9	2003	CONCLUSIONS: This study demonstrates that hyperketonemia increases IL-6 levels in the blood of type 1 diabetic patients and that NAC can inhibit IL-6 secretion by U937 monocytic cells cultured in a ketotic medium.	Acetylcysteine	129-132	interleukin 6	Homo sapiens	145-149
12818576-5	2003	N-acetylcysteine (NAC, 10 mM) and probucol (50 microM), and to a lesser extent, vitamin C (500 microM) and reduced glutathione (1 mM), inhibited AngII-induced [(3)H]-leucine uptake and atrial natriuretic factor (ANF) promoter activity.	Acetylcysteine	0-16	angiotensinogen	Rattus norvegicus	145-150
12882449-2	2003	Therefore the current study investigated whether N-acetylcysteine (NAC), an antioxidative agent, inhibits the interleukin (IL)-1beta-induced expression and production of eotaxin and monocyte chemotactic protein (MCP)-1 in human airway smooth muscle cells (HASMC).	Acetylcysteine	49-65	interleukin 1 beta	Homo sapiens	110-132
12882449-2	2003	Therefore the current study investigated whether N-acetylcysteine (NAC), an antioxidative agent, inhibits the interleukin (IL)-1beta-induced expression and production of eotaxin and monocyte chemotactic protein (MCP)-1 in human airway smooth muscle cells (HASMC).	Acetylcysteine	49-65	C-C motif chemokine ligand 11	Homo sapiens	170-177
12882449-2	2003	Therefore the current study investigated whether N-acetylcysteine (NAC), an antioxidative agent, inhibits the interleukin (IL)-1beta-induced expression and production of eotaxin and monocyte chemotactic protein (MCP)-1 in human airway smooth muscle cells (HASMC).	Acetylcysteine	67-70	interleukin 1 beta	Homo sapiens	110-132
12882449-2	2003	Therefore the current study investigated whether N-acetylcysteine (NAC), an antioxidative agent, inhibits the interleukin (IL)-1beta-induced expression and production of eotaxin and monocyte chemotactic protein (MCP)-1 in human airway smooth muscle cells (HASMC).	Acetylcysteine	67-70	C-C motif chemokine ligand 11	Homo sapiens	170-177
12882449-3	2003	NAC (10 mM) decreased the expression of eotaxin and MCP-1, by 46 +/- 11% (n=7) and 87 +/- 4% (n=6), respectively; the eotaxin release was inhibited by 75 +/- 5% (n=7), whereas the MCP-1 release was decreased by 69 +/- 41% (n=10).	Acetylcysteine	0-3	C-C motif chemokine ligand 11	Homo sapiens	40-47
12882449-3	2003	NAC (10 mM) decreased the expression of eotaxin and MCP-1, by 46 +/- 11% (n=7) and 87 +/- 4% (n=6), respectively; the eotaxin release was inhibited by 75 +/- 5% (n=7), whereas the MCP-1 release was decreased by 69 +/- 41% (n=10).	Acetylcysteine	0-3	C-C motif chemokine ligand 11	Homo sapiens	118-125
12882449-4	2003	NAC (1 mM) also decreased the IL-1beta-induced activation of p38 MAPK.	Acetylcysteine	0-3	interleukin 1 beta	Homo sapiens	30-38
12882449-5	2003	Compared with unstimulated cells, a four-fold increase in 8-isoprostane production in IL-1beta-stimulated HASMC was observed, which could be inhibited by NAC in a concentration-dependent way, with a maximum inhibition of 39 +/- 12%, with 1 mM NAC.	Acetylcysteine	154-157	interleukin 1 beta	Homo sapiens	86-94
12882449-5	2003	Compared with unstimulated cells, a four-fold increase in 8-isoprostane production in IL-1beta-stimulated HASMC was observed, which could be inhibited by NAC in a concentration-dependent way, with a maximum inhibition of 39 +/- 12%, with 1 mM NAC.	Acetylcysteine	243-246	interleukin 1 beta	Homo sapiens	86-94
12882449-6	2003	The present study demonstrated that N-acetylcysteine inhibits the interleukin-1beta-induced eotaxin and monocyte chemotactic protein 1 expression and production due to a decreased activation of p38 mitogen-activated protein kinase.	Acetylcysteine	36-52	interleukin 1 beta	Homo sapiens	66-83
12882449-6	2003	The present study demonstrated that N-acetylcysteine inhibits the interleukin-1beta-induced eotaxin and monocyte chemotactic protein 1 expression and production due to a decreased activation of p38 mitogen-activated protein kinase.	Acetylcysteine	36-52	C-C motif chemokine ligand 11	Homo sapiens	92-99
12882449-7	2003	This study has also shown that N-acetylcysteine decreases the interleukin-1beta-induced production of reactive oxygen species, as suggested by a reduction in the 8-isoprostane production.	Acetylcysteine	31-47	interleukin 1 beta	Homo sapiens	62-79
12818576-5	2003	N-acetylcysteine (NAC, 10 mM) and probucol (50 microM), and to a lesser extent, vitamin C (500 microM) and reduced glutathione (1 mM), inhibited AngII-induced [(3)H]-leucine uptake and atrial natriuretic factor (ANF) promoter activity.	Acetylcysteine	18-21	angiotensinogen	Rattus norvegicus	145-150
12818576-8	2003	Furthermore, NAC blocked AngII-induced increase in myocardial oxidative stress, decreased the expression of ANF and myosin light chain-2v, and inhibited the re-organization of cytoskeletal proteins, desmin and alpha-actinin.	Acetylcysteine	13-16	angiotensinogen	Rattus norvegicus	25-30
12818576-10	2003	Indeed, co-administration of losartan (10 mg/kg/d, 14 d) or NAC (200 mg/kg/d, 14 d) inhibited AngII-induced O(2)(-).	Acetylcysteine	60-63	angiotensinogen	Rattus norvegicus	94-99
12794160-5	2003	This effect was mediated via specific LTB(4) receptors and was inhibited by pretreating the cells with N-acetylcysteine (NAC), an oxygen free radical scavenger, with diphenylene iodonium (DPI), an inhibitor of NADPH oxidase-like flavoproteins, or with PD98059, an extracellular signal-regulated kinase (ERK) inhibitor.	Acetylcysteine	103-119	mitogen-activated protein kinase 1	Homo sapiens	264-301
12929751-3	2003	The antioxidants N-acetyl cysteine, NAC, epigallocathin gallate, EGCG, butylated hydroxyanisole (BHA) and vitamin C could reduce UVB-induced TNF-alpha mRNA levels to various degrees; vitamin E (alpha-tocopherol) had no effect.	Acetylcysteine	17-34	tumor necrosis factor	Homo sapiens	141-150
12794160-5	2003	This effect was mediated via specific LTB(4) receptors and was inhibited by pretreating the cells with N-acetylcysteine (NAC), an oxygen free radical scavenger, with diphenylene iodonium (DPI), an inhibitor of NADPH oxidase-like flavoproteins, or with PD98059, an extracellular signal-regulated kinase (ERK) inhibitor.	Acetylcysteine	103-119	mitogen-activated protein kinase 1	Homo sapiens	303-306
12794160-5	2003	This effect was mediated via specific LTB(4) receptors and was inhibited by pretreating the cells with N-acetylcysteine (NAC), an oxygen free radical scavenger, with diphenylene iodonium (DPI), an inhibitor of NADPH oxidase-like flavoproteins, or with PD98059, an extracellular signal-regulated kinase (ERK) inhibitor.	Acetylcysteine	121-124	mitogen-activated protein kinase 1	Homo sapiens	264-301
12794160-5	2003	This effect was mediated via specific LTB(4) receptors and was inhibited by pretreating the cells with N-acetylcysteine (NAC), an oxygen free radical scavenger, with diphenylene iodonium (DPI), an inhibitor of NADPH oxidase-like flavoproteins, or with PD98059, an extracellular signal-regulated kinase (ERK) inhibitor.	Acetylcysteine	121-124	mitogen-activated protein kinase 1	Homo sapiens	303-306
12794160-6	2003	Consistent with those findings, LTB(4)-induced ERK phosphorylation was completely blocked by pretreating cells with NAC or DPI.	Acetylcysteine	116-119	mitogen-activated protein kinase 1	Homo sapiens	47-50
12870650-7	2003	Antioxidants, such as superoxide dismutase (SOD), N-acetylcysteine (NAC) and pyrrolidine dithiocarbamate (PDTC), blocked silica-induced PI3-kinase activation, suggesting that reactive oxygen species may be important regulatory molecules in NF-kappaB activation by mediating PI3-kinase activation.	Acetylcysteine	68-71	serine (or cysteine) peptidase inhibitor, clade A, member 1C	Mus musculus	136-139
12802283-7	2003	Moreover, cytochrome c release, caspase-3 activation and cell death can be completely abrogated by a previous incubation with the antioxidant N-acetyl-cysteine.	Acetylcysteine	142-159	cytochrome c, somatic	Homo sapiens	10-22
12802283-7	2003	Moreover, cytochrome c release, caspase-3 activation and cell death can be completely abrogated by a previous incubation with the antioxidant N-acetyl-cysteine.	Acetylcysteine	142-159	caspase 3	Homo sapiens	32-41
12576300-8	2003	Finally, antioxidant agents (N-acetyl cysteine and pyrrolidine dithiocarbamate), which inhibited NF-kappaB activation but failed to affect STAT6 activation, almost completely attenuated DEP-induced eotaxin production, whereas these agents failed to attenuate IL-13-induced eotaxin production.	Acetylcysteine	29-46	C-C motif chemokine ligand 11	Homo sapiens	198-205
12857601-8	2003	The release of IL-8 from SAA-stimulated neutrophils is strongly suppressed by the addition of N-acetyl-l-cysteine, alpha-mercaptoethanol, glutathione, and dexamethasone.	Acetylcysteine	94-113	C-X-C motif chemokine ligand 8	Homo sapiens	15-19
12754095-0	2003	N-Acetylcysteine enhances UV-mediated caspase-3 activation, fragmentation of E2F-4, and apoptosis in human C8161 melanoma: inhibition by ectopic Bcl-2 expression.	Acetylcysteine	0-16	caspase 3	Homo sapiens	38-47
12754095-0	2003	N-Acetylcysteine enhances UV-mediated caspase-3 activation, fragmentation of E2F-4, and apoptosis in human C8161 melanoma: inhibition by ectopic Bcl-2 expression.	Acetylcysteine	0-16	BCL2 apoptosis regulator	Homo sapiens	145-150
12754095-5	2003	Compared to treatment with UV radiation alone, combination treatment with NAC doubled the ratio of activated caspase-3 to pro-caspase-3 and produced greater fragmentation of the retinoblastoma protein and the E2F-4 transcription factor without affecting the E2F-1 protein.	Acetylcysteine	74-77	caspase 3	Homo sapiens	109-118
12754095-5	2003	Compared to treatment with UV radiation alone, combination treatment with NAC doubled the ratio of activated caspase-3 to pro-caspase-3 and produced greater fragmentation of the retinoblastoma protein and the E2F-4 transcription factor without affecting the E2F-1 protein.	Acetylcysteine	74-77	caspase 3	Homo sapiens	122-135
12754095-6	2003	These effects of joint NAC-UV radiation treatment were counteracted by the overexpression of the bcl-2 gene.	Acetylcysteine	23-26	BCL2 apoptosis regulator	Homo sapiens	97-102
12754095-7	2003	To our knowledge, this report is the first to: (i) demonstrate a synergy between DNA-damaging agents, like UV radiation, and antioxidants, like NAC, and (ii) show that a Bcl-2-inhibitable E2F-4 fragmentation occurs concurrently with caspase-3 activation and apoptosis.	Acetylcysteine	144-147	BCL2 apoptosis regulator	Homo sapiens	170-175
12684028-5	2003	Antioxidants such as alpha-tocopherol and N-acetylcysteine prevent completely either neuronal apoptosis or activation of JNKs and p38(MAPK) elicited by Abeta or by simultaneous HNE and H(2)O(2) addition.	Acetylcysteine	42-58	mitogen-activated protein kinase 14	Homo sapiens	130-139
12691831-10	2003	NAC treatment also blocked the ischemia/reperfusion-induced expression of tumor necrosis factor and inducible nitric oxide synthase.	Acetylcysteine	0-3	nitric oxide synthase 2	Rattus norvegicus	100-131
12682719-0	2003	Prophylactic N-acetylcysteine decreases serum CRP but not PCT levels and microalbuminuria following major abdominal surgery.	Acetylcysteine	13-29	C-reactive protein	Homo sapiens	46-49
12682719-12	2003	Significantly lower CRP levels were found in the NAC group on days 1 and 2 (t(24): median: 84.5 interquartile range: [62-120] vs. 118 [86-137] mg/l; p=0.020; t(48): 136 [103-232] vs. 195 [154-252] mg/l; p=0.013, NAC vs. placebo respectively).	Acetylcysteine	49-52	C-reactive protein	Homo sapiens	20-23
12682719-12	2003	Significantly lower CRP levels were found in the NAC group on days 1 and 2 (t(24): median: 84.5 interquartile range: [62-120] vs. 118 [86-137] mg/l; p=0.020; t(48): 136 [103-232] vs. 195 [154-252] mg/l; p=0.013, NAC vs. placebo respectively).	Acetylcysteine	212-215	C-reactive protein	Homo sapiens	20-23
12682719-13	2003	CONCLUSION: In this study, short-term NAC treatment decreased CRP levels, but failed to attenuate any other inflammatory response, as monitored by serum PCT and microalbuminuria.	Acetylcysteine	38-41	C-reactive protein	Homo sapiens	62-65
12711260-8	2003	An anti-oxidant, N-acetylcysteine, or PEDF completely prevented the leptin-induced upregulation of vascular endothelial growth factor (VEGF) mRNA levels as well as any increase in DNA synthesis in microvascular EC.	Acetylcysteine	17-33	vascular endothelial growth factor A	Homo sapiens	99-133
12711260-8	2003	An anti-oxidant, N-acetylcysteine, or PEDF completely prevented the leptin-induced upregulation of vascular endothelial growth factor (VEGF) mRNA levels as well as any increase in DNA synthesis in microvascular EC.	Acetylcysteine	17-33	vascular endothelial growth factor A	Homo sapiens	135-139
12754411-6	2003	Addition of n-acetyl cysteine (NAC) or diphenyleneiodonium (DPI) effectively protected cells from apoptosis and significantly lowered As(2)O(3)-induced activation of caspase-3.	Acetylcysteine	12-29	caspase 3	Homo sapiens	166-175
12754411-6	2003	Addition of n-acetyl cysteine (NAC) or diphenyleneiodonium (DPI) effectively protected cells from apoptosis and significantly lowered As(2)O(3)-induced activation of caspase-3.	Acetylcysteine	31-34	caspase 3	Homo sapiens	166-175
12704789-4	2003	We have shown that apoptosis induced by TGFbeta1 is accompanied by ROS generation and the ROS-trapping agent N-acetylcysteine (NAC) inhibits TGFbeta1-induced apoptosis.	Acetylcysteine	109-125	transforming growth factor, beta 1	Rattus norvegicus	141-149
12704789-4	2003	We have shown that apoptosis induced by TGFbeta1 is accompanied by ROS generation and the ROS-trapping agent N-acetylcysteine (NAC) inhibits TGFbeta1-induced apoptosis.	Acetylcysteine	127-130	transforming growth factor, beta 1	Rattus norvegicus	141-149
12684028-5	2003	Antioxidants such as alpha-tocopherol and N-acetylcysteine prevent completely either neuronal apoptosis or activation of JNKs and p38(MAPK) elicited by Abeta or by simultaneous HNE and H(2)O(2) addition.	Acetylcysteine	42-58	amyloid beta precursor protein	Homo sapiens	152-157
12679464-9	2003	Treatment of fetal membranes with NAC significantly suppressed lipopolysaccharide-stimulated type II phospholipase A(2) release and content; PGF(2alpha), IL-6, IL-8, TNFalpha, and 8-isoprostane release; and matrix metalloproteinase-9 and urokinase-type plasminogen activator enzyme activity and suppressed NF-kappaB DNA-binding activity (by ANOVA, P &lt; 0.05).	Acetylcysteine	34-37	interleukin 6	Homo sapiens	154-158
12679464-9	2003	Treatment of fetal membranes with NAC significantly suppressed lipopolysaccharide-stimulated type II phospholipase A(2) release and content; PGF(2alpha), IL-6, IL-8, TNFalpha, and 8-isoprostane release; and matrix metalloproteinase-9 and urokinase-type plasminogen activator enzyme activity and suppressed NF-kappaB DNA-binding activity (by ANOVA, P &lt; 0.05).	Acetylcysteine	34-37	C-X-C motif chemokine ligand 8	Homo sapiens	160-164
12679464-9	2003	Treatment of fetal membranes with NAC significantly suppressed lipopolysaccharide-stimulated type II phospholipase A(2) release and content; PGF(2alpha), IL-6, IL-8, TNFalpha, and 8-isoprostane release; and matrix metalloproteinase-9 and urokinase-type plasminogen activator enzyme activity and suppressed NF-kappaB DNA-binding activity (by ANOVA, P &lt; 0.05).	Acetylcysteine	34-37	tumor necrosis factor	Homo sapiens	166-174
12679464-9	2003	Treatment of fetal membranes with NAC significantly suppressed lipopolysaccharide-stimulated type II phospholipase A(2) release and content; PGF(2alpha), IL-6, IL-8, TNFalpha, and 8-isoprostane release; and matrix metalloproteinase-9 and urokinase-type plasminogen activator enzyme activity and suppressed NF-kappaB DNA-binding activity (by ANOVA, P &lt; 0.05).	Acetylcysteine	34-37	plasminogen activator, urokinase	Homo sapiens	238-274
12688549-8	2003	The MPO activity and MDA levels in lung homogenates were found to be increased in CLP group and the administration of NAC prevented their increase significantly (P &lt; 0.05).	Acetylcysteine	118-121	myeloperoxidase	Homo sapiens	4-7
12688549-10	2003	The number of apoptotic cells was significantly lower in CLP+NAC group than CLP group, and this finding was supported by M30 and caspase 3 expression in lung (P &lt; 0.05).	Acetylcysteine	61-64	caspase 3	Homo sapiens	129-138
12688549-12	2003	In conclusion, the chronic use of NAC inhibited MPO activity and lipid peroxidation, which resulted in reduction of apoptosis in lung in this CLP model.	Acetylcysteine	34-37	myeloperoxidase	Homo sapiens	48-51
12594272-5	2003	We also show that loss of mitochondrial membrane potential, cytochrome c release, as well as caspase-3 activation induced by DEX are attenuated by NAC treatment.	Acetylcysteine	147-150	cytochrome c, somatic	Homo sapiens	60-72
12824000-8	2003	The NAC and the intracellularly delivered SOD1 were found to suppress the IL-4+/-crude gliadin or Glilys-induced IgE production by normal human PBMC.	Acetylcysteine	4-7	interleukin 4	Homo sapiens	74-78
12649745-5	2003	The L-PAM-induced accumulation of B7-1 mRNA was prevented with the antioxidant N-acetyl- L-cysteine (NAC), indicating that reactive oxygen species are important for the transcriptional regulation.	Acetylcysteine	79-99	CD80 antigen	Mus musculus	34-38
12649745-5	2003	The L-PAM-induced accumulation of B7-1 mRNA was prevented with the antioxidant N-acetyl- L-cysteine (NAC), indicating that reactive oxygen species are important for the transcriptional regulation.	Acetylcysteine	101-104	CD80 antigen	Mus musculus	34-38
12631578-5	2003	Furthermore, N-acetyl cysteine, a free radical inhibitor, blocked the mechanical stretch-induced NF-kappaB activation, suggesting the involvement of free radicals.	Acetylcysteine	13-30	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	97-106
12609744-6	2003	Shear stress at 15 dyn/cm(2) for 30 min induced a significant increase in the intracellular peroxide concentration, and the down-regulation of ECE-1 and ET-1 mRNA expression by shear stress was attenuated almost completely on treatment with N-acetyl cysteine (NAC), an antioxidant (20 mM).	Acetylcysteine	241-258	endothelin 1	Homo sapiens	153-157
12609744-6	2003	Shear stress at 15 dyn/cm(2) for 30 min induced a significant increase in the intracellular peroxide concentration, and the down-regulation of ECE-1 and ET-1 mRNA expression by shear stress was attenuated almost completely on treatment with N-acetyl cysteine (NAC), an antioxidant (20 mM).	Acetylcysteine	260-263	endothelin 1	Homo sapiens	153-157
12628482-5	2003	Inhibition of NO production and/or NOS expression by incubating macrophages with different drugs inhibiting NOS activity or modulating the redox state of the cell, such as N-acetylcysteine (NAC) resulted in inhibition of HO-1 expression, suggesting that NO is an endogenous mediator of this stress response.	Acetylcysteine	172-188	heme oxygenase 1	Mus musculus	221-225
12628482-5	2003	Inhibition of NO production and/or NOS expression by incubating macrophages with different drugs inhibiting NOS activity or modulating the redox state of the cell, such as N-acetylcysteine (NAC) resulted in inhibition of HO-1 expression, suggesting that NO is an endogenous mediator of this stress response.	Acetylcysteine	190-193	heme oxygenase 1	Mus musculus	221-225
12514114-6	2003	This postulation is supported by the following findings: Ferrocene generates H2O2 by autooxidation; N-acetylcysteine, a free-radical scavenger, reduces its antitumor effect; and it stimulates GTPase activity catalyzed by pure recombinant p21ras and activates ERK 1/2 in wild Jurkat T cells but fails to do so in the Jurkat T cells expressing p21ras in which cysteine 118 was replaced by serine.	Acetylcysteine	100-116	mitogen-activated protein kinase 3	Homo sapiens	259-266
12581860-5	2003	Although NF-kappaB is known to be a redox-sensitive transcription factor, the antioxidant agents N-acetyl-cysteine (NAC) and 6-hydroxy-2,5,7,8-tetramethyl-chroman-2-carboxylic acid (trolox) showed no suppression and treatment with H(2)O(2) showed only slight enhancement of IFN-gamma-induced NO production.	Acetylcysteine	116-119	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	9-18
12600912-6	2003	Patients were randomly assigned either to receive acetylcysteine (600 mg BID) or placebo.	Acetylcysteine	50-64	BH3 interacting domain death agonist	Homo sapiens	73-76
12600912-11	2003	CONCLUSIONS: In hemodialysis patients, treatment with acetylcysteine (600 mg BID) reduces composite cardiovascular end points.	Acetylcysteine	54-68	BH3 interacting domain death agonist	Homo sapiens	77-80
12406911-4	2003	However, only partial inhibition of Raf-1 and ERK1 stimulation was observed with the antioxidant N-acetylcysteine (N-Ac).	Acetylcysteine	97-113	mitogen-activated protein kinase 3	Homo sapiens	46-50
12406911-4	2003	However, only partial inhibition of Raf-1 and ERK1 stimulation was observed with the antioxidant N-acetylcysteine (N-Ac).	Acetylcysteine	115-119	mitogen-activated protein kinase 3	Homo sapiens	46-50
12604218-7	2003	Pretreatment of SMC with N-acetyl-L-cysteine significantly suppressed the MG-induced AR expression, while DL-buthionine-(S,R)-sulfoximine further augmented the MG-induced increase in AR mRNA level.	Acetylcysteine	25-44	aldo-keto reductase family 1 member B	Homo sapiens	85-87
12521669-8	2003	In addition, in all groups pretreated with NAC, hepatic GSH concentration was significantly increased, as were hepatic and blood glutathione peroxidase (GPx) and catalase (CAT) activities.	Acetylcysteine	43-46	catalase	Mus musculus	162-170
12521669-8	2003	In addition, in all groups pretreated with NAC, hepatic GSH concentration was significantly increased, as were hepatic and blood glutathione peroxidase (GPx) and catalase (CAT) activities.	Acetylcysteine	43-46	catalase	Mus musculus	172-175
12566471-7	2003	In all cell lines studied, alpha-tocopherol and N-acetylcysteine inhibited the effects of beta-carotene on NF-kappaB, cell growth and apoptosis, and normalized the increased expression of c-myc induced by the carotenoid.	Acetylcysteine	48-64	nuclear factor kappa B subunit 1	Homo sapiens	107-116
12682423-5	2003	Limited knowledge showing benefits of preconditioning with anti- oxidants (vitamin C, E, a-lipoic acid, N-acetylcysteine) in order to protect insulin action under oxidative stress prompted the author to discuss the theoretical background to this approach.	Acetylcysteine	104-120	insulin	Homo sapiens	142-149
12601528-8	2003	N-acetylcysteine had no significant effect on growth hormone and IGF-1 levels but caused a significant decrease in plasma TNF-alpha.	Acetylcysteine	0-16	tumor necrosis factor	Homo sapiens	122-131
12206715-7	2002	The JNK/p38 activation by EGCG was also potently inhibited by NAC, whereas those by VP16 and TNF were either not or only minimally affected by NAC.	Acetylcysteine	62-65	mitogen-activated protein kinase 14	Homo sapiens	8-11
12631112-13	2003	These AGE-induced inhibition of protein synthesis and PGE2 secretion as well as the up-regulation of TGF-beta mRNA were found to be completely prevented by N-acetylcysteine.	Acetylcysteine	156-172	transforming growth factor beta 1	Homo sapiens	101-109
12524169-4	2003	Concomitantly, the late activation of apoptosis signal-regulating kinase 1 (ASK1) and c-Jun N-terminal protein kinase (JNK) was also prevented by Naspm or NAC.	Acetylcysteine	155-158	mitogen-activated protein kinase kinase kinase 5	Rattus norvegicus	38-74
12524169-4	2003	Concomitantly, the late activation of apoptosis signal-regulating kinase 1 (ASK1) and c-Jun N-terminal protein kinase (JNK) was also prevented by Naspm or NAC.	Acetylcysteine	155-158	mitogen-activated protein kinase kinase kinase 5	Rattus norvegicus	76-80
12476359-10	2003	A role for free radicals and reactive oxygen species (ROS) in mediating ultrafine inflammation is further strengthened by the ability of the antioxidants N-acetylcysteine (NAC) and glutathione monoethyl ester (GSHme) to block the particle induced release of tumour necrosis factor-alpha (TNF-alpha) from alveolar macrophages in vitro.	Acetylcysteine	154-170	tumor necrosis factor	Rattus norvegicus	288-297
12538039-7	2003	The decrease in chemotaxis and the increase in adherence, ingestion, superoxide anion production, and TNFalpha release shown by macrophages from animals with oxidative stress were counteracted by NAC injection.	Acetylcysteine	196-199	tumor necrosis factor	Mus musculus	102-110
12538039-8	2003	These data suggest that NAC administration may be useful for the treatment of oxidative stress-linked endotoxic shock, modulating the function of macrophages, specifically in decreasing the production of ROS and of inflammatory cytokines such as TNFalpha.	Acetylcysteine	24-27	tumor necrosis factor	Mus musculus	246-254
12631128-7	2003	NAC also reduced renal vascular resistance by 16% when given during angiotensin II infusion (P &lt; 0.05).	Acetylcysteine	0-3	angiotensinogen	Rattus norvegicus	68-82
12560087-12	2003	NO-stabilized HIF-1 alpha was susceptible to the addition of N-acetyl-cysteine that destabilized HIF-1 alpha in close correlation to the disappearance of S-nitrosated HIF-1 alpha.	Acetylcysteine	61-78	hypoxia inducible factor 1 subunit alpha	Homo sapiens	14-25
12560087-12	2003	NO-stabilized HIF-1 alpha was susceptible to the addition of N-acetyl-cysteine that destabilized HIF-1 alpha in close correlation to the disappearance of S-nitrosated HIF-1 alpha.	Acetylcysteine	61-78	hypoxia inducible factor 1 subunit alpha	Homo sapiens	97-108
12560087-12	2003	NO-stabilized HIF-1 alpha was susceptible to the addition of N-acetyl-cysteine that destabilized HIF-1 alpha in close correlation to the disappearance of S-nitrosated HIF-1 alpha.	Acetylcysteine	61-78	hypoxia inducible factor 1 subunit alpha	Homo sapiens	97-108
12504894-9	2003	Cotreatment of cells with antioxidant reagent N-acetylcysteine (NAC) inhibited MGO-BSA-induced TNFalpha secretion.	Acetylcysteine	46-62	tumor necrosis factor	Mus musculus	95-103
12504894-9	2003	Cotreatment of cells with antioxidant reagent N-acetylcysteine (NAC) inhibited MGO-BSA-induced TNFalpha secretion.	Acetylcysteine	64-67	tumor necrosis factor	Mus musculus	95-103
12504894-14	2003	The MGO-BSA-induced NFkappaB activation was prevented in the presence of PD98059, NAC, and parthenolide, a selective inhibitor of NFkappaB.	Acetylcysteine	82-85	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	20-28
12504894-14	2003	The MGO-BSA-induced NFkappaB activation was prevented in the presence of PD98059, NAC, and parthenolide, a selective inhibitor of NFkappaB.	Acetylcysteine	82-85	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	130-138
12414812-5	2003	N-Acetylcysteine and ebselen (but not other antioxidants such as diphenyleneiodonium, Tiron, catalase, ascorbic acid, and vitamin E) reduced EGFR activation by Aplidin.	Acetylcysteine	0-16	epidermal growth factor receptor	Homo sapiens	141-145
12414812-6	2003	N-Acetylcysteine and PP2 also partially inhibited JNK and p38 MAPK activation.	Acetylcysteine	0-16	mitogen-activated protein kinase 8	Homo sapiens	50-53
12414812-6	2003	N-Acetylcysteine and PP2 also partially inhibited JNK and p38 MAPK activation.	Acetylcysteine	0-16	mitogen-activated protein kinase 14	Homo sapiens	58-61
12388243-3	2003	Antioxidants, such as pyrrolidine dithiocarbamate (PDTC) and N-acetylcysteine (NAC), significantly inhibited IL-4-induced MCP-1 mRNA expression.	Acetylcysteine	61-77	interleukin 4	Homo sapiens	109-113
12388243-3	2003	Antioxidants, such as pyrrolidine dithiocarbamate (PDTC) and N-acetylcysteine (NAC), significantly inhibited IL-4-induced MCP-1 mRNA expression.	Acetylcysteine	79-82	interleukin 4	Homo sapiens	109-113
15018304-5	2003	TNF-alpha inhibited EC proliferation, which was significantly blocked by nifedipine or antioxidant N-acetylcysteine (NAC).	Acetylcysteine	99-115	tumor necrosis factor	Homo sapiens	0-9
15018304-5	2003	TNF-alpha inhibited EC proliferation, which was significantly blocked by nifedipine or antioxidant N-acetylcysteine (NAC).	Acetylcysteine	117-120	tumor necrosis factor	Homo sapiens	0-9
15018304-6	2003	Nifedipine or NAC was also found to significantly inhibit apoptotic cell death of TNF-alpha-exposed HUVECs.	Acetylcysteine	14-17	tumor necrosis factor	Homo sapiens	82-91
14521055-5	2003	Besides, H2O2-induced activation of EGF receptor, and STAT factors was fully prevented by NAC pretreatment.	Acetylcysteine	90-93	epidermal growth factor receptor	Homo sapiens	36-48
12206715-7	2002	The JNK/p38 activation by EGCG was also potently inhibited by NAC, whereas those by VP16 and TNF were either not or only minimally affected by NAC.	Acetylcysteine	62-65	mitogen-activated protein kinase 8	Homo sapiens	4-7
12206715-11	2002	Taken together these results strongly suggest that EGCG executed apoptotic cell death via an ASK1, MKK and JNK/p38 cascade which is triggered by NAC-sensitive intracellular oxidative events in a manner distinct from chemically induced or receptor-mediated apoptosis.	Acetylcysteine	145-148	mitogen-activated protein kinase 8	Homo sapiens	107-110
12206715-11	2002	Taken together these results strongly suggest that EGCG executed apoptotic cell death via an ASK1, MKK and JNK/p38 cascade which is triggered by NAC-sensitive intracellular oxidative events in a manner distinct from chemically induced or receptor-mediated apoptosis.	Acetylcysteine	145-148	mitogen-activated protein kinase 14	Homo sapiens	111-114
12616822-8	2002	Significantly lower CRP levels were found in the NAC group on day one and two [t24: median: 84.5 interquartile range: (62.48-120.25) vs. 118 (86-137) mg/l; p = 0.020; t48: 136 (103-232) vs. 195 (154.5-252) mg/l p = 0.013, NAC vs. placebo].	Acetylcysteine	49-52	C-reactive protein	Homo sapiens	20-23
12699247-5	2002	In addition, we show that the redox-sensitive transcription factor Nrf2 is highly expressed in the nuclear fraction of cells exposed to the NO- generator and that this effect is totally abolished by the presence of N-acetyl-L-cysteine.	Acetylcysteine	215-234	NFE2 like bZIP transcription factor 2	Homo sapiens	67-71
12368297-4	2002	This strain-induced PYK2 and Src phosphorylation was inhibited by pretreating ECs with an antioxidant N-acetylcysteine.	Acetylcysteine	102-118	SRC proto-oncogene, non-receptor tyrosine kinase	Bos taurus	29-32
12444151-7	2002	To determine whether ROS induced by M-CSF played a role in Erk activation, we found that N-acetylcysteine and diphenyleneiodonium both suppressed Erk activation in M-CSF-treated monocytes.	Acetylcysteine	89-105	mitogen-activated protein kinase 1	Homo sapiens	59-62
12444151-7	2002	To determine whether ROS induced by M-CSF played a role in Erk activation, we found that N-acetylcysteine and diphenyleneiodonium both suppressed Erk activation in M-CSF-treated monocytes.	Acetylcysteine	89-105	mitogen-activated protein kinase 1	Homo sapiens	146-149
12616822-8	2002	Significantly lower CRP levels were found in the NAC group on day one and two [t24: median: 84.5 interquartile range: (62.48-120.25) vs. 118 (86-137) mg/l; p = 0.020; t48: 136 (103-232) vs. 195 (154.5-252) mg/l p = 0.013, NAC vs. placebo].	Acetylcysteine	222-225	C-reactive protein	Homo sapiens	20-23
12460740-6	2002	These data suggest that pulmonary oxidative stress-related lipid peroxidation may play an important role in developing airway remodeling through activating lung fibroblasts to further produce extracellular matrices, such as fibronectin, partly via activation of an EGFR-linked Erk1/2 signal transduction pathway, and that the antioxidant NAC and the EGFR tyrosine kinase inhibitor AG-1478 can be potentially useful in pulmonary diseases involving airway remodeling.	Acetylcysteine	338-341	fibronectin 1	Homo sapiens	224-235
12421841-0	2002	Supplementation of N-acetylcysteine normalizes lipopolysaccharide-induced nuclear factor kappaB activation and proinflammatory cytokine production during early rehabilitation of protein malnourished mice.	Acetylcysteine	19-35	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	74-95
12421841-10	2002	However, early supplementation of NAC to protein malnourished mice without replenishing with dietary protein restored GSH levels and reduction potential, and normalized NFkappaB activation and proinflammatory cytokine production.	Acetylcysteine	34-37	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	169-177
12446176-7	2002	NAC preincubation (5 x 10(-5)M, 24h) significantly reduced (-21%) the ONOO(-) production in formyl Met-Leu-Phe (fMLP)-activated cells and slightly reduced it under resting conditions, whereas NAC preincubation was unable to modify the release of O(2)(-) both in basal condition and in fMLP-stimulated cells.	Acetylcysteine	0-3	formyl peptide receptor 1	Homo sapiens	112-116
12446176-7	2002	NAC preincubation (5 x 10(-5)M, 24h) significantly reduced (-21%) the ONOO(-) production in formyl Met-Leu-Phe (fMLP)-activated cells and slightly reduced it under resting conditions, whereas NAC preincubation was unable to modify the release of O(2)(-) both in basal condition and in fMLP-stimulated cells.	Acetylcysteine	0-3	formyl peptide receptor 1	Homo sapiens	285-289
12460740-6	2002	These data suggest that pulmonary oxidative stress-related lipid peroxidation may play an important role in developing airway remodeling through activating lung fibroblasts to further produce extracellular matrices, such as fibronectin, partly via activation of an EGFR-linked Erk1/2 signal transduction pathway, and that the antioxidant NAC and the EGFR tyrosine kinase inhibitor AG-1478 can be potentially useful in pulmonary diseases involving airway remodeling.	Acetylcysteine	338-341	epidermal growth factor receptor	Homo sapiens	265-269
12387954-0	2002	N-acetylcysteine for paracetamol poisoning: effect on prothrombin.	Acetylcysteine	0-16	coagulation factor II, thrombin	Homo sapiens	54-65
12171932-10	2002	The inhibition of PDGF-BB-induced Akt phosphorylation by NEM was completely reversed by PP2A inhibitors fostriecin and okadaic acid, ceramide synthase inhibitor fumonisin B1, and ROS scavenger N-acetylcysteine (NAC).	Acetylcysteine	193-209	AKT serine/threonine kinase 1	Homo sapiens	34-37
12171932-10	2002	The inhibition of PDGF-BB-induced Akt phosphorylation by NEM was completely reversed by PP2A inhibitors fostriecin and okadaic acid, ceramide synthase inhibitor fumonisin B1, and ROS scavenger N-acetylcysteine (NAC).	Acetylcysteine	211-214	AKT serine/threonine kinase 1	Homo sapiens	34-37
12138118-9	2002	N-Acetyl-l-cysteine or GADD153 antisense significantly protected the cells from 4HPR-induced apoptosis, accompanying by the inhibition of GADD153 overexpression.	Acetylcysteine	0-19	DNA damage inducible transcript 3	Homo sapiens	138-145
12387824-7	2002	N-acetylcysteine, an antioxidant, could abrogate the production of pro-MMP-9, H(2)O(2) generation, and activation of NF-kappaB and MMP-9 promoter.	Acetylcysteine	0-16	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	117-126
12386145-5	2002	PDGF and H2O2 time-dependently suppressed VDUP-1 expression (13-fold and 30-fold reduction after 1 hour, respectively; P&lt;0.001), and this was inhibited by the cell-permeable antioxidants N-acetylcysteine and 4,5-dihydroxy-1,3-benzene-disulfonic acid (Tiron).	Acetylcysteine	190-206	thioredoxin interacting protein	Homo sapiens	42-48
12387966-0	2002	Effect of acetylcysteine on prothrombin index in paracetamol poisoning without hepatocellular injury.	Acetylcysteine	10-24	coagulation factor II, thrombin	Homo sapiens	28-39
12387966-1	2002	Acetylcysteine treatment reduces liver damage after paracetamol overdose, but can affect the prothrombin index, which is used to assess the progress of overdose patients.	Acetylcysteine	0-14	coagulation factor II, thrombin	Homo sapiens	93-104
12387966-2	2002	We aimed to assess retrospectively the effect of intravenous acetylcysteine on the prothrombin index in patients with paracetamol poisoning without signs of hepatocellular injury.	Acetylcysteine	61-75	coagulation factor II, thrombin	Homo sapiens	83-94
12387966-4	2002	After initiation of treatment, prothrombin index decreased (mean 0.33, 95% CI 0.29-0.38) in all patients, and was strongly associated with the start of acetylcysteine infusion.	Acetylcysteine	152-166	coagulation factor II, thrombin	Homo sapiens	31-42
12237255-9	2002	4 Antioxidants (pyrrolidine dithiocarbamate and N-acetyl-L-cysteine) inhibited GPI-80 release by TNF-alpha stimulation, but superoxide dismutase did not.	Acetylcysteine	48-67	tumor necrosis factor	Homo sapiens	97-106
12372563-0	2002	Protection of cultured oligodendrocytes against tumor necrosis factor-alpha by the antioxidants coenzyme Q(10) and N-acetyl cysteine.	Acetylcysteine	115-132	tumor necrosis factor	Homo sapiens	48-75
12372563-7	2002	If TNF-alpha treatment causes oxidative damage by compromising oxidative metabolism in oligodendrocytes, increasing products of lipid peroxidation and/or generating radical oxygen species that can interfere with maturation signals, CoQ(10) and NAC may protect oligodendrocytes by reversing one or more of those destructive processes during terminal maturation.	Acetylcysteine	244-247	tumor necrosis factor	Homo sapiens	3-12
12151057-0	2002	Preconditioning with millimolar concentrations of vitamin C or N-acetylcysteine protects L6 muscle cells insulin-stimulated viability and DNA synthesis under oxidative stress.	Acetylcysteine	63-79	insulin	Homo sapiens	105-112
12168106-8	2002	Co-treatment with NAC markedly prevented dephosphorylation of Akt, activation of caspase 3, and down-regulation of cIAP1.	Acetylcysteine	18-21	AKT serine/threonine kinase 1	Homo sapiens	62-65
12168106-8	2002	Co-treatment with NAC markedly prevented dephosphorylation of Akt, activation of caspase 3, and down-regulation of cIAP1.	Acetylcysteine	18-21	caspase 3	Homo sapiens	81-90
12193733-7	2002	DNA binding capacity as well as the transactivating capability of PPARgamma were attenuated by addition of the antioxidant N-acetyl-cysteine or in the presence of the NO scavenger 2-phenyl-4,4,5,6-tetramethyl-imidazoline-1-oxyl 3-oxide.	Acetylcysteine	123-140	peroxisome proliferator activated receptor gamma	Homo sapiens	66-75
12359191-2	2002	The subsequent treatment of lead-exposed animals with DMSA, MiADMS, or NAC reversed the lead-induced alterations in blood delta-aminolevulinic acid dehydratase, catalase, malondialdehyde (MDA), reduced glutathione, oxidized glutathione, and brain MDA levels.	Acetylcysteine	71-74	catalase	Rattus norvegicus	161-169
12165419-4	2002	Both of the increases of ASK1 activation and autophosphorylation were suppressed by N-acetylcysteine, a well-known antioxidant, which was administered to the Sprague-Dawley rat 20 min before cerebral ischemia.	Acetylcysteine	84-100	mitogen-activated protein kinase kinase kinase 5	Rattus norvegicus	25-29
12186804-10	2002	This reactive oxygen species-dependent effect of CD40L stimulation was reversed with vitamin C or N-acetylcysteine.	Acetylcysteine	98-114	CD40 ligand	Homo sapiens	49-54
12208513-3	2002	The stimulating effects on IL-8 promoter and AP-1 were reduced by N-acetylcysteine, glutathione, diphenyleneiodonium, rotenone and antimycin A.	Acetylcysteine	66-82	C-X-C motif chemokine ligand 8	Homo sapiens	27-31
12191879-4	2002	The two subjects showed similar peak levels of MA and PGA, as well as 4-vinylphenol conjugates, whereas mercapturic acids were five times higher in the subject bearing the GSTM1pos than in the GSTM1null subject.	Acetylcysteine	104-121	glutathione S-transferase mu 1	Homo sapiens	172-177
12023963-6	2002	In addition, a fusion between p47(phox) and the TRAF4 C terminus constitutively activated JNK, and this activation was decreased by the antioxidant N-acetyl cysteine.	Acetylcysteine	148-165	mitogen-activated protein kinase 8	Homo sapiens	90-93
12191879-4	2002	The two subjects showed similar peak levels of MA and PGA, as well as 4-vinylphenol conjugates, whereas mercapturic acids were five times higher in the subject bearing the GSTM1pos than in the GSTM1null subject.	Acetylcysteine	104-121	glutathione S-transferase mu 1	Homo sapiens	193-198
12191879-5	2002	Also, relative proportions of diasteroisomers of mercapturic acids were influenced by the GSTM1 polymorphism.	Acetylcysteine	49-66	glutathione S-transferase mu 1	Homo sapiens	90-95
12006557-3	2002	IFN-gamma-induced HLA-DRA expression was inhibited by nitric oxide (NO) and antioxidants such as superoxide dismutase, catalase, pyrrolidine dithiocarbamate, and N-acetylcysteine.	Acetylcysteine	162-178	interferon gamma	Homo sapiens	0-9
12165081-5	2002	In contrast, NAC up-regulated interferon-gamma (IFN-gamma) production.	Acetylcysteine	13-16	interferon gamma	Homo sapiens	30-46
12165081-5	2002	In contrast, NAC up-regulated interferon-gamma (IFN-gamma) production.	Acetylcysteine	13-16	interferon gamma	Homo sapiens	48-57
12163654-5	2002	The reduction of HcyT-induced apoptosis by NAC, Vit C or Vit E occurred simultaneously with a significant decrease in intracellular H(2)O(2) levels and reduced caspase-3 enzymatic activity.	Acetylcysteine	43-46	caspase 3	Homo sapiens	160-169
12055096-9	2002	N-acetylcysteine, but not diphenyleneiodonium, attenuated ERK activation mediated by diazoxide.	Acetylcysteine	0-16	mitogen-activated protein kinase 1	Homo sapiens	58-61
12086962-8	2002	Third, exogenous addition of dibutyryl cAMP, endogenous stimulation of cAMP production by forskolin, and antioxidant N-acetylcysteine (NAC) prevented stimulation of TNF-alpha secretion caused by AA alone or with high glucose.	Acetylcysteine	117-133	tumor necrosis factor	Homo sapiens	165-174
12086962-8	2002	Third, exogenous addition of dibutyryl cAMP, endogenous stimulation of cAMP production by forskolin, and antioxidant N-acetylcysteine (NAC) prevented stimulation of TNF-alpha secretion caused by AA alone or with high glucose.	Acetylcysteine	135-138	tumor necrosis factor	Homo sapiens	165-174
12086962-9	2002	Similarly, NAC prevented the elevation of TNF-alpha secretion and lowering of cAMP levels in H(2)O(2)-treated U937 cells.	Acetylcysteine	11-14	tumor necrosis factor	Homo sapiens	42-51
12082021-11	2002	In addition, the number of inducible nitric oxide synthase (iNOS)-positive inflammatory cells in the non-cancerous mucosa of the distal colon was markedly decreased by NAC.	Acetylcysteine	168-171	nitric oxide synthase 2, inducible	Mus musculus	27-58
12096208-0	2002	P-selectin upregulation in bleomycin induced lung injury in rats: effect of N-acetyl-L-cysteine.	Acetylcysteine	76-95	selectin P	Rattus norvegicus	0-10
11940570-10	2002	In contrast, NAC reduced ERK activity to 60% and decreased p38 activity to the basal level, but JNK activity was induced 2-fold.	Acetylcysteine	13-16	mitogen-activated protein kinase 14	Homo sapiens	59-62
12003789-10	2002	The antioxidant N-acetyl-cysteine abolished the p38 response to hypoxia, presumably by scavenging H(2)O(2), but the mitogen extracellular receptor kinase inhibitor PD-98059 did not inhibit p38 phosphorylation during hypoxia.	Acetylcysteine	16-33	mitogen-activated protein kinase 14	Homo sapiens	48-51
12082021-11	2002	In addition, the number of inducible nitric oxide synthase (iNOS)-positive inflammatory cells in the non-cancerous mucosa of the distal colon was markedly decreased by NAC.	Acetylcysteine	168-171	nitric oxide synthase 2, inducible	Mus musculus	60-64
12008116-4	2002	The surface expression of Ro52 induced by UVB irradiation was concentration-dependently inhibited by N-acetyl-L-cysteine, an antioxidant.	Acetylcysteine	101-120	tripartite motif containing 21	Homo sapiens	26-30
12057717-0	2002	N-acetyl-cysteine treatment improves insulin sensitivity in women with polycystic ovary syndrome.	Acetylcysteine	0-17	insulin	Homo sapiens	37-44
12057717-1	2002	OBJECTIVE: To evaluate the effect of N-acetyl-cysteine (NAC) on insulin secretion and peripheral insulin resistance in subjects with polycystic ovary syndrome (PCOS).	Acetylcysteine	37-54	insulin	Homo sapiens	64-71
12057717-1	2002	OBJECTIVE: To evaluate the effect of N-acetyl-cysteine (NAC) on insulin secretion and peripheral insulin resistance in subjects with polycystic ovary syndrome (PCOS).	Acetylcysteine	56-59	insulin	Homo sapiens	64-71
12057717-10	2002	Insulin AUC after OGTT was significantly reduced, and the peripheral insulin sensitivity increased after NAC administration, whereas the hepatic insulin extraction was unaffected.	Acetylcysteine	105-108	insulin	Homo sapiens	69-76
12057717-13	2002	CONCLUSION(S): NAC may be a new treatment for the improvement of insulin circulating levels and insulin sensitivity in hyperinsulinemic patients with polycystic ovary syndrome.	Acetylcysteine	15-18	insulin	Homo sapiens	65-72
12057717-13	2002	CONCLUSION(S): NAC may be a new treatment for the improvement of insulin circulating levels and insulin sensitivity in hyperinsulinemic patients with polycystic ovary syndrome.	Acetylcysteine	15-18	insulin	Homo sapiens	96-103
11970911-6	2002	In addition, pretreatment of cells with N-acetyl-cysteine blocked tumor necrosis factor (TNF)-alpha-induced IL-6 release, suggesting that endogenously produced ROS participate in IL-6 production.	Acetylcysteine	40-57	tumor necrosis factor	Mus musculus	66-99
11959652-5	2002	EGTA, N-acetyl-cysteine, and superoxide dismutase attenuated the hyperplastic response to substance P.	Acetylcysteine	6-23	tachykinin precursor 1	Homo sapiens	90-101
11970911-6	2002	In addition, pretreatment of cells with N-acetyl-cysteine blocked tumor necrosis factor (TNF)-alpha-induced IL-6 release, suggesting that endogenously produced ROS participate in IL-6 production.	Acetylcysteine	40-57	interleukin 6	Mus musculus	108-112
12076959-13	2002	Pretreatment of C6 cells with N-acetyl-l-cysteine (NAC), an antioxidant, nullified the inhibitory effect of iNOS on HIF-1 binding.	Acetylcysteine	30-49	nitric oxide synthase 2	Rattus norvegicus	108-112
11970911-6	2002	In addition, pretreatment of cells with N-acetyl-cysteine blocked tumor necrosis factor (TNF)-alpha-induced IL-6 release, suggesting that endogenously produced ROS participate in IL-6 production.	Acetylcysteine	40-57	interleukin 6	Mus musculus	179-183
11980715-4	2002	N-acetyl-L-cysteine, an ROS inhibitor, rescued p21-induced senescence, showing that ROS elevation is necessary for induction of the permanent growth arrest phenotype.	Acetylcysteine	0-19	cyclin dependent kinase inhibitor 1A	Homo sapiens	47-50
12076959-13	2002	Pretreatment of C6 cells with N-acetyl-l-cysteine (NAC), an antioxidant, nullified the inhibitory effect of iNOS on HIF-1 binding.	Acetylcysteine	51-54	nitric oxide synthase 2	Rattus norvegicus	108-112
12113286-6	2002	In NAC-treated patients hematocrit remained stable and an increase in CD4 cell count took place earlier than that in the control group.	Acetylcysteine	3-6	CD4 molecule	Homo sapiens	70-73
12086016-6	2002	However, such severe cell death was effectively (approximately 85%) prevented with N-acetylcysteine (NAC), a precursor of reduced glutathione (GSH) that is an essential cofactor for Gly-I, accompanied by the intact Gly-I and G3PDH activities.	Acetylcysteine	83-99	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	225-230
11994710-14	2002	Preincubation with N-acetylcysteine completely abrogated DEPex-driven basophil IL-4 expression.	Acetylcysteine	19-35	interleukin 4	Homo sapiens	79-83
11994710-16	2002	N-acetylcysteine inhibition of DEPex-driven IL-4 expression provides evidence that generation of reactive oxygen species is required for the effects observed.	Acetylcysteine	0-16	interleukin 4	Homo sapiens	44-48
11978899-2	2002	N-acetylcysteine (NAC) is a safe compound that inhibits tumour necrosis factor (TNF) and impedes cytoadherence, both of which have been implicated in the pathogenesis of malaria complications.	Acetylcysteine	0-16	tumor necrosis factor	Homo sapiens	56-78
11978899-2	2002	N-acetylcysteine (NAC) is a safe compound that inhibits tumour necrosis factor (TNF) and impedes cytoadherence, both of which have been implicated in the pathogenesis of malaria complications.	Acetylcysteine	0-16	tumor necrosis factor	Homo sapiens	80-83
11978899-2	2002	N-acetylcysteine (NAC) is a safe compound that inhibits tumour necrosis factor (TNF) and impedes cytoadherence, both of which have been implicated in the pathogenesis of malaria complications.	Acetylcysteine	18-21	tumor necrosis factor	Homo sapiens	56-78
11978899-2	2002	N-acetylcysteine (NAC) is a safe compound that inhibits tumour necrosis factor (TNF) and impedes cytoadherence, both of which have been implicated in the pathogenesis of malaria complications.	Acetylcysteine	18-21	tumor necrosis factor	Homo sapiens	80-83
12086016-6	2002	However, such severe cell death was effectively (approximately 85%) prevented with N-acetylcysteine (NAC), a precursor of reduced glutathione (GSH) that is an essential cofactor for Gly-I, accompanied by the intact Gly-I and G3PDH activities.	Acetylcysteine	101-104	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	225-230
11897769-8	2002	Methylglyoxal activated NF-kappaB p65 and increased ICAM-1 expression in hypertensive cells, which was inhibited by N-acetylcysteine.	Acetylcysteine	116-132	synaptotagmin 1	Rattus norvegicus	34-37
11909699-8	2002	Finally, simultaneous treatment with NAC inhibited both indomethacin-induced release of Nrf2 from KIAA0132 and indomethacin-induced nuclear translocation of Nrf2.	Acetylcysteine	37-40	NFE2 like bZIP transcription factor 2	Homo sapiens	88-92
11909699-8	2002	Finally, simultaneous treatment with NAC inhibited both indomethacin-induced release of Nrf2 from KIAA0132 and indomethacin-induced nuclear translocation of Nrf2.	Acetylcysteine	37-40	NFE2 like bZIP transcription factor 2	Homo sapiens	157-161
11867563-6	2002	In addition, there was an increased rat mast cell protease (RMCP) II concentration in the serum after HgCl(2) injection and the elevated levels of RMCP II stimulated by HgCl(2) were totally abolished by the administration NAC in the HgCl(2) + NAC group.	Acetylcysteine	222-225	mast cell protease 2	Rattus norvegicus	147-154
12079021-0	2002	Inhibition of polymethylmethacrylate particle-induced monocyte activation and IL-1beta and TNF-alpha expression by the antioxidant agent N-acetylcysteine.	Acetylcysteine	137-153	interleukin 1 beta	Homo sapiens	78-86
12079021-0	2002	Inhibition of polymethylmethacrylate particle-induced monocyte activation and IL-1beta and TNF-alpha expression by the antioxidant agent N-acetylcysteine.	Acetylcysteine	137-153	tumor necrosis factor	Homo sapiens	91-100
12079021-6	2002	NAC treatment reduced TNFalpha and IL-1beta expression by the monocyte-macrophages.	Acetylcysteine	0-3	tumor necrosis factor	Homo sapiens	22-30
12079021-6	2002	NAC treatment reduced TNFalpha and IL-1beta expression by the monocyte-macrophages.	Acetylcysteine	0-3	interleukin 1 beta	Homo sapiens	35-43
12079021-9	2002	Our findings demonstrate the effectiveness of the antioxidant N-acetylcysteine in suppressing the cell activation and TNFalpha release seen on exposure to wear debris.	Acetylcysteine	62-78	tumor necrosis factor	Homo sapiens	118-126
11866476-3	2002	Inhibition of cytochrome P450 enzymes responsible for NAPQI formation might be useful--besides N-acetylcysteine treatment--in managing acetaminophen overdose.	Acetylcysteine	95-111	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	14-29
11867563-6	2002	In addition, there was an increased rat mast cell protease (RMCP) II concentration in the serum after HgCl(2) injection and the elevated levels of RMCP II stimulated by HgCl(2) were totally abolished by the administration NAC in the HgCl(2) + NAC group.	Acetylcysteine	243-246	mast cell protease 2	Rattus norvegicus	147-154
11859152-4	2002	Of the six agents tested, only the thiol antioxidants, BUC and NAC, were effective at preventing a decrease in intracellular reduced glutathione:glutathione disulfide ratios, protecting cells from protein and lipid oxidation, and preventing heme oxygenase 1 expression.	Acetylcysteine	63-66	heme oxygenase 1	Mus musculus	241-257
12047048-10	2002	Synergistic interactions of mox-LDL with 5-HT, Ang-II, ET-1, or U-II were significantly inhibited by NAC (400 micromol/l).	Acetylcysteine	101-104	angiotensinogen	Homo sapiens	47-53
11858955-5	2002	The presence of N-acetyl-L-cysteine or pyrrolidine dithiocarbamate during H(2)O(2) treatment prevented the nuclear localization of NF-kappaB.	Acetylcysteine	16-35	nuclear factor kappa B subunit 1	Homo sapiens	131-140
12034042-5	2002	LSN-B-inducing activity was inhibited by (1) N-acetyl-L-cysteine, a well-characterized antioxidant, (2) cationic amphiphilic drugs, inhibitors of acidic sphingomyelinase (A-SMase), and (3) D609, an inhibitor of phosphatidylcholine-specific phospholipase C (PC-PLC).	Acetylcysteine	45-64	sphingomyelin phosphodiesterase 1	Homo sapiens	171-178
11854523-2	2002	This selective induction of apoptosis, which we detect by FACS analysis of intracellular HIV/p24 and concomitant surface and apoptosis marker expression, is abrogated by the glutathione precursor, N-acetyl-l-cysteine.	Acetylcysteine	197-216	transmembrane p24 trafficking protein 2	Homo sapiens	93-96
11820781-7	2002	Suppression of ROS formation by antioxidant N-acetylcysteine (NAC) downregulated the induction of MRP1 and MRP3 expression.	Acetylcysteine	44-60	ATP binding cassette subfamily C member 1	Homo sapiens	98-102
11820781-7	2002	Suppression of ROS formation by antioxidant N-acetylcysteine (NAC) downregulated the induction of MRP1 and MRP3 expression.	Acetylcysteine	62-65	ATP binding cassette subfamily C member 1	Homo sapiens	98-102
11820937-7	2002	On the addition of a plant-specific peptide, phytochelatin [PC(7), (gammaGlu-Cys)(7)-Gly], to the medium, the detoxification of Cd(2+) and cooperation with Bcl-2 were more intense than in the cases of GSH and NAC.	Acetylcysteine	209-212	BCL2 apoptosis regulator	Homo sapiens	156-161
11886167-8	2002	In contrast, N-acetylcysteine (NAC), a scavenger of reactive oxygen species, abolished the cobalt induction of HIF-1alpha and that of the VEGF and a HRE-driven reporter genes.	Acetylcysteine	13-29	hypoxia inducible factor 1 subunit alpha	Homo sapiens	111-121
11851362-8	2002	Preincubation of n-acetyl cysteine (NAC), an antioxidant, prior to TNF-alpha treatment, abolished TNF-alpha -induced ROS generation.	Acetylcysteine	17-34	tumor necrosis factor	Rattus norvegicus	67-76
11851362-8	2002	Preincubation of n-acetyl cysteine (NAC), an antioxidant, prior to TNF-alpha treatment, abolished TNF-alpha -induced ROS generation.	Acetylcysteine	17-34	tumor necrosis factor	Rattus norvegicus	98-107
11851362-8	2002	Preincubation of n-acetyl cysteine (NAC), an antioxidant, prior to TNF-alpha treatment, abolished TNF-alpha -induced ROS generation.	Acetylcysteine	36-39	tumor necrosis factor	Rattus norvegicus	67-76
11851362-8	2002	Preincubation of n-acetyl cysteine (NAC), an antioxidant, prior to TNF-alpha treatment, abolished TNF-alpha -induced ROS generation.	Acetylcysteine	36-39	tumor necrosis factor	Rattus norvegicus	98-107
11851362-9	2002	NAC abolished TNF-alpha-induced NF-kappa B activation and hypertrophic responses.	Acetylcysteine	0-3	tumor necrosis factor	Rattus norvegicus	14-23
11862160-10	2002	NAC pretreatment significantly attenuates the effects of endotoxin on BUN, creatinine and TNF-a levels in cirrhotic rats with no improvement in systemic toxicity symptoms.	Acetylcysteine	0-3	tumor necrosis factor	Rattus norvegicus	90-95
11707430-3	2002	We found that treatment of myeloma cells with the antioxidant N-acetylcysteine completely blocked cisplatin-dependent intracellular GSH oxidation, reactive oxygen species (ROS) generation, poly(ADP-ribose) polymerase cleavage, and apoptosis.	Acetylcysteine	62-78	poly(ADP-ribose) polymerase 1	Homo sapiens	189-216
11841797-10	2002	Pretreatment of HL-60 cells with N-acetyl-cysteine or catalase efficiently inhibited H(2)O(2) (200 microM)-induced apoptosis, but showed no inhibitory effect on wogonin- and fisetin-induced DNA ladders, caspase 3 activation, or bax protein induction.	Acetylcysteine	33-50	caspase 3	Homo sapiens	203-212
11841797-10	2002	Pretreatment of HL-60 cells with N-acetyl-cysteine or catalase efficiently inhibited H(2)O(2) (200 microM)-induced apoptosis, but showed no inhibitory effect on wogonin- and fisetin-induced DNA ladders, caspase 3 activation, or bax protein induction.	Acetylcysteine	33-50	BCL2 associated X, apoptosis regulator	Homo sapiens	228-231
11755158-5	2002	ERK1/2 activity was only partly inhibited by green tea catechins alone or in combination with N-acetylcysteine (P&lt;0.05).	Acetylcysteine	94-110	mitogen-activated protein kinase 3	Homo sapiens	0-6
11886167-8	2002	In contrast, N-acetylcysteine (NAC), a scavenger of reactive oxygen species, abolished the cobalt induction of HIF-1alpha and that of the VEGF and a HRE-driven reporter genes.	Acetylcysteine	13-29	vascular endothelial growth factor A	Homo sapiens	138-142
11886167-8	2002	In contrast, N-acetylcysteine (NAC), a scavenger of reactive oxygen species, abolished the cobalt induction of HIF-1alpha and that of the VEGF and a HRE-driven reporter genes.	Acetylcysteine	31-34	hypoxia inducible factor 1 subunit alpha	Homo sapiens	111-121
11886167-8	2002	In contrast, N-acetylcysteine (NAC), a scavenger of reactive oxygen species, abolished the cobalt induction of HIF-1alpha and that of the VEGF and a HRE-driven reporter genes.	Acetylcysteine	31-34	vascular endothelial growth factor A	Homo sapiens	138-142
11815388-2	2002	It was hypothesized that the involvement of the MAPK pathway in regulating LPS-mediated TNF-alpha secretion is redox-dependent, NF-kappaB-sensitive and attenuated by N-acetyl-L-cysteine (NAC) and other antioxidants.	Acetylcysteine	166-185	tumor necrosis factor	Homo sapiens	88-97
12361192-0	2002	N-acetylcysteine potentiates the antihypertensive effect of ACE inhibitors in hypertensive patients.	Acetylcysteine	0-16	angiotensin I converting enzyme	Homo sapiens	60-63
11815388-2	2002	It was hypothesized that the involvement of the MAPK pathway in regulating LPS-mediated TNF-alpha secretion is redox-dependent, NF-kappaB-sensitive and attenuated by N-acetyl-L-cysteine (NAC) and other antioxidants.	Acetylcysteine	187-190	tumor necrosis factor	Homo sapiens	88-97
11815388-9	2002	LPS up-regulated ROS, an effect abrogated by 4"-hydroxy-3"-methoxy-acetophenone and NAC, which reduced TNF-alpha secretion, induced the accumulation of GSH, reduced the concentration of GSSG, and blockaded the phosphorylation/activation of MAPK(p38) pathway.	Acetylcysteine	84-87	tumor necrosis factor	Homo sapiens	103-112
11815388-9	2002	LPS up-regulated ROS, an effect abrogated by 4"-hydroxy-3"-methoxy-acetophenone and NAC, which reduced TNF-alpha secretion, induced the accumulation of GSH, reduced the concentration of GSSG, and blockaded the phosphorylation/activation of MAPK(p38) pathway.	Acetylcysteine	84-87	mitogen-activated protein kinase 14	Homo sapiens	245-248
11999701-5	2002	In the present work, we have studied the in vitro effect of several concentrations of NAC (0.001, 0.01, 0.1, 1 and 2.5 mM) on the following functions: adherence to substrate, chemotaxis, ingestion of particles, ROS production and the release of tumor necrosis factor (TNFalpha) of peritoneal macrophages from BALB/c mice at 2, 4,12 and 24 h after LPS injection.	Acetylcysteine	86-89	tumor necrosis factor	Mus musculus	268-276
11999701-6	2002	The results show that the administration of NAC (especially at 0.1 mM) decreases raised adherence, ingestion, ROS production and TNFalpha levels in macrophages from animals injected with LPS, bringing these functions to values near those of control animals.	Acetylcysteine	44-47	tumor necrosis factor	Mus musculus	129-137
11999701-7	2002	These effects which seem to be linked to a modulation of NF-kappaB, suggest that the improvement of immune functions observed in previous work after injection of NAC to animals with endotoxic shock could be due to a direct action of this thiol antioxidant on immune cells.	Acetylcysteine	162-165	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	57-66
12502184-2	2002	We found that the inhibitory properties of IL-1 on STAT signalling cascade in human hepatoma HepG2 cells are considerably decreased not only in the presence of MAP kinase inhibitors SB203580 and PD98059 but also by some antioxidants (N-acetyl cysteine and pyrrolidine dithiocarbamate) and by anti-inflammatory cytokine IL-4.	Acetylcysteine	234-251	signal transducer and activator of transcription 3	Homo sapiens	51-55
12397613-6	2002	The addition of antioxidant N-acetylcysteine (NAC; 20 mM) 30 min prior to stimulation with TNF-alpha attenuated the inhibition of BSP mRNA levels.	Acetylcysteine	28-44	tumor necrosis factor	Rattus norvegicus	91-100
11799073-9	2002	Incubation of VSMCs with the antioxidant N-acetylcysteine suppressed GSA-elicited mRNA induction of MCP-1 and IL-6.	Acetylcysteine	41-57	interleukin 6	Homo sapiens	110-114
11740866-2	2002	We found that activation of ECV-304 cells by TNFalpha was accompanied by a transient burst of oxidants and activation of JNK, both of which were suppressed by two distinct inhibitors of the phagocyte NADPH oxidase and the thiol antioxidant N-acetyl cysteine (NAC).	Acetylcysteine	240-257	tumor necrosis factor	Homo sapiens	45-53
11740866-2	2002	We found that activation of ECV-304 cells by TNFalpha was accompanied by a transient burst of oxidants and activation of JNK, both of which were suppressed by two distinct inhibitors of the phagocyte NADPH oxidase and the thiol antioxidant N-acetyl cysteine (NAC).	Acetylcysteine	240-257	mitogen-activated protein kinase 8	Homo sapiens	121-124
11740866-2	2002	We found that activation of ECV-304 cells by TNFalpha was accompanied by a transient burst of oxidants and activation of JNK, both of which were suppressed by two distinct inhibitors of the phagocyte NADPH oxidase and the thiol antioxidant N-acetyl cysteine (NAC).	Acetylcysteine	259-262	tumor necrosis factor	Homo sapiens	45-53
11740866-2	2002	We found that activation of ECV-304 cells by TNFalpha was accompanied by a transient burst of oxidants and activation of JNK, both of which were suppressed by two distinct inhibitors of the phagocyte NADPH oxidase and the thiol antioxidant N-acetyl cysteine (NAC).	Acetylcysteine	259-262	mitogen-activated protein kinase 8	Homo sapiens	121-124
12397613-6	2002	The addition of antioxidant N-acetylcysteine (NAC; 20 mM) 30 min prior to stimulation with TNF-alpha attenuated the inhibition of BSP mRNA levels.	Acetylcysteine	28-44	integrin-binding sialoprotein	Rattus norvegicus	130-133
12397613-6	2002	The addition of antioxidant N-acetylcysteine (NAC; 20 mM) 30 min prior to stimulation with TNF-alpha attenuated the inhibition of BSP mRNA levels.	Acetylcysteine	46-49	tumor necrosis factor	Rattus norvegicus	91-100
12397613-6	2002	The addition of antioxidant N-acetylcysteine (NAC; 20 mM) 30 min prior to stimulation with TNF-alpha attenuated the inhibition of BSP mRNA levels.	Acetylcysteine	46-49	integrin-binding sialoprotein	Rattus norvegicus	130-133
12086398-7	2002	As a result, H. pylori induced a time-dependent expression of mRNA and protein for COX-2 via activation of NF-kappaB, which was inhibited by GSH, NAC, and PDTC in the cells.	Acetylcysteine	146-149	nuclear factor kappa B subunit 1	Homo sapiens	107-116
12397613-8	2002	Further deletion analysis of the BSP promoter showed that a region within nts -84 to -60 was targeted by TNF-alpha, the effects which were inhibited by NAC and the tyrosine kinase inhibitor, herbimycin A (HA).	Acetylcysteine	152-155	integrin-binding sialoprotein	Rattus norvegicus	33-36
12397613-8	2002	Further deletion analysis of the BSP promoter showed that a region within nts -84 to -60 was targeted by TNF-alpha, the effects which were inhibited by NAC and the tyrosine kinase inhibitor, herbimycin A (HA).	Acetylcysteine	152-155	tumor necrosis factor	Rattus norvegicus	105-114
12397613-11	2002	Further, the inhibitory effect of TNF-alpha on CRE DNA-protein complex was completely abolished by NAC or HA treatment.	Acetylcysteine	99-102	tumor necrosis factor	Rattus norvegicus	34-43
11710721-15	2001	In contrast, treatment of SSc fibroblasts with the membrane-permeant antioxidant N-acetyl-L-cysteine inhibited ROS production, and this was accompanied by decreased proliferation of these cells and down-regulation of alpha1(I) and alpha2(I) collagen messenger RNA.	Acetylcysteine	81-100	collagen type I alpha 2 chain	Homo sapiens	231-249
11704541-4	2001	Increased expression of MMP-9 and NF-kappa B activation induced by TNF-alpha were inhibited by pyrrolidine dithiocarbamate and N-acetyl-L-cysteine but were not inhibited by curcumin.	Acetylcysteine	127-146	nuclear factor kappa B subunit 1	Homo sapiens	34-44
11704541-4	2001	Increased expression of MMP-9 and NF-kappa B activation induced by TNF-alpha were inhibited by pyrrolidine dithiocarbamate and N-acetyl-L-cysteine but were not inhibited by curcumin.	Acetylcysteine	127-146	tumor necrosis factor	Homo sapiens	67-76
11813981-2	2001	In this report, surface expression of CD21 on B and T cells was shown to be suppressed by a thiol-antioxidant, N-acetylcysteine (NAC), in a dose- and time-dependent manner.	Acetylcysteine	111-127	complement C3d receptor 2	Homo sapiens	38-42
11813981-2	2001	In this report, surface expression of CD21 on B and T cells was shown to be suppressed by a thiol-antioxidant, N-acetylcysteine (NAC), in a dose- and time-dependent manner.	Acetylcysteine	129-132	complement C3d receptor 2	Homo sapiens	38-42
11813981-6	2001	Immunoprecipitation study revealed that NAC causes a loss of anti-CD21 monoclonal antibody (HB5) binding to both membrane and soluble CD21, suggesting that NAC modulates the structure of CD21.	Acetylcysteine	40-43	complement C3d receptor 2	Homo sapiens	66-70
11813981-6	2001	Immunoprecipitation study revealed that NAC causes a loss of anti-CD21 monoclonal antibody (HB5) binding to both membrane and soluble CD21, suggesting that NAC modulates the structure of CD21.	Acetylcysteine	40-43	complement C3d receptor 2	Homo sapiens	134-138
11813981-6	2001	Immunoprecipitation study revealed that NAC causes a loss of anti-CD21 monoclonal antibody (HB5) binding to both membrane and soluble CD21, suggesting that NAC modulates the structure of CD21.	Acetylcysteine	40-43	complement C3d receptor 2	Homo sapiens	134-138
11813981-6	2001	Immunoprecipitation study revealed that NAC causes a loss of anti-CD21 monoclonal antibody (HB5) binding to both membrane and soluble CD21, suggesting that NAC modulates the structure of CD21.	Acetylcysteine	156-159	complement C3d receptor 2	Homo sapiens	66-70
11813981-6	2001	Immunoprecipitation study revealed that NAC causes a loss of anti-CD21 monoclonal antibody (HB5) binding to both membrane and soluble CD21, suggesting that NAC modulates the structure of CD21.	Acetylcysteine	156-159	complement C3d receptor 2	Homo sapiens	134-138
11813981-6	2001	Immunoprecipitation study revealed that NAC causes a loss of anti-CD21 monoclonal antibody (HB5) binding to both membrane and soluble CD21, suggesting that NAC modulates the structure of CD21.	Acetylcysteine	156-159	complement C3d receptor 2	Homo sapiens	134-138
11813981-7	2001	Other thiol-antioxidants, such as 2-mercaptoethanol, pyrrolidine dithiocarbamate, and glutathione, showed similar effect to NAC on CD21 expression.	Acetylcysteine	124-127	complement C3d receptor 2	Homo sapiens	131-135
12043846-4	2001	N-acetylcysteine, a ROS scavenger, inhibited NRG-induced activation of Ras and Erk and PC12-ErbB-4 cell differentiation.	Acetylcysteine	0-16	Eph receptor B1	Rattus norvegicus	79-82
12043846-4	2001	N-acetylcysteine, a ROS scavenger, inhibited NRG-induced activation of Ras and Erk and PC12-ErbB-4 cell differentiation.	Acetylcysteine	0-16	erb-b2 receptor tyrosine kinase 4	Rattus norvegicus	92-98
11709424-5	2001	IL-1 beta treatment stimulated superoxide production in VSM cells that was inhibited by pretreatment of cells with the superoxide scavenger N-acetyl-L-cysteine (NAC) and also by overexpression of the human manganese superoxide dismutase (MnSOD) gene.	Acetylcysteine	140-159	interleukin 1 beta	Homo sapiens	0-9
11709424-5	2001	IL-1 beta treatment stimulated superoxide production in VSM cells that was inhibited by pretreatment of cells with the superoxide scavenger N-acetyl-L-cysteine (NAC) and also by overexpression of the human manganese superoxide dismutase (MnSOD) gene.	Acetylcysteine	161-164	interleukin 1 beta	Homo sapiens	0-9
11709424-6	2001	Treatment of VSM cells with NAC selectively inhibited the sustained phase of ERK activation without influencing the transient phase, suggesting a role for reactive oxygen species in sustained ERK activation.	Acetylcysteine	28-31	mitogen-activated protein kinase 1	Homo sapiens	77-80
11709424-6	2001	Treatment of VSM cells with NAC selectively inhibited the sustained phase of ERK activation without influencing the transient phase, suggesting a role for reactive oxygen species in sustained ERK activation.	Acetylcysteine	28-31	mitogen-activated protein kinase 1	Homo sapiens	192-195
11709424-7	2001	In addition, both NAC treatment and MnSOD overexpression significantly inhibited IL-1 beta-stimulated MMP-9 induction (P &lt; 0.05).	Acetylcysteine	18-21	interleukin 1 beta	Homo sapiens	81-90
12214018-5	2001	Both vitamin E and NAC prevented Abeta-induced ROS generation when applied simultaneously with Abeta, but only NAC prevented Abeta-induced ROS generation when added to cultures that had previously been exposed to Abeta.	Acetylcysteine	19-22	amyloid beta precursor protein	Homo sapiens	33-38
12214018-5	2001	Both vitamin E and NAC prevented Abeta-induced ROS generation when applied simultaneously with Abeta, but only NAC prevented Abeta-induced ROS generation when added to cultures that had previously been exposed to Abeta.	Acetylcysteine	19-22	amyloid beta precursor protein	Homo sapiens	95-100
12214018-5	2001	Both vitamin E and NAC prevented Abeta-induced ROS generation when applied simultaneously with Abeta, but only NAC prevented Abeta-induced ROS generation when added to cultures that had previously been exposed to Abeta.	Acetylcysteine	19-22	amyloid beta precursor protein	Homo sapiens	95-100
12214018-5	2001	Both vitamin E and NAC prevented Abeta-induced ROS generation when applied simultaneously with Abeta, but only NAC prevented Abeta-induced ROS generation when added to cultures that had previously been exposed to Abeta.	Acetylcysteine	19-22	amyloid beta precursor protein	Homo sapiens	95-100
11597988-4	2001	We first confirmed that antioxidant N-acetylcysteine, superoxide scavenger Tiron, and DPI suppressed Ang II-induced IL-6 expression.	Acetylcysteine	36-52	angiotensinogen	Homo sapiens	101-107
11597988-6	2001	Ang II, as well as exogenous H(2)O(2), activated ERK, p38 MAPK, and JNK, which were significantly inhibited by N-acetylcysteine and DPI.	Acetylcysteine	111-127	angiotensinogen	Homo sapiens	0-6
11597988-6	2001	Ang II, as well as exogenous H(2)O(2), activated ERK, p38 MAPK, and JNK, which were significantly inhibited by N-acetylcysteine and DPI.	Acetylcysteine	111-127	mitogen-activated protein kinase 14	Homo sapiens	54-57
11597988-6	2001	Ang II, as well as exogenous H(2)O(2), activated ERK, p38 MAPK, and JNK, which were significantly inhibited by N-acetylcysteine and DPI.	Acetylcysteine	111-127	mitogen-activated protein kinase 8	Homo sapiens	68-71
11578838-7	2001	The AGE-induced increase in oxidized glutathione could be prevented by the radical scavengers N-acetylcysteine, alpha-lipoic acid and 17beta-estradiol or by application of catalase, indicating that superoxide and hydrogen peroxide production precedes the AGE-mediated depletion of reduced glutathione.	Acetylcysteine	94-110	renin binding protein	Homo sapiens	4-7
11597988-4	2001	We first confirmed that antioxidant N-acetylcysteine, superoxide scavenger Tiron, and DPI suppressed Ang II-induced IL-6 expression.	Acetylcysteine	36-52	interleukin 6	Homo sapiens	116-120
11583958-12	2001	In vitro, treatment of cultured canine jugular vein endothelial cells with the reactive oxygen intermediate H2O2 induced a concentration-dependent increase in MCP-1 mRNA levels, which was inhibited by the antioxidant N-acetyl-L-cysteine, a precursor of glutathione, but not pyrrolidine dithiocarbamate, an inhibitor of NF-kappaB and activator of AP-1.	Acetylcysteine	217-236	C-C motif chemokine ligand 2	Canis lupus familiaris	159-164
11532971-9	2001	However, the antioxidants N-acetylcysteine and diphenylene iodonium inhibited both AA- and Ang II-induced Akt/PKB activation.	Acetylcysteine	26-42	angiotensinogen	Homo sapiens	91-97
11557664-7	2001	13-HPODE-induced nuclear factor-kappaB DNA binding activity was blocked by an antioxidant, N-acetylcysteine, as well as an inhibitor of protein kinase C. 13-HPODE, but not the hydroxy product, 13-(S)-hydroxyoctadecadienoic acid, also dose-dependently increased vascular cell adhesion molecule-1 promoter activation.	Acetylcysteine	91-107	vascular cell adhesion molecule 1	Homo sapiens	261-294
11532971-9	2001	However, the antioxidants N-acetylcysteine and diphenylene iodonium inhibited both AA- and Ang II-induced Akt/PKB activation.	Acetylcysteine	26-42	AKT serine/threonine kinase 1	Homo sapiens	106-109
11532971-9	2001	However, the antioxidants N-acetylcysteine and diphenylene iodonium inhibited both AA- and Ang II-induced Akt/PKB activation.	Acetylcysteine	26-42	AKT serine/threonine kinase 1	Homo sapiens	110-113
11642020-4	2001	In these experimental conditions, a prodrug of N-acetylcysteine and beta-mercaptoethylamine, I-152 demonstrated a potent anti-HIV activity, increased intracellular GSH level, and decreased TNF-alpha production.	Acetylcysteine	47-63	tumor necrosis factor	Homo sapiens	189-198
11571584-6	2001	The Ad.CFTR-dependent increase of ICAM-1 mRNA was abolished by inhibitors of NF-kB, such as N-acetyl-L-cysteine, pyrrolidine dithiocarbamate, parthenolide and the synthetic peptide SN50.	Acetylcysteine	92-111	CF transmembrane conductance regulator	Homo sapiens	7-11
11555840-10	2001	In cell-free media, the 2 reductants, dihydrolipoate and N-acetylcysteine, rapidly decreased immunoreactive insulin, but alpha-lipoate was ineffective.	Acetylcysteine	57-73	insulin	Homo sapiens	108-115
11454688-10	2001	In contrast with partial protection by the caspase-3 inhibitor, the antioxidant N-acetyl-L-cysteine gave marked protection from As2O3-induced apoptosis and eliminated the activation of p38, JNK, and caspase-3, and the generation of ROS.	Acetylcysteine	80-99	mitogen-activated protein kinase 14	Homo sapiens	185-188
11438521-8	2001	PBN-induced neurite outgrowth and ERK activation were counteracted by the thiol-based antioxidant N-acetylcysteine.	Acetylcysteine	98-114	Eph receptor B1	Rattus norvegicus	34-37
11544433-0	2001	N-acetylcysteine attenuates the increase in alpha-glutathione S-transferase and circulating ICAM-1 and VCAM-1 after reperfusion in humans undergoing liver transplantation.	Acetylcysteine	0-16	vascular cell adhesion molecule 1	Homo sapiens	103-109
11544433-10	2001	CONCLUSIONS: NAC attenuated the increase in alpha-glutathione S-transferase and circulating ICAM-1 and VCAM-1 after reperfusion of the donor liver, indicating possible cytoprotective effects of NAC.	Acetylcysteine	13-16	vascular cell adhesion molecule 1	Homo sapiens	103-109
11500052-9	2001	Treatment of animals with an antioxidant N-acetylcysteine administered ip greatly diminished the levels of shortened Bcl-2 and Bax proteins.	Acetylcysteine	41-57	BCL2, apoptosis regulator	Rattus norvegicus	117-122
11498281-8	2001	Moreover, N-acetylcysteine effectively blocked caspase-3 activation and the increase of the sub-G(1) population induced by MSC.	Acetylcysteine	10-26	caspase 3	Homo sapiens	47-56
11435216-9	2001	Pretreatment with N-acetylcysteine prevented the CS-induced loss of hrSLPI activity, the decrease in antioxidant defenses, and the elevation of 8-epi-PGF-(2alpha).	Acetylcysteine	18-34	placental growth factor	Homo sapiens	150-153
11768769-7	2001	Free radical scavengers N-acetyl-L-cysteine (NAC), or glutathione (GSH), inhibited ERK2 activation and, to a much lesser extent, JNK1 activation by BHA/tBHQ, implicating the role of oxidative stress.	Acetylcysteine	24-43	mitogen-activated protein kinase 1	Homo sapiens	83-87
11768769-7	2001	Free radical scavengers N-acetyl-L-cysteine (NAC), or glutathione (GSH), inhibited ERK2 activation and, to a much lesser extent, JNK1 activation by BHA/tBHQ, implicating the role of oxidative stress.	Acetylcysteine	24-43	mitogen-activated protein kinase 8	Homo sapiens	129-133
11493611-6	2001	Administration of dimethylthiourea, desferrioxamine, or N-acetylcysteine provoked significant reductions in Ang-II-induced leukocyte-endothelial cell interactions.	Acetylcysteine	56-72	angiotensinogen	Rattus norvegicus	108-114
11749846-4	2001	NAC 4 mmol/L, NDMS 200 micromol/L, CAT 80 kU/L, and Quin 2 20 micromol/L could down-regulate apoptosis variously induced by As2O3.	Acetylcysteine	0-3	catalase	Homo sapiens	35-38
11509327-7	2001	Pretreatment with N-acetyl-cysteine (NAC) (1 to 10 mM) or glutathione (1 to 10 mM) inhibited TNF-alpha-induced activation of NF-kappa B transcriptional activity and IL-8 promoter-mediated reporter gene expression.	Acetylcysteine	18-35	tumor necrosis factor	Homo sapiens	93-102
11509327-7	2001	Pretreatment with N-acetyl-cysteine (NAC) (1 to 10 mM) or glutathione (1 to 10 mM) inhibited TNF-alpha-induced activation of NF-kappa B transcriptional activity and IL-8 promoter-mediated reporter gene expression.	Acetylcysteine	18-35	nuclear factor kappa B subunit 1	Homo sapiens	125-135
11509327-7	2001	Pretreatment with N-acetyl-cysteine (NAC) (1 to 10 mM) or glutathione (1 to 10 mM) inhibited TNF-alpha-induced activation of NF-kappa B transcriptional activity and IL-8 promoter-mediated reporter gene expression.	Acetylcysteine	18-35	C-X-C motif chemokine ligand 8	Homo sapiens	165-169
11509327-7	2001	Pretreatment with N-acetyl-cysteine (NAC) (1 to 10 mM) or glutathione (1 to 10 mM) inhibited TNF-alpha-induced activation of NF-kappa B transcriptional activity and IL-8 promoter-mediated reporter gene expression.	Acetylcysteine	37-40	tumor necrosis factor	Homo sapiens	93-102
11509327-7	2001	Pretreatment with N-acetyl-cysteine (NAC) (1 to 10 mM) or glutathione (1 to 10 mM) inhibited TNF-alpha-induced activation of NF-kappa B transcriptional activity and IL-8 promoter-mediated reporter gene expression.	Acetylcysteine	37-40	nuclear factor kappa B subunit 1	Homo sapiens	125-135
11509327-7	2001	Pretreatment with N-acetyl-cysteine (NAC) (1 to 10 mM) or glutathione (1 to 10 mM) inhibited TNF-alpha-induced activation of NF-kappa B transcriptional activity and IL-8 promoter-mediated reporter gene expression.	Acetylcysteine	37-40	C-X-C motif chemokine ligand 8	Homo sapiens	165-169
11485373-1	2001	This in vivo study evaluates the effect of N-acetylcysteine (NAC) administration on nitric oxide (NO) production by the inducible form of nitric oxide synthase (iNOS).	Acetylcysteine	43-59	nitric oxide synthase 2	Rattus norvegicus	161-165
11485373-1	2001	This in vivo study evaluates the effect of N-acetylcysteine (NAC) administration on nitric oxide (NO) production by the inducible form of nitric oxide synthase (iNOS).	Acetylcysteine	61-64	nitric oxide synthase 2	Rattus norvegicus	161-165
11485373-9	2001	This can be attributed mostly to the inhibitory effect of NAC on one of the events leading to iNOS protein expression.	Acetylcysteine	58-61	nitric oxide synthase 2	Rattus norvegicus	94-98
11448159-6	2001	Both oxidase inhibitors and the thiol antioxidant N-acetyl cysteine decreased Tat-induced JNK1 activation in parallel with reduction in oxidant levels.	Acetylcysteine	50-67	mitogen-activated protein kinase 8	Homo sapiens	90-94
11454704-5	2001	Enhancement of intracellular soluble thiol pools after incubation with N-acetylcysteine (2.5 mM), from 3.27 +/- 0.27 nM/mg protein to 5.34 +/- 0.52 nM/mg protein in cells incubated with N-acetylcysteine 30 min before and assessed 4 h after irradiation, abolished the radiation-induced up-regulation of PAI-1.	Acetylcysteine	71-87	serpin family E member 1	Rattus norvegicus	302-307
11337489-4	2001	We also have shown that TNF induces tyrosine phosphorylation and internalization of the overexpressed EGFR in NIH3T3 cells and the endogenously expressed EGFR in A431 cells and that the transactivation by TNF is suppressed by N-acetyl-l-cysteine or overexpression of an endogenous reducing molecule, thioredoxin, but not by phosphatidylinositol 3-kinase inhibitors and protein kinase C inhibitor.	Acetylcysteine	226-245	tumor necrosis factor	Mus musculus	24-27
11337489-4	2001	We also have shown that TNF induces tyrosine phosphorylation and internalization of the overexpressed EGFR in NIH3T3 cells and the endogenously expressed EGFR in A431 cells and that the transactivation by TNF is suppressed by N-acetyl-l-cysteine or overexpression of an endogenous reducing molecule, thioredoxin, but not by phosphatidylinositol 3-kinase inhibitors and protein kinase C inhibitor.	Acetylcysteine	226-245	tumor necrosis factor	Mus musculus	205-208
11454688-10	2001	In contrast with partial protection by the caspase-3 inhibitor, the antioxidant N-acetyl-L-cysteine gave marked protection from As2O3-induced apoptosis and eliminated the activation of p38, JNK, and caspase-3, and the generation of ROS.	Acetylcysteine	80-99	mitogen-activated protein kinase 8	Homo sapiens	190-193
11454688-10	2001	In contrast with partial protection by the caspase-3 inhibitor, the antioxidant N-acetyl-L-cysteine gave marked protection from As2O3-induced apoptosis and eliminated the activation of p38, JNK, and caspase-3, and the generation of ROS.	Acetylcysteine	80-99	caspase 3	Homo sapiens	199-208
11264281-5	2001	N-Acetylcysteine could reliably decrease inducible MnSOD expression by TNF-alpha, but not IL-1, linking reactive oxygen species (ROS) to the TNF-alpha signaling pathway.	Acetylcysteine	0-16	tumor necrosis factor	Homo sapiens	71-80
11440976-4	2001	A superoxide dismutase mimic (SOD; MnTMPyP, 25 micromol/L) or SOD plus low concentrations of NAC (SODNAC2, 2 mmol/L) increased DCF fluorescence, which was inhibited by catalase or by NAC (10 to 20 mmol/L).	Acetylcysteine	93-96	catalase	Homo sapiens	168-176
11408612-7	2001	The use of the antioxidant N-acetyl cysteine and caspase inhibitors prevents CDDP-induced apoptosis in c-Myc low-expressing clones, demonstrating that ROS, caspase-1, and caspase-3 are required for apoptotic cell death.	Acetylcysteine	27-44	caspase 1	Homo sapiens	156-165
11408612-7	2001	The use of the antioxidant N-acetyl cysteine and caspase inhibitors prevents CDDP-induced apoptosis in c-Myc low-expressing clones, demonstrating that ROS, caspase-1, and caspase-3 are required for apoptotic cell death.	Acetylcysteine	27-44	caspase 3	Homo sapiens	171-180
11390505-6	2001	Antioxidants N-acetylcysteine and pyrrolidine dithiocarbamate inhibited MMP production by AMs from SP-D(-/-) mice.	Acetylcysteine	13-29	surfactant associated protein D	Mus musculus	99-103
11440976-9	2001	p38 Mitogen-activated protein kinase (MAPK) activity was decreased when ROS activity was reduced (NAC, 10 mmol/L) and was augmented when ROS activity was increased (SODNAC2).	Acetylcysteine	98-101	mitogen-activated protein kinase 14	Homo sapiens	0-3
11264281-5	2001	N-Acetylcysteine could reliably decrease inducible MnSOD expression by TNF-alpha, but not IL-1, linking reactive oxygen species (ROS) to the TNF-alpha signaling pathway.	Acetylcysteine	0-16	tumor necrosis factor	Homo sapiens	141-150
11380598-1	2001	BACKGROUND: N-acetyl-L-cysteine, a thiol compound, has been shown to potentiate the inhibition of platelet aggregation exerted by organic nitrates and to increase the anti-aggregating effect of L-arginine, which promotes endogenous synthesis of nitric oxide (NO) acting as substrate of platelet constitutive nitric oxide synthase (NOS).	Acetylcysteine	12-31	nitric oxide synthase 2	Homo sapiens	308-329
11506896-5	2001	The GSNO-stimulated induction of VEGF mRNA was slightly attenuated by MAP protein kinase inhibitors PD98058 and SB203580, but was completely blocked in cells incubated with GSNO in the presence of catalase and superoxide dismutase, enzymes scavenging reactive oxygen species (ROS), or in the presence of thiol-containing antioxidants, N-acetyl cysteine and reduced glutathione.	Acetylcysteine	335-352	vascular endothelial growth factor A	Homo sapiens	33-37
11506896-5	2001	The GSNO-stimulated induction of VEGF mRNA was slightly attenuated by MAP protein kinase inhibitors PD98058 and SB203580, but was completely blocked in cells incubated with GSNO in the presence of catalase and superoxide dismutase, enzymes scavenging reactive oxygen species (ROS), or in the presence of thiol-containing antioxidants, N-acetyl cysteine and reduced glutathione.	Acetylcysteine	335-352	catalase	Homo sapiens	197-205
11384840-7	2001	The free radical scavenging thiol antioxidant N-acetylcysteine (NAC) alleviated partially JNK-1 activation in amino acid-deprived cells.	Acetylcysteine	46-62	mitogen-activated protein kinase 8	Homo sapiens	90-95
11384840-7	2001	The free radical scavenging thiol antioxidant N-acetylcysteine (NAC) alleviated partially JNK-1 activation in amino acid-deprived cells.	Acetylcysteine	64-67	mitogen-activated protein kinase 8	Homo sapiens	90-95
11359799-3	2001	Moreover, the antioxidant N-acetyl-L-cysteine prevented the L-PAM-induced accumulation of B7-1 mRNA in P815 tumor cells, suggesting that reactive oxygen species are involved in the transcriptional regulation of L-PAM-induced B7-1 gene expression.	Acetylcysteine	26-45	CD80 antigen	Mus musculus	90-94
11359799-3	2001	Moreover, the antioxidant N-acetyl-L-cysteine prevented the L-PAM-induced accumulation of B7-1 mRNA in P815 tumor cells, suggesting that reactive oxygen species are involved in the transcriptional regulation of L-PAM-induced B7-1 gene expression.	Acetylcysteine	26-45	CD80 antigen	Mus musculus	225-229
11375274-6	2001	Thrombin-mediated upregulation of IGF-1R mRNA and protein levels was protein kinase C independent but was completely inhibited by the protein tyrosine kinase inhibitor genistein and by the antioxidants N-acetyl-L-cysteine and pyrrolidinedithiocarbamate, suggesting the involvement of reactive oxygen species.	Acetylcysteine	202-221	coagulation factor II	Rattus norvegicus	0-8
11350834-4	2001	Here we show that in a serum-depleted environment (0.1% fetal bovine serum), NAC substantially inhibited lipopolysaccharide (LPS) activation of the mitogen-activated protein kinases (MAPKs), namely extracellular signal-regulated kinase (ERK), p38mapk, and c-Jun NH2-terminal kinase (JNK).	Acetylcysteine	77-80	mitogen-activated protein kinase 8	Homo sapiens	256-281
11350834-4	2001	Here we show that in a serum-depleted environment (0.1% fetal bovine serum), NAC substantially inhibited lipopolysaccharide (LPS) activation of the mitogen-activated protein kinases (MAPKs), namely extracellular signal-regulated kinase (ERK), p38mapk, and c-Jun NH2-terminal kinase (JNK).	Acetylcysteine	77-80	mitogen-activated protein kinase 8	Homo sapiens	283-286
11350834-5	2001	By contrast, in the presence of 10% serum, NAC had no effect on LPS activation of p42 and p44 ERK and in fact enhanced LPS induction of p38mapk and JNK phosphorylation.	Acetylcysteine	43-46	mitogen-activated protein kinase 1	Homo sapiens	136-139
11350834-5	2001	By contrast, in the presence of 10% serum, NAC had no effect on LPS activation of p42 and p44 ERK and in fact enhanced LPS induction of p38mapk and JNK phosphorylation.	Acetylcysteine	43-46	mitogen-activated protein kinase 8	Homo sapiens	148-151
11350834-4	2001	Here we show that in a serum-depleted environment (0.1% fetal bovine serum), NAC substantially inhibited lipopolysaccharide (LPS) activation of the mitogen-activated protein kinases (MAPKs), namely extracellular signal-regulated kinase (ERK), p38mapk, and c-Jun NH2-terminal kinase (JNK).	Acetylcysteine	77-80	mitogen-activated protein kinase 1	Homo sapiens	198-235
11350834-4	2001	Here we show that in a serum-depleted environment (0.1% fetal bovine serum), NAC substantially inhibited lipopolysaccharide (LPS) activation of the mitogen-activated protein kinases (MAPKs), namely extracellular signal-regulated kinase (ERK), p38mapk, and c-Jun NH2-terminal kinase (JNK).	Acetylcysteine	77-80	mitogen-activated protein kinase 1	Homo sapiens	237-240
11385283-9	2001	Inhibitors of NF-kappa B activation such as N-acetylcysteine or N-tosyl-L-phenylalanine chloromethyl ketone can suppress Fc epsilon RI-induced TNF-alpha and MCP-1 release.	Acetylcysteine	44-60	nuclear factor kappa B subunit 1	Homo sapiens	14-24
11306679-8	2001	The stimulatory effect of Zn(2+) on both PI3K and JNK was repressed by the free-radical scavenging agent N-acetylcysteine.	Acetylcysteine	105-121	mitogen-activated protein kinase 8	Homo sapiens	50-53
11278370-6	2001	The ability of IFN-alpha and vanadate to induce apoptosis did not require expression of p53 and was blocked by N-acetyl-l-cysteine.	Acetylcysteine	111-130	interferon alpha 1	Homo sapiens	15-24
11301180-10	2001	Of interest, both N-acetylcysteine and amifostine reduced apoptotic cell death by 45% on average, inhibited the activation/processing of caspase-3, and increased BrdUrd incorporation in postG cultures.	Acetylcysteine	18-34	caspase 3	Homo sapiens	137-146
11322781-9	2001	Antioxidants such as catalase or N-acetyl-cysteine decreased Ang II-activated ERK phosphorylation and inhibited Ang II-induced beta-MyHC promoter activity.	Acetylcysteine	33-50	angiotensinogen	Rattus norvegicus	61-67
11322781-9	2001	Antioxidants such as catalase or N-acetyl-cysteine decreased Ang II-activated ERK phosphorylation and inhibited Ang II-induced beta-MyHC promoter activity.	Acetylcysteine	33-50	Eph receptor B1	Rattus norvegicus	78-81
11322781-9	2001	Antioxidants such as catalase or N-acetyl-cysteine decreased Ang II-activated ERK phosphorylation and inhibited Ang II-induced beta-MyHC promoter activity.	Acetylcysteine	33-50	angiotensinogen	Rattus norvegicus	112-118
11311209-13	2001	These MAPK stimulations were found to be cellular thiol status-dependent events as NAC reversed these stimulations.	Acetylcysteine	83-86	mitogen-activated protein kinase 1	Mus musculus	6-10
11304462-5	2001	Pretreatment of vascular smooth muscle cells with the antioxidants diphenylene iodonium, Tiron, N-acetylcysteine, and ebselen significantly inhibited ( approximately 80% to 90%) tyrosine phosphorylation of the EGF-R by Ang II but not by EGF.	Acetylcysteine	96-112	epidermal growth factor receptor	Homo sapiens	210-215
11304462-5	2001	Pretreatment of vascular smooth muscle cells with the antioxidants diphenylene iodonium, Tiron, N-acetylcysteine, and ebselen significantly inhibited ( approximately 80% to 90%) tyrosine phosphorylation of the EGF-R by Ang II but not by EGF.	Acetylcysteine	96-112	angiotensinogen	Homo sapiens	219-225
11096084-8	2001	N-Acetylcysteine (an antioxidant) and polyvinyl pyridine-N-oxide (an agent that binds to Si-OH groups on silica surfaces) decreased AP-1 activation and phosphorylation of ERKs and p38 kinase.	Acetylcysteine	0-16	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	132-136
11291926-5	2001	Further, heat-induced caspase-3 activity detected by fluorogenic assay in MIAPaCa-2 cells was almost completely inhibited by addition of the antioxidant N-acetyl-L-cysteine.	Acetylcysteine	153-172	caspase 3	Homo sapiens	22-31
11310789-7	2001	These responses of ERK1/2 to UVA irradiation were markedly inhibited when cells were pre-treated with N-acetyl-L-cysteine, an antioxidant, or with suramin, a tyrosine kinase receptor inhibitor.	Acetylcysteine	102-121	mitogen-activated protein kinase 3	Homo sapiens	19-25
11096084-8	2001	N-Acetylcysteine (an antioxidant) and polyvinyl pyridine-N-oxide (an agent that binds to Si-OH groups on silica surfaces) decreased AP-1 activation and phosphorylation of ERKs and p38 kinase.	Acetylcysteine	0-16	mitogen-activated protein kinase 14	Homo sapiens	180-183
11114294-5	2001	Its action was inhibited by inhibitors of the NF-kappaB pathway, including N-acetyl-l-cysteine, pyrrolidine dithiocarbamate, and a synthetic cell-permeable peptide containing the NF-kappaB nuclear localization signal sequence.	Acetylcysteine	75-94	nuclear factor kappa B subunit 1	Homo sapiens	46-55
11226137-6	2001	We conclude: first, that the biphasic changes recorded in mitochondrial inner membrane potential by the effect of cocaine, were parallel to apoptosis; second, that caspase-3 activity and cleavage to it p20 subunit increased sharply in parallel to the translocation of cytochrome c from mitochondria to cytosol; and third, that the antioxidants, NAC or DFO exerted a noticeable protective role in counteracting the cytotoxicity of cocaine, these effects being more pronounced in the case of DFO than NAC.	Acetylcysteine	345-348	heat shock protein family B (small) member 6	Rattus norvegicus	202-205
11245650-10	2001	The combined effects of LPC, H(2)O(2), and 5HT on DNA synthesis were completely reversed by the combined use of an antioxidant, N:-acetylcysteine (400 micromol/L) or butylated hydroxytoluene (20 micromol/L), with a 5HT(2) receptor antagonist, LY281067 (10 microg/mL).	Acetylcysteine	128-145	proprotein convertase subtilisin/kexin type 7	Homo sapiens	24-27
11245650-10	2001	The combined effects of LPC, H(2)O(2), and 5HT on DNA synthesis were completely reversed by the combined use of an antioxidant, N:-acetylcysteine (400 micromol/L) or butylated hydroxytoluene (20 micromol/L), with a 5HT(2) receptor antagonist, LY281067 (10 microg/mL).	Acetylcysteine	128-145	5-hydroxytryptamine receptor 2A	Homo sapiens	215-230
11290857-13	2001	Scavenging ROS by Mn(III)tetrakis(1-methyl-4pyridyl)porphyrin pentachloride and N-acetyl-L-cysteine attenuated chronic EtOH-enhanced TNF-alpha production.	Acetylcysteine	80-99	tumor necrosis factor	Homo sapiens	133-142
11226137-6	2001	We conclude: first, that the biphasic changes recorded in mitochondrial inner membrane potential by the effect of cocaine, were parallel to apoptosis; second, that caspase-3 activity and cleavage to it p20 subunit increased sharply in parallel to the translocation of cytochrome c from mitochondria to cytosol; and third, that the antioxidants, NAC or DFO exerted a noticeable protective role in counteracting the cytotoxicity of cocaine, these effects being more pronounced in the case of DFO than NAC.	Acetylcysteine	499-502	heat shock protein family B (small) member 6	Rattus norvegicus	202-205
11319613-3	2001	In this study, we confirmed that recombinant AIP generated enough H2O2 in culture medium to induce rapid apoptosis in cells and this apoptosis was clearly inhibited by co-cultivation with antioxidants such as catalase and N-acetyl-cysteine.	Acetylcysteine	222-239	aryl hydrocarbon receptor interacting protein	Homo sapiens	45-48
11332652-3	2001	Enhanced INFgamma production was not induced by either anti-CD3 or PMA alone, or anti-CD3 or ConA with anti-CD28, or enhanced by N-acetylcysteine.	Acetylcysteine	129-145	interferon gamma	Homo sapiens	9-17
11159825-7	2001	Inhibition of nuclear factor-kappaB activation by N-acetyl-cysteine and SN50 suppressed Xiap protein expression and enhanced apoptosis induced by TNFalpha.	Acetylcysteine	50-67	tumor necrosis factor	Rattus norvegicus	146-154
11162642-0	2001	N-acetylcysteine inhibits angiotensin ii-mediated activation of extracellular signal-regulated kinase and epidermal growth factor receptor.	Acetylcysteine	0-16	angiotensinogen	Homo sapiens	26-40
11162642-0	2001	N-acetylcysteine inhibits angiotensin ii-mediated activation of extracellular signal-regulated kinase and epidermal growth factor receptor.	Acetylcysteine	0-16	mitogen-activated protein kinase 1	Homo sapiens	64-101
11162642-0	2001	N-acetylcysteine inhibits angiotensin ii-mediated activation of extracellular signal-regulated kinase and epidermal growth factor receptor.	Acetylcysteine	0-16	epidermal growth factor receptor	Homo sapiens	106-138
11162642-3	2001	Here we found that an antioxidant, N-acetylcysteine, inhibited ERK activation and EGF receptor tyrosine phosphorylation induced by Ang II.	Acetylcysteine	35-51	mitogen-activated protein kinase 1	Homo sapiens	63-66
11162642-3	2001	Here we found that an antioxidant, N-acetylcysteine, inhibited ERK activation and EGF receptor tyrosine phosphorylation induced by Ang II.	Acetylcysteine	35-51	epidermal growth factor receptor	Homo sapiens	82-94
11162642-3	2001	Here we found that an antioxidant, N-acetylcysteine, inhibited ERK activation and EGF receptor tyrosine phosphorylation induced by Ang II.	Acetylcysteine	35-51	angiotensinogen	Homo sapiens	131-137
11935096-5	2001	As is the case for MHBs(t167), MHBsKDEL-dependent activation of NFkappaB is inhibited by the antioxidant N-acetyl-L-cysteine indicating the involvement of reactive oxygen intermediates and suggesting a similar mechanism of activation.	Acetylcysteine	105-124	nuclear factor kappa B subunit 1	Homo sapiens	64-72
11230331-8	2001	Ang II-induced ERK activation was inhibited by NAC as well as by PD98059.	Acetylcysteine	47-50	Eph receptor B1	Rattus norvegicus	15-18
11167962-3	2001	It has previously been shown that tumour necrosis factor (TNF)-MA activates p38 mitogen-activated protein (MAP) kinase to produce cytokine, including RANTES, that N-acetylcysteine (NAC) attenuates cytokine production by human bronchial epithelial cells (BECs), and that sensitivity to TNFalpha is inversely correlated with cellular redox state.	Acetylcysteine	163-179	tumor necrosis factor	Homo sapiens	34-56
11167962-3	2001	It has previously been shown that tumour necrosis factor (TNF)-MA activates p38 mitogen-activated protein (MAP) kinase to produce cytokine, including RANTES, that N-acetylcysteine (NAC) attenuates cytokine production by human bronchial epithelial cells (BECs), and that sensitivity to TNFalpha is inversely correlated with cellular redox state.	Acetylcysteine	163-179	tumor necrosis factor	Homo sapiens	58-61
11167962-3	2001	It has previously been shown that tumour necrosis factor (TNF)-MA activates p38 mitogen-activated protein (MAP) kinase to produce cytokine, including RANTES, that N-acetylcysteine (NAC) attenuates cytokine production by human bronchial epithelial cells (BECs), and that sensitivity to TNFalpha is inversely correlated with cellular redox state.	Acetylcysteine	163-179	mitogen-activated protein kinase 14	Homo sapiens	76-79
11167962-3	2001	It has previously been shown that tumour necrosis factor (TNF)-MA activates p38 mitogen-activated protein (MAP) kinase to produce cytokine, including RANTES, that N-acetylcysteine (NAC) attenuates cytokine production by human bronchial epithelial cells (BECs), and that sensitivity to TNFalpha is inversely correlated with cellular redox state.	Acetylcysteine	163-179	tumor necrosis factor	Homo sapiens	285-293
11167962-3	2001	It has previously been shown that tumour necrosis factor (TNF)-MA activates p38 mitogen-activated protein (MAP) kinase to produce cytokine, including RANTES, that N-acetylcysteine (NAC) attenuates cytokine production by human bronchial epithelial cells (BECs), and that sensitivity to TNFalpha is inversely correlated with cellular redox state.	Acetylcysteine	181-184	tumor necrosis factor	Homo sapiens	34-56
11167962-3	2001	It has previously been shown that tumour necrosis factor (TNF)-MA activates p38 mitogen-activated protein (MAP) kinase to produce cytokine, including RANTES, that N-acetylcysteine (NAC) attenuates cytokine production by human bronchial epithelial cells (BECs), and that sensitivity to TNFalpha is inversely correlated with cellular redox state.	Acetylcysteine	181-184	tumor necrosis factor	Homo sapiens	58-61
11167962-3	2001	It has previously been shown that tumour necrosis factor (TNF)-MA activates p38 mitogen-activated protein (MAP) kinase to produce cytokine, including RANTES, that N-acetylcysteine (NAC) attenuates cytokine production by human bronchial epithelial cells (BECs), and that sensitivity to TNFalpha is inversely correlated with cellular redox state.	Acetylcysteine	181-184	mitogen-activated protein kinase 14	Homo sapiens	76-79
11167962-3	2001	It has previously been shown that tumour necrosis factor (TNF)-MA activates p38 mitogen-activated protein (MAP) kinase to produce cytokine, including RANTES, that N-acetylcysteine (NAC) attenuates cytokine production by human bronchial epithelial cells (BECs), and that sensitivity to TNFalpha is inversely correlated with cellular redox state.	Acetylcysteine	181-184	tumor necrosis factor	Homo sapiens	285-293
11230331-5	2001	Preincubation of vascular smooth muscle cells with N:-acetylcysteine (NAC), a potent antioxidant, almost completely inhibited the Ang II-induced downregulation of AT(1)-R mRNA.	Acetylcysteine	51-68	angiotensinogen	Rattus norvegicus	130-136
11230331-5	2001	Preincubation of vascular smooth muscle cells with N:-acetylcysteine (NAC), a potent antioxidant, almost completely inhibited the Ang II-induced downregulation of AT(1)-R mRNA.	Acetylcysteine	70-73	angiotensinogen	Rattus norvegicus	130-136
11230331-6	2001	The effect of NAC was due to stabilization of the AT(1)-R mRNA that was destabilized by Ang II.	Acetylcysteine	14-17	angiotensinogen	Rattus norvegicus	88-94
11230331-8	2001	Ang II-induced ERK activation was inhibited by NAC as well as by PD98059.	Acetylcysteine	47-50	angiotensinogen	Rattus norvegicus	0-6
23886278-8	2001	Monovariate analyses showed that GSTM1 polymorphism was clearly the most significant parameter infiuencing urinary concentrations of mercapturic acids.	Acetylcysteine	133-150	glutathione S-transferase mu 1	Homo sapiens	33-38
11156586-0	2001	N-acetylcysteine attenuates TNF-alpha-induced p38 MAP kinase activation and p38 MAP kinase-mediated IL-8 production by human pulmonary vascular endothelial cells.	Acetylcysteine	0-16	tumor necrosis factor	Homo sapiens	28-37
11156586-0	2001	N-acetylcysteine attenuates TNF-alpha-induced p38 MAP kinase activation and p38 MAP kinase-mediated IL-8 production by human pulmonary vascular endothelial cells.	Acetylcysteine	0-16	mitogen-activated protein kinase 14	Homo sapiens	46-49
11156586-0	2001	N-acetylcysteine attenuates TNF-alpha-induced p38 MAP kinase activation and p38 MAP kinase-mediated IL-8 production by human pulmonary vascular endothelial cells.	Acetylcysteine	0-16	mitogen-activated protein kinase 14	Homo sapiens	76-79
11156586-0	2001	N-acetylcysteine attenuates TNF-alpha-induced p38 MAP kinase activation and p38 MAP kinase-mediated IL-8 production by human pulmonary vascular endothelial cells.	Acetylcysteine	0-16	C-X-C motif chemokine ligand 8	Homo sapiens	100-104
11156586-4	2001	However, the effect of N-acetylcysteine (NAC), which acts as a precursor of glutathione (GSH) synthesis, on TNF-alpha-induced activation of p38 MAP kinase pathway and p38 MAP kinase-mediated IL-8 production by human pulmonary vascular endothelial cells has not been determined.	Acetylcysteine	23-39	tumor necrosis factor	Homo sapiens	108-117
11156586-4	2001	However, the effect of N-acetylcysteine (NAC), which acts as a precursor of glutathione (GSH) synthesis, on TNF-alpha-induced activation of p38 MAP kinase pathway and p38 MAP kinase-mediated IL-8 production by human pulmonary vascular endothelial cells has not been determined.	Acetylcysteine	23-39	mitogen-activated protein kinase 14	Homo sapiens	140-143
11156586-4	2001	However, the effect of N-acetylcysteine (NAC), which acts as a precursor of glutathione (GSH) synthesis, on TNF-alpha-induced activation of p38 MAP kinase pathway and p38 MAP kinase-mediated IL-8 production by human pulmonary vascular endothelial cells has not been determined.	Acetylcysteine	23-39	mitogen-activated protein kinase 14	Homo sapiens	167-170
11156586-4	2001	However, the effect of N-acetylcysteine (NAC), which acts as a precursor of glutathione (GSH) synthesis, on TNF-alpha-induced activation of p38 MAP kinase pathway and p38 MAP kinase-mediated IL-8 production by human pulmonary vascular endothelial cells has not been determined.	Acetylcysteine	23-39	C-X-C motif chemokine ligand 8	Homo sapiens	191-195
11156586-4	2001	However, the effect of N-acetylcysteine (NAC), which acts as a precursor of glutathione (GSH) synthesis, on TNF-alpha-induced activation of p38 MAP kinase pathway and p38 MAP kinase-mediated IL-8 production by human pulmonary vascular endothelial cells has not been determined.	Acetylcysteine	41-44	tumor necrosis factor	Homo sapiens	108-117
11156586-4	2001	However, the effect of N-acetylcysteine (NAC), which acts as a precursor of glutathione (GSH) synthesis, on TNF-alpha-induced activation of p38 MAP kinase pathway and p38 MAP kinase-mediated IL-8 production by human pulmonary vascular endothelial cells has not been determined.	Acetylcysteine	41-44	mitogen-activated protein kinase 14	Homo sapiens	140-143
11156586-4	2001	However, the effect of N-acetylcysteine (NAC), which acts as a precursor of glutathione (GSH) synthesis, on TNF-alpha-induced activation of p38 MAP kinase pathway and p38 MAP kinase-mediated IL-8 production by human pulmonary vascular endothelial cells has not been determined.	Acetylcysteine	41-44	mitogen-activated protein kinase 14	Homo sapiens	167-170
11156586-4	2001	However, the effect of N-acetylcysteine (NAC), which acts as a precursor of glutathione (GSH) synthesis, on TNF-alpha-induced activation of p38 MAP kinase pathway and p38 MAP kinase-mediated IL-8 production by human pulmonary vascular endothelial cells has not been determined.	Acetylcysteine	41-44	C-X-C motif chemokine ligand 8	Homo sapiens	191-195
11156586-5	2001	To clarify these issues, we examined the effect of NAC on TNF-alpha-induced activation of p38 MAP kinase, MAP kinase kinase (MKK) 3 and MKK6 which are upstream regulators of p38 MAP kinase, and p38 MAP kinase-mediated IL-8 production.	Acetylcysteine	51-54	tumor necrosis factor	Homo sapiens	58-67
11156586-5	2001	To clarify these issues, we examined the effect of NAC on TNF-alpha-induced activation of p38 MAP kinase, MAP kinase kinase (MKK) 3 and MKK6 which are upstream regulators of p38 MAP kinase, and p38 MAP kinase-mediated IL-8 production.	Acetylcysteine	51-54	mitogen-activated protein kinase 14	Homo sapiens	90-104
11156586-5	2001	To clarify these issues, we examined the effect of NAC on TNF-alpha-induced activation of p38 MAP kinase, MAP kinase kinase (MKK) 3 and MKK6 which are upstream regulators of p38 MAP kinase, and p38 MAP kinase-mediated IL-8 production.	Acetylcysteine	51-54	mitogen-activated protein kinase kinase 6	Homo sapiens	136-140
11156586-5	2001	To clarify these issues, we examined the effect of NAC on TNF-alpha-induced activation of p38 MAP kinase, MAP kinase kinase (MKK) 3 and MKK6 which are upstream regulators of p38 MAP kinase, and p38 MAP kinase-mediated IL-8 production.	Acetylcysteine	51-54	mitogen-activated protein kinase 14	Homo sapiens	90-93
11156586-5	2001	To clarify these issues, we examined the effect of NAC on TNF-alpha-induced activation of p38 MAP kinase, MAP kinase kinase (MKK) 3 and MKK6 which are upstream regulators of p38 MAP kinase, and p38 MAP kinase-mediated IL-8 production.	Acetylcysteine	51-54	mitogen-activated protein kinase 14	Homo sapiens	174-177
11156586-7	2001	Human pulmonary vascular endothelial cells that had been preincubated with NAC were stimulated with TNF-alpha and then the activation of p38 MAP kinase and MKK3/MKK6 in the cells and IL-8 concentrations in the culture supernatants were determined.	Acetylcysteine	75-78	tumor necrosis factor	Homo sapiens	100-109
11156586-7	2001	Human pulmonary vascular endothelial cells that had been preincubated with NAC were stimulated with TNF-alpha and then the activation of p38 MAP kinase and MKK3/MKK6 in the cells and IL-8 concentrations in the culture supernatants were determined.	Acetylcysteine	75-78	mitogen-activated protein kinase 14	Homo sapiens	137-151
11156586-7	2001	Human pulmonary vascular endothelial cells that had been preincubated with NAC were stimulated with TNF-alpha and then the activation of p38 MAP kinase and MKK3/MKK6 in the cells and IL-8 concentrations in the culture supernatants were determined.	Acetylcysteine	75-78	mitogen-activated protein kinase kinase 6	Homo sapiens	161-165
11156586-7	2001	Human pulmonary vascular endothelial cells that had been preincubated with NAC were stimulated with TNF-alpha and then the activation of p38 MAP kinase and MKK3/MKK6 in the cells and IL-8 concentrations in the culture supernatants were determined.	Acetylcysteine	75-78	C-X-C motif chemokine ligand 8	Homo sapiens	183-187
11156586-11	2001	NAC attenuated TNF-alpha-induced activation of p38 MAP kinase and MKK3/MKK6.	Acetylcysteine	0-3	tumor necrosis factor	Homo sapiens	15-24
11156586-11	2001	NAC attenuated TNF-alpha-induced activation of p38 MAP kinase and MKK3/MKK6.	Acetylcysteine	0-3	mitogen-activated protein kinase 14	Homo sapiens	47-61
11156586-11	2001	NAC attenuated TNF-alpha-induced activation of p38 MAP kinase and MKK3/MKK6.	Acetylcysteine	0-3	mitogen-activated protein kinase kinase 6	Homo sapiens	71-75
11156586-13	2001	NAC attenuated p38 MAP kinase-mediated IL-8 production by TNF-alpha-stimulated cells.	Acetylcysteine	0-3	mitogen-activated protein kinase 14	Homo sapiens	15-18
11156586-13	2001	NAC attenuated p38 MAP kinase-mediated IL-8 production by TNF-alpha-stimulated cells.	Acetylcysteine	0-3	C-X-C motif chemokine ligand 8	Homo sapiens	39-43
11156586-13	2001	NAC attenuated p38 MAP kinase-mediated IL-8 production by TNF-alpha-stimulated cells.	Acetylcysteine	0-3	tumor necrosis factor	Homo sapiens	58-67
11133225-8	2001	Pretreatment of HUVEC with pyrrolidine dithiocarbamate (PDTC) or N-acetylcysteine (NAC) completely prevented IL-4-induced VCAM-1 expression.	Acetylcysteine	65-81	interleukin 4	Homo sapiens	109-113
22387694-5	2001	Both vitamin E and NAC prevented Abeta-induced ROS generation when applied simultaneously with Abeta, but only NAC prevented Abeta-induced ROS generation when added to cultures that had previously been exposed to Abeta.	Acetylcysteine	19-22	amyloid beta precursor protein	Homo sapiens	33-38
22387694-5	2001	Both vitamin E and NAC prevented Abeta-induced ROS generation when applied simultaneously with Abeta, but only NAC prevented Abeta-induced ROS generation when added to cultures that had previously been exposed to Abeta.	Acetylcysteine	19-22	amyloid beta precursor protein	Homo sapiens	95-100
22387694-5	2001	Both vitamin E and NAC prevented Abeta-induced ROS generation when applied simultaneously with Abeta, but only NAC prevented Abeta-induced ROS generation when added to cultures that had previously been exposed to Abeta.	Acetylcysteine	19-22	amyloid beta precursor protein	Homo sapiens	95-100
22387694-5	2001	Both vitamin E and NAC prevented Abeta-induced ROS generation when applied simultaneously with Abeta, but only NAC prevented Abeta-induced ROS generation when added to cultures that had previously been exposed to Abeta.	Acetylcysteine	19-22	amyloid beta precursor protein	Homo sapiens	95-100
11053978-4	2001	The free radical scavengers, dimethylthiourea and N-acetylcysteine inhibited HB-EGF mRNA induction.	Acetylcysteine	50-66	heparin-binding EGF-like growth factor	Rattus norvegicus	77-83
11500943-7	2001	Co-culture of cells with the antioxidants quercetin, dimethyltiourea and N-acetyl cysteine abolished both the iron-induced oxidative damage and the iron-induced increase in calreticulin.	Acetylcysteine	73-90	calreticulin	Homo sapiens	173-185
11133225-8	2001	Pretreatment of HUVEC with pyrrolidine dithiocarbamate (PDTC) or N-acetylcysteine (NAC) completely prevented IL-4-induced VCAM-1 expression.	Acetylcysteine	65-81	vascular cell adhesion molecule 1	Homo sapiens	122-128
11133225-8	2001	Pretreatment of HUVEC with pyrrolidine dithiocarbamate (PDTC) or N-acetylcysteine (NAC) completely prevented IL-4-induced VCAM-1 expression.	Acetylcysteine	83-86	interleukin 4	Homo sapiens	109-113
11133225-8	2001	Pretreatment of HUVEC with pyrrolidine dithiocarbamate (PDTC) or N-acetylcysteine (NAC) completely prevented IL-4-induced VCAM-1 expression.	Acetylcysteine	83-86	vascular cell adhesion molecule 1	Homo sapiens	122-128
11124598-9	2000	In contrast, NAC increased TNF-alpha and IL-10 mRNAs (p &lt; 0.05).	Acetylcysteine	13-16	tumor necrosis factor	Rattus norvegicus	27-36
11087229-4	2000	Adventitial NOS-2 activity largely accounted for 1) the relaxing effect of L-arginine in rings exposed to LPS in vivo, 2) generation of an "NO store" revealed by N-acetylcysteine-induced relaxation, and 3) formation of protein-bound dinitrosyl iron complexes in the medial layer of aortic rings exposed to LPS in vitro.	Acetylcysteine	162-178	nitric oxide synthase 2	Rattus norvegicus	12-17
11112413-5	2000	Furthermore, pretreatment of C6 cells with N-acetyl-l-cysteine (NAC), an antioxidant, nullified the inhibitory effect of iNOS on HIF-1 binding.	Acetylcysteine	43-62	nitric oxide synthase 2	Homo sapiens	121-125
11112413-5	2000	Furthermore, pretreatment of C6 cells with N-acetyl-l-cysteine (NAC), an antioxidant, nullified the inhibitory effect of iNOS on HIF-1 binding.	Acetylcysteine	43-62	hypoxia inducible factor 1 subunit alpha	Homo sapiens	129-134
11024008-6	2000	C5b-9 also induced formation of reactive oxygen species, which, along with IL-6 release, was inhibited by the antioxidant N-acetylcysteine.	Acetylcysteine	122-138	interleukin 6	Homo sapiens	75-79
11428622-7	2000	In this study, we tested the hypotheses that pretreatment with NAC acts through two different pathways to minimize endothelial injury by HD: NAC pretreatment acts via a glutathione (GSH)-dependent pathway; and NAC pretreatment acts to suppress HD-induced activation of the nuclear transcription factor NFkappaB.	Acetylcysteine	63-66	nuclear factor kappa B subunit 1	Homo sapiens	302-310
11428622-19	2000	Paradoxically, treatment of the endothelial cells alone with 50 mM NAC activated NFkappaB, although HD-induced activation of NFkappaB was partially suppressed by NAC at 5 h. Factor NFkappaB is an important transcription factor for a number of cytokine genes (e.g. tumor necrosis factor, TNF), which can be activated following stress in endothelial cells.	Acetylcysteine	67-70	nuclear factor kappa B subunit 1	Homo sapiens	81-89
11428622-19	2000	Paradoxically, treatment of the endothelial cells alone with 50 mM NAC activated NFkappaB, although HD-induced activation of NFkappaB was partially suppressed by NAC at 5 h. Factor NFkappaB is an important transcription factor for a number of cytokine genes (e.g. tumor necrosis factor, TNF), which can be activated following stress in endothelial cells.	Acetylcysteine	162-165	nuclear factor kappa B subunit 1	Homo sapiens	125-133
11428622-19	2000	Paradoxically, treatment of the endothelial cells alone with 50 mM NAC activated NFkappaB, although HD-induced activation of NFkappaB was partially suppressed by NAC at 5 h. Factor NFkappaB is an important transcription factor for a number of cytokine genes (e.g. tumor necrosis factor, TNF), which can be activated following stress in endothelial cells.	Acetylcysteine	162-165	nuclear factor kappa B subunit 1	Homo sapiens	125-133
11428622-19	2000	Paradoxically, treatment of the endothelial cells alone with 50 mM NAC activated NFkappaB, although HD-induced activation of NFkappaB was partially suppressed by NAC at 5 h. Factor NFkappaB is an important transcription factor for a number of cytokine genes (e.g. tumor necrosis factor, TNF), which can be activated following stress in endothelial cells.	Acetylcysteine	162-165	tumor necrosis factor	Homo sapiens	287-290
11428622-22	2000	Under some conditions, NAC may act as an oxidizing agent and thus increase NFkappaB activity.	Acetylcysteine	23-26	nuclear factor kappa B subunit 1	Homo sapiens	75-83
11076697-7	2000	Antioxidants, such as superoxide dismutase (SOD), N-acetylcysteine (NAC), and pyrrolidine dithiocarbamate (PDTC), blocked tyrosine phosphorylation of I kappa B-alpha induced by silica, suggesting reactive oxygen species (ROS) may be important regulatory molecules in NF-kappa B activation through tyrosine phosphorylation of I kappa B-alpha.	Acetylcysteine	50-66	NFKB inhibitor alpha	Homo sapiens	150-165
11102554-9	2000	Addition of the antioxidant N-acetyl-cysteine effectively blocked TNF-alpha-induced granulocyte apoptosis as demonstrated by DNA fragmentation.	Acetylcysteine	28-45	tumor necrosis factor	Homo sapiens	66-75
11063911-9	2000	Pretreatment with N-acetylcysteine, a thiocompound with antioxidant activity and a precursor of glutathione, prevented Cd(2+)-induced (i) reduction in glutathione levels and (ii) induction of HSP72 and diminished (i) Cd(2+) uptake and (ii) Cd(2+)-evoked cell death.	Acetylcysteine	18-34	heat shock protein family A (Hsp70) member 1A	Homo sapiens	192-197
11015349-8	2000	Exogenous TNF-alpha 500 micromol/L increased oxidant production in diaphragm of wild-type mice and caused weakness that was inhibited by N:-acetylcysteine, suggesting that changes observed in the diaphragm of transgenic animals were mediated by TNF-alpha.	Acetylcysteine	137-154	tumor necrosis factor	Mus musculus	10-19
11074303-7	2000	A variety of antioxidants, such as catalase, superoxide dismutase, N-acetyl cysteine (NAC), and pyrrolidine dithiocarbamate, inhibited NF-kappaB activation induced by pervanadate in the presence of silica.	Acetylcysteine	67-84	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	135-144
11074303-7	2000	A variety of antioxidants, such as catalase, superoxide dismutase, N-acetyl cysteine (NAC), and pyrrolidine dithiocarbamate, inhibited NF-kappaB activation induced by pervanadate in the presence of silica.	Acetylcysteine	86-89	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	135-144
11197525-4	2000	The involvement of ROS is suggested by experiments where the stimulation of fibroblasts with TNF-alpha or IL-1alpha are performed in the presence of N-acetylcysteine which increases the intracellular antioxidant potential.	Acetylcysteine	149-165	tumor necrosis factor	Homo sapiens	93-102
11079466-0	2000	Regulation of cyclooxygenase-2 expression in human osteoblastic cells by N-acetylcysteine.	Acetylcysteine	73-89	prostaglandin-endoperoxide synthase 2	Homo sapiens	14-30
11079466-4	2000	We examined whether the antioxidant N-acetylcysteine (NAC) inhibited COX-2 expression induced in the human osteoblastic cell line MG63 by interleukin-1beta (IL-1beta).	Acetylcysteine	36-52	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	69-74
11079466-4	2000	We examined whether the antioxidant N-acetylcysteine (NAC) inhibited COX-2 expression induced in the human osteoblastic cell line MG63 by interleukin-1beta (IL-1beta).	Acetylcysteine	36-52	interleukin 1 beta	Homo sapiens	138-155
11079466-4	2000	We examined whether the antioxidant N-acetylcysteine (NAC) inhibited COX-2 expression induced in the human osteoblastic cell line MG63 by interleukin-1beta (IL-1beta).	Acetylcysteine	36-52	interleukin 1 beta	Homo sapiens	157-165
11079466-4	2000	We examined whether the antioxidant N-acetylcysteine (NAC) inhibited COX-2 expression induced in the human osteoblastic cell line MG63 by interleukin-1beta (IL-1beta).	Acetylcysteine	54-57	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	69-74
11079466-4	2000	We examined whether the antioxidant N-acetylcysteine (NAC) inhibited COX-2 expression induced in the human osteoblastic cell line MG63 by interleukin-1beta (IL-1beta).	Acetylcysteine	54-57	interleukin 1 beta	Homo sapiens	138-155
11079466-4	2000	We examined whether the antioxidant N-acetylcysteine (NAC) inhibited COX-2 expression induced in the human osteoblastic cell line MG63 by interleukin-1beta (IL-1beta).	Acetylcysteine	54-57	interleukin 1 beta	Homo sapiens	157-165
11079466-5	2000	According to Western blot and reverse transcription-polymerase chain reaction (RT-PCR) test results, NAC inhibited IL-1beta-induced COX-2 expression in protein and messenger RNA.	Acetylcysteine	101-104	interleukin 1 beta	Homo sapiens	115-123
11079466-5	2000	According to Western blot and reverse transcription-polymerase chain reaction (RT-PCR) test results, NAC inhibited IL-1beta-induced COX-2 expression in protein and messenger RNA.	Acetylcysteine	101-104	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	132-137
11079466-6	2000	We also demonstrated immunohistochemically that NAC inhibited NFkappaB nuclear translocation.	Acetylcysteine	48-51	nuclear factor kappa B subunit 1	Homo sapiens	62-70
11079466-7	2000	These results suggested that NAC inhibited both COX-2 expression and NFkappaB nuclear translocation in MG63, which in turn indicated that NAC could inhibit the inflammatory process involved in bone resorption by regulating COX-2 expression at the level of transcription.	Acetylcysteine	29-32	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	48-53
11079466-7	2000	These results suggested that NAC inhibited both COX-2 expression and NFkappaB nuclear translocation in MG63, which in turn indicated that NAC could inhibit the inflammatory process involved in bone resorption by regulating COX-2 expression at the level of transcription.	Acetylcysteine	29-32	nuclear factor kappa B subunit 1	Homo sapiens	69-77
11079466-7	2000	These results suggested that NAC inhibited both COX-2 expression and NFkappaB nuclear translocation in MG63, which in turn indicated that NAC could inhibit the inflammatory process involved in bone resorption by regulating COX-2 expression at the level of transcription.	Acetylcysteine	29-32	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	223-228
11079466-7	2000	These results suggested that NAC inhibited both COX-2 expression and NFkappaB nuclear translocation in MG63, which in turn indicated that NAC could inhibit the inflammatory process involved in bone resorption by regulating COX-2 expression at the level of transcription.	Acetylcysteine	138-141	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	48-53
11079466-7	2000	These results suggested that NAC inhibited both COX-2 expression and NFkappaB nuclear translocation in MG63, which in turn indicated that NAC could inhibit the inflammatory process involved in bone resorption by regulating COX-2 expression at the level of transcription.	Acetylcysteine	138-141	nuclear factor kappa B subunit 1	Homo sapiens	69-77
11079466-7	2000	These results suggested that NAC inhibited both COX-2 expression and NFkappaB nuclear translocation in MG63, which in turn indicated that NAC could inhibit the inflammatory process involved in bone resorption by regulating COX-2 expression at the level of transcription.	Acetylcysteine	138-141	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	223-228
11015349-8	2000	Exogenous TNF-alpha 500 micromol/L increased oxidant production in diaphragm of wild-type mice and caused weakness that was inhibited by N:-acetylcysteine, suggesting that changes observed in the diaphragm of transgenic animals were mediated by TNF-alpha.	Acetylcysteine	137-154	tumor necrosis factor	Mus musculus	245-254
11062741-7	2000	Treatment with NAC protected endothelial cells from TGF-beta-induced apoptosis and paraquat-induced cytogenetic damage.	Acetylcysteine	15-18	transforming growth factor beta 1	Homo sapiens	52-60
11029375-7	2000	Pretreatment with the radical scavenger N-acetylcysteine partly protected against LPS-induced AHR.	Acetylcysteine	40-56	toll-like receptor 4	Mus musculus	82-85
11031216-10	2000	Incubation of ECs with N:-acetyl cysteine inhibited production of IL-8 and MCP-1 induced by LDL(-) and oxLDL by &gt;50%.	Acetylcysteine	23-41	C-X-C motif chemokine ligand 8	Homo sapiens	66-70
11029607-9	2000	T cell GSH, adjusted for CD4 T cell count and beta2-microglobulin levels, also increased in the NAC-treated subjects (P = 0.04).	Acetylcysteine	96-99	CD4 molecule	Homo sapiens	25-28
11033415-4	2000	Tempol did not affect the relative levels of Bax and Bcl2, whereas p21(WAF1/CIP1) was enhanced in a concentration- and time-dependent fashion; this effect was partially inhibited by N-acetylcysteine, was maintained for up to 8 h after Tempol removal, and seemed to depend on continuing protein synthesis.	Acetylcysteine	182-198	cyclin dependent kinase inhibitor 1A	Homo sapiens	67-70
11033415-4	2000	Tempol did not affect the relative levels of Bax and Bcl2, whereas p21(WAF1/CIP1) was enhanced in a concentration- and time-dependent fashion; this effect was partially inhibited by N-acetylcysteine, was maintained for up to 8 h after Tempol removal, and seemed to depend on continuing protein synthesis.	Acetylcysteine	182-198	cyclin dependent kinase inhibitor 1A	Homo sapiens	71-75
11033415-4	2000	Tempol did not affect the relative levels of Bax and Bcl2, whereas p21(WAF1/CIP1) was enhanced in a concentration- and time-dependent fashion; this effect was partially inhibited by N-acetylcysteine, was maintained for up to 8 h after Tempol removal, and seemed to depend on continuing protein synthesis.	Acetylcysteine	182-198	cyclin dependent kinase inhibitor 1A	Homo sapiens	76-80
10975858-6	2000	N-acetyl cysteine and the flavonoid, luteolin, inhibited HO-1 protein expression.	Acetylcysteine	0-17	heme oxygenase 1	Mus musculus	57-61
10970698-3	2000	We extend these findings and show that the stimulation of JNK and apoptosis by antagonist G is dependent upon the generation of reactive oxygen species (ROS) being inhibited either by anoxia or the presence of N-acetyl cysteine (n-AC).	Acetylcysteine	210-227	mitogen-activated protein kinase 8	Homo sapiens	58-61
10970698-3	2000	We extend these findings and show that the stimulation of JNK and apoptosis by antagonist G is dependent upon the generation of reactive oxygen species (ROS) being inhibited either by anoxia or the presence of N-acetyl cysteine (n-AC).	Acetylcysteine	229-233	mitogen-activated protein kinase 8	Homo sapiens	58-61
11003618-10	2000	We also found that supplementation of GGT(-/-) mice with N-acetylcysteine (NAC) partially restored liver GSH, but fully restored mitochondrial GSH and respiratory function.	Acetylcysteine	57-73	gamma-glutamyltransferase 1	Mus musculus	38-41
11003618-10	2000	We also found that supplementation of GGT(-/-) mice with N-acetylcysteine (NAC) partially restored liver GSH, but fully restored mitochondrial GSH and respiratory function.	Acetylcysteine	75-78	gamma-glutamyltransferase 1	Mus musculus	38-41
11003618-11	2000	Electron microscopy revealed that the livers of NAC-supplemented GGT(-/-) mice contained fat and glycogen; however, slightly enlarged mitochondria were found in some livers.	Acetylcysteine	48-51	gamma-glutamyltransferase 1	Mus musculus	65-68
10976006-0	2000	Differential effects of N-acetyl-l-cysteine on IL-2- vs IL-12-driven proliferation of a T cell clone: implications for distinct signalling pathways.	Acetylcysteine	24-43	interleukin 2	Homo sapiens	47-51
11042671-6	2000	Reduced glutathione or N-acetylcysteine, which could reduce ceramide formation by inhibiting sphingomyelinase activity, prevented C6 cells from etoposide-induced apoptosis through blockage of caspase-3 activation and change of the Bax/Bcl-2 ratio.	Acetylcysteine	23-39	caspase 3	Homo sapiens	192-201
11042671-6	2000	Reduced glutathione or N-acetylcysteine, which could reduce ceramide formation by inhibiting sphingomyelinase activity, prevented C6 cells from etoposide-induced apoptosis through blockage of caspase-3 activation and change of the Bax/Bcl-2 ratio.	Acetylcysteine	23-39	BCL2 associated X, apoptosis regulator	Homo sapiens	231-234
11042671-6	2000	Reduced glutathione or N-acetylcysteine, which could reduce ceramide formation by inhibiting sphingomyelinase activity, prevented C6 cells from etoposide-induced apoptosis through blockage of caspase-3 activation and change of the Bax/Bcl-2 ratio.	Acetylcysteine	23-39	BCL2 apoptosis regulator	Homo sapiens	235-240
10976006-1	2000	Using a T cell clone (2D6) capable of responding to IL-2 and IL-12, we compared the effects of NAC on IL-2 and IL-12-driven T cell proliferation.	Acetylcysteine	95-98	interleukin 2	Homo sapiens	102-106
10951577-7	2000	The antioxidant N-acetylcysteine and the Cu/Zn superoxide dismutase inhibitor diethyldithiocarbamic acid abolished the hypoxia-induced increases in ROS and p53 levels.	Acetylcysteine	16-32	tumor protein p53	Homo sapiens	156-159
12657201-5	2000	Administration of the antioxidant N-acetylcysteine (NAC,1 g/kg per day, orally) significantly decreased the mortality in infected mice, indicating a role for RO1 in the lethality associated with influenza infection.	Acetylcysteine	34-50	nucleus accumbens associated 1, BEN and BTB (POZ) domain containing	Mus musculus	52-57
10963726-10	2000	NAC treatment markedly reduced the intensity and degree of P-selectin and ICAM-1 in tissue section from SAO-shocked rats.	Acetylcysteine	0-3	selectin P	Rattus norvegicus	59-69
10906152-8	2000	The flavoprotein inhibitor diphenylene iodinium, as well as the antioxidant N-acetylcysteine, prevented AngII-induced p44/42 MAP kinase phosphorylation, indicating involvement of reactive oxygen species generated by membrane-bound NAD(P)H oxidase.	Acetylcysteine	76-92	angiotensinogen	Homo sapiens	104-109
10856288-5	2000	N-Acetyl-l-cysteine, a precursor of anti-oxidant glutathione, canceled both p38 MAPK activation and abnormal cell cycle progression, whereas blockage of the kinase by specific inhibitor SB203580 allowed the appearance of apoptotic cells.	Acetylcysteine	0-19	mitogen-activated protein kinase 14	Homo sapiens	76-79
10801793-4	2000	N-Acetyl-l-cysteine, a glutathione (GSH) precursor and a potent scavenger of reactive oxygen species, induced HIF-1alpha and ameliorated NF-kappaB nuclear abundance and DNA binding activity, respectively, in a dose-dependent manner.	Acetylcysteine	0-19	hypoxia inducible factor 1 subunit alpha	Homo sapiens	110-120
10867640-11	2000	Bcl-2 overexpression or NAC can sustain the activity of NFkappaB.	Acetylcysteine	24-27	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	56-64
10900173-5	2000	This activation of ERK MAPKs was blocked by N-acetylcysteine (NAC), implicating a role for free radicals in the signalling events.	Acetylcysteine	44-60	mitogen-activated protein kinase 1	Homo sapiens	19-22
10900173-5	2000	This activation of ERK MAPKs was blocked by N-acetylcysteine (NAC), implicating a role for free radicals in the signalling events.	Acetylcysteine	62-65	mitogen-activated protein kinase 1	Homo sapiens	19-22
10801894-4	2000	Activation of ERK by ONOO(-) and H(2)O(2) was blocked by the antioxidant N-acetyl-l-cysteine.	Acetylcysteine	73-92	Eph receptor B1	Rattus norvegicus	14-17
10878378-7	2000	The antioxidants N-acetylcysteine and pyrrolidinedithiocarbamic acid abolished the hypoxic activation of NF-kappa B, TNF-alpha gene transcription, and increases in ROS levels.	Acetylcysteine	17-33	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	105-115
10878378-7	2000	The antioxidants N-acetylcysteine and pyrrolidinedithiocarbamic acid abolished the hypoxic activation of NF-kappa B, TNF-alpha gene transcription, and increases in ROS levels.	Acetylcysteine	17-33	tumor necrosis factor	Mus musculus	117-126
10873716-7	2000	Media supplementation with the glutathione precursor N-acetyl-cysteine (NAC) reduced PCB 77-induced JNK/SAPK.	Acetylcysteine	53-70	pyruvate carboxylase	Homo sapiens	85-88
10880232-5	2000	Aphidicolin also synergized with TNF and anti-Fas in inducing cell death which was prevented by reducing atmospheric oxygen or addition of n -acetyl cysteine, a scavenger of oxygen radicals.	Acetylcysteine	139-157	tumor necrosis factor	Homo sapiens	33-36
10913623-6	2000	The addition of NAC (1 mM) to the perfusate during hyperoxia blocked the induction of iNOS and restored GSH levels.	Acetylcysteine	16-19	nitric oxide synthase 2	Rattus norvegicus	86-90
10962206-5	2000	These alterations were delayed in MCF-7/ADR cells transfected with bcl-2 and completely suppressed by treatment with an antioxidant, N-acetyl-L-cysteine.	Acetylcysteine	133-152	BCL2 apoptosis regulator	Homo sapiens	67-72
10873716-7	2000	Media supplementation with the glutathione precursor N-acetyl-cysteine (NAC) reduced PCB 77-induced JNK/SAPK.	Acetylcysteine	53-70	mitogen-activated protein kinase 8	Homo sapiens	100-108
10873716-7	2000	Media supplementation with the glutathione precursor N-acetyl-cysteine (NAC) reduced PCB 77-induced JNK/SAPK.	Acetylcysteine	72-75	pyruvate carboxylase	Homo sapiens	85-88
10873716-7	2000	Media supplementation with the glutathione precursor N-acetyl-cysteine (NAC) reduced PCB 77-induced JNK/SAPK.	Acetylcysteine	72-75	mitogen-activated protein kinase 8	Homo sapiens	100-108
10925209-5	2000	The thiol antioxidant, N-acetylcysteine (NAC) abolished the synergism between IL-1beta or IL-6 and 1,25(OH)(2)D(3), but had only a small protective effect when the cytokines acted alone.	Acetylcysteine	23-39	interleukin 1 beta	Homo sapiens	78-86
10837337-9	2000	Cellular levels of reduced thiols correlated with cell death, and pretreatment with N-acetylcysteine (NAC) fully protected from cell death in either PAPA/NO or SIN-1 exposure.	Acetylcysteine	84-100	MAPK associated protein 1	Homo sapiens	160-165
10837337-9	2000	Cellular levels of reduced thiols correlated with cell death, and pretreatment with N-acetylcysteine (NAC) fully protected from cell death in either PAPA/NO or SIN-1 exposure.	Acetylcysteine	102-105	MAPK associated protein 1	Homo sapiens	160-165
10837337-10	2000	NAC given within the first 3 h posttreatment further delayed cell death and increased the intracellular thiol level in SIN-1 but not.	Acetylcysteine	0-3	MAPK associated protein 1	Homo sapiens	119-124
10925209-5	2000	The thiol antioxidant, N-acetylcysteine (NAC) abolished the synergism between IL-1beta or IL-6 and 1,25(OH)(2)D(3), but had only a small protective effect when the cytokines acted alone.	Acetylcysteine	23-39	interleukin 6	Homo sapiens	90-100
10894110-10	2000	Both N-acetylcysteine and pyrrolidine dithiocarbamate attenuated the action of DEP on IL-8 mRNA expression, suggesting that oxidant-mediated pathway might be involved in its processes.	Acetylcysteine	5-21	C-X-C motif chemokine ligand 8	Homo sapiens	86-90
10771256-9	2000	NAC improved markedly and stabilized the neurological symptoms in patients with EPM 1 but had a doubtful effect in the patient with EPM 2.	Acetylcysteine	0-3	cystatin B	Homo sapiens	80-85
10777712-7	2000	The antioxidant and GSH precursor N-acetyl-l-cysteine favored Bcl-2 at the expense of Bax/p53, whereas pyrrolidine dithiocarbamate induced Bax against Bcl-2, with mild effect on p53.	Acetylcysteine	34-53	BCL2 apoptosis regulator	Homo sapiens	62-67
11876867-0	2000	[The effects of NAC on the expression and activity of SPA in rats inflicted by smoke inhalation injury].	Acetylcysteine	16-19	surfactant protein A1	Rattus norvegicus	54-57
11876867-1	2000	OBJECTIVE: To investigate the effects of NAC (N-acetyl-L-cysteine) on the expression and activity of SPA (surfactant-associated protein A) in rats inflicted by smoke inhalation injury.	Acetylcysteine	41-44	surfactant protein A1	Rattus norvegicus	101-104
11876867-1	2000	OBJECTIVE: To investigate the effects of NAC (N-acetyl-L-cysteine) on the expression and activity of SPA (surfactant-associated protein A) in rats inflicted by smoke inhalation injury.	Acetylcysteine	41-44	surfactant protein A1	Rattus norvegicus	106-137
11876867-1	2000	OBJECTIVE: To investigate the effects of NAC (N-acetyl-L-cysteine) on the expression and activity of SPA (surfactant-associated protein A) in rats inflicted by smoke inhalation injury.	Acetylcysteine	46-65	surfactant protein A1	Rattus norvegicus	101-104
11876867-1	2000	OBJECTIVE: To investigate the effects of NAC (N-acetyl-L-cysteine) on the expression and activity of SPA (surfactant-associated protein A) in rats inflicted by smoke inhalation injury.	Acetylcysteine	46-65	surfactant protein A1	Rattus norvegicus	106-137
11876867-4	2000	RESULTS: After the application of NAC, there exhibited an increase in SPA mRNA expression and static pulmonary compliance, and the restoration of the BAL surface tension to normal.	Acetylcysteine	34-37	surfactant protein A1	Rattus norvegicus	70-73
11876867-5	2000	CONCLUSION: The application of NAC could promote the expression of SPA mRNA after smoke inhalation injury and improve the SPA-related function.	Acetylcysteine	31-34	surfactant protein A1	Rattus norvegicus	67-70
11876867-5	2000	CONCLUSION: The application of NAC could promote the expression of SPA mRNA after smoke inhalation injury and improve the SPA-related function.	Acetylcysteine	31-34	surfactant protein A1	Rattus norvegicus	122-125
10807739-6	2000	JNK and ERK were activated by ET-1 binding to a single receptor (ET-1A) but differed in their downstream mechanisms: only JNK activation was sensitive to the radical scavenger N-acetylcysteine and diphenylene iodonium, an inhibitor of NADPH oxidase, indicating a role for ROS.	Acetylcysteine	176-192	Eph receptor B1	Rattus norvegicus	8-11
10807739-6	2000	JNK and ERK were activated by ET-1 binding to a single receptor (ET-1A) but differed in their downstream mechanisms: only JNK activation was sensitive to the radical scavenger N-acetylcysteine and diphenylene iodonium, an inhibitor of NADPH oxidase, indicating a role for ROS.	Acetylcysteine	176-192	endothelin 1	Rattus norvegicus	30-34
10748142-5	2000	Both PDGF-BB- and AngII-induced phosphorylation of the Shc.PDGFbeta-R complex was inhibited by antioxidants such as N-acetylcysteine and Tiron, but not by calcium chelation.	Acetylcysteine	116-132	angiotensinogen	Homo sapiens	18-23
10843427-5	2000	RESULTS: The results showed that 1) NAC attenuated TNF-alpha-induced p38MAP kinase activation and RANTES production 2) SB 203580 as the specific inhibitor of p38 MAP kinase activity attenuated TNF-alpha-induced RANTES production 3) BSO facilitated TNF-alpha-induced p38 MAP kinase activation and RANTES production 4) SB 203580 attenuated BSO-mediated facilitation of TNF-alpha-induced RANTES production.	Acetylcysteine	36-39	tumor necrosis factor	Homo sapiens	51-60
10843427-5	2000	RESULTS: The results showed that 1) NAC attenuated TNF-alpha-induced p38MAP kinase activation and RANTES production 2) SB 203580 as the specific inhibitor of p38 MAP kinase activity attenuated TNF-alpha-induced RANTES production 3) BSO facilitated TNF-alpha-induced p38 MAP kinase activation and RANTES production 4) SB 203580 attenuated BSO-mediated facilitation of TNF-alpha-induced RANTES production.	Acetylcysteine	36-39	mitogen-activated protein kinase 14	Homo sapiens	69-72
10843427-5	2000	RESULTS: The results showed that 1) NAC attenuated TNF-alpha-induced p38MAP kinase activation and RANTES production 2) SB 203580 as the specific inhibitor of p38 MAP kinase activity attenuated TNF-alpha-induced RANTES production 3) BSO facilitated TNF-alpha-induced p38 MAP kinase activation and RANTES production 4) SB 203580 attenuated BSO-mediated facilitation of TNF-alpha-induced RANTES production.	Acetylcysteine	36-39	mitogen-activated protein kinase 14	Homo sapiens	158-161
10843427-5	2000	RESULTS: The results showed that 1) NAC attenuated TNF-alpha-induced p38MAP kinase activation and RANTES production 2) SB 203580 as the specific inhibitor of p38 MAP kinase activity attenuated TNF-alpha-induced RANTES production 3) BSO facilitated TNF-alpha-induced p38 MAP kinase activation and RANTES production 4) SB 203580 attenuated BSO-mediated facilitation of TNF-alpha-induced RANTES production.	Acetylcysteine	36-39	tumor necrosis factor	Homo sapiens	193-202
10843427-5	2000	RESULTS: The results showed that 1) NAC attenuated TNF-alpha-induced p38MAP kinase activation and RANTES production 2) SB 203580 as the specific inhibitor of p38 MAP kinase activity attenuated TNF-alpha-induced RANTES production 3) BSO facilitated TNF-alpha-induced p38 MAP kinase activation and RANTES production 4) SB 203580 attenuated BSO-mediated facilitation of TNF-alpha-induced RANTES production.	Acetylcysteine	36-39	tumor necrosis factor	Homo sapiens	193-202
10843427-5	2000	RESULTS: The results showed that 1) NAC attenuated TNF-alpha-induced p38MAP kinase activation and RANTES production 2) SB 203580 as the specific inhibitor of p38 MAP kinase activity attenuated TNF-alpha-induced RANTES production 3) BSO facilitated TNF-alpha-induced p38 MAP kinase activation and RANTES production 4) SB 203580 attenuated BSO-mediated facilitation of TNF-alpha-induced RANTES production.	Acetylcysteine	36-39	mitogen-activated protein kinase 14	Homo sapiens	158-161
10843427-5	2000	RESULTS: The results showed that 1) NAC attenuated TNF-alpha-induced p38MAP kinase activation and RANTES production 2) SB 203580 as the specific inhibitor of p38 MAP kinase activity attenuated TNF-alpha-induced RANTES production 3) BSO facilitated TNF-alpha-induced p38 MAP kinase activation and RANTES production 4) SB 203580 attenuated BSO-mediated facilitation of TNF-alpha-induced RANTES production.	Acetylcysteine	36-39	tumor necrosis factor	Homo sapiens	193-202
10857766-0	2000	Suppression of interleukin 2 biosynthesis by three modes of oxidative cellular stress: selective prevention by N-acetyl cysteine.	Acetylcysteine	111-128	interleukin 2	Homo sapiens	15-28
10857766-4	2000	N-acetyl cysteine (NAC) prevented oxidative stress-induced suppression of IL-2 biosynthesis, except for that induced by acute stress at 100 microM and above.	Acetylcysteine	0-17	interleukin 2	Homo sapiens	74-78
10857766-4	2000	N-acetyl cysteine (NAC) prevented oxidative stress-induced suppression of IL-2 biosynthesis, except for that induced by acute stress at 100 microM and above.	Acetylcysteine	19-22	interleukin 2	Homo sapiens	74-78
10788575-7	2000	The enhanced effects of DDC on the release of NO and TNF-alpha from Kupffer cells was inhibited by N-acetyl-L-cysteine (an inhibitor of transcription factor NF-kappaB activation).	Acetylcysteine	99-118	tumor necrosis factor	Rattus norvegicus	53-62
10788610-0	2000	N-acetylcysteine suppresses TNF-induced NF-kappaB activation through inhibition of IkappaB kinases.	Acetylcysteine	0-16	tumor necrosis factor	Homo sapiens	28-31
10788610-0	2000	N-acetylcysteine suppresses TNF-induced NF-kappaB activation through inhibition of IkappaB kinases.	Acetylcysteine	0-16	nuclear factor kappa B subunit 1	Homo sapiens	40-49
10777712-7	2000	The antioxidant and GSH precursor N-acetyl-l-cysteine favored Bcl-2 at the expense of Bax/p53, whereas pyrrolidine dithiocarbamate induced Bax against Bcl-2, with mild effect on p53.	Acetylcysteine	34-53	BCL2 associated X, apoptosis regulator	Homo sapiens	86-89
10777712-7	2000	The antioxidant and GSH precursor N-acetyl-l-cysteine favored Bcl-2 at the expense of Bax/p53, whereas pyrrolidine dithiocarbamate induced Bax against Bcl-2, with mild effect on p53.	Acetylcysteine	34-53	tumor protein p53	Homo sapiens	90-93
10766859-0	2000	Distinct effects of N-acetylcysteine and nitric oxide on angiotensin II-induced epidermal growth factor receptor phosphorylation and intracellular Ca(2+) levels.	Acetylcysteine	20-36	angiotensinogen	Homo sapiens	57-71
10772898-4	2000	The inhibitory effect of an antioxidant, N-acetyl-cysteine, on PYK2 activation by its specific agonists further suggests the pivotal role of PYK2 in vascular remodeling associated with enhanced ROS production.	Acetylcysteine	41-58	protein tyrosine kinase 2 beta	Rattus norvegicus	63-67
10772898-4	2000	The inhibitory effect of an antioxidant, N-acetyl-cysteine, on PYK2 activation by its specific agonists further suggests the pivotal role of PYK2 in vascular remodeling associated with enhanced ROS production.	Acetylcysteine	41-58	protein tyrosine kinase 2 beta	Rattus norvegicus	141-145
10766859-0	2000	Distinct effects of N-acetylcysteine and nitric oxide on angiotensin II-induced epidermal growth factor receptor phosphorylation and intracellular Ca(2+) levels.	Acetylcysteine	20-36	epidermal growth factor receptor	Homo sapiens	80-112
10766859-4	2000	The transactivation of the epidermal growth factor receptor by angiotensin II, a process required for the activation of ERK, was inhibited by N-acetylcysteine but not by nitric oxide.	Acetylcysteine	142-158	epidermal growth factor receptor	Homo sapiens	27-59
10766859-4	2000	The transactivation of the epidermal growth factor receptor by angiotensin II, a process required for the activation of ERK, was inhibited by N-acetylcysteine but not by nitric oxide.	Acetylcysteine	142-158	angiotensinogen	Homo sapiens	63-77
10766859-4	2000	The transactivation of the epidermal growth factor receptor by angiotensin II, a process required for the activation of ERK, was inhibited by N-acetylcysteine but not by nitric oxide.	Acetylcysteine	142-158	mitogen-activated protein kinase 1	Homo sapiens	120-123
10766859-8	2000	N-Acetylcysteine did inhibit the phosphorylation of the calcium sensitive tyrosine kinases PYK2 and Src, effects that also occurred using nitric oxide.	Acetylcysteine	0-16	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	100-103
10749740-6	2000	N-acetyl-L-cysteine, diphenyleneiodonium, and tetramethylpiperidine-N-oxyl, used to reduce ROS, inhibited (86)Rb uptake, thus mimicking the hypoxic effects, whereas deferoxamine, superoxide dismutase, and catalase were ineffective.	Acetylcysteine	0-19	catalase	Homo sapiens	205-213
10771087-4	2000	By the effect of NAC and DFO, significant increases were detected in the levels of mRNA of catalase, manganese superoxide dismutase and glutathione peroxidase.	Acetylcysteine	17-20	catalase	Rattus norvegicus	91-99
10805219-1	2000	N-acetylcysteine downregulates VEGF production in vitro.	Acetylcysteine	0-16	vascular endothelial growth factor A	Homo sapiens	31-35
10727667-9	2000	An antioxidant N-acetyl-L-cysteine and a selective protein kinase C (PKC) inhibitor GF109203X significantly suppressed the TNFalpha-induced NF-kappaB activation, and abrogated potentiation of TNFalpha-induced NF-kappaB activity caused by high glucose (27.5 mmol/l).	Acetylcysteine	15-34	tumor necrosis factor	Homo sapiens	123-131
10727667-9	2000	An antioxidant N-acetyl-L-cysteine and a selective protein kinase C (PKC) inhibitor GF109203X significantly suppressed the TNFalpha-induced NF-kappaB activation, and abrogated potentiation of TNFalpha-induced NF-kappaB activity caused by high glucose (27.5 mmol/l).	Acetylcysteine	15-34	nuclear factor kappa B subunit 1	Homo sapiens	140-149
10727667-9	2000	An antioxidant N-acetyl-L-cysteine and a selective protein kinase C (PKC) inhibitor GF109203X significantly suppressed the TNFalpha-induced NF-kappaB activation, and abrogated potentiation of TNFalpha-induced NF-kappaB activity caused by high glucose (27.5 mmol/l).	Acetylcysteine	15-34	tumor necrosis factor	Homo sapiens	192-200
10727667-9	2000	An antioxidant N-acetyl-L-cysteine and a selective protein kinase C (PKC) inhibitor GF109203X significantly suppressed the TNFalpha-induced NF-kappaB activation, and abrogated potentiation of TNFalpha-induced NF-kappaB activity caused by high glucose (27.5 mmol/l).	Acetylcysteine	15-34	nuclear factor kappa B subunit 1	Homo sapiens	209-218
10805219-5	2000	We also studied the inhibiting effect of one antioxidant, N-acetylcysteine, on VEGF production in three human melanoma cell lines.	Acetylcysteine	58-74	vascular endothelial growth factor A	Homo sapiens	79-83
10727932-7	2000	In contrast, the reductants N-acetyl-L-cysteine [Cys(Ac)] and dithiothreitol markedly suppressed EGF-induced dimerization and activation of the EGF receptor in cells.	Acetylcysteine	28-47	epidermal growth factor receptor	Homo sapiens	144-156
10805219-8	2000	Human melanoma cell lines secreted VEGF in basal conditions (550-963 +/- 125 pg/ml) and N-acetylcysteine (0.5-20 mM) significantly decreased the VEGF production in a dose-dependent manner.	Acetylcysteine	88-104	vascular endothelial growth factor A	Homo sapiens	145-149
10805219-10	2000	N-acetylcysteine inhibits VEGF production in three human melanoma cell lines.	Acetylcysteine	0-16	vascular endothelial growth factor A	Homo sapiens	26-30
10775561-0	2000	N-Acetyl-L-cysteine potentiates interleukin-1beta induction of nitric oxide synthase : role of p44/42 mitogen-activated protein kinases.	Acetylcysteine	0-19	interleukin 1 beta	Rattus norvegicus	32-49
10708808-6	2000	Also, IL-6 stimulated the proliferation of FLSs, and this IL-6 driven proliferation was inhibited with the treatment of MTX or N-acetylcysteine (NAC, 1 mM).	Acetylcysteine	127-143	interleukin 6	Homo sapiens	6-10
10708808-6	2000	Also, IL-6 stimulated the proliferation of FLSs, and this IL-6 driven proliferation was inhibited with the treatment of MTX or N-acetylcysteine (NAC, 1 mM).	Acetylcysteine	127-143	interleukin 6	Homo sapiens	58-62
10775561-1	2000	We have reported previously that N-acetyl-L-cysteine facilitated interleukin-1beta-induced nitric oxide synthase (iNOS) expression in rat vascular smooth muscle cells.	Acetylcysteine	33-52	nitric oxide synthase 2	Rattus norvegicus	65-112
10708808-6	2000	Also, IL-6 stimulated the proliferation of FLSs, and this IL-6 driven proliferation was inhibited with the treatment of MTX or N-acetylcysteine (NAC, 1 mM).	Acetylcysteine	145-148	interleukin 6	Homo sapiens	6-10
10708808-6	2000	Also, IL-6 stimulated the proliferation of FLSs, and this IL-6 driven proliferation was inhibited with the treatment of MTX or N-acetylcysteine (NAC, 1 mM).	Acetylcysteine	145-148	interleukin 6	Homo sapiens	58-62
10775566-4	2000	Preincubation of VSMCs with either N-acetyl-L-cysteine and/or alpha-lipoic acid significantly decreased bradykinin-induced cytosolic and nuclear phosphorylation of p42(mapk) and p44(mapk).	Acetylcysteine	35-54	kininogen 1	Homo sapiens	104-114
10775566-5	2000	In addition, the induction c-fos mRNA levels by bradykinin was completely abolished by N-acetyl-L-cysteine and alpha-lipoic acid.	Acetylcysteine	87-106	kininogen 1	Homo sapiens	48-58
10708808-7	2000	Furthermore, ROS production in FLSs was increased significantly by IL-6, and its effect was also abrogated in the presence of MTX or NAC.	Acetylcysteine	133-136	interleukin 6	Homo sapiens	67-71
10775561-1	2000	We have reported previously that N-acetyl-L-cysteine facilitated interleukin-1beta-induced nitric oxide synthase (iNOS) expression in rat vascular smooth muscle cells.	Acetylcysteine	33-52	nitric oxide synthase 2	Rattus norvegicus	114-118
10775561-2	2000	The present study compares the effect of N-acetyl-L-cysteine with other antioxidants and tested the possibility that N-acetyl-L-cysteine potentiates iNOS induction by a mechanism involving activation of p44/42 mitogen-activated protein kinases (MAPKs).	Acetylcysteine	117-136	nitric oxide synthase 2	Rattus norvegicus	149-153
10775561-3	2000	The effect of N-acetyl-L-cysteine on potentiating interleukin-1beta-induced nitrite production and iNOS expression was mimicked either by the enantiomers, L-cysteine and D-cysteine, or by a non-thiol-containing antioxidant, L-ascorbic acid.	Acetylcysteine	14-33	interleukin 1 beta	Rattus norvegicus	50-67
10775561-3	2000	The effect of N-acetyl-L-cysteine on potentiating interleukin-1beta-induced nitrite production and iNOS expression was mimicked either by the enantiomers, L-cysteine and D-cysteine, or by a non-thiol-containing antioxidant, L-ascorbic acid.	Acetylcysteine	14-33	nitric oxide synthase 2	Rattus norvegicus	99-103
10775561-4	2000	Interleukin-1beta activated p44/42 MAPK, and this activation was enhanced in the presence of N-acetyl-L-cysteine.	Acetylcysteine	93-112	interleukin 1 beta	Rattus norvegicus	0-17
10775561-5	2000	Inhibition of p44/42 MAPK phosphorylation by the selective inhibitor PD98059 clearly inhibited iNOS expression induced by interleukin-1beta either in the absence or in the presence of N-acetyl-L-cysteine.	Acetylcysteine	184-203	nitric oxide synthase 2	Rattus norvegicus	95-99
10718115-6	2000	In addition, the increase in MIP-2 mRNA expression by vanadium was attenuated by co-treatment with the antioxidant N-acetylcysteine (NAC), at the doses of 10 and 20 mM, suggesting that the induction of MIP-2 mRNA is mediated via the generation of reactive oxygen species (ROS).	Acetylcysteine	115-131	chemokine (C-X-C motif) ligand 2	Mus musculus	29-34
10775561-6	2000	These observations, combined with previous results, indicate that p44/42 MAPK activation is required for interleukin-1beta induction of iNOS and that N-acetyl-L-cysteine may act as a reducing agent and facilitate interleukin-1beta-induced iNOS expression through a reduction/oxidation-related mechanism involving potentiation of cytokine activation of the p44/42 MAPK signaling pathway.	Acetylcysteine	150-169	interleukin 1 beta	Rattus norvegicus	213-230
10718115-6	2000	In addition, the increase in MIP-2 mRNA expression by vanadium was attenuated by co-treatment with the antioxidant N-acetylcysteine (NAC), at the doses of 10 and 20 mM, suggesting that the induction of MIP-2 mRNA is mediated via the generation of reactive oxygen species (ROS).	Acetylcysteine	115-131	chemokine (C-X-C motif) ligand 2	Mus musculus	202-207
10775561-6	2000	These observations, combined with previous results, indicate that p44/42 MAPK activation is required for interleukin-1beta induction of iNOS and that N-acetyl-L-cysteine may act as a reducing agent and facilitate interleukin-1beta-induced iNOS expression through a reduction/oxidation-related mechanism involving potentiation of cytokine activation of the p44/42 MAPK signaling pathway.	Acetylcysteine	150-169	nitric oxide synthase 2	Rattus norvegicus	239-243
10718115-6	2000	In addition, the increase in MIP-2 mRNA expression by vanadium was attenuated by co-treatment with the antioxidant N-acetylcysteine (NAC), at the doses of 10 and 20 mM, suggesting that the induction of MIP-2 mRNA is mediated via the generation of reactive oxygen species (ROS).	Acetylcysteine	133-136	chemokine (C-X-C motif) ligand 2	Mus musculus	29-34
10718115-6	2000	In addition, the increase in MIP-2 mRNA expression by vanadium was attenuated by co-treatment with the antioxidant N-acetylcysteine (NAC), at the doses of 10 and 20 mM, suggesting that the induction of MIP-2 mRNA is mediated via the generation of reactive oxygen species (ROS).	Acetylcysteine	133-136	chemokine (C-X-C motif) ligand 2	Mus musculus	202-207
10725743-6	2000	This potentiating effect was mediated by reactive oxygen species (ROS) released by PMN during the coculture; it did not require direct cell contact between PMN and PBMC, it was enhanced when PMN were stimulated by fMLP (a chemotactic peptide), and it was inhibited by two antioxidants, N-acetyl cysteine and pyrrolidine dithiocarbamate.	Acetylcysteine	286-303	formyl peptide receptor 1	Homo sapiens	214-218
10706725-3	2000	Following stimulation with TNF-alpha, pyrrolidine dithiocarbamate (PDTC), N-acetylcysteine, and dexamethasone prevented I kappa B kinase-induced I kappa B-alpha, but not I kappa B-beta or I kappa B-epsilon phosphorylation and degradation.	Acetylcysteine	74-90	NFKB inhibitor alpha	Homo sapiens	145-160
10734112-4	2000	Interestingly, pretreatment with the antioxidants, N-acetyl-L-cysteine, dithiothreitol, and glutathione, impaired chelerythrine-induced JNK1 and p38 activation.	Acetylcysteine	51-70	mitogen-activated protein kinase 8	Homo sapiens	136-140
10734112-4	2000	Interestingly, pretreatment with the antioxidants, N-acetyl-L-cysteine, dithiothreitol, and glutathione, impaired chelerythrine-induced JNK1 and p38 activation.	Acetylcysteine	51-70	mitogen-activated protein kinase 14	Homo sapiens	145-148
10707932-16	2000	In addition, NAC pretreatment also reduced hepatic IL-6 production at 3 and 6 hours after starting cerulein challenge.	Acetylcysteine	13-16	interleukin 6	Mus musculus	51-55
10696066-7	2000	Antioxidants, pyrrolidine dithiocarbamate, and N-acetyl-L-cysteine significantly inhibited IL-8 mRNA and protein levels by BET-1A cells.	Acetylcysteine	47-66	C-X-C motif chemokine ligand 8	Homo sapiens	91-95
10754270-4	2000	Only glutathione, N-acetylcysteine, and vitamin E prevented apoptosis measured by the occurrence of cells with condensed and/or fragmented nuclei, as well as the loss of DeltaPsim, and the release of cytochrome c.	Acetylcysteine	18-34	cytochrome c, somatic	Homo sapiens	200-212
10788318-5	2000	Acetylcysteine but not SOD also counteracted the phosphorylation of Ikappab and thus the transcriptional activation of NFkappab.	Acetylcysteine	0-14	nuclear factor kappa B subunit 1	Homo sapiens	119-127
10679488-8	2000	Induction of eNOS by H(2)O(2) was not affected by the hydroxyl radical scavenger DMSO, mannitol, or N-tert-butyl-alpha-phenylnitrone, but it was inhibited by the antioxidants N-acetylcysteine, ebselen, and exogenously added catalase.	Acetylcysteine	175-191	nitric oxide synthase 3	Bos taurus	13-17
10669634-8	2000	However, simultaneous blockade of the ERK1/2 and ROS pathways by using PD098059 combined with diphenylene iodonium or N-acetylcysteine potently enhanced the ability of MAPK kinase inhibitors to abrogate MCP-1 mRNA expression (100+/-2% inhibition).	Acetylcysteine	118-134	mitogen-activated protein kinase 3	Homo sapiens	38-44
10653697-10	2000	The biological significance of this process is demonstrated by observations that retention of the N-acetyl-cysteine in ACT88F affects the flight muscle function of mod(-) flies.	Acetylcysteine	98-115	Actin 88F	Drosophila melanogaster	119-125
10669634-8	2000	However, simultaneous blockade of the ERK1/2 and ROS pathways by using PD098059 combined with diphenylene iodonium or N-acetylcysteine potently enhanced the ability of MAPK kinase inhibitors to abrogate MCP-1 mRNA expression (100+/-2% inhibition).	Acetylcysteine	118-134	mitogen-activated protein kinase 3	Homo sapiens	168-172
10619832-0	2000	Diesel exhaust particles activate p38 MAP kinase to produce interleukin 8 and RANTES by human bronchial epithelial cells and N-acetylcysteine attenuates p38 MAP kinase activation.	Acetylcysteine	125-141	mitogen-activated protein kinase 14	Homo sapiens	153-156
10652256-7	2000	The HNE-mediated activation of caspases, cleavage of PARP and DNA fragmentation were blocked by antioxidants cysteine, N-acety-L-cysteine and dithiothreitol, but not by two other HNE-reactive amino acids lysine and histidine, or by cystine, the oxidized form of cysteine.	Acetylcysteine	119-137	poly(ADP-ribose) polymerase 1	Homo sapiens	53-57
10656697-5	2000	Bcl-2 overproduction in PC12 cells is associated with increased functional thiol reserves, increased reductive activation of chemotherapeutic prodrugs, and GSH accumulation after treatment with N-acetylcysteine.	Acetylcysteine	194-210	BCL2, apoptosis regulator	Rattus norvegicus	0-5
10619832-4	2000	In addition, we also examined the effect of a thiol-reducing agent, N-acetylcysteine (NAC), on DEP-induced p38 MAP kinase activation and cytokine production in order to clarify the redox control mechanism in DEP-induced p38 MAP kinase activation and IL-8 and RANTES production.	Acetylcysteine	86-89	mitogen-activated protein kinase 14	Homo sapiens	107-110
10619832-7	2000	NAC inhibited DEP-induced p38 MAP kinase activation and IL-8 and RANTES production.	Acetylcysteine	0-3	mitogen-activated protein kinase 14	Homo sapiens	26-29
10619832-7	2000	NAC inhibited DEP-induced p38 MAP kinase activation and IL-8 and RANTES production.	Acetylcysteine	0-3	C-X-C motif chemokine ligand 8	Homo sapiens	56-60
10640773-5	2000	Neutrophil supernatant-induced EGFR tyrosine phosphorylation, activation of p44/42mapk, and MUC5AC synthesis were inhibited by antioxidants (N-acetyl-cysteine, DMSO, dimethyl thiourea, or superoxide dismutase); neutralizing Abs to EGFR ligands (EGF and TGF-alpha) were without effect, and no TGF-alpha protein was found in the neutrophil supernatant.	Acetylcysteine	141-158	epidermal growth factor receptor	Homo sapiens	31-35
10636889-5	2000	Cadmium-induced apoptosis and mdr1 up-regulation depended on ROS, since co-incubation with the ROS scavengers N-acetylcysteine (15 mM) or pyrrolidine dithiocarbamate (0.1 mM) abolished both responses.	Acetylcysteine	110-126	ATP binding cassette subfamily B member 1	Homo sapiens	30-34
10636889-6	2000	Moreover, cadmium- and ROS-associated mdr1 up-regulation was linked to activation of the transcription factor NF-kappaB; N-acetylcysteine, pyrrolidine dithiocarbamate, and the IkappaB-alpha kinase inhibitor Bay 11-7082 (20 microM) prevented both, mdr1 overexpression and degradation of the inhibitory NF-kappaB subunit, IkappaB-alpha, induced by cadmium.	Acetylcysteine	121-137	ATP binding cassette subfamily B member 1	Homo sapiens	38-42
10636889-6	2000	Moreover, cadmium- and ROS-associated mdr1 up-regulation was linked to activation of the transcription factor NF-kappaB; N-acetylcysteine, pyrrolidine dithiocarbamate, and the IkappaB-alpha kinase inhibitor Bay 11-7082 (20 microM) prevented both, mdr1 overexpression and degradation of the inhibitory NF-kappaB subunit, IkappaB-alpha, induced by cadmium.	Acetylcysteine	121-137	nuclear factor kappa B subunit 1	Homo sapiens	110-119
10619832-4	2000	In addition, we also examined the effect of a thiol-reducing agent, N-acetylcysteine (NAC), on DEP-induced p38 MAP kinase activation and cytokine production in order to clarify the redox control mechanism in DEP-induced p38 MAP kinase activation and IL-8 and RANTES production.	Acetylcysteine	68-84	mitogen-activated protein kinase 14	Homo sapiens	107-110
10634825-6	2000	The combined incubation with reduced glutathione diethyl ester or N-acetylcysteine, antioxidants, suppressed the upregulation of uPA and uPAR mRNA and the increase in plasminogen activator activity by lysoPC.	Acetylcysteine	66-82	plasminogen activator, urokinase	Homo sapiens	129-132
11032359-5	2000	Our results allow us to conclude that neurological disorders associated with an IL-1beta-induced oxidative stress could be, at least experimentally, reversible in the presence of one antioxidant, N-acetylcysteine.	Acetylcysteine	196-212	interleukin 1 beta	Homo sapiens	80-88
10585590-5	2000	Additional treatment of cells with the anti-oxidant and glutathione (GSH) precursor N-acetylcysteine (NAC) resulted in inhibition of p53-induced ROIs production and in partial restoration of intracellular GSH levels, which was associated with the ability of NAC to inhibit p53-modulated TNF-induced cytotoxicity.	Acetylcysteine	84-100	tumor protein p53	Homo sapiens	133-136
10585590-5	2000	Additional treatment of cells with the anti-oxidant and glutathione (GSH) precursor N-acetylcysteine (NAC) resulted in inhibition of p53-induced ROIs production and in partial restoration of intracellular GSH levels, which was associated with the ability of NAC to inhibit p53-modulated TNF-induced cytotoxicity.	Acetylcysteine	84-100	tumor protein p53	Homo sapiens	273-276
10585590-5	2000	Additional treatment of cells with the anti-oxidant and glutathione (GSH) precursor N-acetylcysteine (NAC) resulted in inhibition of p53-induced ROIs production and in partial restoration of intracellular GSH levels, which was associated with the ability of NAC to inhibit p53-modulated TNF-induced cytotoxicity.	Acetylcysteine	84-100	tumor necrosis factor	Homo sapiens	287-290
10585590-5	2000	Additional treatment of cells with the anti-oxidant and glutathione (GSH) precursor N-acetylcysteine (NAC) resulted in inhibition of p53-induced ROIs production and in partial restoration of intracellular GSH levels, which was associated with the ability of NAC to inhibit p53-modulated TNF-induced cytotoxicity.	Acetylcysteine	102-105	tumor protein p53	Homo sapiens	133-136
10585590-5	2000	Additional treatment of cells with the anti-oxidant and glutathione (GSH) precursor N-acetylcysteine (NAC) resulted in inhibition of p53-induced ROIs production and in partial restoration of intracellular GSH levels, which was associated with the ability of NAC to inhibit p53-modulated TNF-induced cytotoxicity.	Acetylcysteine	102-105	tumor protein p53	Homo sapiens	273-276
10585590-5	2000	Additional treatment of cells with the anti-oxidant and glutathione (GSH) precursor N-acetylcysteine (NAC) resulted in inhibition of p53-induced ROIs production and in partial restoration of intracellular GSH levels, which was associated with the ability of NAC to inhibit p53-modulated TNF-induced cytotoxicity.	Acetylcysteine	102-105	tumor necrosis factor	Homo sapiens	287-290
10585590-5	2000	Additional treatment of cells with the anti-oxidant and glutathione (GSH) precursor N-acetylcysteine (NAC) resulted in inhibition of p53-induced ROIs production and in partial restoration of intracellular GSH levels, which was associated with the ability of NAC to inhibit p53-modulated TNF-induced cytotoxicity.	Acetylcysteine	258-261	tumor protein p53	Homo sapiens	133-136
10601882-12	1999	The action of PBN and N-acetyl cysteine to suppress the activation of p38 was demonstrated in cultured astrocytes.	Acetylcysteine	22-39	mitogen-activated protein kinase 14	Homo sapiens	70-73
10935502-0	1999	p53-independent inhibition of proliferation and p21(WAF1/Cip1)-modulated induction of cell death by the antioxidants N-acetylcysteine and vitamin E.	Acetylcysteine	117-133	tumor protein p53	Homo sapiens	0-3
10935502-0	1999	p53-independent inhibition of proliferation and p21(WAF1/Cip1)-modulated induction of cell death by the antioxidants N-acetylcysteine and vitamin E.	Acetylcysteine	117-133	cyclin dependent kinase inhibitor 1A	Homo sapiens	48-51
10935502-0	1999	p53-independent inhibition of proliferation and p21(WAF1/Cip1)-modulated induction of cell death by the antioxidants N-acetylcysteine and vitamin E.	Acetylcysteine	117-133	cyclin dependent kinase inhibitor 1A	Homo sapiens	52-56
10935502-0	1999	p53-independent inhibition of proliferation and p21(WAF1/Cip1)-modulated induction of cell death by the antioxidants N-acetylcysteine and vitamin E.	Acetylcysteine	117-133	cyclin dependent kinase inhibitor 1A	Homo sapiens	57-61
10935502-5	1999	The antioxidants, N-acetylcysteine (NAC) and vitamin E either inhibited proliferation in a p53-independent manner without affecting cell viability or induced cell death.	Acetylcysteine	18-34	tumor protein p53	Homo sapiens	91-94
10935502-5	1999	The antioxidants, N-acetylcysteine (NAC) and vitamin E either inhibited proliferation in a p53-independent manner without affecting cell viability or induced cell death.	Acetylcysteine	36-39	tumor protein p53	Homo sapiens	91-94
10653978-6	2000	By exploiting the same transfection assay, we demonstrated that the up-regulation of the grp78 promoter by the protein phosphatase inhibitors is suppressed in the presence of the cytoplasmic calcium chelator bis(aminophenoxy)ethane N,N"-tetraacetic acid, the mitochondria calcium uniporter inhibitor ruthenium red as well as the antioxidants N-acetyl cysteine and pyrrolidinedithiocarbamate.	Acetylcysteine	342-359	heat shock protein family A (Hsp70) member 5	Homo sapiens	89-94
10605034-8	2000	N-Acetylcysteine or glutathione could also completely revert the mycobacteriostatic effects of PA or PA plus IFN-gamma.	Acetylcysteine	0-16	interferon gamma	Mus musculus	109-118
10506589-0	1999	Supplementation of N-acetylcysteine inhibits NFkappaB activation and protects against alloxan-induced diabetes in CD-1 mice.	Acetylcysteine	19-35	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	45-53
10564154-7	1999	N-acetylcysteine (NAC) a membrane-permeant antioxidant, which augmented intracellular sulfhydryl content and inhibited H(2)O(2)-induced DCF fluorescence, had no effect on cytokine-induced NF-kappaB activation.	Acetylcysteine	0-16	nuclear factor kappa B subunit 1	Homo sapiens	188-197
10564154-7	1999	N-acetylcysteine (NAC) a membrane-permeant antioxidant, which augmented intracellular sulfhydryl content and inhibited H(2)O(2)-induced DCF fluorescence, had no effect on cytokine-induced NF-kappaB activation.	Acetylcysteine	18-21	nuclear factor kappa B subunit 1	Homo sapiens	188-197
10592469-9	1999	IL-8 production was significantly inhibited by N-acetyl-L-cysteine, FK506 and MG-132, inhibitors of NF-kappaB activation and translocation.	Acetylcysteine	47-66	C-X-C motif chemokine ligand 8	Homo sapiens	0-4
10592469-9	1999	IL-8 production was significantly inhibited by N-acetyl-L-cysteine, FK506 and MG-132, inhibitors of NF-kappaB activation and translocation.	Acetylcysteine	47-66	nuclear factor kappa B subunit 1	Homo sapiens	100-109
10567349-11	1999	Treatment of the cells with N-acetylcysteine resulted in increased TGF-beta production.	Acetylcysteine	28-44	transforming growth factor, beta 1	Rattus norvegicus	67-75
10564823-8	1999	Expression of Rbtg3 was induced by H(2)O(2) (500mM) up to fourfold in PC12 cells and was blocked by pretreatment of NAC (N-acetyl-L-cysteine, 10mM).	Acetylcysteine	116-119	BTG anti-proliferation factor 3	Rattus norvegicus	14-19
10564823-8	1999	Expression of Rbtg3 was induced by H(2)O(2) (500mM) up to fourfold in PC12 cells and was blocked by pretreatment of NAC (N-acetyl-L-cysteine, 10mM).	Acetylcysteine	121-140	BTG anti-proliferation factor 3	Rattus norvegicus	14-19
10548500-4	1999	Furthermore, the antioxidants vitamin E (alpha-tocopherol) and N-acetyl cysteine prevented both the arachidonic acid-induced increase in intracellular ROS and TBARS, and the activation of AP1 and NFkappaB.	Acetylcysteine	63-80	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	188-191
10548500-4	1999	Furthermore, the antioxidants vitamin E (alpha-tocopherol) and N-acetyl cysteine prevented both the arachidonic acid-induced increase in intracellular ROS and TBARS, and the activation of AP1 and NFkappaB.	Acetylcysteine	63-80	nuclear factor kappa B subunit 1	Homo sapiens	196-204
10545417-7	1999	The antioxidants Trolox and N-acetyl cysteine were both able to inhibit UVB-induced AP-1 transactivation and Trolox was able to inhibit the potentiation of UVB-induced AP-1 by FeCl(3).	Acetylcysteine	28-45	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	84-88
10506589-10	1999	Supplementation with N-acetylcysteine (NAC, 500 mg/kg), a GSH precursor, inhibited alloxan-induced NFkappaB activation and reduced hyperglycemia.	Acetylcysteine	21-37	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	99-107
10506589-10	1999	Supplementation with N-acetylcysteine (NAC, 500 mg/kg), a GSH precursor, inhibited alloxan-induced NFkappaB activation and reduced hyperglycemia.	Acetylcysteine	39-42	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	99-107
10506589-12	1999	Inhibition of NF-kappaB activation by NAC attenuated the severity of IDDM.	Acetylcysteine	38-41	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	14-23
10549609-6	1999	Treatment with NAC clearly restrained TNF-alpha-induced ICAM expression on HUVEC, while preincubation of cells with PDTC showed synergistic effects.	Acetylcysteine	15-18	tumor necrosis factor	Homo sapiens	38-47
10523329-0	1999	N-acetyl-L-cysteine enhances interleukin-1beta-induced nitric oxide synthase expression.	Acetylcysteine	0-19	interleukin 1 beta	Rattus norvegicus	29-46
10523329-1	1999	The effect of N-acetyl-L-cysteine on interleukin-1beta-induced nitric oxide synthase expression was studied in rat vascular smooth muscle cells to determine if the reduction/oxidation state would modulate cytokine-induced changes.	Acetylcysteine	14-33	interleukin 1 beta	Rattus norvegicus	37-54
10523329-5	1999	Northern and Western blot analyses revealed that the upregulation of interleukin-1beta-induced nitric oxide production by N-acetyl-L-cysteine resulted from an enhanced expression of inducible nitric oxide synthase.	Acetylcysteine	122-141	interleukin 1 beta	Rattus norvegicus	69-86
10523329-8	1999	N-Acetyl-L-cysteine upregulated nitrite production and inducible nitric oxide synthase expression induced by combination treatment with interleukin-1beta and either interferon-gamma or tumor necrosis factor-alpha.	Acetylcysteine	0-19	interleukin 1 beta	Rattus norvegicus	136-153
10549609-9	1999	The inhibition of TNF-alpha-induced ICAM-1 expression by NAC might have clinical implications because this substance is used as a radioprotector in radiotherapy.	Acetylcysteine	57-60	tumor necrosis factor	Homo sapiens	18-27
10479653-2	1999	In rat aortic smooth muscle cells, the antioxidants N-acetyl-L-cysteine (5 mmol/L) and pyrrolidine dithiocarbamate (100 micromol/L) completely inhibited angiotensin II-stimulated increases in IGF-1R mRNA and protein levels, suggesting the involvement of reactive oxygen species.	Acetylcysteine	52-71	angiotensinogen	Rattus norvegicus	153-167
10464319-5	1999	N-acetyl cysteine (a scavenger of reactive oxygen intermediates) abolished the ability of all oxidative stressors tested to activate JNK1, but failed to affect the activation of JNK1 by UV-B or by another ribotoxic stressor, the antibiotic anisomycin.	Acetylcysteine	0-17	mitogen-activated protein kinase 8	Homo sapiens	133-137
10485916-4	1999	Addition of NAC or AG to the culture medium at least partially prevented decreases in insulin mRNA, insulin gene promoter activity, DNA binding of two important insulin promoter transcription factors (PDX-1/STF-1 and RIPE-3b1 activator), insulin content, and glucose-induced insulin secretion.	Acetylcysteine	12-15	pancreatic and duodenal homeobox 1	Rattus norvegicus	201-206
10485916-4	1999	Addition of NAC or AG to the culture medium at least partially prevented decreases in insulin mRNA, insulin gene promoter activity, DNA binding of two important insulin promoter transcription factors (PDX-1/STF-1 and RIPE-3b1 activator), insulin content, and glucose-induced insulin secretion.	Acetylcysteine	12-15	pancreatic and duodenal homeobox 1	Rattus norvegicus	207-212
10494766-8	1999	Furthermore, a synthetic compound that inhibits signaling from the thrombin receptor, 4-cyano-5,5-bis (4-methoxyphenyl)-4-pentanoic acid (E5510), and the antioxidant N-acetyl L-cysteine (NAC), efficiently prevented thrombin-induced Neuro-2a cell death.	Acetylcysteine	187-190	coagulation factor II	Mus musculus	67-75
10469636-3	1999	In this report we demonstrate that the antioxidant N-acetylcysteine (NAC), a well-known chemopreventive agent, induces p16(INK4a) and p21(WAF1/CIP1) gene expression and prolongs cell-cycle transition through G(1) phase.	Acetylcysteine	51-67	cyclin dependent kinase inhibitor 2A	Homo sapiens	119-122
10469636-3	1999	In this report we demonstrate that the antioxidant N-acetylcysteine (NAC), a well-known chemopreventive agent, induces p16(INK4a) and p21(WAF1/CIP1) gene expression and prolongs cell-cycle transition through G(1) phase.	Acetylcysteine	51-67	cyclin dependent kinase inhibitor 2A	Homo sapiens	123-128
10469636-3	1999	In this report we demonstrate that the antioxidant N-acetylcysteine (NAC), a well-known chemopreventive agent, induces p16(INK4a) and p21(WAF1/CIP1) gene expression and prolongs cell-cycle transition through G(1) phase.	Acetylcysteine	51-67	cyclin dependent kinase inhibitor 1A	Homo sapiens	134-137
10469636-3	1999	In this report we demonstrate that the antioxidant N-acetylcysteine (NAC), a well-known chemopreventive agent, induces p16(INK4a) and p21(WAF1/CIP1) gene expression and prolongs cell-cycle transition through G(1) phase.	Acetylcysteine	51-67	cyclin dependent kinase inhibitor 1A	Homo sapiens	138-147
10469636-3	1999	In this report we demonstrate that the antioxidant N-acetylcysteine (NAC), a well-known chemopreventive agent, induces p16(INK4a) and p21(WAF1/CIP1) gene expression and prolongs cell-cycle transition through G(1) phase.	Acetylcysteine	69-72	cyclin dependent kinase inhibitor 2A	Homo sapiens	119-122
10469636-3	1999	In this report we demonstrate that the antioxidant N-acetylcysteine (NAC), a well-known chemopreventive agent, induces p16(INK4a) and p21(WAF1/CIP1) gene expression and prolongs cell-cycle transition through G(1) phase.	Acetylcysteine	69-72	cyclin dependent kinase inhibitor 2A	Homo sapiens	123-128
10469636-3	1999	In this report we demonstrate that the antioxidant N-acetylcysteine (NAC), a well-known chemopreventive agent, induces p16(INK4a) and p21(WAF1/CIP1) gene expression and prolongs cell-cycle transition through G(1) phase.	Acetylcysteine	69-72	cyclin dependent kinase inhibitor 1A	Homo sapiens	134-137
10469636-3	1999	In this report we demonstrate that the antioxidant N-acetylcysteine (NAC), a well-known chemopreventive agent, induces p16(INK4a) and p21(WAF1/CIP1) gene expression and prolongs cell-cycle transition through G(1) phase.	Acetylcysteine	69-72	cyclin dependent kinase inhibitor 1A	Homo sapiens	138-147
10469636-4	1999	A portion of the G(1) arrest by NAC is governed by p16(INK4a); it is independent of p53.	Acetylcysteine	32-35	cyclin dependent kinase inhibitor 2A	Homo sapiens	51-54
10469636-4	1999	A portion of the G(1) arrest by NAC is governed by p16(INK4a); it is independent of p53.	Acetylcysteine	32-35	cyclin dependent kinase inhibitor 2A	Homo sapiens	55-60
10489835-6	1999	Addition of GSH and NAC significantly reduced the secretion of TNF-alpha (mean+/-SEM 21.2+/-5 and 44.7+/-4.4% inhibition, respectively) as well as LPS-induced IL-6 and IL-8 (p&lt;0.05).	Acetylcysteine	20-23	tumor necrosis factor	Homo sapiens	63-72
10497896-10	1999	The result shows that vanadate-induced TNFalpha production is elevated by NADPH, which enhances vanadate-mediated generation of ROS, but is inhibited by an antioxidant, N-acetyl-L-cysteine (NAC).	Acetylcysteine	169-188	tumor necrosis factor	Mus musculus	39-47
10497896-10	1999	The result shows that vanadate-induced TNFalpha production is elevated by NADPH, which enhances vanadate-mediated generation of ROS, but is inhibited by an antioxidant, N-acetyl-L-cysteine (NAC).	Acetylcysteine	190-193	tumor necrosis factor	Mus musculus	39-47
10497896-11	1999	Modification of TNFalpha production is associated with an enhancement or a repression of NF-kappaB activity by NADPH or NAC, respectively.	Acetylcysteine	120-123	tumor necrosis factor	Mus musculus	16-24
10497896-11	1999	Modification of TNFalpha production is associated with an enhancement or a repression of NF-kappaB activity by NADPH or NAC, respectively.	Acetylcysteine	120-123	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	89-98
10400652-7	1999	Both vanadate-induced degradation of IkappaBalpha and activation of JNK were potently inhibited by pretreatment of cells with N-acetylcysteine or dimercaprol.	Acetylcysteine	126-142	NFKB inhibitor alpha	Homo sapiens	37-49
10400652-7	1999	Both vanadate-induced degradation of IkappaBalpha and activation of JNK were potently inhibited by pretreatment of cells with N-acetylcysteine or dimercaprol.	Acetylcysteine	126-142	mitogen-activated protein kinase 8	Homo sapiens	68-71
10403520-8	1999	The treatment of A2780 cells with N-acetyl-L-cysteine increased the intracellular GSH concentration, and profoundly suppressed hsp72 mRNA induction and HSF activation by CdCl2.	Acetylcysteine	34-53	heat shock protein family A (Hsp70) member 1A	Homo sapiens	127-132
10403520-8	1999	The treatment of A2780 cells with N-acetyl-L-cysteine increased the intracellular GSH concentration, and profoundly suppressed hsp72 mRNA induction and HSF activation by CdCl2.	Acetylcysteine	34-53	interleukin 6	Homo sapiens	152-155
10446212-1	1999	In a previous study, we showed that nitric oxide donors and N-acetylcysteine, either alone or in combination, inhibited the activation of several mitogen-activated protein kinases by angiotensin II in rat cardiac fibroblasts (Wang, D., Yu, X., and Brecher, P. (1998) J. Biol.	Acetylcysteine	60-76	angiotensinogen	Rattus norvegicus	183-197
10438654-3	1999	Treatment with dimethyl sulfoxide, extracellular glutathione, or N-acetyl-L-cysteine (NAC) decreased cristobalite-induced tumor necrosis factor (TNF)-alpha mRNA levels by 40%, 20%, and 42%, respectively.	Acetylcysteine	65-84	tumor necrosis factor	Mus musculus	122-155
10438654-3	1999	Treatment with dimethyl sulfoxide, extracellular glutathione, or N-acetyl-L-cysteine (NAC) decreased cristobalite-induced tumor necrosis factor (TNF)-alpha mRNA levels by 40%, 20%, and 42%, respectively.	Acetylcysteine	86-89	tumor necrosis factor	Mus musculus	122-155
10438654-5	1999	Cristobalite-induced macrophage inflammatory protein (MIP)-2 mRNA levels were reduced by 52%, 38%, and 57%, with DMSO, GSH, and NAC treatment, respectively.	Acetylcysteine	128-131	chemokine (C-X-C motif) ligand 2	Mus musculus	21-60
10489835-6	1999	Addition of GSH and NAC significantly reduced the secretion of TNF-alpha (mean+/-SEM 21.2+/-5 and 44.7+/-4.4% inhibition, respectively) as well as LPS-induced IL-6 and IL-8 (p&lt;0.05).	Acetylcysteine	20-23	interleukin 6	Homo sapiens	159-163
10489835-6	1999	Addition of GSH and NAC significantly reduced the secretion of TNF-alpha (mean+/-SEM 21.2+/-5 and 44.7+/-4.4% inhibition, respectively) as well as LPS-induced IL-6 and IL-8 (p&lt;0.05).	Acetylcysteine	20-23	C-X-C motif chemokine ligand 8	Homo sapiens	168-172
10489835-7	1999	Similarly, NAC inhibited the production of TNF-alpha, IL-6 and IL-8 in GSH-depleted AMs obtained by BSO pretreatment.	Acetylcysteine	11-14	tumor necrosis factor	Homo sapiens	43-52
10489835-7	1999	Similarly, NAC inhibited the production of TNF-alpha, IL-6 and IL-8 in GSH-depleted AMs obtained by BSO pretreatment.	Acetylcysteine	11-14	interleukin 6	Homo sapiens	54-58
10489835-7	1999	Similarly, NAC inhibited the production of TNF-alpha, IL-6 and IL-8 in GSH-depleted AMs obtained by BSO pretreatment.	Acetylcysteine	11-14	C-X-C motif chemokine ligand 8	Homo sapiens	63-67
10489835-8	1999	In conclusion, N-acetylcysteine and glutathione inhibit the production of tumour necrosis factor-alpha, interleukin-8 and interleukin-6 by alveolar macrophages by a mechanism independent of glutathione metabolism.	Acetylcysteine	15-31	C-X-C motif chemokine ligand 8	Homo sapiens	104-117
10489835-8	1999	In conclusion, N-acetylcysteine and glutathione inhibit the production of tumour necrosis factor-alpha, interleukin-8 and interleukin-6 by alveolar macrophages by a mechanism independent of glutathione metabolism.	Acetylcysteine	15-31	interleukin 6	Homo sapiens	122-135
10362686-9	1999	Moreover, the oxygen-induced rise could be mimicked by addition of H2O2 to normoxic cells, and the oxygen-induced expression of VCAM-1 but not of ICAM-1 was inhibited by addition of the free radical scavengers superoxide dismutase, N-acetyl-L-cysteine, and pyrrolidinedithiocarbamate.	Acetylcysteine	232-251	vascular cell adhesion molecule 1	Homo sapiens	128-134
10385691-3	1999	We found that the antioxidants nordihydroguaiaretic acid (NDGA), catechol, glutaryl probucol, and N-acetylcysteine increased eNOS expression in cultured bovine aortic endothelial cells (BAECs).	Acetylcysteine	98-114	nitric oxide synthase 3	Bos taurus	125-129
10349860-6	1999	Hypoxia-mediated induction of this splice variant was blocked by pretreatment of neuroblastoma cells with the protein synthesis inhibitor cycloheximide or antioxidants such as N-acetylcysteine and diphenyl iodonium, suggesting that hypoxia-mediated oxidant stress might, at least in part, underlie the alternative splicing of PS-2 mRNA through de novo protein synthesis.	Acetylcysteine	176-192	presenilin 2	Homo sapiens	326-330
10354065-5	1999	UVB-induced cyclooxygenase-2 mRNA expression was partly inhibited by the antioxidant N-acetylcysteine and by H-7, a non-specific inhibitor of protein kinase C. Solar-simulated irradiation (40 mJ/cm2) was found to induce in vivo both cyclooxygenase-2 mRNA and protein expression in human skin, whereas the expression of cyclooxygenase-1 mRNA remained at the basal level.	Acetylcysteine	85-101	prostaglandin-endoperoxide synthase 2	Homo sapiens	12-28
10448899-5	1999	Calcium release by thrombin from internal stores of UV-irradiated and neomycin-treated cells was completely abolished by pretreatment with N-acetyl cysteine and dexamethasone.	Acetylcysteine	139-156	coagulation factor II, thrombin	Homo sapiens	19-27
10202011-7	1999	Finally, both N-acetylcysteine and pyrrolidine dithiocarbamate attenuated the action of DEP on IL-8 mRNA expression, suggesting that oxidant-mediated pathway might be involved in its processes.	Acetylcysteine	14-30	C-X-C motif chemokine ligand 8	Homo sapiens	95-99
10456252-3	1999	Treatment with N-acetyl cysteine, i.e. a thiol-containing antioxidant, was found to increase the plasma albumin level and to ameliorate the loss of body cell mass in cancer patients and healthy individuals.	Acetylcysteine	15-32	albumin	Homo sapiens	104-111
10205148-13	1999	This strain-induced ERK activity was attenuated after ECs were treated with N-acetylcysteine or catalase.	Acetylcysteine	76-92	mitogen-activated protein kinase 1	Homo sapiens	20-23
10026227-4	1999	NAC inhibited agonist-induced ERK2, JNK1, and p38 MAP kinase activation and c-Fos, c-Jun, and JunB expression except for platelet-derived growth factor BB-induced ERK2 activation.	Acetylcysteine	0-3	mitogen-activated protein kinase 1	Homo sapiens	30-34
10223197-8	1999	N-acetylcysteine, a thiol-containing antioxidant, decreased activation, further showing that vanadate-induced AP-1 activation involved redox reactions.	Acetylcysteine	0-16	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	110-114
10220113-6	1999	Pretreatment of cells with either PBN or NAC at 1.0 mM suppressed IL1beta H2O2, and sorbitol-mediated activation of p38 and significantly increased phosphatase activity.	Acetylcysteine	41-44	interleukin 1 beta	Rattus norvegicus	66-73
10051543-6	1999	However, both PKC activation and oxidant generation were necessary for ICAM-1 mRNA expression because the pretreatment of HPAE cells with either calphostin C or N-acetylcysteine inhibited the TNF-alpha-induced activation of NF-kappaB and prevented the activation of ICAM-1 promoter.	Acetylcysteine	161-177	tumor necrosis factor	Homo sapiens	192-201
9927752-1	1999	We have investigated by electrophoretic mobility shift assay (EMSA) the level of GATA-1 DNA-binding activity in nuclear extracts prepared from the human erythroleukaemic cell line, K562, after erythroid induction by hemin, sodium butyrate (NaB) or Trichostatin A or treatment with N -acetylcysteine (NAC).	Acetylcysteine	281-298	GATA binding protein 1	Homo sapiens	81-87
9927752-1	1999	We have investigated by electrophoretic mobility shift assay (EMSA) the level of GATA-1 DNA-binding activity in nuclear extracts prepared from the human erythroleukaemic cell line, K562, after erythroid induction by hemin, sodium butyrate (NaB) or Trichostatin A or treatment with N -acetylcysteine (NAC).	Acetylcysteine	300-303	GATA binding protein 1	Homo sapiens	81-87
10209264-9	1999	Pretreatment of CDDP-sensitive A2780 cells with N-acetyl-L-cysteine, a precursor of GSH, effectively enhanced induction of the Hsp72 mRNA by the mild heat stress.	Acetylcysteine	48-67	heat shock protein family A (Hsp70) member 1A	Homo sapiens	127-132
10194176-8	1999	N-Acetylcysteine and glutathione each significantly reversed the inhibitory effect of SIN-1 on isoprenaline-induced bronchoprotection in a dose-dependent manner.	Acetylcysteine	0-16	MAPK associated protein 1	Homo sapiens	86-91
10203355-10	1999	Pyrrolidine dithiocarbamate (PDTC), N-acetyl-L-cysteine, dexamethasone (Dex), HerA, and AG490 partially inhibited LPS/ IFN-gamma- or TNF-alpha/IFN-gamma-induced nitrite production.	Acetylcysteine	36-55	tumor necrosis factor	Rattus norvegicus	133-142
10070106-7	1999	The inhibition of both TNF-alpha production and NF-kappaB activation by N-acetyl-L-cysteine, an antioxidant, indicates that generation of oxidants may contribute to the induction of this cytokine and activation of this transcription factor by glass fibers.	Acetylcysteine	72-91	tumor necrosis factor	Mus musculus	23-32
10026227-4	1999	NAC inhibited agonist-induced ERK2, JNK1, and p38 MAP kinase activation and c-Fos, c-Jun, and JunB expression except for platelet-derived growth factor BB-induced ERK2 activation.	Acetylcysteine	0-3	mitogen-activated protein kinase 8	Homo sapiens	36-40
10026227-4	1999	NAC inhibited agonist-induced ERK2, JNK1, and p38 MAP kinase activation and c-Fos, c-Jun, and JunB expression except for platelet-derived growth factor BB-induced ERK2 activation.	Acetylcysteine	0-3	mitogen-activated protein kinase 1	Homo sapiens	46-49
9922324-9	1999	Similar results were obtained when N-acetyl-L-cysteine was used as an inhibitor of NF-kappaB activation.	Acetylcysteine	35-54	nuclear factor kappa B subunit 1	Homo sapiens	83-92
10063910-5	1999	N-Acetylcysteine (NAC) or dimethylsulfoxide inhibited IL-8 expression induced by tumor necrosis factor-alpha (TNF-alpha) or interleukin-1beta (IL-1beta).	Acetylcysteine	0-16	C-X-C motif chemokine ligand 8	Homo sapiens	54-58
10063910-5	1999	N-Acetylcysteine (NAC) or dimethylsulfoxide inhibited IL-8 expression induced by tumor necrosis factor-alpha (TNF-alpha) or interleukin-1beta (IL-1beta).	Acetylcysteine	0-16	tumor necrosis factor	Homo sapiens	81-108
10063910-5	1999	N-Acetylcysteine (NAC) or dimethylsulfoxide inhibited IL-8 expression induced by tumor necrosis factor-alpha (TNF-alpha) or interleukin-1beta (IL-1beta).	Acetylcysteine	0-16	tumor necrosis factor	Homo sapiens	110-119
10063910-5	1999	N-Acetylcysteine (NAC) or dimethylsulfoxide inhibited IL-8 expression induced by tumor necrosis factor-alpha (TNF-alpha) or interleukin-1beta (IL-1beta).	Acetylcysteine	0-16	interleukin 1 beta	Homo sapiens	124-141
10063910-5	1999	N-Acetylcysteine (NAC) or dimethylsulfoxide inhibited IL-8 expression induced by tumor necrosis factor-alpha (TNF-alpha) or interleukin-1beta (IL-1beta).	Acetylcysteine	0-16	interleukin 1 beta	Homo sapiens	143-151
10063910-5	1999	N-Acetylcysteine (NAC) or dimethylsulfoxide inhibited IL-8 expression induced by tumor necrosis factor-alpha (TNF-alpha) or interleukin-1beta (IL-1beta).	Acetylcysteine	18-21	C-X-C motif chemokine ligand 8	Homo sapiens	54-58
10063910-5	1999	N-Acetylcysteine (NAC) or dimethylsulfoxide inhibited IL-8 expression induced by tumor necrosis factor-alpha (TNF-alpha) or interleukin-1beta (IL-1beta).	Acetylcysteine	18-21	tumor necrosis factor	Homo sapiens	81-108
10063910-5	1999	N-Acetylcysteine (NAC) or dimethylsulfoxide inhibited IL-8 expression induced by tumor necrosis factor-alpha (TNF-alpha) or interleukin-1beta (IL-1beta).	Acetylcysteine	18-21	tumor necrosis factor	Homo sapiens	110-119
10063910-5	1999	N-Acetylcysteine (NAC) or dimethylsulfoxide inhibited IL-8 expression induced by tumor necrosis factor-alpha (TNF-alpha) or interleukin-1beta (IL-1beta).	Acetylcysteine	18-21	interleukin 1 beta	Homo sapiens	124-141
10063910-5	1999	N-Acetylcysteine (NAC) or dimethylsulfoxide inhibited IL-8 expression induced by tumor necrosis factor-alpha (TNF-alpha) or interleukin-1beta (IL-1beta).	Acetylcysteine	18-21	interleukin 1 beta	Homo sapiens	143-151
9895238-4	1999	N-acetyl cysteine inhibited RV-induced NF-kappaB activation and IL-8 elaboration.	Acetylcysteine	0-17	C-X-C motif chemokine ligand 8	Homo sapiens	64-68
10063910-7	1999	TNF-alpha-induced activation of NF-kappaB activity was suppressed by NAC, and H2O2 caused significant activation of NF-kappaB.	Acetylcysteine	69-72	tumor necrosis factor	Homo sapiens	0-9
10063910-7	1999	TNF-alpha-induced activation of NF-kappaB activity was suppressed by NAC, and H2O2 caused significant activation of NF-kappaB.	Acetylcysteine	69-72	nuclear factor kappa B subunit 1	Homo sapiens	32-41
9990295-7	1999	The antioxidant N-acetylcysteine (NAC) blocks cell death and NF-kappa B activation induced by Fas ligation, suggesting a potential role for NF-kappa B in Fas-induced apoptosis in these cells.	Acetylcysteine	16-32	nuclear factor kappa B subunit 1	Homo sapiens	61-71
9973431-5	1999	Inhibition of p38-MAPK by SB203580 and an antisense oligonucleotide delayed apoptosis by approximately 24 h. The antioxidants catalase and N-acetylcysteine delayed neutrophil apoptosis, but failed to inhibit phosphorylation and activation of p38-MAPK.	Acetylcysteine	139-155	mitogen-activated protein kinase 14	Homo sapiens	14-17
9973431-5	1999	Inhibition of p38-MAPK by SB203580 and an antisense oligonucleotide delayed apoptosis by approximately 24 h. The antioxidants catalase and N-acetylcysteine delayed neutrophil apoptosis, but failed to inhibit phosphorylation and activation of p38-MAPK.	Acetylcysteine	139-155	mitogen-activated protein kinase 14	Homo sapiens	18-22
9990295-7	1999	The antioxidant N-acetylcysteine (NAC) blocks cell death and NF-kappa B activation induced by Fas ligation, suggesting a potential role for NF-kappa B in Fas-induced apoptosis in these cells.	Acetylcysteine	16-32	nuclear factor kappa B subunit 1	Homo sapiens	140-150
9990295-7	1999	The antioxidant N-acetylcysteine (NAC) blocks cell death and NF-kappa B activation induced by Fas ligation, suggesting a potential role for NF-kappa B in Fas-induced apoptosis in these cells.	Acetylcysteine	34-37	nuclear factor kappa B subunit 1	Homo sapiens	61-71
9990295-7	1999	The antioxidant N-acetylcysteine (NAC) blocks cell death and NF-kappa B activation induced by Fas ligation, suggesting a potential role for NF-kappa B in Fas-induced apoptosis in these cells.	Acetylcysteine	34-37	nuclear factor kappa B subunit 1	Homo sapiens	140-150
9990295-8	1999	The effects of NAC on TNF-alpha-induced cell death are more complex, with NAC being marginally protective and itself enhancing the formation of c-Rel containing complexes at higher concentrations (25 mM).	Acetylcysteine	15-18	tumor necrosis factor	Homo sapiens	22-31
9990295-8	1999	The effects of NAC on TNF-alpha-induced cell death are more complex, with NAC being marginally protective and itself enhancing the formation of c-Rel containing complexes at higher concentrations (25 mM).	Acetylcysteine	74-77	tumor necrosis factor	Homo sapiens	22-31
10365774-4	1999	The biological activity of TGFbeta (following activation) released into the medium from cultured BPAEC was significantly reduced when the cells were cultured in the presence of 10 mM GSH or 10 mM NAC for 24 h (10 mM GSH: 85.7 +/- 50 pg/ml/10(6) cells and 10 mM NAC: 127.3 +/- 35 pg/ml/10(6) cells, compared with control: 541 +/- 8.9 pg/ml/10(6) cells; p &lt; 0.05).	Acetylcysteine	196-199	transforming growth factor beta 1	Homo sapiens	27-34
10619702-5	1999	The increase in adherence, ingestion and superoxide anion and TNF alpha production shown by macrophages from animals with endotoxic shock was counteracted by NAC injection.	Acetylcysteine	158-161	tumor necrosis factor	Mus musculus	62-71
10619702-7	1999	These data suggest that NAC, administered intraperitoneally, may be useful for the treatment of irreversible endotoxic shock by modulation of the function of macrophages with decreased superoxide anion and TNF alpha production and concomitant increase of survival time.	Acetylcysteine	24-27	tumor necrosis factor	Mus musculus	206-215
10365774-4	1999	The biological activity of TGFbeta (following activation) released into the medium from cultured BPAEC was significantly reduced when the cells were cultured in the presence of 10 mM GSH or 10 mM NAC for 24 h (10 mM GSH: 85.7 +/- 50 pg/ml/10(6) cells and 10 mM NAC: 127.3 +/- 35 pg/ml/10(6) cells, compared with control: 541 +/- 8.9 pg/ml/10(6) cells; p &lt; 0.05).	Acetylcysteine	261-264	transforming growth factor beta 1	Homo sapiens	27-34
9837905-5	1998	The glutathione precursor N-acetylcysteine, an antioxidant, abolished AA-stimulated MKP-1 gene expression, whereas inhibition of protein kinase C by calphostin C had no influence on MKP-1 induction.	Acetylcysteine	26-42	dual specificity phosphatase 1	Homo sapiens	84-89
9892811-15	1999	These results show that NAC inhibits iNOS induction and NO synthesis in this model, and suppresses ROS synthesis and injury.	Acetylcysteine	24-27	nitric oxide synthase 2	Rattus norvegicus	37-41
9886415-6	1999	In contrast, blockade of all three kinases with N-acetylcysteine completely blocked the induction of iNOS expression.	Acetylcysteine	48-64	nitric oxide synthase 2, inducible	Mus musculus	101-105
9843778-9	1998	In particular, NAC inhibited intrapancreatic trypsin activation and mRNA expression of cytokines interleukin-6 and KC, which were dramatically induced by cerulein.	Acetylcysteine	15-18	interleukin 6	Rattus norvegicus	97-110
9830056-0	1998	Nitric oxide and N-acetylcysteine inhibit the activation of mitogen-activated protein kinases by angiotensin II in rat cardiac fibroblasts.	Acetylcysteine	17-33	angiotensinogen	Rattus norvegicus	97-111
9830056-5	1998	Pretreatment of cardiac fibroblasts with either N-acetylcysteine for 8 h or nitric oxide for 10 min suppressed this activation by angiotensin II in a dose-dependent manner.	Acetylcysteine	48-64	angiotensinogen	Rattus norvegicus	130-144
9833950-0	1998	Reduction of oxidative stress by oral N-acetyl-L-cysteine treatment decreases plasma soluble vascular cell adhesion molecule-1 concentrations in non-obese, non-dyslipidaemic, normotensive, patients with non-insulin-dependent diabetes.	Acetylcysteine	38-57	vascular cell adhesion molecule 1	Homo sapiens	93-126
9862355-5	1998	Blocking ROI production by preincubation with the antioxidant N-acetyl-L-cysteine inhibits JNK activation, NF-kappaB-driven luciferase activity, and IL-6 secretion following CD40 ligation, suggesting a role for ROI in CD40-mediated signaling events.	Acetylcysteine	62-81	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	107-116
9862355-5	1998	Blocking ROI production by preincubation with the antioxidant N-acetyl-L-cysteine inhibits JNK activation, NF-kappaB-driven luciferase activity, and IL-6 secretion following CD40 ligation, suggesting a role for ROI in CD40-mediated signaling events.	Acetylcysteine	62-81	interleukin 6	Mus musculus	149-153
9856964-11	1998	N-Acetylcysteine also completely blocked ERK activation and the increase of thymidine incorporation in response to oleic acid.	Acetylcysteine	0-16	mitogen-activated protein kinase 1	Homo sapiens	41-44
9825739-7	1998	Incubation of BSP with selenite in the presence of a thiol, namely glutathione, cysteine or N-acetylcysteine (which convert selenite into nucleophilic products, i.e. the respective selenopersulfides and hydrogen selenide) resulted in product(s) chromatographically identical to the biliary selenium-containing BSP metabolite(s) of peak Y, irrespective of the nature of the thiol used.	Acetylcysteine	92-108	integrin-binding sialoprotein	Rattus norvegicus	14-17
9825739-7	1998	Incubation of BSP with selenite in the presence of a thiol, namely glutathione, cysteine or N-acetylcysteine (which convert selenite into nucleophilic products, i.e. the respective selenopersulfides and hydrogen selenide) resulted in product(s) chromatographically identical to the biliary selenium-containing BSP metabolite(s) of peak Y, irrespective of the nature of the thiol used.	Acetylcysteine	92-108	integrin-binding sialoprotein	Rattus norvegicus	310-313
9833940-1	1998	Free-radical scavengers and inhibitors of tumour necrosis factor-alpha (TNF-alpha) such as N-acetylcysteine and pentoxifylline have been shown to inhibit the development of peripheral neuropathy in streptozotocin(STZ)-induced diabetic rats.	Acetylcysteine	91-107	tumor necrosis factor	Rattus norvegicus	72-81
9826428-8	1998	The presence of 5 mM N-acetylcysteine prevented induction of iNOS in crocidolite-treated A549 cells.	Acetylcysteine	21-37	nitric oxide synthase 2	Homo sapiens	61-65
9840292-6	1998	In particular, a significant correlation was found between the decrease in number of CD4+ lymphocytes in patients at different stages of disease and the susceptibility of their PBMCs to oxidative stress; (2) preincubation with NAC was able to preserve partially the ultrastructural characteristics of PBMCs isolated from HIV+ patients.	Acetylcysteine	227-230	CD4 molecule	Homo sapiens	85-88
9840292-7	1998	In particular, a direct relationship was found between the efficacy of NAC protection and CD4 counts; (3) evaluation of the plasma index of peroxidation and the number of circulating CD4 lymphocytes indicates the existence of a positive correlation between "systemic" oxidative imbalance and stage of the disease; and (4) cells from LTNPs display either oxidative susceptibility or oxidative markers similar to those of healthy donor cells.	Acetylcysteine	71-74	CD4 molecule	Homo sapiens	90-93
9833950-7	1998	Treatment with N-acetyl-L-cysteine decreased plasma VCAM-1 (p = 0.01) and intraerythrocytic GSSG (p = 0.006) but increased GSH concentrations (p = 0.04) and the GSH:GSSG ratio (p = 0.004) in non-insulin dependent diabetic patients.	Acetylcysteine	15-34	vascular cell adhesion molecule 1	Homo sapiens	52-58
9714697-5	1998	In vitro administration of N-acetylcysteine (NAC) not only restored intracellular GSH levels but also enhanced the IL-2-stimulated cytotoxicity of liver MNC in HCC patients.	Acetylcysteine	27-43	interleukin 2	Homo sapiens	115-119
9788899-8	1998	Further, PLD activation by ROS was attenuated by N-acetylcysteine, indicating that intracellular thiol status is critical to ROS-mediated signal transduction.	Acetylcysteine	49-65	glycosylphosphatidylinositol specific phospholipase D1	Homo sapiens	9-12
9721806-2	1998	The present study was designed to investigate whether the antioxidants butylated hydroxytoluene (BHT) and N-acetylcysteine (NAC) modified TNF-alpha production in stimulated and unstimulated alveolar macrophages from lung transplant recipients in vitro.	Acetylcysteine	106-122	tumor necrosis factor	Homo sapiens	138-147
9721806-2	1998	The present study was designed to investigate whether the antioxidants butylated hydroxytoluene (BHT) and N-acetylcysteine (NAC) modified TNF-alpha production in stimulated and unstimulated alveolar macrophages from lung transplant recipients in vitro.	Acetylcysteine	124-127	tumor necrosis factor	Homo sapiens	138-147
9721806-3	1998	METHODS: The effects of BHT and NAC on TNF-alpha production were studied both with and without lipopolysaccharide (LPS) activation of alveolar macrophages from bronchoalveolar lavage fluid.	Acetylcysteine	32-35	tumor necrosis factor	Homo sapiens	39-48
9721806-6	1998	RESULTS: In unstimulated alveolar macrophages, TNF-alpha levels were significantly reduced by incubation with BHT or NAC.	Acetylcysteine	117-120	tumor necrosis factor	Homo sapiens	47-56
9721806-8	1998	A significant reduction of TNF-alpha levels in LPS-stimulated alveolar macrophages was obtained in the presence of BHT or NAC.	Acetylcysteine	122-125	tumor necrosis factor	Homo sapiens	27-36
9730864-5	1998	Cytokine secretion was preceded by activation of the transcription factor nuclear factor-kappaB (NF-kappaB) and was reduced by treatment of cultures with superoxide dismutase, deferoxamine, or N-acetylcysteine.	Acetylcysteine	193-209	nuclear factor kappa B subunit 1	Homo sapiens	74-95
9730864-5	1998	Cytokine secretion was preceded by activation of the transcription factor nuclear factor-kappaB (NF-kappaB) and was reduced by treatment of cultures with superoxide dismutase, deferoxamine, or N-acetylcysteine.	Acetylcysteine	193-209	nuclear factor kappa B subunit 1	Homo sapiens	97-106
9714697-5	1998	In vitro administration of N-acetylcysteine (NAC) not only restored intracellular GSH levels but also enhanced the IL-2-stimulated cytotoxicity of liver MNC in HCC patients.	Acetylcysteine	45-48	interleukin 2	Homo sapiens	115-119
9707512-6	1998	IL-8 and MIP-2 secretion induced either by the metals or H2O2 were inhibited by antioxidants such as tetramethyl-thiourea and N-acetyl-cysteine.	Acetylcysteine	126-143	C-X-C motif chemokine ligand 8	Homo sapiens	0-4
9718198-9	1998	An antioxidant, N-acetyl-L-cysteine, significantly attenuated the TNF-alpha-dependent increase in these mRNAs, and simultaneously reduced the activation of NF-kappaB by TNF-alpha, indicating that NF-kappaB mediates the TNF-alpha-dependent expression of IL-6 and ICAM-1 in ROS17/2.8 cells.	Acetylcysteine	16-35	tumor necrosis factor	Rattus norvegicus	66-75
9718198-9	1998	An antioxidant, N-acetyl-L-cysteine, significantly attenuated the TNF-alpha-dependent increase in these mRNAs, and simultaneously reduced the activation of NF-kappaB by TNF-alpha, indicating that NF-kappaB mediates the TNF-alpha-dependent expression of IL-6 and ICAM-1 in ROS17/2.8 cells.	Acetylcysteine	16-35	tumor necrosis factor	Rattus norvegicus	169-178
9718198-9	1998	An antioxidant, N-acetyl-L-cysteine, significantly attenuated the TNF-alpha-dependent increase in these mRNAs, and simultaneously reduced the activation of NF-kappaB by TNF-alpha, indicating that NF-kappaB mediates the TNF-alpha-dependent expression of IL-6 and ICAM-1 in ROS17/2.8 cells.	Acetylcysteine	16-35	tumor necrosis factor	Rattus norvegicus	169-178
9718198-9	1998	An antioxidant, N-acetyl-L-cysteine, significantly attenuated the TNF-alpha-dependent increase in these mRNAs, and simultaneously reduced the activation of NF-kappaB by TNF-alpha, indicating that NF-kappaB mediates the TNF-alpha-dependent expression of IL-6 and ICAM-1 in ROS17/2.8 cells.	Acetylcysteine	16-35	interleukin 6	Rattus norvegicus	253-257
9726445-7	1998	Both IL-8 and MIP-2 secretion were inhibited, although to varying degrees, by such antioxidants as TMTU, DMSO, catalase, and N-acetylcysteine.	Acetylcysteine	125-141	C-X-C motif chemokine ligand 8	Homo sapiens	5-9
9711995-1	1998	N-acetylcysteine and pentoxifylline, free radical scavengers and inhibitors of tumor necrosis factor-alpha (TNF-alpha) production, inhibit the development of peripheral neuropathy in streptozotocin (STZ)-induced diabetic rats.	Acetylcysteine	0-16	tumor necrosis factor	Rattus norvegicus	79-106
9651337-10	1998	TNFalpha or hydrogen peroxide treatment increased the dimeric form of ASK1, and pretreatment with N-acetylcysteine decreased it.	Acetylcysteine	98-114	tumor necrosis factor	Homo sapiens	0-8
9670954-6	1998	The activation of JNK by HIV-tat appears to be mediated through generation of free radical species, since pretreatment of cells with N-acetylcysteine (NAC) abolished the effect.	Acetylcysteine	133-149	mitogen-activated protein kinase 8	Homo sapiens	18-21
9670954-6	1998	The activation of JNK by HIV-tat appears to be mediated through generation of free radical species, since pretreatment of cells with N-acetylcysteine (NAC) abolished the effect.	Acetylcysteine	151-154	mitogen-activated protein kinase 8	Homo sapiens	18-21
9660850-8	1998	The same GSH and NAC conjugates were also observed when DMBI was oxidized by HOCl or by the MPO system, followed by addition of GSH or NAC.	Acetylcysteine	17-20	myeloperoxidase	Homo sapiens	92-95
9651185-8	1998	The IL-6 response was inhibited by the metal chelator deferoxamine and the free radical scavenger N-acetyl-L-cysteine, suggesting that the activation of NF-kappaB may be mediated through reactive oxygen intermediates generated by transition metals found in ROFA.	Acetylcysteine	98-117	interleukin 6	Homo sapiens	4-8
9651185-8	1998	The IL-6 response was inhibited by the metal chelator deferoxamine and the free radical scavenger N-acetyl-L-cysteine, suggesting that the activation of NF-kappaB may be mediated through reactive oxygen intermediates generated by transition metals found in ROFA.	Acetylcysteine	98-117	nuclear factor kappa B subunit 1	Homo sapiens	153-162
9592085-4	1998	We show that NAC activates the Ras-extracellular signal-regulated kinase (ERK) pathway in PC12 cells.	Acetylcysteine	13-16	Eph receptor B1	Rattus norvegicus	31-72
9620307-8	1998	Phosphorylation of EGFR was inhibited by the structurally unrelated antioxidants butylated hydroxyanisole, N-acetyl-L-cysteine, and pyrrolidine dithiocarbamate, or by the H2O2-degrading enzyme catalase.	Acetylcysteine	107-126	epidermal growth factor receptor	Homo sapiens	19-23
9592085-4	1998	We show that NAC activates the Ras-extracellular signal-regulated kinase (ERK) pathway in PC12 cells.	Acetylcysteine	13-16	Eph receptor B1	Rattus norvegicus	74-77
9592085-6	1998	Promotion of PC12 cell survival by NAC is totally blocked by PD98059, an inhibitor of the ERK-activating MAP kinase/ERK kinase, suggesting a required role for ERK activation in the NAC mechanism.	Acetylcysteine	35-38	Eph receptor B1	Rattus norvegicus	90-93
9592085-6	1998	Promotion of PC12 cell survival by NAC is totally blocked by PD98059, an inhibitor of the ERK-activating MAP kinase/ERK kinase, suggesting a required role for ERK activation in the NAC mechanism.	Acetylcysteine	35-38	Eph receptor B1	Rattus norvegicus	116-119
9592085-6	1998	Promotion of PC12 cell survival by NAC is totally blocked by PD98059, an inhibitor of the ERK-activating MAP kinase/ERK kinase, suggesting a required role for ERK activation in the NAC mechanism.	Acetylcysteine	35-38	Eph receptor B1	Rattus norvegicus	116-119
9592085-6	1998	Promotion of PC12 cell survival by NAC is totally blocked by PD98059, an inhibitor of the ERK-activating MAP kinase/ERK kinase, suggesting a required role for ERK activation in the NAC mechanism.	Acetylcysteine	181-184	Eph receptor B1	Rattus norvegicus	90-93
9592085-6	1998	Promotion of PC12 cell survival by NAC is totally blocked by PD98059, an inhibitor of the ERK-activating MAP kinase/ERK kinase, suggesting a required role for ERK activation in the NAC mechanism.	Acetylcysteine	181-184	Eph receptor B1	Rattus norvegicus	116-119
9592085-6	1998	Promotion of PC12 cell survival by NAC is totally blocked by PD98059, an inhibitor of the ERK-activating MAP kinase/ERK kinase, suggesting a required role for ERK activation in the NAC mechanism.	Acetylcysteine	181-184	Eph receptor B1	Rattus norvegicus	116-119
9592085-11	1998	These findings highlight the role of Ras-ERK activation in the mechanism by which NAC prevents neuronal death after loss of trophic support.	Acetylcysteine	82-85	Eph receptor B1	Rattus norvegicus	41-44
9692856-1	1998	Mycothiol (MSH) is a glycosylated derivative of N-acetylcysteine that may have antioxidant functions in mycobacteria and other actinomycetes.	Acetylcysteine	48-64	msh homeobox 2	Homo sapiens	11-14
12671299-5	1998	Pretreatment with free radical scavengers N-acetyl-L-cysteine (NAC), glutathione (GSH), or vitamin E, inhibited ERK2 activation and, to a much lesser extent, JNK 1 activation by BHA and tBHQ, implicating the role of oxidative stress.	Acetylcysteine	42-61	mitogen-activated protein kinase 1	Homo sapiens	112-116
12671299-5	1998	Pretreatment with free radical scavengers N-acetyl-L-cysteine (NAC), glutathione (GSH), or vitamin E, inhibited ERK2 activation and, to a much lesser extent, JNK 1 activation by BHA and tBHQ, implicating the role of oxidative stress.	Acetylcysteine	42-61	mitogen-activated protein kinase 8	Homo sapiens	158-163
9564042-5	1998	Treatment of cells with N-acetyl-L-cysteine also inhibited serum withdrawal-, TNF-alpha- and hydrogen peroxide-induced activation of ASK1 as well as apoptosis.	Acetylcysteine	24-43	tumor necrosis factor	Homo sapiens	78-87
9581680-7	1998	On the other hand, kinetic analysis showed that production of nitric oxide (NO) and tumor necrosis factor alpha (TNF-alpha) by lipopolysaccharide-stimulated Kupffer cells was strongly inhibited by resveratrol and quercetin but not by NAC.	Acetylcysteine	234-237	tumor necrosis factor	Rattus norvegicus	84-111
9581680-7	1998	On the other hand, kinetic analysis showed that production of nitric oxide (NO) and tumor necrosis factor alpha (TNF-alpha) by lipopolysaccharide-stimulated Kupffer cells was strongly inhibited by resveratrol and quercetin but not by NAC.	Acetylcysteine	234-237	tumor necrosis factor	Rattus norvegicus	113-122
9575216-11	1998	Treatment of cultured rat fibroblast and human breast cancer cell lines with N-acetylcysteine resulted in a substantial loss of Ca2+- and PS- dependent PKC activity in the cells within 30 min.	Acetylcysteine	77-93	protein kinase C alpha	Homo sapiens	152-155
9556624-6	1998	Pretreatment of cells with GSH, GSH-methylester, or N-acetylcysteine, a precursor of GSH biosynthesis, inhibited the TNFalpha-induced sphingomyelin hydrolysis and ceramide generation as well as cell death.	Acetylcysteine	52-68	tumor necrosis factor	Homo sapiens	117-125
9581775-5	1998	Inhibition of TNFalpha-induced NF-kappaB activation using the antioxidant N-acetylcysteine (NAC) resulted in increased apoptosis in both U937 and U9-IIIB cells, while preactivation of NF-kappaB with the non-apoptotic inducer IL-1beta caused a relative decrease in apoptosis.	Acetylcysteine	74-90	tumor necrosis factor	Homo sapiens	14-22
9581775-5	1998	Inhibition of TNFalpha-induced NF-kappaB activation using the antioxidant N-acetylcysteine (NAC) resulted in increased apoptosis in both U937 and U9-IIIB cells, while preactivation of NF-kappaB with the non-apoptotic inducer IL-1beta caused a relative decrease in apoptosis.	Acetylcysteine	74-90	interleukin 1 beta	Homo sapiens	225-233
9581775-5	1998	Inhibition of TNFalpha-induced NF-kappaB activation using the antioxidant N-acetylcysteine (NAC) resulted in increased apoptosis in both U937 and U9-IIIB cells, while preactivation of NF-kappaB with the non-apoptotic inducer IL-1beta caused a relative decrease in apoptosis.	Acetylcysteine	92-95	tumor necrosis factor	Homo sapiens	14-22
9581775-5	1998	Inhibition of TNFalpha-induced NF-kappaB activation using the antioxidant N-acetylcysteine (NAC) resulted in increased apoptosis in both U937 and U9-IIIB cells, while preactivation of NF-kappaB with the non-apoptotic inducer IL-1beta caused a relative decrease in apoptosis.	Acetylcysteine	92-95	interleukin 1 beta	Homo sapiens	225-233
9581775-7	1998	TNFalpha plus NAC treatment resulted in a marked decrease in Bcl-2 protein levels in HIV-1-infected cells, coupled with an increase in Bax protein compared to uninfected cells, suggesting that the difference in susceptibility to TNFalpha-induced apoptosis may relate to the differences in relative levels of Bcl-2 and Bax.	Acetylcysteine	14-17	BCL2 apoptosis regulator	Homo sapiens	61-66
9581775-7	1998	TNFalpha plus NAC treatment resulted in a marked decrease in Bcl-2 protein levels in HIV-1-infected cells, coupled with an increase in Bax protein compared to uninfected cells, suggesting that the difference in susceptibility to TNFalpha-induced apoptosis may relate to the differences in relative levels of Bcl-2 and Bax.	Acetylcysteine	14-17	tumor necrosis factor	Homo sapiens	229-237
9581775-7	1998	TNFalpha plus NAC treatment resulted in a marked decrease in Bcl-2 protein levels in HIV-1-infected cells, coupled with an increase in Bax protein compared to uninfected cells, suggesting that the difference in susceptibility to TNFalpha-induced apoptosis may relate to the differences in relative levels of Bcl-2 and Bax.	Acetylcysteine	14-17	BCL2 apoptosis regulator	Homo sapiens	308-313
9563752-6	1998	In vitro, TNF production and DNA binding of nuclear factor kappa B (NF-kappaB) in human Mono Mac 6 cells was only inhibited at concentrations of NAC above 20 mM.	Acetylcysteine	145-148	tumor necrosis factor	Homo sapiens	10-13
9563490-7	1998	N-Acetylcysteine elevated p53 expression posttranscriptionally by increasing the rate of p53 mRNA translation rather than by altering the protein stability.	Acetylcysteine	0-16	tumor protein p53	Homo sapiens	26-29
9563490-7	1998	N-Acetylcysteine elevated p53 expression posttranscriptionally by increasing the rate of p53 mRNA translation rather than by altering the protein stability.	Acetylcysteine	0-16	tumor protein p53	Homo sapiens	89-92
9563752-6	1998	In vitro, TNF production and DNA binding of nuclear factor kappa B (NF-kappaB) in human Mono Mac 6 cells was only inhibited at concentrations of NAC above 20 mM.	Acetylcysteine	145-148	nuclear factor kappa B subunit 1	Homo sapiens	44-66
9563752-6	1998	In vitro, TNF production and DNA binding of nuclear factor kappa B (NF-kappaB) in human Mono Mac 6 cells was only inhibited at concentrations of NAC above 20 mM.	Acetylcysteine	145-148	nuclear factor kappa B subunit 1	Homo sapiens	68-77
9546365-9	1998	These findings provide direct evidence for a major role of GGT in regulating the tissue distribution and elimination of methylmercury and inorganic mercury and provide additional support for the use of NAC as an antidote in methylmercury poisoning.	Acetylcysteine	202-205	gamma-glutamyltransferase 1	Mus musculus	59-62
9566715-7	1998	The nucleotide depletion likely reflected the action of ROS, since the nucleotide depletion caused by TNF or oxidants such as menadione or H2O2 in cells with active c-Myc was partly inhibited by the anti-oxidant N-acetylcysteine.	Acetylcysteine	212-228	tumor necrosis factor	Rattus norvegicus	102-105
9535218-4	1998	Exposure to N-acetylcysteine before treatment with oxLDL, C2-ceramide, TNF-alpha, or H2O2 reversed a decrease in cellular glutathione concentrations as well as the enhanced production of p53 and MnSOD mRNA and protein.	Acetylcysteine	12-28	tumor necrosis factor	Homo sapiens	71-80
9535218-4	1998	Exposure to N-acetylcysteine before treatment with oxLDL, C2-ceramide, TNF-alpha, or H2O2 reversed a decrease in cellular glutathione concentrations as well as the enhanced production of p53 and MnSOD mRNA and protein.	Acetylcysteine	12-28	tumor protein p53	Homo sapiens	187-190
9529157-11	1998	Experiments performed in the presence of the antioxidant N-acetylcysteine demonstrated that the expression of vascular cell adhesion molecule-1 could be almost totally abolished, whereas that of intercellular adhesion molecule-1 was typically reduced by approximately 70%.	Acetylcysteine	57-73	vascular cell adhesion molecule 1	Homo sapiens	110-143
9521863-2	1998	Recently we demonstrated the thiol antioxidant N-acetylcysteine (NAC) inhibits constitutive NF-kappa B/Rel activity and growth of vascular SMCs.	Acetylcysteine	47-63	nuclear factor kappa B subunit 1	Homo sapiens	92-102
9521863-2	1998	Recently we demonstrated the thiol antioxidant N-acetylcysteine (NAC) inhibits constitutive NF-kappa B/Rel activity and growth of vascular SMCs.	Acetylcysteine	65-68	nuclear factor kappa B subunit 1	Homo sapiens	92-102
9571990-9	1998	NAC prevented activation of mitogen-activated protein (MAP) kinases p42MAPK and p44MAPK and inhibited expression of cyclin D1, but had no effect on the levels of proliferating cell nuclear antigen.	Acetylcysteine	0-3	mitogen-activated protein kinase 1	Mus musculus	68-75
9518260-11	1998	In addition, provision of the GSH precursor, N-acetylcysteine during TNF-alpha challenge only diminished MnSOD activity and mitochondrial compartmentalization in the AIDS-KS cells, a finding that likely reflects the lower levels of reduced thiols in this cellular population.	Acetylcysteine	45-61	tumor necrosis factor	Homo sapiens	69-78
9501919-3	1998	Addition of either N-acetyl-L-cysteine or glutathione ester (GSE), but not L-2-oxothiazolidine 4-carboxylate, partially restored intracellular GSH levels and resulted in loss of extracellular FGF-1.	Acetylcysteine	19-38	fibroblast growth factor 1	Homo sapiens	192-197
9580328-4	1998	Overexpression of Bcl-2 and pretreatment with either the immunosuppressant cyclosporin A or the glutathione precursor N-acetyl-L-cysteine blocked deltapsi(m) disruption and apoptosis, but not the generation of ROS induced by these compounds.	Acetylcysteine	118-137	BCL2 apoptosis regulator	Homo sapiens	18-23
9489720-7	1998	The ROS- and NO-enhanced tyrosine phosphorylation and activation of p42 MAPK and p44 MAPK were inhibited by pretreatment with the antioxidant N-acetyl-L-cysteine.	Acetylcysteine	142-161	mitogen-activated protein kinase 1	Homo sapiens	68-76
9489720-7	1998	The ROS- and NO-enhanced tyrosine phosphorylation and activation of p42 MAPK and p44 MAPK were inhibited by pretreatment with the antioxidant N-acetyl-L-cysteine.	Acetylcysteine	142-161	mitogen-activated protein kinase 3	Homo sapiens	81-89
9446561-9	1998	Inhibition of ceramide and LPS-mediated induction of iNOS by antioxidant inhibitors of NF-kappaB (N-acetylcysteine and pyrrolidine dithiocarbamate) suggest that the stimulatory effect of ceramide on the induction of iNOS is due to the stimulation of NF-kappaB activation and that cellular redox plays a role in the activation of NF-kappaB and induction of iNOS.	Acetylcysteine	98-114	nitric oxide synthase 2	Rattus norvegicus	53-57
9452508-7	1998	Anti-oxidants N-acetylcysteine and catalase, which serve as scavengers of reactive oxygen species generated by metabolic DA oxidation, effectively block DA-induced JNK activation and subsequent apoptosis.	Acetylcysteine	14-30	mitogen-activated protein kinase 8	Homo sapiens	164-167
9476910-15	1998	Treatment of cells with the antioxidants N-acetyl-L-cysteine (NAC) and dimethyl sulfoxide (DMSO) not only blunts LPS-induced production of ROI, but also significantly attenuates LPS-induced HO-1 messenger RNA (mRNA) expression and gene transcription.	Acetylcysteine	41-60	heme oxygenase 1	Mus musculus	190-194
9476910-15	1998	Treatment of cells with the antioxidants N-acetyl-L-cysteine (NAC) and dimethyl sulfoxide (DMSO) not only blunts LPS-induced production of ROI, but also significantly attenuates LPS-induced HO-1 messenger RNA (mRNA) expression and gene transcription.	Acetylcysteine	62-65	heme oxygenase 1	Mus musculus	190-194
9692114-0	1998	N-acetylcysteine inhibits IL-1 alpha-induced IL-8 secretion by bronchial epithelial cells.	Acetylcysteine	0-16	C-X-C motif chemokine ligand 8	Homo sapiens	45-49
9446561-9	1998	Inhibition of ceramide and LPS-mediated induction of iNOS by antioxidant inhibitors of NF-kappaB (N-acetylcysteine and pyrrolidine dithiocarbamate) suggest that the stimulatory effect of ceramide on the induction of iNOS is due to the stimulation of NF-kappaB activation and that cellular redox plays a role in the activation of NF-kappaB and induction of iNOS.	Acetylcysteine	98-114	nitric oxide synthase 2	Rattus norvegicus	216-220
9446561-9	1998	Inhibition of ceramide and LPS-mediated induction of iNOS by antioxidant inhibitors of NF-kappaB (N-acetylcysteine and pyrrolidine dithiocarbamate) suggest that the stimulatory effect of ceramide on the induction of iNOS is due to the stimulation of NF-kappaB activation and that cellular redox plays a role in the activation of NF-kappaB and induction of iNOS.	Acetylcysteine	98-114	nitric oxide synthase 2	Rattus norvegicus	216-220
9419178-4	1998	However, lipopolysaccharide-induced IL-8 production was increased in a dose-dependent manner by a combination of sodium nitroprusside and N-acetylcysteine (P = .03) or by S-nitrosoglutathione (P = .004).	Acetylcysteine	138-154	C-X-C motif chemokine ligand 8	Homo sapiens	36-40
9457054-5	1998	N-Acetylcysteine (1 mM) interfered with NO-mediated apoptotic signaling, blocking DNA fragmentation as well as PARP and U1 snRNP cleavage.	Acetylcysteine	0-16	poly(ADP-ribose) polymerase 1	Homo sapiens	111-115
9436612-4	1998	The decrease in NO production by NAC was accompanied by a decrease in inducible nitric oxide synthase (iNOS) activity, in iNOS protein detected by immunoblot analysis with antibodies against iNOS, and in iNOS mRNA determined by reverse-transcriptase coupled polymerase chain reaction (RT-PCR).	Acetylcysteine	33-36	nitric oxide synthase 2	Rattus norvegicus	70-101
9436612-4	1998	The decrease in NO production by NAC was accompanied by a decrease in inducible nitric oxide synthase (iNOS) activity, in iNOS protein detected by immunoblot analysis with antibodies against iNOS, and in iNOS mRNA determined by reverse-transcriptase coupled polymerase chain reaction (RT-PCR).	Acetylcysteine	33-36	nitric oxide synthase 2	Rattus norvegicus	103-107
9436612-4	1998	The decrease in NO production by NAC was accompanied by a decrease in inducible nitric oxide synthase (iNOS) activity, in iNOS protein detected by immunoblot analysis with antibodies against iNOS, and in iNOS mRNA determined by reverse-transcriptase coupled polymerase chain reaction (RT-PCR).	Acetylcysteine	33-36	nitric oxide synthase 2	Rattus norvegicus	122-126
9436612-4	1998	The decrease in NO production by NAC was accompanied by a decrease in inducible nitric oxide synthase (iNOS) activity, in iNOS protein detected by immunoblot analysis with antibodies against iNOS, and in iNOS mRNA determined by reverse-transcriptase coupled polymerase chain reaction (RT-PCR).	Acetylcysteine	33-36	nitric oxide synthase 2	Rattus norvegicus	122-126
9436612-4	1998	The decrease in NO production by NAC was accompanied by a decrease in inducible nitric oxide synthase (iNOS) activity, in iNOS protein detected by immunoblot analysis with antibodies against iNOS, and in iNOS mRNA determined by reverse-transcriptase coupled polymerase chain reaction (RT-PCR).	Acetylcysteine	33-36	nitric oxide synthase 2	Rattus norvegicus	122-126
9436612-8	1998	Inhibition of LPS-induced activation of NF-kappaB by NAC in rat peritoneal macrophages suggests that the inhibitory effect of NAC on the induction of iNOS is due to the inhibition of NF-kappaB.	Acetylcysteine	126-129	nitric oxide synthase 2	Rattus norvegicus	150-154
9436612-9	1998	Besides NO, NAC also blocked the production of TNF-alpha in rat peritoneal macrophages activated with endotoxin.	Acetylcysteine	12-15	tumor necrosis factor	Rattus norvegicus	47-56
9430725-6	1998	Isothiocyanate-induced JNK activation was blocked by the antioxidants 2-mercaptoethanol and N-acetyl-L-cysteine, suggesting that the death signaling was triggered by oxidative stress.	Acetylcysteine	92-111	mitogen-activated protein kinase 8	Homo sapiens	23-26
9417094-6	1998	Inclusion of N-acetylcysteine in the culture medium during the recovery period following diamide treatment increased the extent of restoration of NFI activity.	Acetylcysteine	13-29	nuclear factor I C	Homo sapiens	146-149
18370551-2	1998	OBJECTIVE: This trial reports the 6-month results of a pilot study using lymphoblastoid interferon alpha (IFNalpha) and acetylcysteine (N-acetylcysteine) separately and in combination in patients with chronic hepatitis C, genotype 1b, who were nonresponders to previous treatment with recombinant IFNalpha alone.	Acetylcysteine	120-134	interferon alpha 1	Homo sapiens	297-305
18370551-2	1998	OBJECTIVE: This trial reports the 6-month results of a pilot study using lymphoblastoid interferon alpha (IFNalpha) and acetylcysteine (N-acetylcysteine) separately and in combination in patients with chronic hepatitis C, genotype 1b, who were nonresponders to previous treatment with recombinant IFNalpha alone.	Acetylcysteine	136-152	interferon alpha 1	Homo sapiens	297-305
9452125-4	1998	NAC and alpha-TOC also markedly suppressed LPS-induced tumor necrosis factor-alpha (TNF-alpha) mRNA levels and secretion.	Acetylcysteine	0-3	tumor necrosis factor	Rattus norvegicus	55-82
9452125-4	1998	NAC and alpha-TOC also markedly suppressed LPS-induced tumor necrosis factor-alpha (TNF-alpha) mRNA levels and secretion.	Acetylcysteine	0-3	tumor necrosis factor	Rattus norvegicus	84-93
9358747-0	1997	N-acetyl cysteine blocks mesangial VCAM-1 and NF-kappa B expression in vivo.	Acetylcysteine	0-17	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	46-56
9440542-3	1997	In both cell lines, n-acetyl-L-cysteine (NAC), a potent thiol antioxidant, inhibited the triggering of the nuclear expression of NF-kappaB by IL-4 and by anti-CD40 monoclonal antibody.	Acetylcysteine	20-39	nuclear factor kappa B subunit 1	Homo sapiens	129-138
9440542-3	1997	In both cell lines, n-acetyl-L-cysteine (NAC), a potent thiol antioxidant, inhibited the triggering of the nuclear expression of NF-kappaB by IL-4 and by anti-CD40 monoclonal antibody.	Acetylcysteine	20-39	interleukin 4	Homo sapiens	142-146
9440542-3	1997	In both cell lines, n-acetyl-L-cysteine (NAC), a potent thiol antioxidant, inhibited the triggering of the nuclear expression of NF-kappaB by IL-4 and by anti-CD40 monoclonal antibody.	Acetylcysteine	41-44	nuclear factor kappa B subunit 1	Homo sapiens	129-138
9440542-3	1997	In both cell lines, n-acetyl-L-cysteine (NAC), a potent thiol antioxidant, inhibited the triggering of the nuclear expression of NF-kappaB by IL-4 and by anti-CD40 monoclonal antibody.	Acetylcysteine	41-44	interleukin 4	Homo sapiens	142-146
9440542-4	1997	Although IL-4 activated signal transducers and activators of transcription (STAT) 6 in addition to NF-kappaB, NAC treatment or the transfection of decoy oligodeoxynucleotides for NF-kappaB or STAT6 only partly blocked IL-4-induced germline Cepsilon transcription.	Acetylcysteine	110-113	interleukin 4	Homo sapiens	9-13
9440542-6	1997	Of note, CD40-mediated enhancement of IL-4-driven germline Cepsilon transcription was markedly decreased by NAC or by a decoy oligodeoxynucleotide for NF-kappaB.	Acetylcysteine	108-111	interleukin 4	Homo sapiens	38-42
9360968-9	1997	Pretreatment with N-acetyl-L-cysteine, glutathione, or vitamin E attenuated ERK2 but not JNK1 activation by BHA and tBHQ.	Acetylcysteine	18-37	mitogen-activated protein kinase 1	Homo sapiens	76-80
9360968-9	1997	Pretreatment with N-acetyl-L-cysteine, glutathione, or vitamin E attenuated ERK2 but not JNK1 activation by BHA and tBHQ.	Acetylcysteine	18-37	mitogen-activated protein kinase 8	Homo sapiens	89-93
9440542-8	1997	NAC inhibited the generation of Smu/Sepsilon switch fragments in normal human B cells costimulated with IL-4 and anti-CD40 monoclonal antibody.	Acetylcysteine	0-3	interleukin 4	Homo sapiens	104-108
9421857-9	1997	Although neutrophil influx was unaffected, neutrophil activation as assessed by surface CD11b expression and chemiluminescence was significantly down-regulated by NAC.	Acetylcysteine	163-166	integrin subunit alpha M	Rattus norvegicus	88-93
9354637-5	1997	The sodium nitroprusside-induced stimulation of JNK1 activity was abolished by treatment of cells with N-acetylcysteine.	Acetylcysteine	103-119	mitogen-activated protein kinase 8	Homo sapiens	48-52
9352875-8	1997	N-Acetylcysteine and allopurinol dramatically decreased TNF (-64% and -62%) and IL-10 (-49% and -57%) levels in the effluents, as did an inhibitor of the transcription factor NF-kappaB mobilization (-73% and -76% for TNF and IL-10, respectively).	Acetylcysteine	0-16	tumor necrosis factor	Mus musculus	56-59
9351437-10	1997	Pretreatment of cells with 500 mumol/L NAC for 1 hour attenuated approximately 50% of Aug II-induced JNK activation, suggesting that ROIs, at least partially, mediate Ang II-induced JNK activation.	Acetylcysteine	39-42	angiotensinogen	Rattus norvegicus	167-173
9351451-8	1997	The sustained activation of NF-kappa B was abolished by cotreatment with N-acetylcysteine or PDTC.	Acetylcysteine	73-89	nuclear factor kappa B subunit 1	Homo sapiens	28-38
9374731-6	1997	Moreover, chelation of surface iron from crocidolite fibers or addition of N-acetyl-L-cysteine prevented ERK activation and apoptosis by crocidolite, indicating an oxidative mechanism of cell signaling.	Acetylcysteine	75-94	Eph receptor B1	Rattus norvegicus	105-108
9352875-8	1997	N-Acetylcysteine and allopurinol dramatically decreased TNF (-64% and -62%) and IL-10 (-49% and -57%) levels in the effluents, as did an inhibitor of the transcription factor NF-kappaB mobilization (-73% and -76% for TNF and IL-10, respectively).	Acetylcysteine	0-16	interleukin 10	Mus musculus	80-85
9352875-8	1997	N-Acetylcysteine and allopurinol dramatically decreased TNF (-64% and -62%) and IL-10 (-49% and -57%) levels in the effluents, as did an inhibitor of the transcription factor NF-kappaB mobilization (-73% and -76% for TNF and IL-10, respectively).	Acetylcysteine	0-16	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	175-184
9352875-8	1997	N-Acetylcysteine and allopurinol dramatically decreased TNF (-64% and -62%) and IL-10 (-49% and -57%) levels in the effluents, as did an inhibitor of the transcription factor NF-kappaB mobilization (-73% and -76% for TNF and IL-10, respectively).	Acetylcysteine	0-16	tumor necrosis factor	Mus musculus	217-220
9352875-8	1997	N-Acetylcysteine and allopurinol dramatically decreased TNF (-64% and -62%) and IL-10 (-49% and -57%) levels in the effluents, as did an inhibitor of the transcription factor NF-kappaB mobilization (-73% and -76% for TNF and IL-10, respectively).	Acetylcysteine	0-16	interleukin 10	Mus musculus	225-230
9277499-0	1997	Distinct mechanisms for N-acetylcysteine inhibition of cytokine-induced E-selectin and VCAM-1 expression.	Acetylcysteine	24-40	vascular cell adhesion molecule 1	Homo sapiens	87-93
9378980-3	1997	IL-6 induction was dependent on the intracellular redox-oxidative state, since intracellular hydroxyl scavengers and N-acetylcysteine, a precursor of glutathione, abrogated IL-6 secretion by asbestos or H2O2.	Acetylcysteine	117-133	interleukin 6	Homo sapiens	0-4
9378980-3	1997	IL-6 induction was dependent on the intracellular redox-oxidative state, since intracellular hydroxyl scavengers and N-acetylcysteine, a precursor of glutathione, abrogated IL-6 secretion by asbestos or H2O2.	Acetylcysteine	117-133	interleukin 6	Homo sapiens	173-177
9323023-4	1997	At low thiol:ONOO- concentration ratios, several thiols (captopril, penicillamine, cysteine, cystine and penicillamine disulphide) aggravated inactivation of alpha1AP by ONOO- , whereas GSH, GSSG, homocysteine, ergothioneine, N-acetylcysteine, lipoate and dihydrolipoate did not.	Acetylcysteine	226-242	serpin family A member 1	Homo sapiens	158-166
9298175-0	1997	N-acetylcysteine attenuates TNF-alpha-dependent reduction of IL-4-induced Fc epsilon RII expression in human monocytes.	Acetylcysteine	0-16	tumor necrosis factor	Homo sapiens	28-37
9298175-0	1997	N-acetylcysteine attenuates TNF-alpha-dependent reduction of IL-4-induced Fc epsilon RII expression in human monocytes.	Acetylcysteine	0-16	interleukin 4	Homo sapiens	61-65
9298175-2	1997	It has been shown that TNF-alpha activates nuclear transcriptional factors through the generation of reactive oxygen intermediates (ROIs), and antioxidant N-acetylcysteine (NAC) inhibits TNF-alpha-induced activation of nuclear transcriptional factors.	Acetylcysteine	155-171	tumor necrosis factor	Homo sapiens	187-196
9298175-2	1997	It has been shown that TNF-alpha activates nuclear transcriptional factors through the generation of reactive oxygen intermediates (ROIs), and antioxidant N-acetylcysteine (NAC) inhibits TNF-alpha-induced activation of nuclear transcriptional factors.	Acetylcysteine	173-176	tumor necrosis factor	Homo sapiens	187-196
9298175-4	1997	In the present study, to test our hypothesis, we examined the effect of NAC on TNF-alpha-dependent reduction of IL-4-induced Fc epsilon RII expression in human monocytes.	Acetylcysteine	72-75	tumor necrosis factor	Homo sapiens	79-88
9298175-4	1997	In the present study, to test our hypothesis, we examined the effect of NAC on TNF-alpha-dependent reduction of IL-4-induced Fc epsilon RII expression in human monocytes.	Acetylcysteine	72-75	interleukin 4	Homo sapiens	112-116
9298175-5	1997	NAC attenuated TNF-alpha-dependent reduction of IL-4-induced Fc epsilon RII expression by attenuating TNF-alpha-dependent reduction of Fc epsilon RII mRNA expression.	Acetylcysteine	0-3	tumor necrosis factor	Homo sapiens	15-24
9298175-5	1997	NAC attenuated TNF-alpha-dependent reduction of IL-4-induced Fc epsilon RII expression by attenuating TNF-alpha-dependent reduction of Fc epsilon RII mRNA expression.	Acetylcysteine	0-3	interleukin 4	Homo sapiens	48-52
9298175-5	1997	NAC attenuated TNF-alpha-dependent reduction of IL-4-induced Fc epsilon RII expression by attenuating TNF-alpha-dependent reduction of Fc epsilon RII mRNA expression.	Acetylcysteine	0-3	tumor necrosis factor	Homo sapiens	102-111
9343371-21	1997	p21 induction in HT29 cells was also inhibited by DTPA, a metal chelator, and N-acetylcysteine, a potent cellular anti-oxidant, suggesting that HO.	Acetylcysteine	78-94	cyclin dependent kinase inhibitor 1A	Homo sapiens	0-3
9375974-16	1997	LTB4 undergoes a H2O2-dependent oxidation that is inhibited by NAC but this is unlikely to account fully for the increased levels of LTB4, suggesting that NAC may increase LTB4 production by blocking the H2O2-dependent inhibition of a synthetic enzyme, such as 5-lipoxygenase.	Acetylcysteine	155-158	arachidonate 5-lipoxygenase	Homo sapiens	261-275
9268159-3	1997	N-Acetylcysteine (NAC), pyrrolidinedithiocarbamate (PDTC), and Trimidox (TD) at various concentrations inhibited TNF-alpha-induced NF-kappaB binding in Jurkat cells.	Acetylcysteine	0-16	tumor necrosis factor	Homo sapiens	113-122
9268159-3	1997	N-Acetylcysteine (NAC), pyrrolidinedithiocarbamate (PDTC), and Trimidox (TD) at various concentrations inhibited TNF-alpha-induced NF-kappaB binding in Jurkat cells.	Acetylcysteine	18-21	tumor necrosis factor	Homo sapiens	113-122
9268159-7	1997	Synergistic induction of HIV-1 LTR-mediated gene expression by TNF-alpha and the HIV-1 transactivator Tat in Jurkat cells was significantly suppressed in the presence of NAC and TD, but not PDTC.	Acetylcysteine	170-173	tumor necrosis factor	Homo sapiens	63-72
16465270-4	1997	In contrast, the anti-oxidants desferrioxamine, butylated hydroxyanisol and N-acetyl cysteine all inhibited TNF-induced apoptosis in a concentration-dependent fashion.	Acetylcysteine	76-93	tumor necrosis factor	Homo sapiens	108-111
9242544-0	1997	N-acetyl-L-cysteine exhibits antitumoral activity by increasing tumor necrosis factor alpha-dependent T-cell cytotoxicity.	Acetylcysteine	0-19	tumor necrosis factor	Mus musculus	64-91
9234735-5	1997	We identified the intracellular glutathione (GSH) level as critical for JNK/SAPK activation by MMS: enhancing the GSH level by pretreatment of the cells with GSH or N-acetylcysteine inhibits, whereas depletion of the cellular GSH pool causes hyperinduction of JNK/SAPK activity by MMS.	Acetylcysteine	165-181	mitogen-activated protein kinase 8	Homo sapiens	72-80
9288612-10	1997	In addition, NAC treatment resulted in significant preservation of membrane fluidity and of the activities of catalase, mitochondrial SOD and the different forms of GPx.	Acetylcysteine	13-16	catalase	Rattus norvegicus	110-118
9234735-5	1997	We identified the intracellular glutathione (GSH) level as critical for JNK/SAPK activation by MMS: enhancing the GSH level by pretreatment of the cells with GSH or N-acetylcysteine inhibits, whereas depletion of the cellular GSH pool causes hyperinduction of JNK/SAPK activity by MMS.	Acetylcysteine	165-181	mitogen-activated protein kinase 8	Homo sapiens	72-75
9234735-5	1997	We identified the intracellular glutathione (GSH) level as critical for JNK/SAPK activation by MMS: enhancing the GSH level by pretreatment of the cells with GSH or N-acetylcysteine inhibits, whereas depletion of the cellular GSH pool causes hyperinduction of JNK/SAPK activity by MMS.	Acetylcysteine	165-181	mitogen-activated protein kinase 9	Homo sapiens	76-80
9437769-3	1997	Albumin, reduced glutathione (GSH), cysteine and N-acetylcysteine, but not other amino acids lowered the amount of NO2- as detected by Griess" method no matter whether sodium nitrite or 3-morpholinosydnonimine (SIN-1) were used as a source of NO2-.	Acetylcysteine	49-65	MAPK associated protein 1	Homo sapiens	211-216
9257692-5	1997	Simulated solar UV radiation increased p53, and agents that scavenge active oxygen species, N-acetylcysteine, ascorbate and alpha-tocopherol, inhibited the increase.	Acetylcysteine	92-108	tumor protein p53	Homo sapiens	39-42
9240427-6	1997	The inhibition of PON activity by the CSE was reversed by the addition of glutathione or N-acetyl cysteine.	Acetylcysteine	89-106	paraoxonase 1	Homo sapiens	18-21
9091316-3	1997	Expression of iNOS in HeLa G cells induces apoptosis which can be prevented by co-expression of bcl-2 or by addition of reduced glutathione or N-acetylcysteine.	Acetylcysteine	143-159	nitric oxide synthase 2	Homo sapiens	14-18
9218489-7	1997	N-Acetyl-L-cysteine and aminoguanidine suppressed both dicarbonyl-increased HB-EGF mRNA and intracellular peroxide levels in RASMC.	Acetylcysteine	0-19	heparin-binding EGF-like growth factor	Rattus norvegicus	76-82
9207456-12	1997	The effect of sin-1 on apoptosis and hematopoiesis in LTMC was largely prevented by NAC.	Acetylcysteine	84-87	MAPK associated protein 1	Homo sapiens	14-19
9182816-7	1997	The antioxidant N-acetylcysteine impaired the UVB- and EGF-induced activation of JNK1.	Acetylcysteine	16-32	mitogen-activated protein kinase 8	Homo sapiens	81-85
9152014-9	1997	Depleting GSH by treatment of cells with buthionine sulfoximine (BSO) enhanced Cd-induced expression of MT, GST, and HO whereas thiol supplementation, by treatment with N-acetyl cysteine (NAC), had an attenuating effect.	Acetylcysteine	169-186	metallothionein 1	Rattus norvegicus	104-106
9178189-13	1997	In conclusion, N-acetylcysteine reduces superoxide generation in response to FMLP and phorbol myristate acetate and partially protects against lipid peroxidation in PMN from man.	Acetylcysteine	15-31	formyl peptide receptor 1	Homo sapiens	77-81
9107159-10	1997	The antioxidants N-acetylcysteine and the combination of vitamins C and E prevented oxLDL-induced apoptosis, abrogated the enhancement of CPP32-like protease activity, and inhibited the proteolytic cleavage of CPP32 into its active subunit p17.	Acetylcysteine	17-33	caspase 3	Homo sapiens	138-143
9107159-10	1997	The antioxidants N-acetylcysteine and the combination of vitamins C and E prevented oxLDL-induced apoptosis, abrogated the enhancement of CPP32-like protease activity, and inhibited the proteolytic cleavage of CPP32 into its active subunit p17.	Acetylcysteine	17-33	caspase 3	Homo sapiens	210-215
9210957-0	1997	Suppression of nitric oxide-induced apoptosis by N-acetyl-L-cysteine through modulation of glutathione, bcl-2, and bax protein levels.	Acetylcysteine	49-68	BCL2 apoptosis regulator	Homo sapiens	104-109
9210957-0	1997	Suppression of nitric oxide-induced apoptosis by N-acetyl-L-cysteine through modulation of glutathione, bcl-2, and bax protein levels.	Acetylcysteine	49-68	BCL2 associated X, apoptosis regulator	Homo sapiens	115-118
9183012-6	1997	Furthermore, TPA-induced and serum-induced p21(waf1/cip1) mRNA accumulation was blocked by pretreating the cells with the antioxidant compound N-acetylcysteine, suggesting that oxidative stress is involved in these responses.	Acetylcysteine	143-159	cyclin dependent kinase inhibitor 1A	Homo sapiens	43-56
9178189-3	1997	This study examines the activity of N-acetylcysteine, a known antioxidant, in the protection of PMN exposed in-vitro to the chemoattractant peptide fMet-Leu-Phe (FMLP), the protein kinase C activator phorbol myristate acetate or the lipid peroxidation promoter t-butyl hydroperoxide.	Acetylcysteine	36-52	formyl peptide receptor 1	Homo sapiens	148-160
9178189-3	1997	This study examines the activity of N-acetylcysteine, a known antioxidant, in the protection of PMN exposed in-vitro to the chemoattractant peptide fMet-Leu-Phe (FMLP), the protein kinase C activator phorbol myristate acetate or the lipid peroxidation promoter t-butyl hydroperoxide.	Acetylcysteine	36-52	formyl peptide receptor 1	Homo sapiens	162-166
9178189-5	1997	Pre-treatment with N-acetylcysteine (33-333 microM) resulted in concentration-related inhibition of superoxide production induced by FMLP (30 nM) or phorbol myristate acetate (16 nM);-log IC50 values were 3.97 +/- 0.07 and 3.91 +/- 0.10, respectively.	Acetylcysteine	19-35	formyl peptide receptor 1	Homo sapiens	133-137
9099744-7	1997	This effect of IL-1beta is abrogated by pretreating cells with the antioxidants N-acetyl-L-cysteine or dithiothreitol.	Acetylcysteine	80-99	interleukin 1 beta	Homo sapiens	15-23
9115810-3	1997	Pretreatment of ACH-2 T cells by NAC followed by stimulation with PMA, TNF-alpha, or hydrogen peroxide (H2O2) resulted in strong suppression of NF-kappa B activation.	Acetylcysteine	33-36	nuclear factor kappa B subunit 1	Homo sapiens	144-154
9044846-11	1997	Both gadd153 mRNA level increase and internucleosomal DNA fragmentation were inhibited by N-tosyl-L-phenylalanine chloromethylketone, a serine threonine protease inhibitor, N-acetyl-leucyl-leucyl-norleucinal, an inhibitor of calpain, N-acetylcysteine, an inhibitor of oxidative metabolism, and overexpression of Bcl-2.	Acetylcysteine	234-250	DNA damage inducible transcript 3	Homo sapiens	5-12
8977531-5	1996	n-Acetyl-L-cysteine (NAC), a potent antioxidant, blocked NF-kappa B activation caused by IL-4 and by anti-CD40 mAb.	Acetylcysteine	0-19	nuclear factor kappa B subunit 1	Homo sapiens	57-67
9201246-9	1997	The antioxidants N-acetylcysteine, nordihydroguaiaretic acid and mepacrine dose-dependently inhibited gamma-irradiation-mediated TNF alpha production.	Acetylcysteine	17-33	tumor necrosis factor	Homo sapiens	129-138
9110071-12	1997	The use of NAC, NAM or LAC seems to rescue cells through a protective effect on mitochondria, a well-known target for the action of TNF-alpha and for reactive oxygen species, the production of which is strongly induced by this cytokine.	Acetylcysteine	11-14	tumor necrosis factor	Homo sapiens	132-141
9000534-0	1997	N-acetyl-L-cysteine-induced up-regulation of HIV-1 gene expression in monocyte-derived macrophages correlates with increased NF-kappaB DNA binding activity.	Acetylcysteine	0-19	nuclear factor kappa B subunit 1	Homo sapiens	125-134
9000534-2	1997	In T cells, N-acetyl-L-cysteine (NAC) inhibits the induction of NF-kappaB and transcription of HIV-1.	Acetylcysteine	12-31	nuclear factor kappa B subunit 1	Homo sapiens	64-73
8943236-13	1996	p21 induction elicited by the above quinones was inhibited by N-acetylcysteine, whereas the non-sulfur analog, N-acetylalanine, was without effect.	Acetylcysteine	62-78	cyclin dependent kinase inhibitor 1A	Homo sapiens	0-3
8977111-4	1996	IL-8 production in oxidized-LDL-treated cells was mediated by reactive oxygen species, as it was partially inhibited by catalase and completely inhibited by glutathione peroxidase and N-acetylcysteine (p &lt; 0.01).	Acetylcysteine	184-200	C-X-C motif chemokine ligand 8	Homo sapiens	0-4
8977531-5	1996	n-Acetyl-L-cysteine (NAC), a potent antioxidant, blocked NF-kappa B activation caused by IL-4 and by anti-CD40 mAb.	Acetylcysteine	0-19	interleukin 4	Homo sapiens	89-93
8977531-5	1996	n-Acetyl-L-cysteine (NAC), a potent antioxidant, blocked NF-kappa B activation caused by IL-4 and by anti-CD40 mAb.	Acetylcysteine	21-24	nuclear factor kappa B subunit 1	Homo sapiens	57-67
8977531-5	1996	n-Acetyl-L-cysteine (NAC), a potent antioxidant, blocked NF-kappa B activation caused by IL-4 and by anti-CD40 mAb.	Acetylcysteine	21-24	interleukin 4	Homo sapiens	89-93
8977531-6	1996	Although inhibition of IL-4-driven germline C epsilon transcription by NAC was not sufficient, the agent remarkably diminished anti-CD40 mAb-mediated up-regulation of germline C epsilon transcription.	Acetylcysteine	71-74	interleukin 4	Homo sapiens	23-27
8977531-10	1996	These results indicate that NF-kappa B activity is commonly inducible in DND39 cells by IL-4 and anti-CD40 mAb and suggest that NF-kappa B sensitive to NAC may play a role in regulating IgE synthesis in B cells.	Acetylcysteine	152-155	nuclear factor kappa B subunit 1	Homo sapiens	28-38
8977531-10	1996	These results indicate that NF-kappa B activity is commonly inducible in DND39 cells by IL-4 and anti-CD40 mAb and suggest that NF-kappa B sensitive to NAC may play a role in regulating IgE synthesis in B cells.	Acetylcysteine	152-155	interleukin 4	Homo sapiens	88-92
8977531-10	1996	These results indicate that NF-kappa B activity is commonly inducible in DND39 cells by IL-4 and anti-CD40 mAb and suggest that NF-kappa B sensitive to NAC may play a role in regulating IgE synthesis in B cells.	Acetylcysteine	152-155	nuclear factor kappa B subunit 1	Homo sapiens	128-138
9216201-2	1996	N-acetylcysteine, an antioxidant, decreased the TNF alpha-induced expression of intercellular adhesion molecule-1 on cultured epithelial cells from human bronchi (BEAS-2A), and inhibited IL-8 production by those cells.	Acetylcysteine	0-16	tumor necrosis factor	Homo sapiens	48-57
9216201-2	1996	N-acetylcysteine, an antioxidant, decreased the TNF alpha-induced expression of intercellular adhesion molecule-1 on cultured epithelial cells from human bronchi (BEAS-2A), and inhibited IL-8 production by those cells.	Acetylcysteine	0-16	C-X-C motif chemokine ligand 8	Homo sapiens	187-191
8950199-6	1996	The AO, N-acetylcysteine (NAC), decreased the extent of cartilage PG depletion caused by TNF-alpha and IL-1 alpha and by the ROS, hydrogen peroxide and superoxide anion, confirming that the cytokines operate through ROS and that ROS can initiate cartilage PG depletion.	Acetylcysteine	8-24	tumor necrosis factor	Homo sapiens	89-98
8940042-5	1996	c-Jun kinase activation and the action of bcl-2 and other survival agents, such as cell cycle blockers, a NO generator, N-acetylcysteine, aurintricarboxylic acid, and actinomycin D occurred at a point further upstream in the apoptotic pathway compared with the aspartase activation.	Acetylcysteine	120-136	BCL2, apoptosis regulator	Rattus norvegicus	42-47
8950199-6	1996	The AO, N-acetylcysteine (NAC), decreased the extent of cartilage PG depletion caused by TNF-alpha and IL-1 alpha and by the ROS, hydrogen peroxide and superoxide anion, confirming that the cytokines operate through ROS and that ROS can initiate cartilage PG depletion.	Acetylcysteine	26-29	tumor necrosis factor	Homo sapiens	89-98
8950199-7	1996	NAC at 0.1 and 1 mM, totally suppressed PG depletion caused by a highly potent amino-terminal 29-kDa fibronectin fragment (Fn-f) for 14 days in culture.	Acetylcysteine	0-3	fibronectin 1	Homo sapiens	101-112
8896414-3	1996	Thus, we have explored the effect of two inhibitors of the NF-kappa B activation, pyrrolidine dithiocarbamate (PDTC) and N-acetylcysteine (NAC), on the production of these cytokines by EC.	Acetylcysteine	139-142	nuclear factor kappa B subunit 1	Homo sapiens	59-69
8917554-5	1996	We found that treatment of such macrophages with N-acetylcysteine, known as antioxidant compound, prevented the decrease of CD3 zeta.	Acetylcysteine	49-65	CD247 antigen	Mus musculus	124-132
8896414-4	1996	Both PDTC and NAC inhibited, in a dose-dependent manner, the synthesis of IL-6, IL-8, and GM-CSF induced by tumor necrosis factor (TNF)-alpha or bacterial lipopolysaccharides (LPS) in human umbilical vein endothelial cells (HUVEC).	Acetylcysteine	14-17	interleukin 6	Homo sapiens	74-78
8896414-4	1996	Both PDTC and NAC inhibited, in a dose-dependent manner, the synthesis of IL-6, IL-8, and GM-CSF induced by tumor necrosis factor (TNF)-alpha or bacterial lipopolysaccharides (LPS) in human umbilical vein endothelial cells (HUVEC).	Acetylcysteine	14-17	C-X-C motif chemokine ligand 8	Homo sapiens	80-84
8896414-4	1996	Both PDTC and NAC inhibited, in a dose-dependent manner, the synthesis of IL-6, IL-8, and GM-CSF induced by tumor necrosis factor (TNF)-alpha or bacterial lipopolysaccharides (LPS) in human umbilical vein endothelial cells (HUVEC).	Acetylcysteine	14-17	tumor necrosis factor	Homo sapiens	108-141
8906868-4	1996	Furthermore, N-acetylcysteine markedly reduced the activation of SAPK in response to NO.	Acetylcysteine	13-29	mitogen-activated protein kinase 9	Rattus norvegicus	65-69
8787669-7	1996	AGE-beta2M reduced cytochrome c and the elaboration of TNF by MPs was inhibited by N-acetylcysteine.	Acetylcysteine	83-99	tumor necrosis factor	Homo sapiens	55-58
8824287-3	1996	In this study we show that the structurally unrelated antioxidant agents pyrrolidine dithiocarbamate (PDTC), butylated hydroxyanisole, and Nacetylcysteine activated JNK (c-Jun NH2-terminal kinase) in Jurkat T cells.	Acetylcysteine	139-154	mitogen-activated protein kinase 8	Homo sapiens	165-168
8824287-3	1996	In this study we show that the structurally unrelated antioxidant agents pyrrolidine dithiocarbamate (PDTC), butylated hydroxyanisole, and Nacetylcysteine activated JNK (c-Jun NH2-terminal kinase) in Jurkat T cells.	Acetylcysteine	139-154	mitogen-activated protein kinase 8	Homo sapiens	170-195
8871608-0	1996	The suppression of T cell function and NF(kappa)B expression by serine protease inhibitors is blocked by N-acetylcysteine.	Acetylcysteine	105-121	nuclear factor kappa B subunit 1	Homo sapiens	39-49
8871608-0	1996	The suppression of T cell function and NF(kappa)B expression by serine protease inhibitors is blocked by N-acetylcysteine.	Acetylcysteine	105-121	coagulation factor II, thrombin	Homo sapiens	64-79
8871608-1	1996	Direct evidence that N-acetylcysteine (NAC) enhances the immune response of peripheral blood T cells at the level of NF(kappa)B is presented.	Acetylcysteine	21-37	nuclear factor kappa B subunit 1	Homo sapiens	117-127
8871608-1	1996	Direct evidence that N-acetylcysteine (NAC) enhances the immune response of peripheral blood T cells at the level of NF(kappa)B is presented.	Acetylcysteine	39-42	nuclear factor kappa B subunit 1	Homo sapiens	117-127
8871608-8	1996	Our data support the notion that NF(kappa)B and I(kappa)B proteases play obligate roles in T cell activation and mitogenesis, roles that are enhanced significantly by NAC.	Acetylcysteine	167-170	nuclear factor kappa B subunit 1	Homo sapiens	33-43
8781560-3	1996	N-acetyl-cysteine (NAC), a precursor of glutathione (GSH), an intracellular free radical scavenger, abolishes the UVB-stimulated POMC peptide production and secretion.	Acetylcysteine	0-17	proopiomelanocortin	Homo sapiens	129-133
8806670-2	1996	In response to stimulation with hydrogen peroxide (100-400 microM), gene expression of HB-EGF and AR increased in a dose-dependent manner, peaked at 3 h, and returned to the base line at 7 h. Hydrogen peroxide-induced HB-EGF and AR gene expression was blocked by pretreatment with an antioxidant N-acetyl-cysteine.	Acetylcysteine	296-313	heparin-binding EGF-like growth factor	Rattus norvegicus	87-93
8806670-2	1996	In response to stimulation with hydrogen peroxide (100-400 microM), gene expression of HB-EGF and AR increased in a dose-dependent manner, peaked at 3 h, and returned to the base line at 7 h. Hydrogen peroxide-induced HB-EGF and AR gene expression was blocked by pretreatment with an antioxidant N-acetyl-cysteine.	Acetylcysteine	296-313	heparin-binding EGF-like growth factor	Rattus norvegicus	218-224
8781560-3	1996	N-acetyl-cysteine (NAC), a precursor of glutathione (GSH), an intracellular free radical scavenger, abolishes the UVB-stimulated POMC peptide production and secretion.	Acetylcysteine	19-22	proopiomelanocortin	Homo sapiens	129-133
8761454-7	1996	Increased AtFer1 transcript abundance in response to iron is inhibited by the antioxidant N-acetylcysteine.	Acetylcysteine	90-106	ferretin 1	Arabidopsis thaliana	10-16
8853906-0	1996	Transforming growth factor beta 1-induced apoptosis in human ovarian carcinoma cells: protection by the antioxidant N-acetylcysteine and bcl-2.	Acetylcysteine	116-132	transforming growth factor beta 1	Homo sapiens	0-33
8758915-4	1996	N-acetylcysteine and o-phenanthroline abolished ERK activation by BHTOOH, consistent with a requirement for metal-dependent formation of reactive intermediates.	Acetylcysteine	0-16	Eph receptor B1	Rattus norvegicus	48-51
8853906-3	1996	We found that both TGF-beta 1 and an oxidant, hydrogen peroxide, rapidly increase the expression of c-fos and c-jun genes and induce cell death by apoptosis; these effects are inhibited by the antioxidant N-acetylcysteine.	Acetylcysteine	205-221	transforming growth factor beta 1	Homo sapiens	19-29
8760145-3	1996	Pretreatment of human pulmonary adenocarcinoma cells H441 with the antioxidants N-acetyl-L-cysteine (NAC) and nordihydroguaiaretic acid (NDGA) blocked MnSOD induction by TNF-alpha, implicating ROS as a signaling agent in this pathway.	Acetylcysteine	80-99	tumor necrosis factor	Homo sapiens	170-179
8774698-7	1996	The extent of transcriptional activation of the fos, jun and HO genes in M1 cells treated with LPS was strongly reduced by a scavenger of oxygen radicals (N-acetyl-L-cysteine), but a specific inhibitor of protein kinase C only reduced transcriptional activation by 10-20%.	Acetylcysteine	155-174	toll-like receptor 4	Mus musculus	95-98
8760145-3	1996	Pretreatment of human pulmonary adenocarcinoma cells H441 with the antioxidants N-acetyl-L-cysteine (NAC) and nordihydroguaiaretic acid (NDGA) blocked MnSOD induction by TNF-alpha, implicating ROS as a signaling agent in this pathway.	Acetylcysteine	101-104	tumor necrosis factor	Homo sapiens	170-179
8760145-7	1996	TNF-alpha increased nuclear factor (NF)-kappa B-DNA binding, an effect blocked by pretreatment with NAC.	Acetylcysteine	100-103	tumor necrosis factor	Homo sapiens	0-9
8670069-4	1996	GADD153 mRNA induction by both H2O2 and arsenite was potentiated by GSH depletion, and completely inhibited by N-acetyl-cysteine.	Acetylcysteine	111-128	DNA damage inducible transcript 3	Homo sapiens	0-7
8670763-5	1996	Furthermore, 10.54 ng/ml of TGF-beta1 and 2.98 ng/ml of TGF-beta2 were detected in tears treated with the mucolytic agent, acetylcysteine.	Acetylcysteine	123-137	transforming growth factor beta 1	Homo sapiens	28-43
8670763-11	1996	A high molecular weight (MW) TGF-beta band (&gt;203 dD) was noted in untreated tears; however, this band disappeared following treatment with acetylcysteine.	Acetylcysteine	142-156	transforming growth factor beta 1	Homo sapiens	29-37
8901051-1	1996	N-acetyl cysteine is an agent which has been shown to interrupt signal transduction processes linking a wide range of stimuli to the activation of NF-kappa B in mammalian cells.	Acetylcysteine	0-17	nuclear factor kappa B subunit 1	Homo sapiens	147-157
8639020-0	1996	N-acetylcysteine inhibits production of tumor necrosis factor alpha and interleukin-1 beta.	Acetylcysteine	0-16	tumor necrosis factor	Homo sapiens	40-67
8639020-0	1996	N-acetylcysteine inhibits production of tumor necrosis factor alpha and interleukin-1 beta.	Acetylcysteine	0-16	interleukin 1 beta	Homo sapiens	72-90
8743957-6	1996	Pretreatment of cells with N-acetylcysteine, an agent known to counteract oxidative stress, attenuates the cellular p53 response to ultraviolet light by reducing the number of cells with high p53 levels but does not affect the response to ionizing radiation.	Acetylcysteine	27-43	tumor protein p53	Homo sapiens	116-119
8743957-6	1996	Pretreatment of cells with N-acetylcysteine, an agent known to counteract oxidative stress, attenuates the cellular p53 response to ultraviolet light by reducing the number of cells with high p53 levels but does not affect the response to ionizing radiation.	Acetylcysteine	27-43	tumor protein p53	Homo sapiens	192-195
8602587-6	1996	Pretreatment of endothelial cells with vitamin E and N-acetyl cysteine inhibited the fatty acid-induced activation of NF-kappa B and formation of lipid hydroperoxides.	Acetylcysteine	53-70	nuclear factor kappa B subunit 1	Homo sapiens	118-128
8669050-3	1996	In this study the effect von N-acetylcysteine (NAC) on the release of interleukin-1 alpha and beta (IL-1), interleukin-2 (IL-2), interferon-gamma (IFN-gamma) and tumornecrosisfactor-alpha (TNF-alpha) was assessed in an in vitro assay.	Acetylcysteine	47-50	interleukin 2	Homo sapiens	107-120
8721770-1	1996	N-acetylcysteine (NAC) is a precursor of glutathione (GSH) synthesis, a free radical scavenger and an inhibitor of tumour necrosis factor alpha (TNF).	Acetylcysteine	0-16	tumor necrosis factor	Rattus norvegicus	145-148
8721770-1	1996	N-acetylcysteine (NAC) is a precursor of glutathione (GSH) synthesis, a free radical scavenger and an inhibitor of tumour necrosis factor alpha (TNF).	Acetylcysteine	18-21	tumor necrosis factor	Rattus norvegicus	145-148
8721770-6	1996	NAC treatment had no effect on blood glucose levels or on the nerve glucose, sorbitol and cAMP contents, whereas it corrected the decreased GSH levels in erythrocytes, the increased lipid peroxide levels in plasma and the increased lipopolysaccharide-induced TNF activity in sera of diabetic rats.	Acetylcysteine	0-3	tumor necrosis factor	Rattus norvegicus	259-262
8631978-4	1996	In addition, overexpression of Bcl-2 suppressed vascular smooth muscle cell death caused by PDTC and NAC.	Acetylcysteine	101-104	BCL2, apoptosis regulator	Rattus norvegicus	31-36
8669050-9	1996	IFN-gamma and TNF-alpha: Until 12 mmol/l NAC no changes were observed.	Acetylcysteine	41-44	tumor necrosis factor	Homo sapiens	14-23
8669050-11	1996	CONCLUSION: N-acetylcysteine is capable to co-stimulate radioprotective cytokines like IL-1 alpha and IL-1 beta and to enhance IL-2 in vitro, whereas higher doses result in a suppression.	Acetylcysteine	12-28	interleukin 1 beta	Homo sapiens	102-111
8669050-11	1996	CONCLUSION: N-acetylcysteine is capable to co-stimulate radioprotective cytokines like IL-1 alpha and IL-1 beta and to enhance IL-2 in vitro, whereas higher doses result in a suppression.	Acetylcysteine	12-28	interleukin 2	Homo sapiens	127-131
8669050-3	1996	In this study the effect von N-acetylcysteine (NAC) on the release of interleukin-1 alpha and beta (IL-1), interleukin-2 (IL-2), interferon-gamma (IFN-gamma) and tumornecrosisfactor-alpha (TNF-alpha) was assessed in an in vitro assay.	Acetylcysteine	47-50	interferon gamma	Homo sapiens	129-145
8669050-3	1996	In this study the effect von N-acetylcysteine (NAC) on the release of interleukin-1 alpha and beta (IL-1), interleukin-2 (IL-2), interferon-gamma (IFN-gamma) and tumornecrosisfactor-alpha (TNF-alpha) was assessed in an in vitro assay.	Acetylcysteine	47-50	interferon gamma	Homo sapiens	147-156
8669050-3	1996	In this study the effect von N-acetylcysteine (NAC) on the release of interleukin-1 alpha and beta (IL-1), interleukin-2 (IL-2), interferon-gamma (IFN-gamma) and tumornecrosisfactor-alpha (TNF-alpha) was assessed in an in vitro assay.	Acetylcysteine	47-50	tumor necrosis factor	Homo sapiens	162-187
8669050-3	1996	In this study the effect von N-acetylcysteine (NAC) on the release of interleukin-1 alpha and beta (IL-1), interleukin-2 (IL-2), interferon-gamma (IFN-gamma) and tumornecrosisfactor-alpha (TNF-alpha) was assessed in an in vitro assay.	Acetylcysteine	47-50	tumor necrosis factor	Homo sapiens	189-198
8869738-4	1996	Substrates for MRP include thioether-linked conjugates of lipophilic compounds with glutathione, cysteinyl glycine, cysteine, and N-acetyl cysteine, but also glutathione disulfide, and glucuronate conjugates such as etoposide glucuronide.	Acetylcysteine	130-147	ATP binding cassette subfamily C member 1	Homo sapiens	15-18
8858271-4	1996	RESULTS: After treatment the low plasma cysteine level in the NAC group increased to normal, and the decline of the CD4+ lymphocyte count before the study start, was less steep in the NAC group than in the placebo group after treatment.	Acetylcysteine	184-187	CD4 molecule	Homo sapiens	116-119
8975632-5	1996	Enzymes of the mercapturic acid pathway cleave DCVG to the corresponding cysteine S-conjugate, which is, after translocation to the kidney, cleaved by renal cysteine S-conjugate beta -lyase to the electrophile chlorothioketene.	Acetylcysteine	15-31	kynurenine aminotransferase 1	Homo sapiens	157-189
8546677-16	1996	The effect of NAC was shown to be mediated largely by the AP1 site, since mutation of this site abolished the induction by NAC.	Acetylcysteine	14-17	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	58-61
8546677-16	1996	The effect of NAC was shown to be mediated largely by the AP1 site, since mutation of this site abolished the induction by NAC.	Acetylcysteine	123-126	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	58-61
8858271-6	1996	However, NAC had no effect on the radical production by neutrophils, and although it did not increase the CD4+ cell count, it may have decreased the decline in CD4+ cells.	Acetylcysteine	9-12	CD4 molecule	Homo sapiens	160-163
8902524-8	1996	The antioxidants, N-acetylcysteine or dimethylfumaric acid, increased intracellular thiol status and prevented both oxidant formation and translocation of NF-kappa B binding proteins in response to arsenite.	Acetylcysteine	18-34	nuclear factor kappa B subunit 1	Homo sapiens	155-165
8831801-5	1996	N-acetyl-L-cysteine also reacted with hydroxyl radicals (1.28 +/- 0.14 x 10(10) M-1S-1) but not with superoxide radical.	Acetylcysteine	0-19	tumor associated calcium signal transducer 2	Homo sapiens	80-86
7588208-4	1995	Inhibitors of NFkappaB, diethyldithiocarbamate, pyrrolidine dithiocarbamate, and N-acetyl cysteine prevent IL-1-induced iNOS expression at the level of messenger RNA, protein, and nitrite generation.	Acetylcysteine	81-98	nitric oxide synthase 2	Rattus norvegicus	120-124
8826530-3	1996	In the former case, NAC prevented the death of oligodendrocytes induced by glutamate or tumor necrosis factor-alpha (TNF-alpha), and also prevented TNF-alpha-induced death of L929 cells.	Acetylcysteine	20-23	tumor necrosis factor	Mus musculus	88-115
7493974-4	1995	The fact that N-acetylcysteine, a precursor of GSH that blocks oxidative stress, prevented WAF1/CIP1 induction by DEM suggests that WAF1/CIP1 induction probably was a consequence of the ability of DEM to reduce intracellular GSH levels.	Acetylcysteine	14-30	cyclin dependent kinase inhibitor 1A	Homo sapiens	91-95
8747803-13	1995	N-acetylcysteine inhibits angiotensin converting enzyme and counteracts nitrate-induced stimulation of the renin angiotensin system in vivo.	Acetylcysteine	0-16	renin	Homo sapiens	107-112
8826530-3	1996	In the former case, NAC prevented the death of oligodendrocytes induced by glutamate or tumor necrosis factor-alpha (TNF-alpha), and also prevented TNF-alpha-induced death of L929 cells.	Acetylcysteine	20-23	tumor necrosis factor	Mus musculus	117-126
8826530-3	1996	In the former case, NAC prevented the death of oligodendrocytes induced by glutamate or tumor necrosis factor-alpha (TNF-alpha), and also prevented TNF-alpha-induced death of L929 cells.	Acetylcysteine	20-23	tumor necrosis factor	Mus musculus	148-157
8826530-4	1996	NAC also acted in synergy with ciliary neurotrophic factor (CNTF) to prevent killing of oligodendrocytes by TNF-alpha.	Acetylcysteine	0-3	tumor necrosis factor	Mus musculus	108-117
7493974-4	1995	The fact that N-acetylcysteine, a precursor of GSH that blocks oxidative stress, prevented WAF1/CIP1 induction by DEM suggests that WAF1/CIP1 induction probably was a consequence of the ability of DEM to reduce intracellular GSH levels.	Acetylcysteine	14-30	cyclin dependent kinase inhibitor 1A	Homo sapiens	96-100
7493974-4	1995	The fact that N-acetylcysteine, a precursor of GSH that blocks oxidative stress, prevented WAF1/CIP1 induction by DEM suggests that WAF1/CIP1 induction probably was a consequence of the ability of DEM to reduce intracellular GSH levels.	Acetylcysteine	14-30	cyclin dependent kinase inhibitor 1A	Homo sapiens	132-136
7493974-4	1995	The fact that N-acetylcysteine, a precursor of GSH that blocks oxidative stress, prevented WAF1/CIP1 induction by DEM suggests that WAF1/CIP1 induction probably was a consequence of the ability of DEM to reduce intracellular GSH levels.	Acetylcysteine	14-30	cyclin dependent kinase inhibitor 1A	Homo sapiens	137-141
7500023-2	1995	In vitro, NAC and GSH have been shown to act on T cells by increasing interleukin (IL) 2 production, synthesis and turnover of IL-2 receptors, proliferation, cytotoxic properties, and resistance to apoptosis.	Acetylcysteine	10-13	interleukin 2	Homo sapiens	70-88
7500023-2	1995	In vitro, NAC and GSH have been shown to act on T cells by increasing interleukin (IL) 2 production, synthesis and turnover of IL-2 receptors, proliferation, cytotoxic properties, and resistance to apoptosis.	Acetylcysteine	10-13	interleukin 2	Homo sapiens	127-131
7500023-3	1995	We report here that NAC and GSH decrease in a dose-dependent manner human IL-4 production by stimulated peripheral blood T cells and by T helper (Th) 0- and Th2-like T cell clones.	Acetylcysteine	20-23	interleukin 4	Homo sapiens	74-78
7500023-6	1995	A functional consequence was the capacity of NAC and GSH to selectively decrease in a dose-dependent manner IL-4-induced immunoglobulin (Ig) E and IgG4 production by human peripheral blood mononuclear cells.	Acetylcysteine	45-48	interleukin 4	Homo sapiens	108-112
7500023-11	1995	Finally, when given orally to mice, NAC decreased both IgE and IgG1 antibody responses to ovalbumin.	Acetylcysteine	36-39	immunoglobulin heavy constant gamma 1 (G1m marker)	Mus musculus	63-67
7500023-12	1995	These results demonstrate that NAC, GSH, and other thiols may control the production of both the Th2-derived cytokine IL-4 and IL-4-induced Ig in vitro and in vivo.	Acetylcysteine	31-34	interleukin 4	Homo sapiens	118-122
7500023-12	1995	These results demonstrate that NAC, GSH, and other thiols may control the production of both the Th2-derived cytokine IL-4 and IL-4-induced Ig in vitro and in vivo.	Acetylcysteine	31-34	interleukin 4	Homo sapiens	127-131
7592595-5	1995	N-Acetylcysteine (NAC) and glutathione, as well as superoxide dismutase and catalase, inhibited both the increase in endogenous MT-1 mRNA and the activation of reporter gene activity by heme-hemopexin, CoPP-hemopexin, and phorbol 12-myristate 13-acetate.	Acetylcysteine	0-16	metallothionein 1	Mus musculus	128-132
7593644-10	1995	The anti-oxidants N-acetyl cysteine (NAC) or pentoxifylline (PTX), which are used clinically to reduce NF-kappa B/Rel activity, inhibited NF-kappa B driven promoter transactivation, and SMC-Rel binding activity.	Acetylcysteine	18-35	nuclear factor kappa B subunit 1	Homo sapiens	103-113
7593644-10	1995	The anti-oxidants N-acetyl cysteine (NAC) or pentoxifylline (PTX), which are used clinically to reduce NF-kappa B/Rel activity, inhibited NF-kappa B driven promoter transactivation, and SMC-Rel binding activity.	Acetylcysteine	18-35	nuclear factor kappa B subunit 1	Homo sapiens	138-148
7593644-10	1995	The anti-oxidants N-acetyl cysteine (NAC) or pentoxifylline (PTX), which are used clinically to reduce NF-kappa B/Rel activity, inhibited NF-kappa B driven promoter transactivation, and SMC-Rel binding activity.	Acetylcysteine	37-40	nuclear factor kappa B subunit 1	Homo sapiens	103-113
7593644-10	1995	The anti-oxidants N-acetyl cysteine (NAC) or pentoxifylline (PTX), which are used clinically to reduce NF-kappa B/Rel activity, inhibited NF-kappa B driven promoter transactivation, and SMC-Rel binding activity.	Acetylcysteine	37-40	nuclear factor kappa B subunit 1	Homo sapiens	138-148
7592595-5	1995	N-Acetylcysteine (NAC) and glutathione, as well as superoxide dismutase and catalase, inhibited both the increase in endogenous MT-1 mRNA and the activation of reporter gene activity by heme-hemopexin, CoPP-hemopexin, and phorbol 12-myristate 13-acetate.	Acetylcysteine	18-21	metallothionein 1	Mus musculus	128-132
7592595-7	1995	Induction of heme oxygenase-1 expression, in contrast to MT-1, is significantly less sensitive to NAC.	Acetylcysteine	98-101	heme oxygenase 1	Mus musculus	13-29
8801863-9	1995	On the other hand, NAC partially protected against TNF-induced injury to endothelial monolayers.	Acetylcysteine	19-22	tumor necrosis factor	Homo sapiens	51-54
7664840-4	1995	In fact, the antioxidant N-acetylcysteine (NAC) seems to be capable of impairing the apoptotic program, replenishing intracellular reduced glutathione content in cells exposed to tumor necrosis factor-alpha (TNF) as apoptotic inducer.	Acetylcysteine	25-41	tumor necrosis factor	Homo sapiens	179-206
7545088-5	1995	We have also demonstrated that the adhesion of tumor cells to IL-1 beta-treated human umbilical vein endothelial cells can be inhibited by anti-NF kappa B reagents such as N-acetyl L-cysteine, aspirin, or pentoxifylline.	Acetylcysteine	172-191	interleukin 1 beta	Homo sapiens	62-71
7545088-5	1995	We have also demonstrated that the adhesion of tumor cells to IL-1 beta-treated human umbilical vein endothelial cells can be inhibited by anti-NF kappa B reagents such as N-acetyl L-cysteine, aspirin, or pentoxifylline.	Acetylcysteine	172-191	nuclear factor kappa B subunit 1	Homo sapiens	144-154
7664840-4	1995	In fact, the antioxidant N-acetylcysteine (NAC) seems to be capable of impairing the apoptotic program, replenishing intracellular reduced glutathione content in cells exposed to tumor necrosis factor-alpha (TNF) as apoptotic inducer.	Acetylcysteine	25-41	tumor necrosis factor	Homo sapiens	208-211
7664840-4	1995	In fact, the antioxidant N-acetylcysteine (NAC) seems to be capable of impairing the apoptotic program, replenishing intracellular reduced glutathione content in cells exposed to tumor necrosis factor-alpha (TNF) as apoptotic inducer.	Acetylcysteine	43-46	tumor necrosis factor	Homo sapiens	179-206
7664840-4	1995	In fact, the antioxidant N-acetylcysteine (NAC) seems to be capable of impairing the apoptotic program, replenishing intracellular reduced glutathione content in cells exposed to tumor necrosis factor-alpha (TNF) as apoptotic inducer.	Acetylcysteine	43-46	tumor necrosis factor	Homo sapiens	208-211
7664840-7	1995	Our results show that TNF exposure is capable of altering the mitochondria and that NAC protection from CHX + TNF-induced apoptosis could be due to a direct effect of the drug on mitochondrial integrity and function.	Acetylcysteine	84-87	tumor necrosis factor	Homo sapiens	110-113
7739519-0	1995	Tumor necrosis factor alpha-induced apoptosis in human neuronal cells: protection by the antioxidant N-acetylcysteine and the genes bcl-2 and crmA.	Acetylcysteine	101-117	tumor necrosis factor	Homo sapiens	0-27
7544803-5	1995	The inhibitory effect of anti-RAGE IgG, a truncated form of the receptor (soluble RAGE) or N-acetylcysteine on VCAM-1 expression indicated that AGE-RAGE-induced oxidant stress was central to VCAM-1 induction.	Acetylcysteine	91-107	vascular cell adhesion molecule 1	Homo sapiens	111-117
7544803-5	1995	The inhibitory effect of anti-RAGE IgG, a truncated form of the receptor (soluble RAGE) or N-acetylcysteine on VCAM-1 expression indicated that AGE-RAGE-induced oxidant stress was central to VCAM-1 induction.	Acetylcysteine	91-107	vascular cell adhesion molecule 1	Homo sapiens	191-197
7544803-6	1995	Electrophoretic mobility shift assays on nuclear extracts from AGE-treated ECs showed induction of specific DNA binding activity for NF-kB in the VCAM-1 promoter, which was blocked by anti-RAGE IgG or N-acetylcysteine.	Acetylcysteine	201-217	vascular cell adhesion molecule 1	Homo sapiens	146-152
7576405-0	1995	N-acetylcysteine potentiates the antihypertensive effect of angiotensin converting enzyme inhibitors.	Acetylcysteine	0-16	angiotensin I converting enzyme	Homo sapiens	60-89
7739519-4	1995	Finally, overexpression of bcl-2 or crmA conferred resistance to apoptosis mediated by TNF-alpha, as did the addition of the antioxidant N-acetylcysteine.	Acetylcysteine	137-153	BCL2 apoptosis regulator	Homo sapiens	27-32
7733896-8	1995	Consistently, expression of the adipocyte phenotype induced by insulin, dexamethasone and isobutylmethylxanthine was enhanced in the presence of exogenous hypoxanthine/xanthine oxidase, whereas antioxidants, such as N-acetylcysteine or ascorbate, suppressed the process of differentiation.	Acetylcysteine	216-232	insulin	Homo sapiens	63-70
8866668-5	1995	In addition, TNF produced minor changes of the levels of reduced and oxidized glutathione in the cell lines, and its cytotoxic effects were not inluenced by agents that modify the cell glutathione content such as buthionine sulfoximine, ethacrynic acid, or N-acetyl cysteine.	Acetylcysteine	257-274	tumor necrosis factor	Homo sapiens	13-16
7705924-10	1995	Spontaneous metastasis formation by B16-F10 and B16-BL6 tumors was slightly yet significantly reduced by oral administration of NAC.	Acetylcysteine	128-131	coagulation factor X	Mus musculus	36-55
7873605-5	1995	N-Acetylcysteine (NAC), which counteracts the effects of DEM by increasing GSH biosynthesis, prevents the decrease of GR-DNA binding in cells treated with DEM.	Acetylcysteine	0-16	nuclear receptor subfamily 3 group C member 1	Homo sapiens	118-120
7873605-5	1995	N-Acetylcysteine (NAC), which counteracts the effects of DEM by increasing GSH biosynthesis, prevents the decrease of GR-DNA binding in cells treated with DEM.	Acetylcysteine	18-21	nuclear receptor subfamily 3 group C member 1	Homo sapiens	118-120
7840217-4	1995	IL-1-induced tolerance to IL-1-mediated lung leak and the associated increases in lung catalase, lung G6PDH, and serum catalase activities were all prevented by treating rats with the IL-1-receptor antagonist or with N-acetyl-L-cysteine, an agent that increases intracellular glutathione levels.	Acetylcysteine	217-236	catalase	Rattus norvegicus	87-95
7840217-4	1995	IL-1-induced tolerance to IL-1-mediated lung leak and the associated increases in lung catalase, lung G6PDH, and serum catalase activities were all prevented by treating rats with the IL-1-receptor antagonist or with N-acetyl-L-cysteine, an agent that increases intracellular glutathione levels.	Acetylcysteine	217-236	catalase	Rattus norvegicus	119-127
8574146-5	1995	Interestingly, 5 mM N-acetylcysteine (NAC) acts as an immunoenhancer; mitogenesis was enhanced 2 fold or more in general for control and HIV+ CD4+ T-cells and IL-2 production was enhanced 2-3 fold for anti-CD3 (with PMA or anti-CD28) for both controls and HIV+ CD4+ cells.	Acetylcysteine	20-36	CD4 molecule	Homo sapiens	142-145
8574146-5	1995	Interestingly, 5 mM N-acetylcysteine (NAC) acts as an immunoenhancer; mitogenesis was enhanced 2 fold or more in general for control and HIV+ CD4+ T-cells and IL-2 production was enhanced 2-3 fold for anti-CD3 (with PMA or anti-CD28) for both controls and HIV+ CD4+ cells.	Acetylcysteine	20-36	interleukin 2	Homo sapiens	159-163
8574146-5	1995	Interestingly, 5 mM N-acetylcysteine (NAC) acts as an immunoenhancer; mitogenesis was enhanced 2 fold or more in general for control and HIV+ CD4+ T-cells and IL-2 production was enhanced 2-3 fold for anti-CD3 (with PMA or anti-CD28) for both controls and HIV+ CD4+ cells.	Acetylcysteine	20-36	CD4 molecule	Homo sapiens	261-264
8574146-5	1995	Interestingly, 5 mM N-acetylcysteine (NAC) acts as an immunoenhancer; mitogenesis was enhanced 2 fold or more in general for control and HIV+ CD4+ T-cells and IL-2 production was enhanced 2-3 fold for anti-CD3 (with PMA or anti-CD28) for both controls and HIV+ CD4+ cells.	Acetylcysteine	38-41	CD4 molecule	Homo sapiens	142-145
8574146-5	1995	Interestingly, 5 mM N-acetylcysteine (NAC) acts as an immunoenhancer; mitogenesis was enhanced 2 fold or more in general for control and HIV+ CD4+ T-cells and IL-2 production was enhanced 2-3 fold for anti-CD3 (with PMA or anti-CD28) for both controls and HIV+ CD4+ cells.	Acetylcysteine	38-41	interleukin 2	Homo sapiens	159-163
8574146-5	1995	Interestingly, 5 mM N-acetylcysteine (NAC) acts as an immunoenhancer; mitogenesis was enhanced 2 fold or more in general for control and HIV+ CD4+ T-cells and IL-2 production was enhanced 2-3 fold for anti-CD3 (with PMA or anti-CD28) for both controls and HIV+ CD4+ cells.	Acetylcysteine	38-41	CD4 molecule	Homo sapiens	261-264
8574146-6	1995	However, NAC suppressed IL-4 production induced by anti-CD3 and anti-CD28 in both control and HIV+ CD4+ T cells.	Acetylcysteine	9-12	interleukin 4	Homo sapiens	24-28
8574146-6	1995	However, NAC suppressed IL-4 production induced by anti-CD3 and anti-CD28 in both control and HIV+ CD4+ T cells.	Acetylcysteine	9-12	CD4 molecule	Homo sapiens	99-102
7841193-5	1995	Similarly, N-acetylcysteine only proved inhibitory in hydrogen peroxide and TNF treated Jurkat and failed to inhibit IL1 and TNF-activated NF kappa B in EL4.NOB-1 and KB cells respectively.	Acetylcysteine	11-27	tumor necrosis factor	Mus musculus	76-79
7851416-4	1995	Induction of HSP27 kinase activity by TNF or H2O2 was completely inhibited by first treating the cells with the antioxidant N-acetyl-L-cysteine, suggesting that generation of reactive oxygen metabolites was the key triggering element of this induction.	Acetylcysteine	124-143	tumor necrosis factor	Homo sapiens	38-41
8574146-0	1995	N-acetylcysteine (NAC) enhances interleukin-2 but suppresses interleukin-4 secretion from normal and HIV+ CD4+ T-cells.	Acetylcysteine	0-16	interleukin 2	Homo sapiens	32-45
8574146-0	1995	N-acetylcysteine (NAC) enhances interleukin-2 but suppresses interleukin-4 secretion from normal and HIV+ CD4+ T-cells.	Acetylcysteine	0-16	interleukin 4	Homo sapiens	61-74
8574146-0	1995	N-acetylcysteine (NAC) enhances interleukin-2 but suppresses interleukin-4 secretion from normal and HIV+ CD4+ T-cells.	Acetylcysteine	0-16	CD4 molecule	Homo sapiens	106-109
8574146-0	1995	N-acetylcysteine (NAC) enhances interleukin-2 but suppresses interleukin-4 secretion from normal and HIV+ CD4+ T-cells.	Acetylcysteine	18-21	interleukin 2	Homo sapiens	32-45
8574146-0	1995	N-acetylcysteine (NAC) enhances interleukin-2 but suppresses interleukin-4 secretion from normal and HIV+ CD4+ T-cells.	Acetylcysteine	18-21	interleukin 4	Homo sapiens	61-74
8574146-0	1995	N-acetylcysteine (NAC) enhances interleukin-2 but suppresses interleukin-4 secretion from normal and HIV+ CD4+ T-cells.	Acetylcysteine	18-21	CD4 molecule	Homo sapiens	106-109
7550551-2	1995	In case of SIN-1 generation of nitrites run in parallel to disappearance of sulfhydryl groups of N-acetylcysteine and glutathione, however, for a pair of SIN-1 and cysteine the rate of formation of nitrites was much slower than the rate of consumption of sulfhydryl groups.	Acetylcysteine	97-113	MAPK associated protein 1	Homo sapiens	11-16
8144975-5	1994	However, LPS-dependent TNF-alpha production was increased by exposure to SNP (p &lt; 0.05); this effect was further increased by the addition of NAC (p &lt; 0.02).	Acetylcysteine	145-148	tumor necrosis factor	Homo sapiens	23-32
7998983-8	1994	NAC also reduced HO-1 mRNA accumulation when administered to mice in which glutathione was depleted and its synthesis blocked by BSO (1.6 g/kg).	Acetylcysteine	0-3	heme oxygenase 1	Mus musculus	17-21
7798616-5	1994	We found that N-acetyl-L-cysteine treatment reduced ICAM-1 mRNA levels when keratinocytes were stimulated with either IFN-gamma or TNF-alpha; however, pyrrolidine dithiocarbamate and alpha-tocopherol had no effect on either IFN-gamma- or TNF-alpha-induced ICAM-1 mRNA levels.	Acetylcysteine	14-33	interferon gamma	Homo sapiens	118-127
7798616-5	1994	We found that N-acetyl-L-cysteine treatment reduced ICAM-1 mRNA levels when keratinocytes were stimulated with either IFN-gamma or TNF-alpha; however, pyrrolidine dithiocarbamate and alpha-tocopherol had no effect on either IFN-gamma- or TNF-alpha-induced ICAM-1 mRNA levels.	Acetylcysteine	14-33	tumor necrosis factor	Homo sapiens	131-140
7798616-5	1994	We found that N-acetyl-L-cysteine treatment reduced ICAM-1 mRNA levels when keratinocytes were stimulated with either IFN-gamma or TNF-alpha; however, pyrrolidine dithiocarbamate and alpha-tocopherol had no effect on either IFN-gamma- or TNF-alpha-induced ICAM-1 mRNA levels.	Acetylcysteine	14-33	interferon gamma	Homo sapiens	224-233
7798616-5	1994	We found that N-acetyl-L-cysteine treatment reduced ICAM-1 mRNA levels when keratinocytes were stimulated with either IFN-gamma or TNF-alpha; however, pyrrolidine dithiocarbamate and alpha-tocopherol had no effect on either IFN-gamma- or TNF-alpha-induced ICAM-1 mRNA levels.	Acetylcysteine	14-33	tumor necrosis factor	Homo sapiens	238-247
27414179-0	1994	N-acetylcysteine prevents TNF-induced mitochondrial damage, apoptosis and viral particle production in HIV-infected U937 cells.	Acetylcysteine	0-16	tumor necrosis factor	Homo sapiens	26-29
27414179-6	1994	In the present work, we demonstrate (a) that apoptosis can be easily induced by TNF only in infected U937 cells and not in control wild-type cells, (b) that daily treatment of TNF-exposed cells with low concentrations of NAC is able to impair viral progeny formation as early as 24 h, (c) that the mitochondrial damage induced by TNF is counteracted by preexposure to NAC, and (d) that NAC alone exerts changes in mitochondria which may be responsible for the protective effects exerted by this compound.	Acetylcysteine	221-224	tumor necrosis factor	Homo sapiens	80-83
27414179-6	1994	In the present work, we demonstrate (a) that apoptosis can be easily induced by TNF only in infected U937 cells and not in control wild-type cells, (b) that daily treatment of TNF-exposed cells with low concentrations of NAC is able to impair viral progeny formation as early as 24 h, (c) that the mitochondrial damage induced by TNF is counteracted by preexposure to NAC, and (d) that NAC alone exerts changes in mitochondria which may be responsible for the protective effects exerted by this compound.	Acetylcysteine	221-224	tumor necrosis factor	Homo sapiens	176-179
27414179-6	1994	In the present work, we demonstrate (a) that apoptosis can be easily induced by TNF only in infected U937 cells and not in control wild-type cells, (b) that daily treatment of TNF-exposed cells with low concentrations of NAC is able to impair viral progeny formation as early as 24 h, (c) that the mitochondrial damage induced by TNF is counteracted by preexposure to NAC, and (d) that NAC alone exerts changes in mitochondria which may be responsible for the protective effects exerted by this compound.	Acetylcysteine	221-224	tumor necrosis factor	Homo sapiens	176-179
27414179-6	1994	In the present work, we demonstrate (a) that apoptosis can be easily induced by TNF only in infected U937 cells and not in control wild-type cells, (b) that daily treatment of TNF-exposed cells with low concentrations of NAC is able to impair viral progeny formation as early as 24 h, (c) that the mitochondrial damage induced by TNF is counteracted by preexposure to NAC, and (d) that NAC alone exerts changes in mitochondria which may be responsible for the protective effects exerted by this compound.	Acetylcysteine	368-371	tumor necrosis factor	Homo sapiens	176-179
27414179-6	1994	In the present work, we demonstrate (a) that apoptosis can be easily induced by TNF only in infected U937 cells and not in control wild-type cells, (b) that daily treatment of TNF-exposed cells with low concentrations of NAC is able to impair viral progeny formation as early as 24 h, (c) that the mitochondrial damage induced by TNF is counteracted by preexposure to NAC, and (d) that NAC alone exerts changes in mitochondria which may be responsible for the protective effects exerted by this compound.	Acetylcysteine	368-371	tumor necrosis factor	Homo sapiens	176-179
27414179-6	1994	In the present work, we demonstrate (a) that apoptosis can be easily induced by TNF only in infected U937 cells and not in control wild-type cells, (b) that daily treatment of TNF-exposed cells with low concentrations of NAC is able to impair viral progeny formation as early as 24 h, (c) that the mitochondrial damage induced by TNF is counteracted by preexposure to NAC, and (d) that NAC alone exerts changes in mitochondria which may be responsible for the protective effects exerted by this compound.	Acetylcysteine	368-371	tumor necrosis factor	Homo sapiens	176-179
27414179-6	1994	In the present work, we demonstrate (a) that apoptosis can be easily induced by TNF only in infected U937 cells and not in control wild-type cells, (b) that daily treatment of TNF-exposed cells with low concentrations of NAC is able to impair viral progeny formation as early as 24 h, (c) that the mitochondrial damage induced by TNF is counteracted by preexposure to NAC, and (d) that NAC alone exerts changes in mitochondria which may be responsible for the protective effects exerted by this compound.	Acetylcysteine	368-371	tumor necrosis factor	Homo sapiens	176-179
27414179-7	1994	Because of the radical producing capacity of TNF, these results seem to indicate that the protective effects of NAC may be due to the specific antioxidant nature of this substance which appears to be capable of impairing both the apoptotic machinery and viral replication by an intracellular mechanism involving mitochondrial integrity and function.	Acetylcysteine	112-115	tumor necrosis factor	Homo sapiens	45-48
8200134-2	1994	In this report we confirmed the enhanced production of TNF in streptozotocin (STZ)-induced diabetes and then attempted to suppress the enhanced TNF production with N-acetylcysteine (NAC), a precursor of glutathione synthesis.	Acetylcysteine	164-180	tumor necrosis factor	Rattus norvegicus	144-147
8200134-2	1994	In this report we confirmed the enhanced production of TNF in streptozotocin (STZ)-induced diabetes and then attempted to suppress the enhanced TNF production with N-acetylcysteine (NAC), a precursor of glutathione synthesis.	Acetylcysteine	182-185	tumor necrosis factor	Rattus norvegicus	144-147
8200134-4	1994	A single, oral administration of NAC (200 or 1000 mg/kg body wt) significantly suppressed the enhanced TNF production in the diabetic rats compared with that in untreated rats in a dose-dependent manner.	Acetylcysteine	33-36	tumor necrosis factor	Rattus norvegicus	103-106
8200134-5	1994	On the other hand, in the long-term (6 or 12 weeks) administrations, smaller doses of NAC (50 or 200 mg/kg/day) also significantly inhibited the enhanced production of TNF regardless of the dose of NAC.	Acetylcysteine	86-89	tumor necrosis factor	Rattus norvegicus	168-171
8200134-8	1994	These results show that NAC administration significantly suppressed the enhanced TNF production in diabetic rats and indicate that NAC might be useful in preventing TNF-mediated pathological conditions in diabetes.	Acetylcysteine	24-27	tumor necrosis factor	Rattus norvegicus	81-84
8200134-8	1994	These results show that NAC administration significantly suppressed the enhanced TNF production in diabetic rats and indicate that NAC might be useful in preventing TNF-mediated pathological conditions in diabetes.	Acetylcysteine	24-27	tumor necrosis factor	Rattus norvegicus	165-168
8200134-8	1994	These results show that NAC administration significantly suppressed the enhanced TNF production in diabetic rats and indicate that NAC might be useful in preventing TNF-mediated pathological conditions in diabetes.	Acetylcysteine	131-134	tumor necrosis factor	Rattus norvegicus	165-168
8006457-6	1994	These results show that N-acetylcysteine antagonizes the development of irritant and contact hypersensitivity reactions and that its action includes a reduction in the expression of tumor necrosis factor-alpha mRNA.	Acetylcysteine	24-40	tumor necrosis factor	Mus musculus	182-209
8006457-7	1994	N-acetylcysteine may be useful in the treatment of cutaneous inflammation mediated by tumor necrosis factor-alpha.	Acetylcysteine	0-16	tumor necrosis factor	Mus musculus	86-113
7798616-4	1994	N-acetyl-L-cysteine also suppressed keratinocyte surface expression of ICAM-1 induced by the cytokines interferon-gamma (IFN-gamma) or tumor necrosis factor-alpha (TNF-alpha), whereas pyrrolidine dithiocarbamate and alpha-tocopherol suppressed IFN-gamma-induced surface expression but not TNF-alpha-induced expression.	Acetylcysteine	0-19	interferon gamma	Homo sapiens	103-119
7798616-4	1994	N-acetyl-L-cysteine also suppressed keratinocyte surface expression of ICAM-1 induced by the cytokines interferon-gamma (IFN-gamma) or tumor necrosis factor-alpha (TNF-alpha), whereas pyrrolidine dithiocarbamate and alpha-tocopherol suppressed IFN-gamma-induced surface expression but not TNF-alpha-induced expression.	Acetylcysteine	0-19	interferon gamma	Homo sapiens	121-130
7798616-4	1994	N-acetyl-L-cysteine also suppressed keratinocyte surface expression of ICAM-1 induced by the cytokines interferon-gamma (IFN-gamma) or tumor necrosis factor-alpha (TNF-alpha), whereas pyrrolidine dithiocarbamate and alpha-tocopherol suppressed IFN-gamma-induced surface expression but not TNF-alpha-induced expression.	Acetylcysteine	0-19	tumor necrosis factor	Homo sapiens	135-162
7798616-4	1994	N-acetyl-L-cysteine also suppressed keratinocyte surface expression of ICAM-1 induced by the cytokines interferon-gamma (IFN-gamma) or tumor necrosis factor-alpha (TNF-alpha), whereas pyrrolidine dithiocarbamate and alpha-tocopherol suppressed IFN-gamma-induced surface expression but not TNF-alpha-induced expression.	Acetylcysteine	0-19	tumor necrosis factor	Homo sapiens	164-173
7798616-4	1994	N-acetyl-L-cysteine also suppressed keratinocyte surface expression of ICAM-1 induced by the cytokines interferon-gamma (IFN-gamma) or tumor necrosis factor-alpha (TNF-alpha), whereas pyrrolidine dithiocarbamate and alpha-tocopherol suppressed IFN-gamma-induced surface expression but not TNF-alpha-induced expression.	Acetylcysteine	0-19	interferon gamma	Homo sapiens	244-253
7798616-4	1994	N-acetyl-L-cysteine also suppressed keratinocyte surface expression of ICAM-1 induced by the cytokines interferon-gamma (IFN-gamma) or tumor necrosis factor-alpha (TNF-alpha), whereas pyrrolidine dithiocarbamate and alpha-tocopherol suppressed IFN-gamma-induced surface expression but not TNF-alpha-induced expression.	Acetylcysteine	0-19	tumor necrosis factor	Homo sapiens	289-298
8082232-2	1994	It was found that L-cysteine, L-cysteine methyl ester and D-penicillamine were very efficient reductants for cytochrome c, whereas N-acetylated amino acids (N-acetyl-L-cysteine and N-acetyl-D-cysteine) reacted considerably slower.	Acetylcysteine	181-200	cytochrome c, somatic	Homo sapiens	109-121
8082232-3	1994	A series of glutathione peroxidase mimetics and related compounds were studied as catalysts for the N-acetyl-L-cysteine reduction of ferric cytochrome c.	Acetylcysteine	100-119	cytochrome c, somatic	Homo sapiens	140-152
8082232-8	1994	In the presence of diaryl ditellurides and N-acetyl-L-cysteine, ferric cytochrome c was also rapidly reduced.	Acetylcysteine	43-62	cytochrome c, somatic	Homo sapiens	71-83
7863231-0	1994	The influence of N-acetylcysteine on the measurement of prothrombin time and activated partial thromboplastin time in healthy subjects.	Acetylcysteine	17-33	coagulation factor II, thrombin	Homo sapiens	56-67
7863231-1	1994	The purpose of the study was to evaluate whether the infusion of N-acetylcysteine decreased the measurement of prothrombin time and activated partial thromboplastin time (APTT) in healthy persons.	Acetylcysteine	65-81	coagulation factor II, thrombin	Homo sapiens	111-122
7863231-8	1994	We conclude that infusion of N-acetylcysteine intraveneously decreases the prothrombin time in healthy subjects.	Acetylcysteine	29-45	coagulation factor II, thrombin	Homo sapiens	75-86
7957773-3	1994	The intracellular oxidation state was increased 60 min after the addition of TNF alpha, and this increase was abolished by a radical scavenger, N-acetylcysteine (NAC), which is also a precursor of glutathione, and by pyrrolidine dithiocarbamate (PDTC).	Acetylcysteine	144-160	tumor necrosis factor	Homo sapiens	77-86
7957773-3	1994	The intracellular oxidation state was increased 60 min after the addition of TNF alpha, and this increase was abolished by a radical scavenger, N-acetylcysteine (NAC), which is also a precursor of glutathione, and by pyrrolidine dithiocarbamate (PDTC).	Acetylcysteine	162-165	tumor necrosis factor	Homo sapiens	77-86
7926024-0	1994	Inhibition by N-acetyl-L-cysteine of interleukin-6 mRNA induction and activation of NF kappa B by tumor necrosis factor alpha in a mouse fibroblastic cell line, Balb/3T3.	Acetylcysteine	14-33	interleukin 6	Mus musculus	37-50
7926024-0	1994	Inhibition by N-acetyl-L-cysteine of interleukin-6 mRNA induction and activation of NF kappa B by tumor necrosis factor alpha in a mouse fibroblastic cell line, Balb/3T3.	Acetylcysteine	14-33	tumor necrosis factor	Mus musculus	98-125
7926024-4	1994	We found that: (i) TNF alpha increased IL-6 mRNA levels and this increase was inhibited by N-acetyl-L-cysteine (NAC), a scavenger of reactive oxygen species.	Acetylcysteine	91-110	tumor necrosis factor	Mus musculus	19-28
7926024-4	1994	We found that: (i) TNF alpha increased IL-6 mRNA levels and this increase was inhibited by N-acetyl-L-cysteine (NAC), a scavenger of reactive oxygen species.	Acetylcysteine	91-110	interleukin 6	Mus musculus	39-43
7926024-4	1994	We found that: (i) TNF alpha increased IL-6 mRNA levels and this increase was inhibited by N-acetyl-L-cysteine (NAC), a scavenger of reactive oxygen species.	Acetylcysteine	112-115	tumor necrosis factor	Mus musculus	19-28
7926024-4	1994	We found that: (i) TNF alpha increased IL-6 mRNA levels and this increase was inhibited by N-acetyl-L-cysteine (NAC), a scavenger of reactive oxygen species.	Acetylcysteine	112-115	interleukin 6	Mus musculus	39-43
7926024-5	1994	(ii) NF kappa B binding activity in this cell line was also increased by TNF alpha, and the increase was inhibited in the presence of NAC.	Acetylcysteine	134-137	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	5-15
7926024-5	1994	(ii) NF kappa B binding activity in this cell line was also increased by TNF alpha, and the increase was inhibited in the presence of NAC.	Acetylcysteine	134-137	tumor necrosis factor	Mus musculus	73-82
7522548-4	1994	PDTC or N-acetylcysteine dose dependently reduced TNF-induced VCAM-1 but not ICAM-1 surface protein (also in human umbilical arterial endothelial cells) and mRNA expression (by 70% at 100 mumol/L PDTC) in HUVECs as assessed by flow cytometry and polymerase chain reaction.	Acetylcysteine	8-24	tumor necrosis factor	Homo sapiens	50-53
7522548-4	1994	PDTC or N-acetylcysteine dose dependently reduced TNF-induced VCAM-1 but not ICAM-1 surface protein (also in human umbilical arterial endothelial cells) and mRNA expression (by 70% at 100 mumol/L PDTC) in HUVECs as assessed by flow cytometry and polymerase chain reaction.	Acetylcysteine	8-24	vascular cell adhesion molecule 1	Homo sapiens	62-68
7521369-10	1994	Activated NF-kappa B was apparent from 20 min and remained for up to 24 h. N-acetylcysteine (NAC) and pyrollidinedithiocarbamate (PDTC), which were shown to inhibit activation of NF-kappa B in Jurkat E6.1 lymphoblasts and EL4.NOB-1 thymoma, failed to block IL-1 activation of NF-kappa B in 1321N1 astrocytoma.	Acetylcysteine	75-91	nuclear factor kappa B subunit 1	Homo sapiens	10-20
7521369-10	1994	Activated NF-kappa B was apparent from 20 min and remained for up to 24 h. N-acetylcysteine (NAC) and pyrollidinedithiocarbamate (PDTC), which were shown to inhibit activation of NF-kappa B in Jurkat E6.1 lymphoblasts and EL4.NOB-1 thymoma, failed to block IL-1 activation of NF-kappa B in 1321N1 astrocytoma.	Acetylcysteine	75-91	nuclear factor kappa B subunit 1	Homo sapiens	179-189
7521369-10	1994	Activated NF-kappa B was apparent from 20 min and remained for up to 24 h. N-acetylcysteine (NAC) and pyrollidinedithiocarbamate (PDTC), which were shown to inhibit activation of NF-kappa B in Jurkat E6.1 lymphoblasts and EL4.NOB-1 thymoma, failed to block IL-1 activation of NF-kappa B in 1321N1 astrocytoma.	Acetylcysteine	75-91	nuclear factor kappa B subunit 1	Homo sapiens	179-189
7521369-10	1994	Activated NF-kappa B was apparent from 20 min and remained for up to 24 h. N-acetylcysteine (NAC) and pyrollidinedithiocarbamate (PDTC), which were shown to inhibit activation of NF-kappa B in Jurkat E6.1 lymphoblasts and EL4.NOB-1 thymoma, failed to block IL-1 activation of NF-kappa B in 1321N1 astrocytoma.	Acetylcysteine	93-96	nuclear factor kappa B subunit 1	Homo sapiens	10-20
7521369-10	1994	Activated NF-kappa B was apparent from 20 min and remained for up to 24 h. N-acetylcysteine (NAC) and pyrollidinedithiocarbamate (PDTC), which were shown to inhibit activation of NF-kappa B in Jurkat E6.1 lymphoblasts and EL4.NOB-1 thymoma, failed to block IL-1 activation of NF-kappa B in 1321N1 astrocytoma.	Acetylcysteine	93-96	nuclear factor kappa B subunit 1	Homo sapiens	179-189
7521369-10	1994	Activated NF-kappa B was apparent from 20 min and remained for up to 24 h. N-acetylcysteine (NAC) and pyrollidinedithiocarbamate (PDTC), which were shown to inhibit activation of NF-kappa B in Jurkat E6.1 lymphoblasts and EL4.NOB-1 thymoma, failed to block IL-1 activation of NF-kappa B in 1321N1 astrocytoma.	Acetylcysteine	93-96	nuclear factor kappa B subunit 1	Homo sapiens	179-189
7521369-12	1994	The induction of VCAM-1 but not of ICAM-1 proved susceptible to inhibition by both PDTC and NAC.	Acetylcysteine	92-95	vascular cell adhesion molecule 1	Homo sapiens	17-23
8022202-7	1994	Raising glutathione levels with N-acetyl cysteine substantially reduced NF-kappa B induction by TNF in two of four samples tested.	Acetylcysteine	32-49	nuclear factor kappa B subunit 1	Homo sapiens	72-82
8022202-7	1994	Raising glutathione levels with N-acetyl cysteine substantially reduced NF-kappa B induction by TNF in two of four samples tested.	Acetylcysteine	32-49	tumor necrosis factor	Homo sapiens	96-99
8006457-2	1994	N-acetylcysteine is an anti-oxidant that inhibits the action of the nuclear factor-kB, which promotes the transcription of many genes, including the gene for tumor necrosis factor-alpha.	Acetylcysteine	0-16	tumor necrosis factor	Mus musculus	158-185
7909525-0	1994	Effect of glutathione depletion and oral N-acetyl-cysteine treatment on CD4+ and CD8+ cells.	Acetylcysteine	41-58	CD4 molecule	Homo sapiens	72-75
7909525-6	1994	NAC caused this relative increase of CD4+ T cell numbers in spite of decreasing glutathione levels and not by increasing the glutathione level.	Acetylcysteine	0-3	CD4 molecule	Homo sapiens	37-40
8299097-9	1994	Treatment of R4, R11, and OVC-8 cells with TNF-alpha in combination with glutathione or N-acetyl-cysteine (NAC) showed an antagonistic cytotoxic effect.	Acetylcysteine	107-110	tumor necrosis factor	Rattus norvegicus	43-52
8106395-10	1994	The antioxidant N-acetylcysteine decreased UVB-induced EGF-R tyrosine phosphorylation and PGE2 synthesis to near-basal levels.	Acetylcysteine	16-32	epidermal growth factor receptor	Homo sapiens	55-60
8152263-7	1994	Acetaminophen, N-acetylcysteine, propylthiouracil, D-penicillamine, mefenamic acid, dapsone, and methimazole all inhibited MPO at clinically achievable concentrations.	Acetylcysteine	15-31	myeloperoxidase	Homo sapiens	123-126
8299097-14	1994	Incubation of R4 cells with glutathione or NAC also down-regulated the expression of TNF-alpha mRNA.	Acetylcysteine	43-46	tumor necrosis factor	Homo sapiens	85-94
8353285-4	1993	We now provide evidence that the tyrosine kinase inhibitor herbimycin A and the free radical scavenger N-acetyl-cysteine inhibit both radiation-induced and H2O2-induced activation of NF-kappa B, indicating that activation triggered by ROI is dependent on tyrosine kinase activity.	Acetylcysteine	103-120	nuclear factor kappa B subunit 1	Homo sapiens	183-193
7691889-3	1993	In cultured human umbilical vein endothelial (HUVE) cells, the cytokine interleukin 1 beta (IL-1 beta) activated VCAM-1 gene expression through a mechanism that was repressed approximately 90% by the antioxidants pyrrolidine dithiocarbamate (PDTC) and N-acetylcysteine (NAC).	Acetylcysteine	252-268	interleukin 1 beta	Homo sapiens	72-90
7691889-3	1993	In cultured human umbilical vein endothelial (HUVE) cells, the cytokine interleukin 1 beta (IL-1 beta) activated VCAM-1 gene expression through a mechanism that was repressed approximately 90% by the antioxidants pyrrolidine dithiocarbamate (PDTC) and N-acetylcysteine (NAC).	Acetylcysteine	252-268	interleukin 1 beta	Homo sapiens	92-101
7691889-3	1993	In cultured human umbilical vein endothelial (HUVE) cells, the cytokine interleukin 1 beta (IL-1 beta) activated VCAM-1 gene expression through a mechanism that was repressed approximately 90% by the antioxidants pyrrolidine dithiocarbamate (PDTC) and N-acetylcysteine (NAC).	Acetylcysteine	252-268	vascular cell adhesion molecule 1	Homo sapiens	113-119
7691889-3	1993	In cultured human umbilical vein endothelial (HUVE) cells, the cytokine interleukin 1 beta (IL-1 beta) activated VCAM-1 gene expression through a mechanism that was repressed approximately 90% by the antioxidants pyrrolidine dithiocarbamate (PDTC) and N-acetylcysteine (NAC).	Acetylcysteine	270-273	interleukin 1 beta	Homo sapiens	72-90
7691889-3	1993	In cultured human umbilical vein endothelial (HUVE) cells, the cytokine interleukin 1 beta (IL-1 beta) activated VCAM-1 gene expression through a mechanism that was repressed approximately 90% by the antioxidants pyrrolidine dithiocarbamate (PDTC) and N-acetylcysteine (NAC).	Acetylcysteine	270-273	interleukin 1 beta	Homo sapiens	92-101
7691889-3	1993	In cultured human umbilical vein endothelial (HUVE) cells, the cytokine interleukin 1 beta (IL-1 beta) activated VCAM-1 gene expression through a mechanism that was repressed approximately 90% by the antioxidants pyrrolidine dithiocarbamate (PDTC) and N-acetylcysteine (NAC).	Acetylcysteine	270-273	vascular cell adhesion molecule 1	Homo sapiens	113-119
8361551-3	1993	Simultaneous incubation with N-acetyl-L-cysteine (0.5-5 mmol/l) protected endothelial cells from tumor necrosis factor-alpha-mediated cytotoxicity and increased viability in a concentration-dependent fashion to 69% of control.	Acetylcysteine	29-48	tumor necrosis factor	Mus musculus	97-124
21573353-9	1993	The protective effect of GSH was shown for TNF-alpha but not for CDDP as treatment of C30 cells with TNF-alpha in combination with GSH or N-acetyl-cysteine (NAC) reduced the cytotoxic effect of TNF-alpha.	Acetylcysteine	157-160	tumor necrosis factor	Homo sapiens	101-110
21573353-9	1993	The protective effect of GSH was shown for TNF-alpha but not for CDDP as treatment of C30 cells with TNF-alpha in combination with GSH or N-acetyl-cysteine (NAC) reduced the cytotoxic effect of TNF-alpha.	Acetylcysteine	157-160	tumor necrosis factor	Homo sapiens	101-110
21573353-13	1993	Further, incubation of C30 cells with TNF-alpha in conjunction with GSH or NAC also downregulated the expression of TNF-alpha mRNA induced by TNF-alpha.	Acetylcysteine	75-78	tumor necrosis factor	Homo sapiens	38-47
21573353-13	1993	Further, incubation of C30 cells with TNF-alpha in conjunction with GSH or NAC also downregulated the expression of TNF-alpha mRNA induced by TNF-alpha.	Acetylcysteine	75-78	tumor necrosis factor	Homo sapiens	116-125
21573353-13	1993	Further, incubation of C30 cells with TNF-alpha in conjunction with GSH or NAC also downregulated the expression of TNF-alpha mRNA induced by TNF-alpha.	Acetylcysteine	75-78	tumor necrosis factor	Homo sapiens	116-125
7687566-4	1993	The present findings, which elucidate a relationship between the percentage of apoptotic cells, reduced glutathione (GSH) depletion and an increase of p24 antigenemia, suggest that pretreatment with N-acetylcysteine (NAC) is capable of decreasing the above-mentioned phenomena in HIV-infected U937 cells.	Acetylcysteine	199-215	transmembrane p24 trafficking protein 2	Homo sapiens	151-154
7687566-4	1993	The present findings, which elucidate a relationship between the percentage of apoptotic cells, reduced glutathione (GSH) depletion and an increase of p24 antigenemia, suggest that pretreatment with N-acetylcysteine (NAC) is capable of decreasing the above-mentioned phenomena in HIV-infected U937 cells.	Acetylcysteine	217-220	transmembrane p24 trafficking protein 2	Homo sapiens	151-154
21573353-9	1993	The protective effect of GSH was shown for TNF-alpha but not for CDDP as treatment of C30 cells with TNF-alpha in combination with GSH or N-acetyl-cysteine (NAC) reduced the cytotoxic effect of TNF-alpha.	Acetylcysteine	138-155	tumor necrosis factor	Homo sapiens	43-52
21573353-9	1993	The protective effect of GSH was shown for TNF-alpha but not for CDDP as treatment of C30 cells with TNF-alpha in combination with GSH or N-acetyl-cysteine (NAC) reduced the cytotoxic effect of TNF-alpha.	Acetylcysteine	157-160	tumor necrosis factor	Homo sapiens	43-52
8228388-6	1993	In IFN-unresponsive patients, the addition of 600 mg tid of oral N-acetyl cysteine (NAC), a glutathione precursor, resulted in a steady decrease of ALT values in all patients, with complete normalization in 41% of cases after 5-6 months of combined therapy.	Acetylcysteine	65-82	interferon alpha 1	Homo sapiens	3-6
8228388-6	1993	In IFN-unresponsive patients, the addition of 600 mg tid of oral N-acetyl cysteine (NAC), a glutathione precursor, resulted in a steady decrease of ALT values in all patients, with complete normalization in 41% of cases after 5-6 months of combined therapy.	Acetylcysteine	84-87	interferon alpha 1	Homo sapiens	3-6
8228388-8	1993	Supplementation of IFN with NAC induced a near normalization of intralymphocytic glutathione, but plasma levels were only moderately increased.	Acetylcysteine	28-31	interferon alpha 1	Homo sapiens	19-22
8228388-10	1993	In conclusion, NAC enhances the response to IFN in CHC.	Acetylcysteine	15-18	interferon alpha 1	Homo sapiens	44-47
8389858-10	1993	Plasma angiotensin II (ANG II) increased during the first 24 hr of isosorbide dinitrate infusion and decreased from 28 +/- 4 to 14 +/- 2 ng/l after 2 hr of NAC infusion (P &lt; .05).	Acetylcysteine	156-159	angiotensinogen	Rattus norvegicus	23-29
8361551-7	1993	These findings demonstrate protection from tumor necrosis factor-alpha-mediated toxicity by N-acetyl-L-cysteine in endothelial cells but not in a tumor cell line.	Acetylcysteine	92-111	tumor necrosis factor	Mus musculus	43-70
8361551-8	1993	It is concluded that N-acetyl-L-cysteine might serve as a therapeutic agent to limit the vascular toxicity of tumor necrosis factor-alpha without affecting its antineoplastic activity.	Acetylcysteine	21-40	tumor necrosis factor	Mus musculus	110-137
8443968-9	1993	Pretreatment with NAC not only inhibited TNF production but also protected against LPS-induced pulmonary oedema, indicating that reactive oxygen intermediates are implicated.	Acetylcysteine	18-21	tumor necrosis factor	Mus musculus	41-44
8318649-4	1993	However, in the presence of glutathione, cysteine, penicillamine, or N-acetylcysteine, Co(II) generated cumene-OOH-derived carbon-centered radicals, cumene alkoxyl radicals, and hydroxyl (.OH) radicals.	Acetylcysteine	69-85	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	87-93
8496812-6	1993	Cardioprotection with the SH-containing compound n-acetyl cysteine (300 microM) was also reversed by glyburide, further demonstrating that ACE inhibition is not a prerequisite.	Acetylcysteine	49-66	angiotensin I converting enzyme	Rattus norvegicus	139-142
8443968-10	1993	NAC also blocked TNF production in blood and in bronchoalveolar lavage.	Acetylcysteine	0-3	tumor necrosis factor	Mus musculus	17-20
1530143-1	1992	Considering the well-documented protection of acetylcysteine (AC) in hepatotoxicity related to acetaminophen, we studied the preventive potential of AC against mild hepatotoxicity of CCl4, potentiated with ethyl alcohol (ETH) and the role of tissue glutathione.	Acetylcysteine	149-151	C-C motif chemokine ligand 4	Rattus norvegicus	183-187
8381319-15	1993	Sodium nitroprusside (80 JAM) or atrial natriuretic factor (ANF, I0- M) increased the levels of cyclic GMP in normal or tolerant SMC or EC to the same extent.5 The anti-platelet effects of GTN (44 JM) were potentiated by the sulphydryl donor N-acetylcysteine(NAC, 0.5mM).	Acetylcysteine	242-258	natriuretic peptide A	Homo sapiens	60-63
1520537-8	1992	Thus, a single pulse exposure of HIV-1-infected monocyte/macrophages with GSH or NAC led to a sustained, concentration-dependent decrease in HIV-1 p24 antigen levels, as well as, reverse transcriptase activity without producing detectable cellular toxicity in monocyte/macrophages.	Acetylcysteine	81-84	transmembrane p24 trafficking protein 2	Homo sapiens	147-150
1326880-6	1992	From the fact that NAC (i) inhibited extracellularly localized myeloperoxidase dependent activities, and (ii) had no effect on neutrophils from patients with chronic granulomatous disease (CGD), we conclude that the scavenger effect of NAC not only reduces the accumulation of oxidative metabolites per se, but also enhances receptor-mediated phagocytosis by protecting Fc(IgG)-receptors from oxidative damage mediated by myeloperoxidase (MPO) and hydrogen peroxide (H2O2).	Acetylcysteine	19-22	myeloperoxidase	Homo sapiens	63-78
33761438-8	2021	Hypoxia- or CoCl2-induced ROS increased HIF-1alpha and Nrf2 levels, which were attenuated by treatment with N-acetyl-L-cysteine (NAC), a ROS scavenger.	Acetylcysteine	108-127	hypoxia inducible factor 1 subunit alpha	Homo sapiens	40-50
1522704-4	1992	The results indicate that the C18 sample preparation technique followed by GC/MS analysis using stable isotopically labeled internal standards provides a rapid and accurate method for quantitation of mercapturic acids at low-ppb levels in the urine.	Acetylcysteine	200-217	Bardet-Biedl syndrome 9	Homo sapiens	30-33
1544168-4	1992	In this study we investigated the effect of NAC on TNF production and LPS lethality in mice.	Acetylcysteine	44-47	tumor necrosis factor	Mus musculus	51-54
1544168-5	1992	The results indicated that oral administration of NAC protects against LPS toxicity and inhibits the increase in serum TNF levels in LPS-treated mice.	Acetylcysteine	50-53	tumor necrosis factor	Mus musculus	119-122
1544168-6	1992	The inhibition was not confined to the released form of TNF, since NAC also inhibited LPS-induced spleen-associated TNF.	Acetylcysteine	67-70	tumor necrosis factor	Mus musculus	116-119
1544168-9	1992	NAC was also active in inhibiting TNF production and hepatotoxicity in mice treated with LPS in association with a sensitizing dose of Actinomycin D.	Acetylcysteine	0-3	tumor necrosis factor	Mus musculus	34-37
1907460-6	1991	Cysteine and NAC also inhibit NF-kappa B activity as determined by electrophoretic mobility shift assays and chloramphenicol acetyl-transferase (CAT) gene expression under control of NF-kappa B binding sites in uninfected cells.	Acetylcysteine	13-16	nuclear factor kappa B subunit 1	Homo sapiens	30-40
1907460-6	1991	Cysteine and NAC also inhibit NF-kappa B activity as determined by electrophoretic mobility shift assays and chloramphenicol acetyl-transferase (CAT) gene expression under control of NF-kappa B binding sites in uninfected cells.	Acetylcysteine	13-16	nuclear factor kappa B subunit 1	Homo sapiens	183-193
2112750-1	1990	We show that the stimulation of human immunodeficiency virus (HIV) brought about by tumor necrosis factor alpha and phorbol 12-myristate 13-acetate can be inhibited by adding N-acetyl-L-cysteine (NAC).	Acetylcysteine	175-194	tumor necrosis factor	Homo sapiens	84-111
33761438-8	2021	Hypoxia- or CoCl2-induced ROS increased HIF-1alpha and Nrf2 levels, which were attenuated by treatment with N-acetyl-L-cysteine (NAC), a ROS scavenger.	Acetylcysteine	108-127	NFE2 like bZIP transcription factor 2	Homo sapiens	55-59
33761438-8	2021	Hypoxia- or CoCl2-induced ROS increased HIF-1alpha and Nrf2 levels, which were attenuated by treatment with N-acetyl-L-cysteine (NAC), a ROS scavenger.	Acetylcysteine	129-132	hypoxia inducible factor 1 subunit alpha	Homo sapiens	40-50
33761438-8	2021	Hypoxia- or CoCl2-induced ROS increased HIF-1alpha and Nrf2 levels, which were attenuated by treatment with N-acetyl-L-cysteine (NAC), a ROS scavenger.	Acetylcysteine	129-132	NFE2 like bZIP transcription factor 2	Homo sapiens	55-59
33772418-6	2021	While NAC treatment improved TAC and IL-10 values, it decreased MDA and TNF-alpha levels in the liver of rats exposed to Cd (P < 0.001).	Acetylcysteine	6-9	tumor necrosis factor	Rattus norvegicus	72-81
33775218-8	2021	NAC, ALA, BM-MNCs and their combination caused a reduction of ALT, AST, while, increase albumin, CAT, TAC, GPx, SOD as compared to CCl4 treated groups.	Acetylcysteine	0-3	glutamic-oxaloacetic transaminase 2	Rattus norvegicus	67-70
33775218-8	2021	NAC, ALA, BM-MNCs and their combination caused a reduction of ALT, AST, while, increase albumin, CAT, TAC, GPx, SOD as compared to CCl4 treated groups.	Acetylcysteine	0-3	catalase	Rattus norvegicus	97-100
33775218-11	2021	BM-MNCs combination with NAC or ALA exerted significant antioxidant, anti-inflammatory and anti-cytogenetical aberrations effect compared to each of them alone.HighlightsCCl4 elevated ALT, AST, TNF-alpha, IL-6 and MDACCl4 reduced ALB, IL-10, SOD, CAT, GPx and TACCCl4 increased the number of DNA breaks in liverNAC, ALA and BM-MNCs reduced ALT, AST, while, increase albumin, CAT, TAC, GPx, SODNAC, ALA and BM-MNCs decreased in MDA, IL-6 and TNF-alpha and increased IL-10.	Acetylcysteine	25-28	glutamic-oxaloacetic transaminase 2	Rattus norvegicus	189-192
33775218-11	2021	BM-MNCs combination with NAC or ALA exerted significant antioxidant, anti-inflammatory and anti-cytogenetical aberrations effect compared to each of them alone.HighlightsCCl4 elevated ALT, AST, TNF-alpha, IL-6 and MDACCl4 reduced ALB, IL-10, SOD, CAT, GPx and TACCCl4 increased the number of DNA breaks in liverNAC, ALA and BM-MNCs reduced ALT, AST, while, increase albumin, CAT, TAC, GPx, SODNAC, ALA and BM-MNCs decreased in MDA, IL-6 and TNF-alpha and increased IL-10.	Acetylcysteine	25-28	tumor necrosis factor	Rattus norvegicus	194-203
33775218-11	2021	BM-MNCs combination with NAC or ALA exerted significant antioxidant, anti-inflammatory and anti-cytogenetical aberrations effect compared to each of them alone.HighlightsCCl4 elevated ALT, AST, TNF-alpha, IL-6 and MDACCl4 reduced ALB, IL-10, SOD, CAT, GPx and TACCCl4 increased the number of DNA breaks in liverNAC, ALA and BM-MNCs reduced ALT, AST, while, increase albumin, CAT, TAC, GPx, SODNAC, ALA and BM-MNCs decreased in MDA, IL-6 and TNF-alpha and increased IL-10.	Acetylcysteine	25-28	interleukin 6	Rattus norvegicus	205-209
33775218-11	2021	BM-MNCs combination with NAC or ALA exerted significant antioxidant, anti-inflammatory and anti-cytogenetical aberrations effect compared to each of them alone.HighlightsCCl4 elevated ALT, AST, TNF-alpha, IL-6 and MDACCl4 reduced ALB, IL-10, SOD, CAT, GPx and TACCCl4 increased the number of DNA breaks in liverNAC, ALA and BM-MNCs reduced ALT, AST, while, increase albumin, CAT, TAC, GPx, SODNAC, ALA and BM-MNCs decreased in MDA, IL-6 and TNF-alpha and increased IL-10.	Acetylcysteine	25-28	catalase	Rattus norvegicus	247-250
33775218-11	2021	BM-MNCs combination with NAC or ALA exerted significant antioxidant, anti-inflammatory and anti-cytogenetical aberrations effect compared to each of them alone.HighlightsCCl4 elevated ALT, AST, TNF-alpha, IL-6 and MDACCl4 reduced ALB, IL-10, SOD, CAT, GPx and TACCCl4 increased the number of DNA breaks in liverNAC, ALA and BM-MNCs reduced ALT, AST, while, increase albumin, CAT, TAC, GPx, SODNAC, ALA and BM-MNCs decreased in MDA, IL-6 and TNF-alpha and increased IL-10.	Acetylcysteine	25-28	glutamic-oxaloacetic transaminase 2	Rattus norvegicus	345-348
33775218-11	2021	BM-MNCs combination with NAC or ALA exerted significant antioxidant, anti-inflammatory and anti-cytogenetical aberrations effect compared to each of them alone.HighlightsCCl4 elevated ALT, AST, TNF-alpha, IL-6 and MDACCl4 reduced ALB, IL-10, SOD, CAT, GPx and TACCCl4 increased the number of DNA breaks in liverNAC, ALA and BM-MNCs reduced ALT, AST, while, increase albumin, CAT, TAC, GPx, SODNAC, ALA and BM-MNCs decreased in MDA, IL-6 and TNF-alpha and increased IL-10.	Acetylcysteine	25-28	catalase	Rattus norvegicus	375-378
33775218-11	2021	BM-MNCs combination with NAC or ALA exerted significant antioxidant, anti-inflammatory and anti-cytogenetical aberrations effect compared to each of them alone.HighlightsCCl4 elevated ALT, AST, TNF-alpha, IL-6 and MDACCl4 reduced ALB, IL-10, SOD, CAT, GPx and TACCCl4 increased the number of DNA breaks in liverNAC, ALA and BM-MNCs reduced ALT, AST, while, increase albumin, CAT, TAC, GPx, SODNAC, ALA and BM-MNCs decreased in MDA, IL-6 and TNF-alpha and increased IL-10.	Acetylcysteine	25-28	interleukin 6	Rattus norvegicus	432-436
33775218-11	2021	BM-MNCs combination with NAC or ALA exerted significant antioxidant, anti-inflammatory and anti-cytogenetical aberrations effect compared to each of them alone.HighlightsCCl4 elevated ALT, AST, TNF-alpha, IL-6 and MDACCl4 reduced ALB, IL-10, SOD, CAT, GPx and TACCCl4 increased the number of DNA breaks in liverNAC, ALA and BM-MNCs reduced ALT, AST, while, increase albumin, CAT, TAC, GPx, SODNAC, ALA and BM-MNCs decreased in MDA, IL-6 and TNF-alpha and increased IL-10.	Acetylcysteine	25-28	tumor necrosis factor	Rattus norvegicus	441-450
33126251-7	2021	The adverse impact of MAPK and c-Src overactivation on the intestinal barrier can be combatted with various antioxidant measures, including phycocyanobilin, phase 2-inducer nutraceuticals, and N-acetylcysteine.	Acetylcysteine	193-209	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	31-36
33771976-7	2021	Increased reactive oxygen species (ROS) levels and the expression of HIF-1alpha and Nrf2 decreased under the hypoxic condition following incubation with N-acetylcysteine, a ROS scavenger, which was associated with a decrease in CXCR4 expression.	Acetylcysteine	153-169	hypoxia inducible factor 1 subunit alpha	Homo sapiens	69-79
33771976-7	2021	Increased reactive oxygen species (ROS) levels and the expression of HIF-1alpha and Nrf2 decreased under the hypoxic condition following incubation with N-acetylcysteine, a ROS scavenger, which was associated with a decrease in CXCR4 expression.	Acetylcysteine	153-169	NFE2 like bZIP transcription factor 2	Homo sapiens	84-88
33806765-7	2021	Pre-treatment with N-acetylcysteine significantly abrogated the expression of nuclear HIF-1alpha, JNK transduction components and fibrotic marker proteins.	Acetylcysteine	19-35	hypoxia inducible factor 1 subunit alpha	Homo sapiens	86-96
33806765-7	2021	Pre-treatment with N-acetylcysteine significantly abrogated the expression of nuclear HIF-1alpha, JNK transduction components and fibrotic marker proteins.	Acetylcysteine	19-35	mitogen-activated protein kinase 8	Homo sapiens	98-101
33819738-7	2021	Following N-acetylcysteine treatment, apoptotic rates of the cancer cell lines decreased from 38.9% to 7.3%, and the expression of Cl-PARP, Cl-Caspase-3 and Cl-Caspase-9 also decreased, confirming that compound 6g induced apoptosis through ROS induction.	Acetylcysteine	10-26	poly(ADP-ribose) polymerase 1	Homo sapiens	134-138
33819738-7	2021	Following N-acetylcysteine treatment, apoptotic rates of the cancer cell lines decreased from 38.9% to 7.3%, and the expression of Cl-PARP, Cl-Caspase-3 and Cl-Caspase-9 also decreased, confirming that compound 6g induced apoptosis through ROS induction.	Acetylcysteine	10-26	caspase 3	Homo sapiens	143-152
33816149-6	2021	The same study has concluded that NAC"s ability to mitigate the impact of the cytokine storm and prevent elevation of liver enzymes, C-reactive protein, and ferritin is associated with higher success rates weaning from the ventilator and return to normal function in COVID-19 patients.	Acetylcysteine	34-37	C-reactive protein	Homo sapiens	133-151
33800932-6	2021	Spike and envelope protein disulfide bonds were reduced by Acetylcysteine.	Acetylcysteine	59-73	envelope protein	Severe acute respiratory syndrome coronavirus 2	10-18
33772418-0	2021	The effect of N-Acetyl cysteine on the expression of Fxr (Nr1h4), LXRalpha (Nr1h3) and Sirt1 genes, oxidative stress, and apoptosis in the liver of rats exposed to different doses of cadmium.	Acetylcysteine	14-31	sirtuin 1	Rattus norvegicus	87-92
33772418-7	2021	NAC decreased Bax/Bcl2 in the liver of G4 and G5 groups (P < 0.001).	Acetylcysteine	0-3	BCL2, apoptosis regulator	Rattus norvegicus	18-22
33772418-9	2021	NAC increased Fxr, LXRalpha, and Sirt1 expression (P < 0.01) and decreased Cd concentrations in both serum and tissue samples in G4 and G5 groups.	Acetylcysteine	0-3	nuclear receptor subfamily 1, group H, member 3	Rattus norvegicus	19-27
33772418-9	2021	NAC increased Fxr, LXRalpha, and Sirt1 expression (P < 0.01) and decreased Cd concentrations in both serum and tissue samples in G4 and G5 groups.	Acetylcysteine	0-3	sirtuin 1	Rattus norvegicus	33-38
33772418-10	2021	Our results suggested that NAC protects liver tissue against Cd toxicity by elevating antioxidant capacity, mitigating oxidative stress, inflammation, apoptosis and up-regulation of FXR, LXR, and SIRT1 genes.	Acetylcysteine	27-30	sirtuin 1	Rattus norvegicus	196-201
33817118-6	2018	Furthermore, the generation of reactive oxygen species (ROS) was up-regulated in KLE cells upon treatment with emodin, while the anti-oxidant agent N-acetyl cysteine (NAC) can inhibit emodin-induced apoptosis and promote the activation of AKT and Bcl-2.	Acetylcysteine	148-165	AKT serine/threonine kinase 1	Homo sapiens	239-242
33426091-11	2020	Nrf2 nuclear translocation was blocked by ROS inhibitor N-acetylcysteine.	Acetylcysteine	56-72	NFE2 like bZIP transcription factor 2	Homo sapiens	0-4
33817118-6	2018	Furthermore, the generation of reactive oxygen species (ROS) was up-regulated in KLE cells upon treatment with emodin, while the anti-oxidant agent N-acetyl cysteine (NAC) can inhibit emodin-induced apoptosis and promote the activation of AKT and Bcl-2.	Acetylcysteine	148-165	BCL2 apoptosis regulator	Homo sapiens	247-252
33817118-6	2018	Furthermore, the generation of reactive oxygen species (ROS) was up-regulated in KLE cells upon treatment with emodin, while the anti-oxidant agent N-acetyl cysteine (NAC) can inhibit emodin-induced apoptosis and promote the activation of AKT and Bcl-2.	Acetylcysteine	167-170	AKT serine/threonine kinase 1	Homo sapiens	239-242
33817118-6	2018	Furthermore, the generation of reactive oxygen species (ROS) was up-regulated in KLE cells upon treatment with emodin, while the anti-oxidant agent N-acetyl cysteine (NAC) can inhibit emodin-induced apoptosis and promote the activation of AKT and Bcl-2.	Acetylcysteine	167-170	BCL2 apoptosis regulator	Homo sapiens	247-252
15033766-3	2003	The antioxidants N-acetylcysteine, glutathione, lipoic acid, and ascorbic acid markedly reduced the effect of the hormone on TNF-induced caspase activation, attesting to the involvement of reactive oxygen species (ROS) in the cross-talk between the hormone and the cytokine.	Acetylcysteine	17-33	tumor necrosis factor	Homo sapiens	125-128
21055460-8	2011	Importantly, NAC treatment caused an early but transient activation of Akt and Erk1/2.	Acetylcysteine	13-16	AKT serine/threonine kinase 1	Homo sapiens	71-74
21055460-8	2011	Importantly, NAC treatment caused an early but transient activation of Akt and Erk1/2.	Acetylcysteine	13-16	mitogen-activated protein kinase 3	Homo sapiens	79-85
21055460-9	2011	The NAC-induced increase in Cyr61 protein levels was suppressed by the PI3K inhibitor (Ly294002) and, to a lesser extent, MEK/Erk1/2 inhibitor (PD98059).	Acetylcysteine	4-7	mitogen-activated protein kinase kinase 7	Homo sapiens	122-125
21055460-9	2011	The NAC-induced increase in Cyr61 protein levels was suppressed by the PI3K inhibitor (Ly294002) and, to a lesser extent, MEK/Erk1/2 inhibitor (PD98059).	Acetylcysteine	4-7	mitogen-activated protein kinase 3	Homo sapiens	126-132
17702197-7	2007	NAC, Se, DVP, MKH and DVPMKH caused a reduction in CAT activity, while DVPSOD and DVPSe caused an increase of the latter.	Acetylcysteine	0-3	catalase	Mus musculus	51-54
21055460-10	2011	Taken together, our data suggest that the antiproliferative effect of NAC is partially mediated by intracellular ROS production, the inhibition of NF-kappaB activity, and the activation of PI3K- and/or MEK/Erk-related intracellular signaling pathways, which lead to up-regulation of Cyr61 expression.	Acetylcysteine	70-73	mitogen-activated protein kinase kinase 7	Homo sapiens	202-205
21055460-10	2011	Taken together, our data suggest that the antiproliferative effect of NAC is partially mediated by intracellular ROS production, the inhibition of NF-kappaB activity, and the activation of PI3K- and/or MEK/Erk-related intracellular signaling pathways, which lead to up-regulation of Cyr61 expression.	Acetylcysteine	70-73	mitogen-activated protein kinase 1	Homo sapiens	206-209
34856342-5	2022	Analysis of the presence of reactive oxygen species (ROS) as well as reduced glutathione (GSH) / oxidized glutathione (GSSG) ratio revealed that treatment with AhR ligands is associated with oxidative stress which can be ameliorated with NAC (N-acetyl cysteine) or diphenyleneiodonium chloride (DPI).	Acetylcysteine	238-241	aryl-hydrocarbon receptor	Mus musculus	160-163
34856342-5	2022	Analysis of the presence of reactive oxygen species (ROS) as well as reduced glutathione (GSH) / oxidized glutathione (GSSG) ratio revealed that treatment with AhR ligands is associated with oxidative stress which can be ameliorated with NAC (N-acetyl cysteine) or diphenyleneiodonium chloride (DPI).	Acetylcysteine	243-260	aryl-hydrocarbon receptor	Mus musculus	160-163
34856342-6	2022	On the other hand, NAC and DPI enhanced melanogenesis induced by AhR ligands by reducing the level of ROS.	Acetylcysteine	19-22	aryl-hydrocarbon receptor	Mus musculus	65-68
34861471-11	2022	Furthermore, c-Jun NH2-terminal kinase inhibition reduced Nix and Bax cleavage, and both signaling pathways were suppressed by N-acetylcysteine treatment.	Acetylcysteine	127-143	BCL2 associated X, apoptosis regulator	Homo sapiens	66-69
34387821-13	2022	In addition, NAC attenuated BaP-induced NF-kappaB activation in A549 cells and mouse lungs.	Acetylcysteine	13-16	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	40-49
34293569-9	2022	However, pretreatment of L-02 cells with antioxidant N-Acetyl-l-cysteine (NAC) and endoplasmic reticulum stress inhibitor 4-PBA inhibited DBDPE-induced oxidative stress, endoplasmic reticulum stress, CYP3A expression decrease, and apoptosis.	Acetylcysteine	53-72	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	200-205
34293569-9	2022	However, pretreatment of L-02 cells with antioxidant N-Acetyl-l-cysteine (NAC) and endoplasmic reticulum stress inhibitor 4-PBA inhibited DBDPE-induced oxidative stress, endoplasmic reticulum stress, CYP3A expression decrease, and apoptosis.	Acetylcysteine	74-77	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	200-205
34847624-7	2022	Moreover, N-acetyl-L-cysteine (NAC, a ROS inhibitor) could significantly reverse the effects of alnustone on the growth inhibition of BEL-7402 and HepG2 cells and the expression of proteins related to apoptosis and PI3K/Akt/mTOR signaling pathway in HepG2 cells.	Acetylcysteine	10-29	AKT serine/threonine kinase 1	Homo sapiens	220-223
34801870-10	2022	We also found that either TSH or NAC enhanced PKA, Akt, mTORC, AMPK, Sirtuins, PGC1alpha, NRF-2, mitofusin-2, TFAM and catalase in the N-TSHR-mAb stressed cells.	Acetylcysteine	33-36	AKT serine/threonine kinase 1	Rattus norvegicus	51-54
34801870-10	2022	We also found that either TSH or NAC enhanced PKA, Akt, mTORC, AMPK, Sirtuins, PGC1alpha, NRF-2, mitofusin-2, TFAM and catalase in the N-TSHR-mAb stressed cells.	Acetylcysteine	33-36	protein kinase AMP-activated catalytic subunit alpha 2	Rattus norvegicus	63-67
34801870-10	2022	We also found that either TSH or NAC enhanced PKA, Akt, mTORC, AMPK, Sirtuins, PGC1alpha, NRF-2, mitofusin-2, TFAM and catalase in the N-TSHR-mAb stressed cells.	Acetylcysteine	33-36	PPARG coactivator 1 alpha	Rattus norvegicus	79-88
34801870-10	2022	We also found that either TSH or NAC enhanced PKA, Akt, mTORC, AMPK, Sirtuins, PGC1alpha, NRF-2, mitofusin-2, TFAM and catalase in the N-TSHR-mAb stressed cells.	Acetylcysteine	33-36	NFE2 like bZIP transcription factor 2	Rattus norvegicus	90-95
34801870-10	2022	We also found that either TSH or NAC enhanced PKA, Akt, mTORC, AMPK, Sirtuins, PGC1alpha, NRF-2, mitofusin-2, TFAM and catalase in the N-TSHR-mAb stressed cells.	Acetylcysteine	33-36	catalase	Rattus norvegicus	119-127
34801870-10	2022	We also found that either TSH or NAC enhanced PKA, Akt, mTORC, AMPK, Sirtuins, PGC1alpha, NRF-2, mitofusin-2, TFAM and catalase in the N-TSHR-mAb stressed cells.	Acetylcysteine	33-36	thyroid stimulating hormone receptor	Rattus norvegicus	137-141
34801870-4	2022	Furthermore, the addition of TSH, or the antioxidant N-acetyl-l-cysteine (NAC), rescued N-TSHR-mAb-induced apoptotic death.	Acetylcysteine	53-72	thyroid stimulating hormone receptor	Rattus norvegicus	90-94
34801870-4	2022	Furthermore, the addition of TSH, or the antioxidant N-acetyl-l-cysteine (NAC), rescued N-TSHR-mAb-induced apoptotic death.	Acetylcysteine	74-77	thyroid stimulating hormone receptor	Rattus norvegicus	90-94
34801870-7	2022	RESULTS: Under starvation conditions with N-TSHR-mAb the addition of TSH or NAC prevented thyroid cell death by enhancing autophagy.	Acetylcysteine	76-79	thyroid stimulating hormone receptor	Rattus norvegicus	44-48
34763314-11	2022	Moreover, these elevated levels of the proteins were inhibited by the antioxidant N-acetylcysteine and the JNK inhibitor SP600125, suggesting the involvement of ROS/JNK-dependent mechanisms in AGS-30-induced apoptosis.	Acetylcysteine	82-98	mitogen-activated protein kinase 8	Homo sapiens	165-168
34847624-7	2022	Moreover, N-acetyl-L-cysteine (NAC, a ROS inhibitor) could significantly reverse the effects of alnustone on the growth inhibition of BEL-7402 and HepG2 cells and the expression of proteins related to apoptosis and PI3K/Akt/mTOR signaling pathway in HepG2 cells.	Acetylcysteine	10-29	mechanistic target of rapamycin kinase	Homo sapiens	224-228
34847624-7	2022	Moreover, N-acetyl-L-cysteine (NAC, a ROS inhibitor) could significantly reverse the effects of alnustone on the growth inhibition of BEL-7402 and HepG2 cells and the expression of proteins related to apoptosis and PI3K/Akt/mTOR signaling pathway in HepG2 cells.	Acetylcysteine	31-34	AKT serine/threonine kinase 1	Homo sapiens	220-223
34847624-7	2022	Moreover, N-acetyl-L-cysteine (NAC, a ROS inhibitor) could significantly reverse the effects of alnustone on the growth inhibition of BEL-7402 and HepG2 cells and the expression of proteins related to apoptosis and PI3K/Akt/mTOR signaling pathway in HepG2 cells.	Acetylcysteine	31-34	mechanistic target of rapamycin kinase	Homo sapiens	224-228
34687772-6	2021	Removal of ROS by N-acetylcysteine significantly reduced ER stress in prostate cancer cells, followed by the decrease of Smad3 phosphorylation and expression of nuclear Snail, resulting in the inhibition of EMT and malignant phenotypic changes of prostate cancer cells.	Acetylcysteine	18-34	snail family transcriptional repressor 1	Homo sapiens	169-174
34971797-5	2022	However, the addition of active oxygen scavenger N-acetylcysteine can significantly reduce the ROS production, improve cell cycle arrest, reduce apoptosis, and the expression of phosphorylated NF-kappaB in BV2 microglia cells.	Acetylcysteine	49-65	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	193-202
34936178-9	2021	CONCLUSION: The RCTs examined suggest that prophylactic administration of corticosteroid agents and NAC can reduce the severity of pancreatitis as indicated by histopathologic markers, serum amylase and IL-6 levels.	Acetylcysteine	100-103	interleukin 6	Homo sapiens	203-207
34948425-11	2021	NAC administration to dams or offspring demonstrated lower brain NF-kappaB p65, nNOS, TNF-alpha and IL-6 protein levels compared to hypoxia alone.	Acetylcysteine	0-3	tumor necrosis factor	Rattus norvegicus	86-95
34948425-11	2021	NAC administration to dams or offspring demonstrated lower brain NF-kappaB p65, nNOS, TNF-alpha and IL-6 protein levels compared to hypoxia alone.	Acetylcysteine	0-3	interleukin 6	Rattus norvegicus	100-104
34924003-8	2021	Exogenous supplementation of NAC or GSH reduced the expression of NRF2 and GCLC, suggesting the NRF2/GCLC-related antioxidant production pathway might be desensitized.	Acetylcysteine	29-32	nuclear factor, erythroid derived 2, like 2	Mus musculus	66-70
34924003-8	2021	Exogenous supplementation of NAC or GSH reduced the expression of NRF2 and GCLC, suggesting the NRF2/GCLC-related antioxidant production pathway might be desensitized.	Acetylcysteine	29-32	nuclear factor, erythroid derived 2, like 2	Mus musculus	96-100
34979328-4	2022	In vitro experiments showed that NAC reduced complement activation and VWF multimerization in HUVECs.	Acetylcysteine	33-36	von Willebrand factor	Homo sapiens	71-74
34954677-8	2021	The ROS scavenger N-acetylcysteine (NAC) attenuated BPA-induced the mTOR/ULK1 pathway activation, apoptosis and autophagy.	Acetylcysteine	18-34	mechanistic target of rapamycin kinase	Homo sapiens	68-72
34954677-8	2021	The ROS scavenger N-acetylcysteine (NAC) attenuated BPA-induced the mTOR/ULK1 pathway activation, apoptosis and autophagy.	Acetylcysteine	36-39	mechanistic target of rapamycin kinase	Homo sapiens	68-72
34926192-8	2021	The expression of RAGE (1.83+-0.11 fold), IL-1beta, and CCAP-3, and the number of apoptotic cells, were reduced by topical NAC treatment.	Acetylcysteine	123-126	interleukin 1 alpha	Rattus norvegicus	42-50
34926192-10	2021	However, the addition of NAC reduced the concentrations of TNF-alpha (153.67+-2.31 pg/mL) and cleaved PARP (5.55+-0.31 fold) and the number of apoptotic cells.	Acetylcysteine	25-28	tumor necrosis factor	Rattus norvegicus	59-68
34619980-9	2021	NAC treatment reduced TGF-beta signaling, p-Smad2 and collagen levels, and mesenchymal transition from Isolectin-B4 and CD45-positive cells in LDLR mice.	Acetylcysteine	0-3	SMAD family member 2	Mus musculus	44-49
34718251-6	2021	H2O2 increased ROS and NAC reduced ROS in a concentration-dependent pattern, but the change was significantly greater in Bmi1+/--NSCs than WT-NSCs.	Acetylcysteine	23-26	Bmi1 polycomb ring finger oncogene	Mus musculus	121-125
34718251-10	2021	After treatment with 1 mM NAC, the number and diameter of neurospheres, Brdu incorporation rate, cell viability, T-AOC and total superoxide dismutase activity of Bmi1+/--NSCs were lower than those of WT-NSCs.	Acetylcysteine	26-29	Bmi1 polycomb ring finger oncogene	Mus musculus	162-166
34468764-11	2021	Eliminating ROS by N-acetyl-l-cysteine abrogated Cd-induced PP2A-JNK pathway disruption and concurrently reinforced MgIG-conferred protective effects, which could be further slightly strengthened by PP2A overexpression.	Acetylcysteine	19-38	mitogen-activated protein kinase 8	Homo sapiens	65-68
34794237-10	2021	TGF-beta-induced upregulation of KCa2.3, KCa3.1, collagen, and alpha-smooth muscle actin and downregulation of catalase were reversed by modafinil, polyethylene glycol catalase, N-acetylcysteine, siRNA against KCa2.3 or KCa3.1, and Epac inhibitors.	Acetylcysteine	178-194	catalase	Homo sapiens	111-119
34899969-0	2021	N-Acetylcysteine (NAC) Inhibits Synthesis of IL-18 in Macrophage by Suppressing NLRP3 Expression to Reduce the Production of IFN-gamma from NK Cells.	Acetylcysteine	0-16	NLR family pyrin domain containing 3	Homo sapiens	80-85
34899969-0	2021	N-Acetylcysteine (NAC) Inhibits Synthesis of IL-18 in Macrophage by Suppressing NLRP3 Expression to Reduce the Production of IFN-gamma from NK Cells.	Acetylcysteine	0-16	interferon gamma	Homo sapiens	125-134
34899969-0	2021	N-Acetylcysteine (NAC) Inhibits Synthesis of IL-18 in Macrophage by Suppressing NLRP3 Expression to Reduce the Production of IFN-gamma from NK Cells.	Acetylcysteine	18-21	NLR family pyrin domain containing 3	Homo sapiens	80-85
34899969-0	2021	N-Acetylcysteine (NAC) Inhibits Synthesis of IL-18 in Macrophage by Suppressing NLRP3 Expression to Reduce the Production of IFN-gamma from NK Cells.	Acetylcysteine	18-21	interferon gamma	Homo sapiens	125-134
34899969-9	2021	Result: NAC could effectively improve the immune status of COPD patients as well as the COPD mouse model by downregulating proinflammation and inflammation cytokines including IL-1beta, interferon- (IFN-) gamma, tumor necrosis factor- (TNF-) alpha, and IL-18.	Acetylcysteine	8-11	interferon gamma	Mus musculus	186-210
34899969-9	2021	Result: NAC could effectively improve the immune status of COPD patients as well as the COPD mouse model by downregulating proinflammation and inflammation cytokines including IL-1beta, interferon- (IFN-) gamma, tumor necrosis factor- (TNF-) alpha, and IL-18.	Acetylcysteine	8-11	tumor necrosis factor	Mus musculus	212-247
34899969-11	2021	Conclusion: NAC could effectively inhibit the production of IL-18 by suppressing NLRP3 expression in macrophages to reduce the production of IFN-gamma in NK cells.	Acetylcysteine	12-15	NLR family pyrin domain containing 3	Homo sapiens	81-86
34899969-11	2021	Conclusion: NAC could effectively inhibit the production of IL-18 by suppressing NLRP3 expression in macrophages to reduce the production of IFN-gamma in NK cells.	Acetylcysteine	12-15	interferon gamma	Homo sapiens	141-150
34544266-10	2021	NAC/AAP also improved the population doubling time of MSCs (first 6-days post isolation) and significantly downregulated the expression of 2 genes (Nox1 and Rag2) associated with oxidative stress compared to placebo treatment.	Acetylcysteine	0-3	recombination activating gene 2	Mus musculus	157-161
34711021-7	2021	Compared to rats that treated to continuous dose of Cd, NAC supplementation enhanced the expression of Nrf2 by 1.67-fold (p<0.001) and reduced the expression of NLRP3 and Caspase 1 genes by 1.39-fold (p<0.001) and 1.58-fold (p<0.001), respectively.	Acetylcysteine	56-59	NFE2 like bZIP transcription factor 2	Rattus norvegicus	103-107
34711021-7	2021	Compared to rats that treated to continuous dose of Cd, NAC supplementation enhanced the expression of Nrf2 by 1.67-fold (p<0.001) and reduced the expression of NLRP3 and Caspase 1 genes by 1.39-fold (p<0.001) and 1.58-fold (p<0.001), respectively.	Acetylcysteine	56-59	NLR family, pyrin domain containing 3	Rattus norvegicus	161-166
34711021-9	2021	NAC protects liver tissue against Cd-induced oxidative injuries via enhancement of Nrf2 expression and reduction of NLRP3 and caspase 1 genes.	Acetylcysteine	0-3	NFE2 like bZIP transcription factor 2	Rattus norvegicus	83-87
34711021-9	2021	NAC protects liver tissue against Cd-induced oxidative injuries via enhancement of Nrf2 expression and reduction of NLRP3 and caspase 1 genes.	Acetylcysteine	0-3	NLR family, pyrin domain containing 3	Rattus norvegicus	116-121
34601074-9	2021	While expression of TNF-alpha and IL-1beta, latency, as well as density of apoptosis cells in caspase-3 evaluation significantly more decreased in HBO+NAC group compared to other groups.	Acetylcysteine	151-154	tumor necrosis factor	Rattus norvegicus	20-29
34601074-9	2021	While expression of TNF-alpha and IL-1beta, latency, as well as density of apoptosis cells in caspase-3 evaluation significantly more decreased in HBO+NAC group compared to other groups.	Acetylcysteine	151-154	interleukin 1 alpha	Rattus norvegicus	34-42
34982438-14	2021	A favorable significant lower concentration of IL-6 was detected in the colchicine plus NAC group vs. the other groups.	Acetylcysteine	88-91	interleukin-6	Oryctolagus cuniculus	47-51
34982438-16	2021	Colchicine, as an NLRP3 inflammasome inhibitor, and NAC, as an agent that directly targets IL-6 signaling, can reduce the inflammatory risk.	Acetylcysteine	52-55	interleukin-6	Oryctolagus cuniculus	91-95
34850077-8	2021	Finally, we demonstrated that NAC selectively normalized uterine leukemia inhibitory factor, osteopontin/secreted phosphoprotein 1, progesterone receptor, and homeobox A11 mRNA expression and placental estrogen related receptor beta and trophoblast specific protein alpha mRNA expression.	Acetylcysteine	30-33	homeobox A11	Rattus norvegicus	159-171
34884437-6	2021	While the addition of extracellular SOD potentiated NAC-induced cell death, extracellular catalase (CAT) prevented cell death in HL-60 cells.	Acetylcysteine	52-55	superoxide dismutase 1	Homo sapiens	36-39
34868392-8	2021	Conclusions: NAC can inhibit AngII-induced CF proliferation and collagen synthesis through the NF-kappaB signaling pathway, alleviate the OS response of myocardial tissue, inhibit the fibrosis of myocardial tissue, and thus slow down the pathological remodeling of the heart.	Acetylcysteine	13-16	angiotensinogen	Rattus norvegicus	29-34
34884437-8	2021	In U937 cells, the weak cytotoxicity of NAC is probably caused by lower expression of NOX2, SOD1, SOD3, and by the absence of MOP expression.	Acetylcysteine	40-43	superoxide dismutase 1	Homo sapiens	92-96
34884437-8	2021	In U937 cells, the weak cytotoxicity of NAC is probably caused by lower expression of NOX2, SOD1, SOD3, and by the absence of MOP expression.	Acetylcysteine	40-43	superoxide dismutase 3	Homo sapiens	98-102
34993544-6	2022	NAC down-regulated the expression of GRP78 after TGF-beta1 treatment.	Acetylcysteine	0-3	heat shock protein family A (Hsp70) member 5	Homo sapiens	37-42
34993544-6	2022	NAC down-regulated the expression of GRP78 after TGF-beta1 treatment.	Acetylcysteine	0-3	transforming growth factor beta 1	Homo sapiens	49-58
34993544-9	2022	NAC abrogated TGF-beta1-induced integrin-beta3 expression.	Acetylcysteine	0-3	transforming growth factor beta 1	Homo sapiens	14-23
34993544-9	2022	NAC abrogated TGF-beta1-induced integrin-beta3 expression.	Acetylcysteine	0-3	integrin subunit beta 3	Homo sapiens	32-46
34993544-11	2022	Furthermore, NAC, 4-PBA and an anti-interin-beta3 antibody attenuated TGF-beta1-induced podocyte adhesion and migration.	Acetylcysteine	13-16	transforming growth factor beta 1	Homo sapiens	70-79
34447990-5	2021	On the other hand, treatment with the antioxidant N-acetylcysteine (NAC) increased glutathione concentration, decreased basal H2O2 production, p53 levels and sensitivity to AA treatment in the XPC-null back to the levels found in XPC-wt cells.	Acetylcysteine	50-66	tumor protein p53	Homo sapiens	143-146
34867200-0	2021	N-Acetyl Cysteine Restores Sirtuin-6 and Decreases HMGB1 Release Following Lipopolysaccharide-Sensitized Hypoxic-Ischemic Brain Injury in Neonatal Mice.	Acetylcysteine	0-17	sirtuin 6	Mus musculus	27-36
34867200-7	2021	Furthermore, we assessed the effect of the antioxidant N-acetyl cysteine (NAC) on sirtuin-6 expression, nuclear to cytoplasmic translocation, and release of HMGB1 in the brain and blood thiol oxidation after LPS+HI.	Acetylcysteine	55-72	sirtuin 6	Mus musculus	82-91
34867200-9	2021	NAC treatment restored sirtuin-6 protein levels, which was associated with reduced extracellular HMGB1 release and reduced thiol oxidation in the blood.	Acetylcysteine	0-3	sirtuin 6	Mus musculus	23-32
34447990-5	2021	On the other hand, treatment with the antioxidant N-acetylcysteine (NAC) increased glutathione concentration, decreased basal H2O2 production, p53 levels and sensitivity to AA treatment in the XPC-null back to the levels found in XPC-wt cells.	Acetylcysteine	68-71	tumor protein p53	Homo sapiens	143-146
34753902-6	2021	RESULTS: The inclusion of NAC increased the activity of mitochondrial complexes I and II + III as well as decreased the concentration of interleukin-1beta, tumor necrosis factor alpha, and caspase-3, but only in the parotid glands of rats with hyperglycemia compared to the HFD group.	Acetylcysteine	26-29	interleukin 1 beta	Rattus norvegicus	137-154
34753902-6	2021	RESULTS: The inclusion of NAC increased the activity of mitochondrial complexes I and II + III as well as decreased the concentration of interleukin-1beta, tumor necrosis factor alpha, and caspase-3, but only in the parotid glands of rats with hyperglycemia compared to the HFD group.	Acetylcysteine	26-29	tumor necrosis factor	Rattus norvegicus	156-183
34510229-8	2021	In addition, treatment with N-acetylcysteine (NAC) improved inflammation and blocked the upregulation of the MAPK/NF-kappaB signaling pathway.	Acetylcysteine	28-44	nuclear factor kappa B subunit 1	Homo sapiens	114-123
34739934-8	2021	The findings demonstrated that NAC relieved NiCl2-induced autophagy and reversed the activation of Akt/AMPK/mTOR pathway.	Acetylcysteine	31-34	thymoma viral proto-oncogene 1	Mus musculus	99-102
34510229-8	2021	In addition, treatment with N-acetylcysteine (NAC) improved inflammation and blocked the upregulation of the MAPK/NF-kappaB signaling pathway.	Acetylcysteine	46-49	nuclear factor kappa B subunit 1	Homo sapiens	114-123
34627931-8	2021	TQ increased the levels of reactive oxygen species (ROS), whereas pretreatment with N-acetyl cysteine (NAC), a ROS scavenger, prevented the suppressive effect of TQ on Jak2/STAT3 activation and protected SK-MEL-28 cells from TQ-induced apoptosis.	Acetylcysteine	84-101	signal transducer and activator of transcription 3	Homo sapiens	173-178
34494136-12	2021	In VIC cultures treated with glucose in combination with reactive oxygen species (ROS) inhibitor (N-acetyl-L-cysteine), the expression of NF-kappaB and BMP-2 was significantly suppressed.	Acetylcysteine	98-117	nuclear factor kappa B subunit 1	Homo sapiens	138-147
34156614-6	2021	NAC also significantly increased the expression and distribution of zonula occludens 1 (ZO-1), decreased the relative mRNA and protein expression levels of Bax, Bid, caspase-3, and caspase-9, and increased Bcl-2 expression level and inhibited the decrease of mitochondrial membrane potential.	Acetylcysteine	0-3	tight junction protein 1	Homo sapiens	68-86
34156614-6	2021	NAC also significantly increased the expression and distribution of zonula occludens 1 (ZO-1), decreased the relative mRNA and protein expression levels of Bax, Bid, caspase-3, and caspase-9, and increased Bcl-2 expression level and inhibited the decrease of mitochondrial membrane potential.	Acetylcysteine	0-3	tight junction protein 1	Homo sapiens	88-92
34156614-6	2021	NAC also significantly increased the expression and distribution of zonula occludens 1 (ZO-1), decreased the relative mRNA and protein expression levels of Bax, Bid, caspase-3, and caspase-9, and increased Bcl-2 expression level and inhibited the decrease of mitochondrial membrane potential.	Acetylcysteine	0-3	BCL2 associated X, apoptosis regulator	Homo sapiens	156-159
34156614-6	2021	NAC also significantly increased the expression and distribution of zonula occludens 1 (ZO-1), decreased the relative mRNA and protein expression levels of Bax, Bid, caspase-3, and caspase-9, and increased Bcl-2 expression level and inhibited the decrease of mitochondrial membrane potential.	Acetylcysteine	0-3	BH3 interacting domain death agonist	Homo sapiens	161-164
34156614-6	2021	NAC also significantly increased the expression and distribution of zonula occludens 1 (ZO-1), decreased the relative mRNA and protein expression levels of Bax, Bid, caspase-3, and caspase-9, and increased Bcl-2 expression level and inhibited the decrease of mitochondrial membrane potential.	Acetylcysteine	0-3	caspase 3	Homo sapiens	166-175
34156614-6	2021	NAC also significantly increased the expression and distribution of zonula occludens 1 (ZO-1), decreased the relative mRNA and protein expression levels of Bax, Bid, caspase-3, and caspase-9, and increased Bcl-2 expression level and inhibited the decrease of mitochondrial membrane potential.	Acetylcysteine	0-3	BCL2 apoptosis regulator	Homo sapiens	206-211
34627931-8	2021	TQ increased the levels of reactive oxygen species (ROS), whereas pretreatment with N-acetyl cysteine (NAC), a ROS scavenger, prevented the suppressive effect of TQ on Jak2/STAT3 activation and protected SK-MEL-28 cells from TQ-induced apoptosis.	Acetylcysteine	103-106	signal transducer and activator of transcription 3	Homo sapiens	173-178
34146182-10	2021	IL-1beta repressed the activation of the PI3K/Akt pathway, but ROS inhibition using N-acetylcysteine (NAC) rescued this pathway.	Acetylcysteine	84-100	AKT serine/threonine kinase 1	Homo sapiens	46-49
34182881-10	2021	NAC improved over time the PO2/FiO2 ratio and decreased the white blood cell, CRP, D-dimers and LDH levels.	Acetylcysteine	0-3	C-reactive protein	Homo sapiens	78-81
34146182-10	2021	IL-1beta repressed the activation of the PI3K/Akt pathway, but ROS inhibition using N-acetylcysteine (NAC) rescued this pathway.	Acetylcysteine	102-105	AKT serine/threonine kinase 1	Homo sapiens	46-49
34745415-6	2021	In addition, blocking of the RIPK1/RIPK3/MLKL signaling by necrostatin-1 (Nec-1), a key inhibitor of RIPK1 kinase in the necroptosis pathway, or antioxidant N-acetylcysteine (NAC), an inhibitor of ROS, could decrease the activation of osteoblast necroptosis and ameliorate alcohol-induced osteopenia both in vivo and in vitro.	Acetylcysteine	157-173	receptor (TNFRSF)-interacting serine-threonine kinase 1	Mus musculus	29-34
34644184-8	2021	Mancozeb reduced viability and increased the level of intracellular ROS, p38 and c-Jun N-terminal kinases (JNK) MAPK proteins phosphorylation, and apoptotic cell death, which could be blocked by NAC as an inhibitor of oxidative stress.	Acetylcysteine	195-198	mitogen-activated protein kinase 14	Homo sapiens	73-76
34644184-8	2021	Mancozeb reduced viability and increased the level of intracellular ROS, p38 and c-Jun N-terminal kinases (JNK) MAPK proteins phosphorylation, and apoptotic cell death, which could be blocked by NAC as an inhibitor of oxidative stress.	Acetylcysteine	195-198	mitogen-activated protein kinase 8	Homo sapiens	81-105
34644184-8	2021	Mancozeb reduced viability and increased the level of intracellular ROS, p38 and c-Jun N-terminal kinases (JNK) MAPK proteins phosphorylation, and apoptotic cell death, which could be blocked by NAC as an inhibitor of oxidative stress.	Acetylcysteine	195-198	mitogen-activated protein kinase 8	Homo sapiens	107-110
34481340-13	2021	Treatment with the ROS scavenger N-acetyl cysteine, effectively reversed the induction of apoptosis, autophagy, JNK activation and DNA damage elicited by RA.	Acetylcysteine	33-50	mitogen-activated protein kinase 8	Homo sapiens	112-115
34776955-5	2021	This was confirmed by which the JNK inhibitor SP600125 partially rescued CRC cells from chaetocin induced apoptosis and the ROS scavenger N-acetyl-L-cysteine (NAC) reversed both the chaetocin induced apoptosis and the JNK/c-Jun pathway activation.	Acetylcysteine	138-157	mitogen-activated protein kinase 8	Homo sapiens	218-221
34776955-5	2021	This was confirmed by which the JNK inhibitor SP600125 partially rescued CRC cells from chaetocin induced apoptosis and the ROS scavenger N-acetyl-L-cysteine (NAC) reversed both the chaetocin induced apoptosis and the JNK/c-Jun pathway activation.	Acetylcysteine	159-162	mitogen-activated protein kinase 8	Homo sapiens	218-221
34745415-6	2021	In addition, blocking of the RIPK1/RIPK3/MLKL signaling by necrostatin-1 (Nec-1), a key inhibitor of RIPK1 kinase in the necroptosis pathway, or antioxidant N-acetylcysteine (NAC), an inhibitor of ROS, could decrease the activation of osteoblast necroptosis and ameliorate alcohol-induced osteopenia both in vivo and in vitro.	Acetylcysteine	175-178	receptor (TNFRSF)-interacting serine-threonine kinase 1	Mus musculus	29-34
34697592-0	2021	The Role of Mesenchymal Stem Cells with Ascorbic Acid and N-Acetylcysteine on TNF-alpha, IL 1beta, and NF-kappabeta Expressions in Acute Pancreatitis in Albino Rats.	Acetylcysteine	58-74	tumor necrosis factor	Rattus norvegicus	78-87
34687223-7	2022	Moreover, pretreatment of 5 mM ROS scavenger N-acetyl-L-cysteine (NAC) ameliorated PFOS-induced NLRP3 inflammasome activation and pyroptosis.	Acetylcysteine	45-64	NLR family, pyrin domain containing 3	Rattus norvegicus	96-101
34687223-7	2022	Moreover, pretreatment of 5 mM ROS scavenger N-acetyl-L-cysteine (NAC) ameliorated PFOS-induced NLRP3 inflammasome activation and pyroptosis.	Acetylcysteine	66-69	NLR family, pyrin domain containing 3	Rattus norvegicus	96-101
34080015-6	2021	We show that a sequential combination of NAC+EE applied after an early-life oxidative insult recovers integrity and function of PVI network in adult Gclm KO, via the inhibition of MMP9/RAGE.	Acetylcysteine	41-44	glutamate-cysteine ligase modifier subunit	Homo sapiens	149-153
34744744-6	2021	An antioxidant N-Acetyl-l-cysteine (NAC) pretreatment could partially suppress the CXCL14 expression in CRC cells treated with H2O2.	Acetylcysteine	15-34	C-X-C motif chemokine ligand 14	Homo sapiens	83-89
34744744-6	2021	An antioxidant N-Acetyl-l-cysteine (NAC) pretreatment could partially suppress the CXCL14 expression in CRC cells treated with H2O2.	Acetylcysteine	36-39	C-X-C motif chemokine ligand 14	Homo sapiens	83-89
34755672-5	2021	The effects of chrysin, LPS, and their combination on the mRNA expressions of iNOS and COX-2 were detected using RT-PCR; Western blotting was performed to examine the changes in cellular expressions of p-AKT, p-PRAS40, p-mTOR, mTOR, p-P70S6k, p-S6RP and S6RP following the treatments with LPS, N-Acetyl-L-cysteine, and chrysin, alone or in combinations.	Acetylcysteine	294-313	nitric oxide synthase 2, inducible	Mus musculus	78-82
34755672-5	2021	The effects of chrysin, LPS, and their combination on the mRNA expressions of iNOS and COX-2 were detected using RT-PCR; Western blotting was performed to examine the changes in cellular expressions of p-AKT, p-PRAS40, p-mTOR, mTOR, p-P70S6k, p-S6RP and S6RP following the treatments with LPS, N-Acetyl-L-cysteine, and chrysin, alone or in combinations.	Acetylcysteine	294-313	thymoma viral proto-oncogene 1	Mus musculus	204-207
34755672-9	2021	Chrysin treatment significantly reduced the generation of endogenous ROS, and treatment with N-Acetyl-L-cysteine to eliminate intracellular ROS obviously reduced the expressions of iNOS and COX-2 (P < 0.05) and blocked the AKT/mTOR pathway (P < 0.05).	Acetylcysteine	93-112	nitric oxide synthase 2, inducible	Mus musculus	181-185
34755672-9	2021	Chrysin treatment significantly reduced the generation of endogenous ROS, and treatment with N-Acetyl-L-cysteine to eliminate intracellular ROS obviously reduced the expressions of iNOS and COX-2 (P < 0.05) and blocked the AKT/mTOR pathway (P < 0.05).	Acetylcysteine	93-112	thymoma viral proto-oncogene 1	Mus musculus	223-226
34697592-0	2021	The Role of Mesenchymal Stem Cells with Ascorbic Acid and N-Acetylcysteine on TNF-alpha, IL 1beta, and NF-kappabeta Expressions in Acute Pancreatitis in Albino Rats.	Acetylcysteine	58-74	interleukin 1 alpha	Rattus norvegicus	89-97
34697592-6	2021	AA and NAC combination with BM-MSCs (group IV) was demonstrated to affect the expression of the inflammatory cytokines: IL 1beta, TNF-alpha, and NF-kappabeta.	Acetylcysteine	7-10	interleukin 1 alpha	Rattus norvegicus	120-128
34697592-6	2021	AA and NAC combination with BM-MSCs (group IV) was demonstrated to affect the expression of the inflammatory cytokines: IL 1beta, TNF-alpha, and NF-kappabeta.	Acetylcysteine	7-10	tumor necrosis factor	Rattus norvegicus	130-139
34652265-1	2021	We investigated the effects of N-acetyl cysteine (NAC) on transient receptor potential melastatin 2 (TRPM2) channel expression in rat kidney and liver tissues following experimental malathion intoxication.	Acetylcysteine	31-48	transient receptor potential cation channel, subfamily M, member 2	Rattus norvegicus	101-106
34652265-0	2021	Effects of N-acetyl cysteine on TRPM2 expression in kidney and liver tissues following malathion intoxication.	Acetylcysteine	11-28	transient receptor potential cation channel, subfamily M, member 2	Rattus norvegicus	32-37
34332247-0	2021	NAC antagonizes arsenic-induced neurotoxicity through TMEM179 by inhibiting oxidative stress in Oli-neu cells.	Acetylcysteine	0-3	transmembrane protein 179	Mus musculus	54-61
34332247-9	2021	We found that TMEM179 played a critical role in mediating the neurotoxic effects of arsenic and the protective role of NAC.	Acetylcysteine	119-122	transmembrane protein 179	Mus musculus	14-21
34652265-1	2021	We investigated the effects of N-acetyl cysteine (NAC) on transient receptor potential melastatin 2 (TRPM2) channel expression in rat kidney and liver tissues following experimental malathion intoxication.	Acetylcysteine	50-53	transient receptor potential cation channel, subfamily M, member 2	Rattus norvegicus	101-106
34652265-5	2021	In kidney tissue, MDA levels, apoptosis and TRPM2 immunoreactivity were increased significantly in the malathion and malathion + NAC groups compared to the control group.	Acetylcysteine	129-132	transient receptor potential cation channel, subfamily M, member 2	Rattus norvegicus	44-49
34690806-9	2021	Additionally, CSE-induced upregulation of STIM1 in PMA-differentiated THP-1 macrophages was inhibited by pretreatment with N-acetylcysteine (NAC), a ROS scavenger.	Acetylcysteine	123-139	stromal interaction molecule 1	Homo sapiens	42-47
34681647-9	2021	Compound 6c-induced DNA damage was characterized by comet assay, p53 phosphorylation, and gammaH2A.X, which was diminished by pretreatment with NAC.	Acetylcysteine	144-147	tumor protein p53	Homo sapiens	65-68
34681610-5	2021	Further study revealed that OTA increased reactive oxygen species (ROS) levels, and N-acetyl cysteine (NAC) could reduce OTA-induced JNK-related apoptosis and ROS levels in HK-2 cells.	Acetylcysteine	84-101	mitogen-activated protein kinase 8	Homo sapiens	133-136
34681610-5	2021	Further study revealed that OTA increased reactive oxygen species (ROS) levels, and N-acetyl cysteine (NAC) could reduce OTA-induced JNK-related apoptosis and ROS levels in HK-2 cells.	Acetylcysteine	103-106	mitogen-activated protein kinase 8	Homo sapiens	133-136
34690806-9	2021	Additionally, CSE-induced upregulation of STIM1 in PMA-differentiated THP-1 macrophages was inhibited by pretreatment with N-acetylcysteine (NAC), a ROS scavenger.	Acetylcysteine	123-139	GLI family zinc finger 2	Homo sapiens	70-75
34690806-9	2021	Additionally, CSE-induced upregulation of STIM1 in PMA-differentiated THP-1 macrophages was inhibited by pretreatment with N-acetylcysteine (NAC), a ROS scavenger.	Acetylcysteine	141-144	stromal interaction molecule 1	Homo sapiens	42-47
34690806-9	2021	Additionally, CSE-induced upregulation of STIM1 in PMA-differentiated THP-1 macrophages was inhibited by pretreatment with N-acetylcysteine (NAC), a ROS scavenger.	Acetylcysteine	141-144	GLI family zinc finger 2	Homo sapiens	70-75
34690806-10	2021	Transfection with small interfering RNA (siRNA) targeting STIM1 and pretreatment with NAC alleviated CSE-induced increase in intracellular Ca2+ levels and IL-8 expression.	Acetylcysteine	86-89	C-X-C motif chemokine ligand 8	Homo sapiens	155-159
34420083-7	2021	Delayed NAC treatment had no effect on APAP-induced liver injury at 24 h but reduced the decline of plasma ALT activities and prevented the shrinkage of the areas of necrosis at 48 h. This effect correlated with down-regulation of key activators of mitochondrial biogenesis (AMPK, PGC-1alpha, Nrf1/2, TFAM) and reduced expression of Tom 20 (mitochondrial mass) and PCNA (cell proliferation).	Acetylcysteine	8-11	nuclear respiratory factor 1	Mus musculus	293-299
34692691-10	2021	Concomitantly, N-acetylcysteine, a ROS scavenger, abolished the inhibition of the mTOR signaling pathway, thus preventing autophagy and restoring cell viability.	Acetylcysteine	15-31	mechanistic target of rapamycin kinase	Homo sapiens	82-86
34420083-7	2021	Delayed NAC treatment had no effect on APAP-induced liver injury at 24 h but reduced the decline of plasma ALT activities and prevented the shrinkage of the areas of necrosis at 48 h. This effect correlated with down-regulation of key activators of mitochondrial biogenesis (AMPK, PGC-1alpha, Nrf1/2, TFAM) and reduced expression of Tom 20 (mitochondrial mass) and PCNA (cell proliferation).	Acetylcysteine	8-11	translocase of outer mitochondrial membrane 20	Mus musculus	333-339
34414459-8	2021	The ROS inhibitor, N-acetyl-l-cysteine, exerted a protective effect on the UA-induced apoptosis of tubular epithelial cells by reducing excess ROS production, which significantly inhibited NEK7 and NLRP3 inflammasome activation.	Acetylcysteine	19-38	NLR family, pyrin domain containing 3	Rattus norvegicus	198-203
34098069-5	2021	Elevated ROS and NLRP3, caspase-1, IL-1beta and IL-18 were detected, which was attenuated by N-acetylcysteine.	Acetylcysteine	93-109	NLR family pyrin domain containing 3	Homo sapiens	17-22
34098069-5	2021	Elevated ROS and NLRP3, caspase-1, IL-1beta and IL-18 were detected, which was attenuated by N-acetylcysteine.	Acetylcysteine	93-109	caspase 1	Homo sapiens	24-33
34343907-12	2021	The antioxidant N-acetylcysteine (NAC) also efficiently blocked CYP2E1-and NOX4-mediated induction of autophagy.	Acetylcysteine	16-32	cytochrome P450 family 2 subfamily E member 1	Homo sapiens	64-70
34402957-6	2021	Treatment with N-acetyl-L-cysteine, a widely used thiol-containing antioxidant, blunted the enhancement of the LPS-induced upregulation of pro-inflammatory cytokine production, iNOS expression, and NO production in macrophages.	Acetylcysteine	15-34	nitric oxide synthase 2	Homo sapiens	177-181
34343907-12	2021	The antioxidant N-acetylcysteine (NAC) also efficiently blocked CYP2E1-and NOX4-mediated induction of autophagy.	Acetylcysteine	34-37	cytochrome P450 family 2 subfamily E member 1	Homo sapiens	64-70
34343907-13	2021	Finally, specific and non-toxic production of H2O2 by the GOX/CAT system as evidenced by elevated peroxiredoxin (Prx-2) also induced LC3B which was efficiently blocked by NAC.	Acetylcysteine	171-174	catalase	Mus musculus	62-65
34703822-10	2021	NAC suppressed TNF-alpha- or poly (I:C)-induced expression of MCP-1 and CX3CL1.	Acetylcysteine	0-3	tumor necrosis factor	Rattus norvegicus	15-24
34703822-10	2021	NAC suppressed TNF-alpha- or poly (I:C)-induced expression of MCP-1 and CX3CL1.	Acetylcysteine	0-3	C-X3-C motif chemokine ligand 1	Rattus norvegicus	72-78
34680443-5	2021	Furthermore, IS and UT mix induced the production of intracellular reactive oxygen species, and caspase-1 activity and IL-1beta secretion were reduced in the presence of antioxidant N-acetylcysteine.	Acetylcysteine	182-198	caspase 1	Homo sapiens	96-105
34684414-8	2021	Moreover, NAC and ALA augmented the expression of GLUT4 and the phosphorylation state of Akt (Ser473) and GSK3beta (Ser9), which improved the intracellular insulin transduction pathway.	Acetylcysteine	10-13	AKT serine/threonine kinase 1	Rattus norvegicus	89-92
34175667-8	2021	General antioxidants such as N-Acetyl Cysteine (NAC) or the mitochondria-specific Mitoquinone prevented HIF-1alpha stabilization, ameliorated hypoxia-related mitochondrial oxidative stress, and suppressed mitophagy.	Acetylcysteine	48-51	hypoxia inducible factor 1 subunit alpha	Homo sapiens	104-114
34510030-4	2021	These effects reflected caspase 3-mediated apoptosis and could be attenuated or abolished by inhibiting ROS production with N-acetyl-L-cysteine, inhibiting autophagy with chloroquine, or silencing ATG7 with targeted siRNA.	Acetylcysteine	124-143	caspase 3	Homo sapiens	24-33
34479474-9	2021	NAC could inhibit cell migration and invasion, elevate E-cadherin expression, the ratio of CD3+, CD4+, CD8+ and CD4+/CD8+T lymphocytes, and levels of IgG, IgA, and IgM, and reduce N-cadherin expression and levels of IL-6 and TNF-alpha in CSE cells and serum of COPD rats.	Acetylcysteine	0-3	interleukin 6	Rattus norvegicus	216-220
34479474-9	2021	NAC could inhibit cell migration and invasion, elevate E-cadherin expression, the ratio of CD3+, CD4+, CD8+ and CD4+/CD8+T lymphocytes, and levels of IgG, IgA, and IgM, and reduce N-cadherin expression and levels of IL-6 and TNF-alpha in CSE cells and serum of COPD rats.	Acetylcysteine	0-3	tumor necrosis factor	Rattus norvegicus	225-234
34763128-7	2021	Inhibiting Nrf2 activation either by reducing ROS levels by N-acetylcysteine or by knocking down of Nrf2 by small interfering RNA attenuated both Notch signaling activation and EMT development.	Acetylcysteine	60-76	NFE2 like bZIP transcription factor 2	Homo sapiens	11-15
34278450-10	2021	Furthermore, the phosphorylated (p-)Akt and p-mTOR levels were significantly decreased in a concentration-dependent manner following treatment with chrysin, while NAC blocked these effects.	Acetylcysteine	163-166	AKT serine/threonine kinase 1	Homo sapiens	36-39
34278450-10	2021	Furthermore, the phosphorylated (p-)Akt and p-mTOR levels were significantly decreased in a concentration-dependent manner following treatment with chrysin, while NAC blocked these effects.	Acetylcysteine	163-166	mechanistic target of rapamycin kinase	Homo sapiens	46-50
34175667-8	2021	General antioxidants such as N-Acetyl Cysteine (NAC) or the mitochondria-specific Mitoquinone prevented HIF-1alpha stabilization, ameliorated hypoxia-related mitochondrial oxidative stress, and suppressed mitophagy.	Acetylcysteine	29-46	hypoxia inducible factor 1 subunit alpha	Homo sapiens	104-114
34544380-11	2021	Median AST on the day of administration of NAC was 1125 U/L interquartile range (IQR) 1653.25 while median ALT was 752 (IQR 459.25).	Acetylcysteine	43-46	solute carrier family 17 member 5	Homo sapiens	7-10
34544380-12	2021	There was a statistically significant reduction of both ALT (p = 0.034) and AST (p = 0.049) from day 1 to 4 after NAC infusion.	Acetylcysteine	114-117	solute carrier family 17 member 5	Homo sapiens	76-79
34214916-6	2021	Nrf2 levels increased after ROS scavenging by N-acetyl-L-cysteine (NAC), which indicated that the Nrf2 pathway may be affected by oxidative stress.	Acetylcysteine	46-65	NFE2 like bZIP transcription factor 2	Homo sapiens	0-4
34214916-6	2021	Nrf2 levels increased after ROS scavenging by N-acetyl-L-cysteine (NAC), which indicated that the Nrf2 pathway may be affected by oxidative stress.	Acetylcysteine	46-65	NFE2 like bZIP transcription factor 2	Homo sapiens	98-102
34214916-6	2021	Nrf2 levels increased after ROS scavenging by N-acetyl-L-cysteine (NAC), which indicated that the Nrf2 pathway may be affected by oxidative stress.	Acetylcysteine	67-70	NFE2 like bZIP transcription factor 2	Homo sapiens	0-4
34214916-6	2021	Nrf2 levels increased after ROS scavenging by N-acetyl-L-cysteine (NAC), which indicated that the Nrf2 pathway may be affected by oxidative stress.	Acetylcysteine	67-70	NFE2 like bZIP transcription factor 2	Homo sapiens	98-102
34576117-5	2021	Treatment with N-acetylcysteine, a pharmacological antioxidant, inhibited the acute glucose shift-induced generation of ROS, activation of NLRP3 inflammasome, and upregulation of MAPK-NF-kappaB.	Acetylcysteine	15-31	NLR family pyrin domain containing 3	Homo sapiens	139-144
34576117-5	2021	Treatment with N-acetylcysteine, a pharmacological antioxidant, inhibited the acute glucose shift-induced generation of ROS, activation of NLRP3 inflammasome, and upregulation of MAPK-NF-kappaB.	Acetylcysteine	15-31	nuclear factor kappa B subunit 1	Homo sapiens	184-193
34572983-8	2021	N-acetylcysteine treatment delayed the onset of SNHL and mitigated cochlear damage, with fewer TUNEL+ HC and lower numbers of spiral ganglion neurons with p-H2AX foci.	Acetylcysteine	0-16	H2A.X variant histone	Mus musculus	157-161
34462463-6	2021	Treatment of the neurons with an antioxidant, N-acetylcysteine, significantly suppressed the Abeta secretion.	Acetylcysteine	46-62	amyloid beta precursor protein	Homo sapiens	93-98
34462463-7	2021	These findings suggest that oxidative stress has an important role in controlling the Abeta level in neurons differentiated from DS patient-derived iPSCs and that N-acetylcysteine can be a potential therapeutic option to ameliorate the Abeta secretion.	Acetylcysteine	163-179	amyloid beta precursor protein	Homo sapiens	86-91
34462463-7	2021	These findings suggest that oxidative stress has an important role in controlling the Abeta level in neurons differentiated from DS patient-derived iPSCs and that N-acetylcysteine can be a potential therapeutic option to ameliorate the Abeta secretion.	Acetylcysteine	163-179	amyloid beta precursor protein	Homo sapiens	236-241
34346218-5	2021	The results from the TC uptake assay using N-acetylcysteine suggested that the inhibitory effect of TF2A and TF2B was attributed to the oxidization of their benzotropolone rings and their covalent bonding with ASBT"s cysteine.	Acetylcysteine	43-59	general transcription factor IIB	Homo sapiens	109-113
34459136-0	2021	N-Acetyl-l-cysteine restores reproductive defects caused by Ggt1 deletion in mice.	Acetylcysteine	0-19	gamma-glutamyltransferase 1	Mus musculus	60-64
34445365-0	2021	Single Dose of N-Acetylcysteine in Local Anesthesia Increases Expression of HIF1alpha, MAPK1, TGFbeta1 and Growth Factors in Rat Wound Healing.	Acetylcysteine	15-31	transforming growth factor, beta 1	Rattus norvegicus	94-102
34445365-7	2021	On the 14th day, the number of cells stained with anti-CD68 and anti-CD31 antibodies was significantly larger in the tissues treated with 0.03% NAC compared with the control.	Acetylcysteine	144-147	platelet and endothelial cell adhesion molecule 1	Rattus norvegicus	69-73
34146943-9	2021	After cells treated with NAC, the effect of raddeanin A was reversed, as evidenced by the apoptosis and ROS generation were suppressed, and the expression of p-STAT3 was promoted.	Acetylcysteine	25-28	signal transducer and activator of transcription 3	Homo sapiens	160-165
34167418-0	2021	The effect of N-acetyl cysteine and doxycycline on TNF-alpha-Rel-a inflammatory pathway and downstream angiogenesis factors in the cornea of rats injured by 2-chloroethyl-ethyl sulfide.	Acetylcysteine	14-31	tumor necrosis factor	Rattus norvegicus	51-60
34753839-9	2021	NAC incorporated at a concentration of 2.5 mM showed higher mineralization and considerably increased gene expression levels of runt-related transcription factor 2 (RUNX2), COL1A1, DSPP, and DMP-1.	Acetylcysteine	0-3	RUNX family transcription factor 2	Homo sapiens	128-163
34753839-9	2021	NAC incorporated at a concentration of 2.5 mM showed higher mineralization and considerably increased gene expression levels of runt-related transcription factor 2 (RUNX2), COL1A1, DSPP, and DMP-1.	Acetylcysteine	0-3	RUNX family transcription factor 2	Homo sapiens	165-170
34236028-10	2021	Immunocytochemical staining confirmed that the isolated and cultured cells were AA-FLS; NAC inhibited the proliferation of AA-FLS treated with H2O2 in a concentration-dependent manner, and the mitochondrial ROS content and the protein expressions of Nrf2 and Keap1 decreased.	Acetylcysteine	88-91	NFE2 like bZIP transcription factor 2	Rattus norvegicus	250-254
34236028-0	2021	(N-acetylcysteine inhibits the proliferation of hydrogen peroxide treated fibroblast-like synoviocytes in rats with adjuvant arthritis (AA) via blocking Nrf2/Keap1 pathway).	Acetylcysteine	1-17	NFE2 like bZIP transcription factor 2	Rattus norvegicus	153-157
34236028-11	2021	Conclusion NAC can inhibit the proliferation of AA-FLS treated with H2O2, which may be related to blocking Nrf2/Keap1 pathway.	Acetylcysteine	11-14	NFE2 like bZIP transcription factor 2	Rattus norvegicus	107-111
34236028-8	2021	The effects of NAC (final concentration 0, 3, 10, 30 mumol/L) on Nrf2 and Keap1 protein expressions in AA-FLS treated with H2O2 at low concentration were detected by Western blotting.	Acetylcysteine	15-18	NFE2 like bZIP transcription factor 2	Rattus norvegicus	65-69
34258270-0	2021	N-Acetylcysteine Improves Inflammatory Response in COPD Patients by Regulating Th17/Treg Balance through Hypoxia Inducible Factor-1alpha Pathway.	Acetylcysteine	0-16	hypoxia inducible factor 1 subunit alpha	Homo sapiens	105-136
34475984-5	2021	The inhibition of ROS generation by N-acetyl-l-cysteine not only recovered cell migration and viability, but also reduced beta-catenin accumulation and JNK and ERK activation.	Acetylcysteine	36-55	mitogen-activated protein kinase 8	Homo sapiens	152-155
34475984-5	2021	The inhibition of ROS generation by N-acetyl-l-cysteine not only recovered cell migration and viability, but also reduced beta-catenin accumulation and JNK and ERK activation.	Acetylcysteine	36-55	mitogen-activated protein kinase 1	Homo sapiens	160-163
34213003-10	2021	Histopathological injury score, plasma MPO, AST, ALT, tissue MPO and tissue MDA values were statistically significantly lower in the treatment groups, prominently in the levosimendan and NAS combination group concerning liver histopathological damage.	Acetylcysteine	187-190	glutamic-oxaloacetic transaminase 2	Rattus norvegicus	44-47
34349610-10	2021	Antioxidant N-acetyl cysteine (NAC) and ML171, a specific NADPH oxidase 1 inhibitor, suppressed cerulein/resistin-induced ROS production, NF-kappaB activation, and IL-6 expression.	Acetylcysteine	12-29	resistin	Rattus norvegicus	105-113
34349610-10	2021	Antioxidant N-acetyl cysteine (NAC) and ML171, a specific NADPH oxidase 1 inhibitor, suppressed cerulein/resistin-induced ROS production, NF-kappaB activation, and IL-6 expression.	Acetylcysteine	12-29	interleukin 6	Rattus norvegicus	164-168
34349610-10	2021	Antioxidant N-acetyl cysteine (NAC) and ML171, a specific NADPH oxidase 1 inhibitor, suppressed cerulein/resistin-induced ROS production, NF-kappaB activation, and IL-6 expression.	Acetylcysteine	31-34	resistin	Rattus norvegicus	105-113
34349610-10	2021	Antioxidant N-acetyl cysteine (NAC) and ML171, a specific NADPH oxidase 1 inhibitor, suppressed cerulein/resistin-induced ROS production, NF-kappaB activation, and IL-6 expression.	Acetylcysteine	31-34	interleukin 6	Rattus norvegicus	164-168
34439408-4	2021	Importantly, we found that a combined treatment with the cell permeant iron chelator deferiprone and the glutathione precursor N-acetyl cysteine promoted the structural repair of mitochondria and ER, decreased mitochondrial labile iron and ROS levels, and restored glucose-stimulated insulin secretion.	Acetylcysteine	127-144	insulin	Homo sapiens	284-291
34356340-8	2021	The protective effects of NAC were, at least, partly due to a decrease in the production of tumor necrosis factor-alpha (TNF-alpha) by acinar cells, which was concomitant with the inhibition of NF-kappaB(p65) nuclear translocation.	Acetylcysteine	26-29	tumor necrosis factor	Mus musculus	92-119
34356340-8	2021	The protective effects of NAC were, at least, partly due to a decrease in the production of tumor necrosis factor-alpha (TNF-alpha) by acinar cells, which was concomitant with the inhibition of NF-kappaB(p65) nuclear translocation.	Acetylcysteine	26-29	tumor necrosis factor	Mus musculus	121-130
34258270-9	2021	In vitro studies, we found that NAC regulated Th17/Treg balance through Hypoxia Inducible Factor-1alpha pathway.	Acetylcysteine	32-35	hypoxia inducible factor 1 subunit alpha	Homo sapiens	72-103
34257541-7	2021	Moreover, pre-incubation of cells with ROS inhibitor N-acetyl-L-cysteine (NAC) significantly reversed beta-elemene-mediated apoptosis effect and down-regulation of JAK2/Src-STAT3 signaling pathway.	Acetylcysteine	53-72	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	169-172
34206987-7	2021	A pronounced stimulation of cell proliferation and interferon-gamma (IFN-gamma) secretion in response to concanavalin A was shown for antioxidant N-acetylcysteine (NAC), polyamine biosynthesis inhibitor 2-difluoromethylornithine (DFMO), and TLR9 agonist CpG ODN 1826 (CpG).	Acetylcysteine	146-162	interferon gamma	Homo sapiens	51-67
34206987-7	2021	A pronounced stimulation of cell proliferation and interferon-gamma (IFN-gamma) secretion in response to concanavalin A was shown for antioxidant N-acetylcysteine (NAC), polyamine biosynthesis inhibitor 2-difluoromethylornithine (DFMO), and TLR9 agonist CpG ODN 1826 (CpG).	Acetylcysteine	146-162	interferon gamma	Homo sapiens	69-78
34206987-7	2021	A pronounced stimulation of cell proliferation and interferon-gamma (IFN-gamma) secretion in response to concanavalin A was shown for antioxidant N-acetylcysteine (NAC), polyamine biosynthesis inhibitor 2-difluoromethylornithine (DFMO), and TLR9 agonist CpG ODN 1826 (CpG).	Acetylcysteine	164-167	interferon gamma	Homo sapiens	51-67
34206987-7	2021	A pronounced stimulation of cell proliferation and interferon-gamma (IFN-gamma) secretion in response to concanavalin A was shown for antioxidant N-acetylcysteine (NAC), polyamine biosynthesis inhibitor 2-difluoromethylornithine (DFMO), and TLR9 agonist CpG ODN 1826 (CpG).	Acetylcysteine	164-167	interferon gamma	Homo sapiens	69-78
34208683-5	2021	As an anti-inflammatory compound, NAC can reduce levels of tumor necrosis factor-alpha (TNF-alpha) and interleukins (IL-6 and IL-1beta) by suppressing the activity of nuclear factor kappa B (NF-kappaB).	Acetylcysteine	34-37	tumor necrosis factor	Homo sapiens	59-86
34208683-5	2021	As an anti-inflammatory compound, NAC can reduce levels of tumor necrosis factor-alpha (TNF-alpha) and interleukins (IL-6 and IL-1beta) by suppressing the activity of nuclear factor kappa B (NF-kappaB).	Acetylcysteine	34-37	tumor necrosis factor	Homo sapiens	88-97
34208683-5	2021	As an anti-inflammatory compound, NAC can reduce levels of tumor necrosis factor-alpha (TNF-alpha) and interleukins (IL-6 and IL-1beta) by suppressing the activity of nuclear factor kappa B (NF-kappaB).	Acetylcysteine	34-37	interleukin 6	Homo sapiens	117-121
34208683-5	2021	As an anti-inflammatory compound, NAC can reduce levels of tumor necrosis factor-alpha (TNF-alpha) and interleukins (IL-6 and IL-1beta) by suppressing the activity of nuclear factor kappa B (NF-kappaB).	Acetylcysteine	34-37	nuclear factor kappa B subunit 1	Homo sapiens	167-189
34208683-5	2021	As an anti-inflammatory compound, NAC can reduce levels of tumor necrosis factor-alpha (TNF-alpha) and interleukins (IL-6 and IL-1beta) by suppressing the activity of nuclear factor kappa B (NF-kappaB).	Acetylcysteine	34-37	nuclear factor kappa B subunit 1	Homo sapiens	191-200
34194603-9	2021	Moreover, pretreatment with N-acetyl-L-cysteine, diphenyleneiodonium chloride, apocynin, or rotenone blocked nuclear translocation and promoter binding activity of Nrf2 induced by CORM-3.	Acetylcysteine	28-47	NFE2 like bZIP transcription factor 2	Rattus norvegicus	164-168
34204067-10	2021	Hydroquinone reduced the intracellular levels of PARP, which were restored by treatment with the ROS scavenger N-acetyl-cysteine (NAC).	Acetylcysteine	111-128	poly(ADP-ribose) polymerase 1	Homo sapiens	49-53
34204067-10	2021	Hydroquinone reduced the intracellular levels of PARP, which were restored by treatment with the ROS scavenger N-acetyl-cysteine (NAC).	Acetylcysteine	130-133	poly(ADP-ribose) polymerase 1	Homo sapiens	49-53
34204067-11	2021	NAC concurrently reduced the NLRP3 levels but had no effect on IL-18 release.	Acetylcysteine	0-3	NLR family pyrin domain containing 3	Homo sapiens	29-34
34064109-4	2021	Inhibition of apigenin-induced reactive oxygen species (ROS) generation by a ROS scavenger N-acetyl-L-cysteine blocked the lipid raft membrane localization and activation of ASM and formation of ceramide-enriched lipid raft membranes, returned PI3K-Akt-GTP-Rac1-modulated CDK1-cyclin B1 activity, and subsequently restored the BCL-2/BCL-xL-regulated ER-mitochondrial bioenergetic activity.	Acetylcysteine	91-110	sphingomyelin phosphodiesterase 1	Homo sapiens	174-177
34064109-4	2021	Inhibition of apigenin-induced reactive oxygen species (ROS) generation by a ROS scavenger N-acetyl-L-cysteine blocked the lipid raft membrane localization and activation of ASM and formation of ceramide-enriched lipid raft membranes, returned PI3K-Akt-GTP-Rac1-modulated CDK1-cyclin B1 activity, and subsequently restored the BCL-2/BCL-xL-regulated ER-mitochondrial bioenergetic activity.	Acetylcysteine	91-110	AKT serine/threonine kinase 1	Homo sapiens	249-252
34064109-4	2021	Inhibition of apigenin-induced reactive oxygen species (ROS) generation by a ROS scavenger N-acetyl-L-cysteine blocked the lipid raft membrane localization and activation of ASM and formation of ceramide-enriched lipid raft membranes, returned PI3K-Akt-GTP-Rac1-modulated CDK1-cyclin B1 activity, and subsequently restored the BCL-2/BCL-xL-regulated ER-mitochondrial bioenergetic activity.	Acetylcysteine	91-110	BCL2 apoptosis regulator	Homo sapiens	327-332
34064109-4	2021	Inhibition of apigenin-induced reactive oxygen species (ROS) generation by a ROS scavenger N-acetyl-L-cysteine blocked the lipid raft membrane localization and activation of ASM and formation of ceramide-enriched lipid raft membranes, returned PI3K-Akt-GTP-Rac1-modulated CDK1-cyclin B1 activity, and subsequently restored the BCL-2/BCL-xL-regulated ER-mitochondrial bioenergetic activity.	Acetylcysteine	91-110	BCL2 like 1	Homo sapiens	333-339
34257541-7	2021	Moreover, pre-incubation of cells with ROS inhibitor N-acetyl-L-cysteine (NAC) significantly reversed beta-elemene-mediated apoptosis effect and down-regulation of JAK2/Src-STAT3 signaling pathway.	Acetylcysteine	53-72	signal transducer and activator of transcription 3	Homo sapiens	173-178
34257541-7	2021	Moreover, pre-incubation of cells with ROS inhibitor N-acetyl-L-cysteine (NAC) significantly reversed beta-elemene-mediated apoptosis effect and down-regulation of JAK2/Src-STAT3 signaling pathway.	Acetylcysteine	74-77	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	169-172
34257541-7	2021	Moreover, pre-incubation of cells with ROS inhibitor N-acetyl-L-cysteine (NAC) significantly reversed beta-elemene-mediated apoptosis effect and down-regulation of JAK2/Src-STAT3 signaling pathway.	Acetylcysteine	74-77	signal transducer and activator of transcription 3	Homo sapiens	173-178
35427795-7	2022	Activating pparg in the wild-type female fish via dietary supplementation with rosiglitazone (a pparg agonist), or reducing oxidative stress in the female pparg mutants via dietary supplementation with N-acetylcysteine (an antioxidant), or promoting mitochondrial fatty acid beta-oxidation in the female pparg mutants via dietary supplementation with l-carnitine, resulted in significantly reduced cellular injury, and improved environmental stress resistance.	Acetylcysteine	202-218	peroxisome proliferator-activated receptor gamma	Danio rerio	155-160
35504092-5	2022	Additionally, supplementation of N-acetylcysteine (NAC), known as an antidote of APAP, mitigated the ALI and downregulated the expression of NADK which was also in a dose-dependent manner.	Acetylcysteine	33-49	NAD kinase	Mus musculus	141-145
35504092-5	2022	Additionally, supplementation of N-acetylcysteine (NAC), known as an antidote of APAP, mitigated the ALI and downregulated the expression of NADK which was also in a dose-dependent manner.	Acetylcysteine	51-54	NAD kinase	Mus musculus	141-145
34744411-1	2021	The kinetic characteristics of the interaction of N-acetylcysteine (ASH) with reactive oxygen species (ROS), peroxyl radicals and hydrogen peroxide were determined.	Acetylcysteine	50-66	arylsulfatase family member H	Homo sapiens	68-71
35403328-12	2022	Moreover, we observed that PM2.5 exposure increased the production of intracellular ROS following OGD/R, while inhibiting ROS production with NAC partially attenuated PM2.5-induced NLRP3 inflammasome activation and pyroptosis under ischemic conditions.	Acetylcysteine	142-145	NLR family pyrin domain containing 3	Homo sapiens	181-186
35430258-8	2022	The use of NAC was found to alleviate the DNA damage, cell apoptosis, and oxidative stress via Nrf2/Sirt3 pathway though without any effect on the mitochondrial membrane potential.	Acetylcysteine	11-14	NFE2 like bZIP transcription factor 2	Homo sapiens	95-99
35489181-11	2022	Treatment with NAC+ASA increased the levels of glutamate transporters xCT and GLT-1 in nucleus accumbens, while Lactobacillus-GG administration increased those of the dopamine transporter (DAT).	Acetylcysteine	15-18	solute carrier family 1 member 2	Rattus norvegicus	78-83
35430258-8	2022	The use of NAC was found to alleviate the DNA damage, cell apoptosis, and oxidative stress via Nrf2/Sirt3 pathway though without any effect on the mitochondrial membrane potential.	Acetylcysteine	11-14	sirtuin 3	Homo sapiens	100-105
35624495-7	2022	The low fluorescence intensity of autophagic flux and the increased phosphorylation of RIP3 induced by CIRI could be attenuated by ROS scavenger, NAC (P < 0.05).	Acetylcysteine	146-149	myosin phosphatase Rho interacting protein	Mus musculus	87-91
35593216-8	2022	In conclusion, NAC can improve erectile function through inhibiting oxidative stress via activating Nrf2 pathways and reducing apoptosis in streptozotocin-induced diabetic mice.	Acetylcysteine	15-18	nuclear factor, erythroid derived 2, like 2	Mus musculus	100-104
35125047-0	2022	The effects of N-acetylcysteine on experimentally created l-asparaginase-induced liver and pancreatic damage in rats.	Acetylcysteine	15-31	asparaginase and isoaspartyl peptidase 1	Rattus norvegicus	58-72
35624854-10	2022	Furthermore, N-acetyl-L-cysteine (NAC) treatment blocked both tomentosin-induced production of ROS and the nuclear translocation of Nrf2.	Acetylcysteine	13-32	NFE2 like bZIP transcription factor 2	Homo sapiens	132-136
35624854-10	2022	Furthermore, N-acetyl-L-cysteine (NAC) treatment blocked both tomentosin-induced production of ROS and the nuclear translocation of Nrf2.	Acetylcysteine	34-37	NFE2 like bZIP transcription factor 2	Homo sapiens	132-136
35550579-14	2022	Pretreatment of NAC in CSE or H2O2-induced HBE mitigated HE4 expression.	Acetylcysteine	16-19	WAP four-disulfide core domain 2	Mus musculus	57-60
35615146-7	2022	Conversely, inhibiting ROS production with N-acetylcysteine (NAC) elevated AD-decreased ER-alpha expression, which could be alleviated by FOXM1 knockdown.	Acetylcysteine	43-59	estrogen receptor 1	Homo sapiens	88-96
35615146-7	2022	Conversely, inhibiting ROS production with N-acetylcysteine (NAC) elevated AD-decreased ER-alpha expression, which could be alleviated by FOXM1 knockdown.	Acetylcysteine	61-64	estrogen receptor 1	Homo sapiens	88-96
35533555-7	2022	Furthermore, N-acetylcysteine (NAC), an ROS scavenger, alleviates HFCS-aggravated colitis in mice and inhibits the ROS-mediated NF-kappaB signaling pathway in RAW264.7 macrophages.	Acetylcysteine	13-29	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	128-137
35533555-7	2022	Furthermore, N-acetylcysteine (NAC), an ROS scavenger, alleviates HFCS-aggravated colitis in mice and inhibits the ROS-mediated NF-kappaB signaling pathway in RAW264.7 macrophages.	Acetylcysteine	31-34	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	128-137
35417750-6	2022	In the P. bovis group, treatment with N-acetyl-l-cysteine (NAC) significantly decreased protein expression in NF-kappaB and the NLRP3 inflammasome pathway, as well as IL-1beta, IL-6 and IL-18, whereas protein expression in the Nrf2 pathway was significantly changed.	Acetylcysteine	38-57	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	110-119
35507947-8	2022	In addition, the expression of Gdf9, Lif, Bax, and Bcl2 genes were increased and Amh was decreased in groups cultured in the presence of NAC compared to groups cultured without NAC.	Acetylcysteine	137-140	B cell leukemia/lymphoma 2	Mus musculus	51-55
35507947-8	2022	In addition, the expression of Gdf9, Lif, Bax, and Bcl2 genes were increased and Amh was decreased in groups cultured in the presence of NAC compared to groups cultured without NAC.	Acetylcysteine	177-180	B cell leukemia/lymphoma 2	Mus musculus	51-55
35513370-0	2022	N-Acetylcysteine improves oocyte quality through modulating the Nrf2 signaling pathway to ameliorate oxidative stress caused by repeated controlled ovarian hyperstimulation.	Acetylcysteine	0-16	nuclear factor, erythroid derived 2, like 2	Mus musculus	64-68
35513370-7	2022	The mechanism of regulation of nuclear factor erythroid 2-related factor 2 (Nrf2) by NAC to ameliorate oxidative stress was also investigated.	Acetylcysteine	85-88	nuclear factor, erythroid derived 2, like 2	Mus musculus	31-74
35513370-7	2022	The mechanism of regulation of nuclear factor erythroid 2-related factor 2 (Nrf2) by NAC to ameliorate oxidative stress was also investigated.	Acetylcysteine	85-88	nuclear factor, erythroid derived 2, like 2	Mus musculus	76-80
35513370-9	2022	In in vitro experiments, it was verified that NAC can promote the nuclear translocation of Nrf2, which transcriptionally activates the expression of superoxide dismutase and glutathione peroxidase, which removed excessive reactive oxygen species that causes mitochondria damage.	Acetylcysteine	46-49	nuclear factor, erythroid derived 2, like 2	Mus musculus	91-95
35629355-8	2022	Pretreatment with N-acetylcysteine (NAC) reduced Apl-1-induced mitochondria-dependent apoptosis and preserved the expression of NOX, HO-1, and HIF-1a.	Acetylcysteine	18-34	hypoxia inducible factor 1 subunit alpha	Homo sapiens	143-149
35629355-8	2022	Pretreatment with N-acetylcysteine (NAC) reduced Apl-1-induced mitochondria-dependent apoptosis and preserved the expression of NOX, HO-1, and HIF-1a.	Acetylcysteine	36-39	hypoxia inducible factor 1 subunit alpha	Homo sapiens	143-149
35635082-7	2022	N-acetyl cysteine (NAC), which is an inhibitor of ROS, was used to confirm whether AF exerted its effects on KLE cells through ROS/AMPK/mTOR signaling.	Acetylcysteine	0-17	mechanistic target of rapamycin kinase	Homo sapiens	136-140
35635082-10	2022	NAC reversed the effects of AF on biological behaviors of KLE cells by inactivating ROS/AMPK/mTOR signaling.	Acetylcysteine	0-3	mechanistic target of rapamycin kinase	Homo sapiens	93-97
35417750-6	2022	In the P. bovis group, treatment with N-acetyl-l-cysteine (NAC) significantly decreased protein expression in NF-kappaB and the NLRP3 inflammasome pathway, as well as IL-1beta, IL-6 and IL-18, whereas protein expression in the Nrf2 pathway was significantly changed.	Acetylcysteine	38-57	nuclear factor, erythroid derived 2, like 2	Mus musculus	227-231
35417750-6	2022	In the P. bovis group, treatment with N-acetyl-l-cysteine (NAC) significantly decreased protein expression in NF-kappaB and the NLRP3 inflammasome pathway, as well as IL-1beta, IL-6 and IL-18, whereas protein expression in the Nrf2 pathway was significantly changed.	Acetylcysteine	59-62	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	110-119
35417750-6	2022	In the P. bovis group, treatment with N-acetyl-l-cysteine (NAC) significantly decreased protein expression in NF-kappaB and the NLRP3 inflammasome pathway, as well as IL-1beta, IL-6 and IL-18, whereas protein expression in the Nrf2 pathway was significantly changed.	Acetylcysteine	59-62	nuclear factor, erythroid derived 2, like 2	Mus musculus	227-231
35473933-9	2022	In addition, we showed that necrotic TECs-induced activation of TLR2/caspase-5/Panx1 axis could be decreased in macrophages when TECs was protected by N-acetylcysteine (NAC).	Acetylcysteine	151-167	toll like receptor 2	Homo sapiens	64-68
35167014-6	2022	Furthermore, the mechanism of action of NAC was evaluated by analysing brain expression levels of some possible key targets: the excitatory amino acid transporter 2, cystine-glutamate antiporter, metabotropic glutamate receptor 2, the mechanistic target of rapamycin and p70S6K as well as levels of total glutathione.	Acetylcysteine	40-43	glutamate metabotropic receptor 2	Rattus norvegicus	196-229
35473809-5	2022	Based on the percentage of CD34+VEGFR2 (CD309)+ endothelial cells (ECs) in bone marrow (BM) detected by flow cytometry at 14 days before conditioning, patients aged 15 to 60 years with acute leukemia undergoing haploidentical HSCT were categorized as low-risk (EC >= 0.1%) or high-risk (EC < 0.1%); patients at high risk were randomly assigned (2:1) to receive NAC prophylaxis or nonprophylaxis.	Acetylcysteine	361-364	CD34 molecule	Homo sapiens	27-31
35473809-9	2022	Consistently, NAC prophylaxis gradually improved BM ECs and CD34+ cells in group A, whereas reduced their reactive oxygen species (ROS) levels post-HSCT.	Acetylcysteine	14-17	CD34 molecule	Homo sapiens	60-64
35473933-9	2022	In addition, we showed that necrotic TECs-induced activation of TLR2/caspase-5/Panx1 axis could be decreased in macrophages when TECs was protected by N-acetylcysteine (NAC).	Acetylcysteine	169-172	toll like receptor 2	Homo sapiens	64-68
35437791-6	2022	Pretreatment of reactive oxygen species scavenger N-acetyl-L-cysteine (NAC), particularly mitochondrial reactive oxygen species scavengers Mito-TEMPO, effectively inhibited the activation of NLRP3 inflammasome, suggesting that nitrosamines could mediate the activation of NLRP3 inflammasome via mitochondrial reactive oxygen species (mtROS).	Acetylcysteine	50-69	NLR family pyrin domain containing 3	Homo sapiens	191-196
35403558-7	2022	Additionally, NAC also maintained mitochondrial functions, enhanced the gene expression of PGC-1alpha and its downstream regulators.	Acetylcysteine	14-17	PPARG coactivator 1 alpha	Rattus norvegicus	91-101
35403558-8	2022	The results of the present study indicate that NAC prevents hepatic mitochondrial dysfunctions and maintains PGC-1alpha signalling.	Acetylcysteine	47-50	PPARG coactivator 1 alpha	Rattus norvegicus	109-119
35437791-6	2022	Pretreatment of reactive oxygen species scavenger N-acetyl-L-cysteine (NAC), particularly mitochondrial reactive oxygen species scavengers Mito-TEMPO, effectively inhibited the activation of NLRP3 inflammasome, suggesting that nitrosamines could mediate the activation of NLRP3 inflammasome via mitochondrial reactive oxygen species (mtROS).	Acetylcysteine	50-69	NLR family pyrin domain containing 3	Homo sapiens	272-277
35437791-6	2022	Pretreatment of reactive oxygen species scavenger N-acetyl-L-cysteine (NAC), particularly mitochondrial reactive oxygen species scavengers Mito-TEMPO, effectively inhibited the activation of NLRP3 inflammasome, suggesting that nitrosamines could mediate the activation of NLRP3 inflammasome via mitochondrial reactive oxygen species (mtROS).	Acetylcysteine	71-74	NLR family pyrin domain containing 3	Homo sapiens	191-196
35437791-6	2022	Pretreatment of reactive oxygen species scavenger N-acetyl-L-cysteine (NAC), particularly mitochondrial reactive oxygen species scavengers Mito-TEMPO, effectively inhibited the activation of NLRP3 inflammasome, suggesting that nitrosamines could mediate the activation of NLRP3 inflammasome via mitochondrial reactive oxygen species (mtROS).	Acetylcysteine	71-74	NLR family pyrin domain containing 3	Homo sapiens	272-277
35293662-8	2022	Inhibition of ROS using N-acetyl-l-cysteine (NAC) inhibited chromium-induced activation of ATF6 and upregulation of PLK4.	Acetylcysteine	24-43	polo like kinase 4	Homo sapiens	116-120
35428330-13	2022	Additionally, the ROS scavengers N-Acetylcysteine (N-Ace) was also found to inhibit the nuclear translocation of NF-kappaB and the mRNA expression of IL-6 and MCP-1 induced by LPS, which suggested that ROS was essential for the nuclear translocation of NF-kappaB.	Acetylcysteine	33-49	interleukin 6	Rattus norvegicus	150-154
35428330-13	2022	Additionally, the ROS scavengers N-Acetylcysteine (N-Ace) was also found to inhibit the nuclear translocation of NF-kappaB and the mRNA expression of IL-6 and MCP-1 induced by LPS, which suggested that ROS was essential for the nuclear translocation of NF-kappaB.	Acetylcysteine	51-56	interleukin 6	Rattus norvegicus	150-154
35453467-14	2022	The binding activity between Nrf2 and HO-1 promoter was attenuated by APO, NAC, Srci II, PF431396, or Go6983.	Acetylcysteine	75-78	NFE2 like bZIP transcription factor 2	Homo sapiens	29-33
35453467-14	2022	The binding activity between Nrf2 and HO-1 promoter was attenuated by APO, NAC, Srci II, PF431396, or Go6983.	Acetylcysteine	75-78	heme oxygenase 1	Mus musculus	38-42
35453441-11	2022	NAC effectively prevented neuronal death and GPx1 downregulation in CA1 neurons, and restored GPx1 expression to the control level in CA1 astrocytes.	Acetylcysteine	0-3	glutathione peroxidase 1	Rattus norvegicus	45-49
35453441-11	2022	NAC effectively prevented neuronal death and GPx1 downregulation in CA1 neurons, and restored GPx1 expression to the control level in CA1 astrocytes.	Acetylcysteine	0-3	glutathione peroxidase 1	Rattus norvegicus	94-98
35453441-13	2022	In contrast, NAC restored GPx1 expression in clasmatodendritic astrocytes and ameliorated this autophagic astroglial death.	Acetylcysteine	13-16	glutathione peroxidase 1	Rattus norvegicus	26-30
35582415-8	2022	NAC inhibited ROS production, decreased cell apoptosis by decreasing the Bax/Bcl-2 ratio and caspase-3 expression in HK-2 cells and regulated oxidative stress indicators in the kidney by decreasing GSH, SOD and CAT activity and increasing MDA levels.	Acetylcysteine	0-3	BCL2, apoptosis regulator	Rattus norvegicus	77-82
35582415-8	2022	NAC inhibited ROS production, decreased cell apoptosis by decreasing the Bax/Bcl-2 ratio and caspase-3 expression in HK-2 cells and regulated oxidative stress indicators in the kidney by decreasing GSH, SOD and CAT activity and increasing MDA levels.	Acetylcysteine	0-3	catalase	Rattus norvegicus	211-214
35419302-10	2022	Notably, FGF2 stimulation produced reactive oxygen species (ROS) accumulation in MDA-MB-231 cells, and FGF2-induced nuclear accumulation of FGFR1 was abrogated by the ROS scavenging agent, N-acetylcysteine.	Acetylcysteine	189-205	fibroblast growth factor 2	Homo sapiens	9-13
35419302-10	2022	Notably, FGF2 stimulation produced reactive oxygen species (ROS) accumulation in MDA-MB-231 cells, and FGF2-induced nuclear accumulation of FGFR1 was abrogated by the ROS scavenging agent, N-acetylcysteine.	Acetylcysteine	189-205	fibroblast growth factor 2	Homo sapiens	103-107
35419302-10	2022	Notably, FGF2 stimulation produced reactive oxygen species (ROS) accumulation in MDA-MB-231 cells, and FGF2-induced nuclear accumulation of FGFR1 was abrogated by the ROS scavenging agent, N-acetylcysteine.	Acetylcysteine	189-205	fibroblast growth factor receptor 1	Homo sapiens	140-145
35383148-7	2022	Antioxidant N-acetylcysteine (NAC) or Cyclosporine A (mPTP inhibitor) blocked the mPTP opening, which significantly attenuated mitochondrial dysfunction and apoptosis induced by glucose oxidative stress.	Acetylcysteine	12-28	protein tyrosine phosphatase, receptor type, U	Mus musculus	82-86
35383148-7	2022	Antioxidant N-acetylcysteine (NAC) or Cyclosporine A (mPTP inhibitor) blocked the mPTP opening, which significantly attenuated mitochondrial dysfunction and apoptosis induced by glucose oxidative stress.	Acetylcysteine	30-33	protein tyrosine phosphatase, receptor type, U	Mus musculus	82-86
35571453-11	2022	BBR-induced, dose-dependent induction of apoptosis was accompanied by sustained phosphorylation of c-jun-NH2-kinase (JNK) and the JNK inhibitor (SP600125) significantly suppressed BBR-induced apoptosis, N-acetyl cysteine (NAC), a ROS scavenger, was sufficient to both suppress apoptosis signal-regulating kinase 1 (ASK1) and JNK activation and disrupt apoptotic induction.	Acetylcysteine	203-220	mitogen-activated protein kinase 8	Homo sapiens	99-115
35571453-11	2022	BBR-induced, dose-dependent induction of apoptosis was accompanied by sustained phosphorylation of c-jun-NH2-kinase (JNK) and the JNK inhibitor (SP600125) significantly suppressed BBR-induced apoptosis, N-acetyl cysteine (NAC), a ROS scavenger, was sufficient to both suppress apoptosis signal-regulating kinase 1 (ASK1) and JNK activation and disrupt apoptotic induction.	Acetylcysteine	203-220	mitogen-activated protein kinase 8	Homo sapiens	117-120
35571453-11	2022	BBR-induced, dose-dependent induction of apoptosis was accompanied by sustained phosphorylation of c-jun-NH2-kinase (JNK) and the JNK inhibitor (SP600125) significantly suppressed BBR-induced apoptosis, N-acetyl cysteine (NAC), a ROS scavenger, was sufficient to both suppress apoptosis signal-regulating kinase 1 (ASK1) and JNK activation and disrupt apoptotic induction.	Acetylcysteine	203-220	mitogen-activated protein kinase 8	Homo sapiens	130-133
35571453-11	2022	BBR-induced, dose-dependent induction of apoptosis was accompanied by sustained phosphorylation of c-jun-NH2-kinase (JNK) and the JNK inhibitor (SP600125) significantly suppressed BBR-induced apoptosis, N-acetyl cysteine (NAC), a ROS scavenger, was sufficient to both suppress apoptosis signal-regulating kinase 1 (ASK1) and JNK activation and disrupt apoptotic induction.	Acetylcysteine	222-225	mitogen-activated protein kinase 8	Homo sapiens	99-115
35571453-11	2022	BBR-induced, dose-dependent induction of apoptosis was accompanied by sustained phosphorylation of c-jun-NH2-kinase (JNK) and the JNK inhibitor (SP600125) significantly suppressed BBR-induced apoptosis, N-acetyl cysteine (NAC), a ROS scavenger, was sufficient to both suppress apoptosis signal-regulating kinase 1 (ASK1) and JNK activation and disrupt apoptotic induction.	Acetylcysteine	222-225	mitogen-activated protein kinase 8	Homo sapiens	117-120
35571453-11	2022	BBR-induced, dose-dependent induction of apoptosis was accompanied by sustained phosphorylation of c-jun-NH2-kinase (JNK) and the JNK inhibitor (SP600125) significantly suppressed BBR-induced apoptosis, N-acetyl cysteine (NAC), a ROS scavenger, was sufficient to both suppress apoptosis signal-regulating kinase 1 (ASK1) and JNK activation and disrupt apoptotic induction.	Acetylcysteine	222-225	mitogen-activated protein kinase 8	Homo sapiens	130-133
34982346-9	2022	ET-1 mediated mRNA expression of GAG synthesizing enzymes C4ST-1 and ChSy-1 was also blocked by TGBFR1 antagonists, SB431542, broad spectrum ET receptor antagonist bosentan, DPI and ROS scavenger N-acetyl-L-cysteine.	Acetylcysteine	196-215	endothelin 1	Homo sapiens	0-4
34982346-9	2022	ET-1 mediated mRNA expression of GAG synthesizing enzymes C4ST-1 and ChSy-1 was also blocked by TGBFR1 antagonists, SB431542, broad spectrum ET receptor antagonist bosentan, DPI and ROS scavenger N-acetyl-L-cysteine.	Acetylcysteine	196-215	chondroitin sulfate synthase 1	Homo sapiens	69-75
35394351-6	2022	However, ROS scavenger N-acetylcysteine (NAC) attenuated the above effects and restored the effects of GO on protein expressions related to apoptosis, autophagy and AMPK/mTOR/ULK1 signal pathways.	Acetylcysteine	23-39	mechanistic target of rapamycin kinase	Homo sapiens	170-174
35394351-6	2022	However, ROS scavenger N-acetylcysteine (NAC) attenuated the above effects and restored the effects of GO on protein expressions related to apoptosis, autophagy and AMPK/mTOR/ULK1 signal pathways.	Acetylcysteine	41-44	mechanistic target of rapamycin kinase	Homo sapiens	170-174
35065218-6	2022	Pre-treatment with NAC was efficient to prevent cell damage at lower Cl2 concentrations in part by averting the formation of apoptotic-like bodies and increasing the expression of the anti-apoptotic proteins clusterin and phosphorylated tumour protein p53(S46).	Acetylcysteine	19-22	tumor protein p53	Homo sapiens	252-255
35293662-8	2022	Inhibition of ROS using N-acetyl-l-cysteine (NAC) inhibited chromium-induced activation of ATF6 and upregulation of PLK4.	Acetylcysteine	45-48	polo like kinase 4	Homo sapiens	116-120
35065167-9	2022	Further studies revealed that beneficial effects of NAC is through targeting the mitochondrial autophagy via regulating the GSK-3beta/Drp1mediated mitochondrial fission and inhibiting the expression of beclin-1 and conversion of LC3, as well as activating the p-Akt pro-survival pathway.	Acetylcysteine	52-55	AKT serine/threonine kinase 1	Rattus norvegicus	262-265
35156537-9	2022	Meanwhile, RPN2 upregulation increased the levels of p-PI3K/PI3K and p-Akt/Akt, which were attenuated by N-acetyl-L-cysteine (NAC), an ROS inhibitor.	Acetylcysteine	105-124	AKT serine/threonine kinase 1	Homo sapiens	71-74
35088107-10	2022	Additionally, the antioxidant N-acetyl-L-cysteine (NAC) pretreatment promoted the activation of antioxidative defense Nrf2/PPARgamma signaling pathways, and prevented the production of cellular ROS, thus protecting the DNA from cleavage.	Acetylcysteine	30-49	NFE2 like bZIP transcription factor 2	Homo sapiens	118-122
35088107-10	2022	Additionally, the antioxidant N-acetyl-L-cysteine (NAC) pretreatment promoted the activation of antioxidative defense Nrf2/PPARgamma signaling pathways, and prevented the production of cellular ROS, thus protecting the DNA from cleavage.	Acetylcysteine	30-49	peroxisome proliferator activated receptor gamma	Homo sapiens	123-132
35088107-10	2022	Additionally, the antioxidant N-acetyl-L-cysteine (NAC) pretreatment promoted the activation of antioxidative defense Nrf2/PPARgamma signaling pathways, and prevented the production of cellular ROS, thus protecting the DNA from cleavage.	Acetylcysteine	51-54	NFE2 like bZIP transcription factor 2	Homo sapiens	118-122
35088107-10	2022	Additionally, the antioxidant N-acetyl-L-cysteine (NAC) pretreatment promoted the activation of antioxidative defense Nrf2/PPARgamma signaling pathways, and prevented the production of cellular ROS, thus protecting the DNA from cleavage.	Acetylcysteine	51-54	peroxisome proliferator activated receptor gamma	Homo sapiens	123-132
35236897-9	2022	NRDC may be also involved in ROS-mediated in vivo thermogenesis because the inhibitory effects of N-acetyl cysteine, an ROS scavenger, on beta3 agonist-induced thermogenesis were stronger in Adipo-KO mice.	Acetylcysteine	98-115	cholinergic receptor, nicotinic, alpha polypeptide 3	Mus musculus	138-143
35434015-5	2022	NLRP3 inflammasome activation was Reactive oxygen species (ROS) dependent, and the protein level was regulated when N-acetylcysteine (NAC) and adenosine triphosphate (ATP) were selected as tools for regulating ROS.	Acetylcysteine	116-132	NLR family pyrin domain containing 3	Homo sapiens	0-5
35434015-5	2022	NLRP3 inflammasome activation was Reactive oxygen species (ROS) dependent, and the protein level was regulated when N-acetylcysteine (NAC) and adenosine triphosphate (ATP) were selected as tools for regulating ROS.	Acetylcysteine	134-137	NLR family pyrin domain containing 3	Homo sapiens	0-5
35434015-7	2022	NLRP3 inflammasome activation was sensitive to both ATP-mediated ROS level increases and NAC-mediated ROS inhibition, suggesting that ROS is associated with the activation of NLRP3 inflammasome in necroptosis.	Acetylcysteine	89-92	NLR family pyrin domain containing 3	Homo sapiens	0-5
35434015-7	2022	NLRP3 inflammasome activation was sensitive to both ATP-mediated ROS level increases and NAC-mediated ROS inhibition, suggesting that ROS is associated with the activation of NLRP3 inflammasome in necroptosis.	Acetylcysteine	89-92	NLR family pyrin domain containing 3	Homo sapiens	175-180
35156537-9	2022	Meanwhile, RPN2 upregulation increased the levels of p-PI3K/PI3K and p-Akt/Akt, which were attenuated by N-acetyl-L-cysteine (NAC), an ROS inhibitor.	Acetylcysteine	105-124	AKT serine/threonine kinase 1	Homo sapiens	75-78
35156537-9	2022	Meanwhile, RPN2 upregulation increased the levels of p-PI3K/PI3K and p-Akt/Akt, which were attenuated by N-acetyl-L-cysteine (NAC), an ROS inhibitor.	Acetylcysteine	126-129	AKT serine/threonine kinase 1	Homo sapiens	71-74
35156537-9	2022	Meanwhile, RPN2 upregulation increased the levels of p-PI3K/PI3K and p-Akt/Akt, which were attenuated by N-acetyl-L-cysteine (NAC), an ROS inhibitor.	Acetylcysteine	126-129	AKT serine/threonine kinase 1	Homo sapiens	75-78
35008006-6	2022	Suppressing ROS with N-acetylcysteine (NAC) or interfering with NOX2 by small interfering RNA weakened the promoting effect of CTRP9 on the NLRP3 inflammasome.	Acetylcysteine	39-42	C1q and tumor necrosis factor related protein 9	Mus musculus	127-132
35217818-11	2022	In vitro, N-acetylcysteine (NAC) inhibited NLRP3 inflammasome activation and NLRP3 knockdown reduced GSDMD expression, in MOVAS cells treated with TNF-alpha.	Acetylcysteine	10-26	tumor necrosis factor	Mus musculus	147-156
35023144-9	2022	After HSP70 stimulation, the expression of ROS, NLRP3, Caspase-1, and interleukin-18 (IL-18) increased significantly and could be reduced by ROS inhibitor NAC.	Acetylcysteine	155-158	NLR family pyrin domain containing 3	Homo sapiens	48-53
35023144-9	2022	After HSP70 stimulation, the expression of ROS, NLRP3, Caspase-1, and interleukin-18 (IL-18) increased significantly and could be reduced by ROS inhibitor NAC.	Acetylcysteine	155-158	caspase 1	Homo sapiens	55-64
35023144-11	2022	In beagle models that received TmLRP, HSP70, NLRP3, Caspase-1, IL-1beta, and IL-18 were highly expressed in the wound tissue or urine, and could also be reduced by NAC pretreatment.	Acetylcysteine	164-167	NLR family pyrin domain containing 3	Homo sapiens	45-50
35023144-11	2022	In beagle models that received TmLRP, HSP70, NLRP3, Caspase-1, IL-1beta, and IL-18 were highly expressed in the wound tissue or urine, and could also be reduced by NAC pretreatment.	Acetylcysteine	164-167	caspase 1	Homo sapiens	52-61
35280167-7	2022	Furthermore, NAC normalized the altered GSH levels displayed by these animals in the hippocampus and nucleus accumbens, and it partially rescued the altered expression of post-synaptic terminal network genes found in VPA-exposed rats, such as NR2a, MGLUR5, GLUR1, and GLUR2 in nucleus accumbens, and CAMK2, NR1, and GLUR2 in cerebellum.	Acetylcysteine	13-16	glutamate ionotropic receptor NMDA type subunit 2A	Rattus norvegicus	243-247
35217818-11	2022	In vitro, N-acetylcysteine (NAC) inhibited NLRP3 inflammasome activation and NLRP3 knockdown reduced GSDMD expression, in MOVAS cells treated with TNF-alpha.	Acetylcysteine	28-31	tumor necrosis factor	Mus musculus	147-156
35280167-7	2022	Furthermore, NAC normalized the altered GSH levels displayed by these animals in the hippocampus and nucleus accumbens, and it partially rescued the altered expression of post-synaptic terminal network genes found in VPA-exposed rats, such as NR2a, MGLUR5, GLUR1, and GLUR2 in nucleus accumbens, and CAMK2, NR1, and GLUR2 in cerebellum.	Acetylcysteine	13-16	glutamate ionotropic receptor AMPA type subunit 1	Rattus norvegicus	257-262
35280167-7	2022	Furthermore, NAC normalized the altered GSH levels displayed by these animals in the hippocampus and nucleus accumbens, and it partially rescued the altered expression of post-synaptic terminal network genes found in VPA-exposed rats, such as NR2a, MGLUR5, GLUR1, and GLUR2 in nucleus accumbens, and CAMK2, NR1, and GLUR2 in cerebellum.	Acetylcysteine	13-16	glutamate ionotropic receptor AMPA type subunit 2	Rattus norvegicus	268-273
35280167-7	2022	Furthermore, NAC normalized the altered GSH levels displayed by these animals in the hippocampus and nucleus accumbens, and it partially rescued the altered expression of post-synaptic terminal network genes found in VPA-exposed rats, such as NR2a, MGLUR5, GLUR1, and GLUR2 in nucleus accumbens, and CAMK2, NR1, and GLUR2 in cerebellum.	Acetylcysteine	13-16	glutamate ionotropic receptor AMPA type subunit 2	Rattus norvegicus	316-321
35085590-13	2022	Crocin promoted apoptosis and increased caspase-3 activity and LDH release, which were reversed by ROS scavenger N-acetyl-L-cysteine (NAC), miR-34a overexpression, and PTPN4 silencing.	Acetylcysteine	113-132	caspase 3	Homo sapiens	40-49
35085590-13	2022	Crocin promoted apoptosis and increased caspase-3 activity and LDH release, which were reversed by ROS scavenger N-acetyl-L-cysteine (NAC), miR-34a overexpression, and PTPN4 silencing.	Acetylcysteine	134-137	caspase 3	Homo sapiens	40-49
35140209-6	2022	Cartilage-specific Sephs1 knockout in adult mice causes aging-associated OA, and augments post-traumatic OA, which is rescued by supplementation of N-acetylcysteine (NAC).	Acetylcysteine	148-164	selenophosphate synthetase 1	Mus musculus	19-25
35215995-9	2022	The ROS scavenger N-acetyl-l-cysteine (NAC) and the p53 specific inhibitor Pifithrin-alpha (PFT-alpha) suppressed PEDV-induced apoptosis and impeded viral replication, suggesting that ROS and p53 play an important role in PEDV-induced apoptosis and viral replication.	Acetylcysteine	39-42	tumor protein p53	Homo sapiens	192-195
35140209-6	2022	Cartilage-specific Sephs1 knockout in adult mice causes aging-associated OA, and augments post-traumatic OA, which is rescued by supplementation of N-acetylcysteine (NAC).	Acetylcysteine	166-169	selenophosphate synthetase 1	Mus musculus	19-25
35086548-10	2022	Co-culture of macrophages pre-treated with NAC-derived tumor exosomes or exosomal miR-155-5p with T-lymphocytes leading to an increased percentage of CD8+ T-lymphocyte and a decreased CD3+ T cell apoptosis through PD-L1 downregulation.	Acetylcysteine	43-46	CD247 antigen	Mus musculus	184-187
35043378-7	2022	Moreover, the expression of the long noncoding RNA (lncRNA) taurine upregulated gene 1 (TUG1) increased, and NAC and TUG1 siRNA inhibited the expression of TUG1/mammalian target of rapamycin (mTOR) in DRGs treated with BP in a high-glucose environment.	Acetylcysteine	109-112	mechanistic target of rapamycin kinase	Homo sapiens	156-190
35043378-7	2022	Moreover, the expression of the long noncoding RNA (lncRNA) taurine upregulated gene 1 (TUG1) increased, and NAC and TUG1 siRNA inhibited the expression of TUG1/mammalian target of rapamycin (mTOR) in DRGs treated with BP in a high-glucose environment.	Acetylcysteine	109-112	mechanistic target of rapamycin kinase	Homo sapiens	192-196
35187102-8	2021	H2O2 (100 muM) recapitulated the effects of (+-)-SKF 38393 and fenoldopam on APs and a ROS-blocker N-acetylcysteine (NAC, 1 mM) abolished the effects, suggesting that the ROS-signaling is involved in the dopamine D1/D5 receptor actions.	Acetylcysteine	99-115	dopamine receptor D1	Homo sapiens	204-227
35186974-6	2021	Conversely, the HIF-1alpha-mediated protective effect was strengthened by scavenger N-acetylcysteine (NAC), a type of reactive oxygen species.	Acetylcysteine	84-100	hypoxia inducible factor 1 subunit alpha	Homo sapiens	16-26
35186974-6	2021	Conversely, the HIF-1alpha-mediated protective effect was strengthened by scavenger N-acetylcysteine (NAC), a type of reactive oxygen species.	Acetylcysteine	102-105	hypoxia inducible factor 1 subunit alpha	Homo sapiens	16-26
34981453-0	2022	Upregulation of Striatal Metabotropic Glutamate Receptor Subtype 1 (mGluR1) in Rats with Excessive Glutamate Release Induced by N-Acetylcysteine.	Acetylcysteine	128-144	glutamate metabotropic receptor 1	Rattus norvegicus	68-74
34981453-4	2022	Similarly, PET studies with (11C)ITDM, a useful radioligand for mGluR1 imaging exhibited that the striatal binding potential (BPND) of (11C)ITDM for mGluR1 in PET assessments was increased in NAC-treated animals at day 7 after implantation (2.30) compared with before implantation (1.92).	Acetylcysteine	192-195	glutamate metabotropic receptor 1	Rattus norvegicus	64-70
34981453-4	2022	Similarly, PET studies with (11C)ITDM, a useful radioligand for mGluR1 imaging exhibited that the striatal binding potential (BPND) of (11C)ITDM for mGluR1 in PET assessments was increased in NAC-treated animals at day 7 after implantation (2.30) compared with before implantation (1.92).	Acetylcysteine	192-195	glutamate metabotropic receptor 1	Rattus norvegicus	149-155
35086548-10	2022	Co-culture of macrophages pre-treated with NAC-derived tumor exosomes or exosomal miR-155-5p with T-lymphocytes leading to an increased percentage of CD8+ T-lymphocyte and a decreased CD3+ T cell apoptosis through PD-L1 downregulation.	Acetylcysteine	43-46	CD274 antigen	Mus musculus	214-219
35083332-11	2022	More importantly, N-acetylcysteine induced reduction of ROS in HPDLCs, downregulated TXNIP expression, inhibited the expression and aggregation of NLRP3 inflammasome-related factors, and abrogated the inflammatory response to hypoxia.	Acetylcysteine	18-34	NLR family, pyrin domain containing 3	Rattus norvegicus	147-152
35052658-0	2022	GlyNAC (Glycine and N-Acetylcysteine) Supplementation Improves Impaired Mitochondrial Fuel Oxidation and Lowers Insulin Resistance in Patients with Type 2 Diabetes: Results of a Pilot Study.	Acetylcysteine	20-36	insulin	Homo sapiens	112-119
32291602-8	2021	Further in vitro studies show that CD21 (20 muM) strongly enhanced the Msr1 mRNA and MSR1 protein levers in RAW264.7 cells and PRX1 internalization in cellular lysosomes, which were significantly reversed by N-acetylcysteine treatment.	Acetylcysteine	208-224	macrophage scavenger receptor 1	Mus musculus	71-75
35296207-7	2022	I/R-induced upregulation of STAT3 phosphorylation and ZIP2 expression was reversed by the ROS scavenger N-acetylcysteine (NAC) and the NOX inhibitor diphenyleneiodonium (DPI).	Acetylcysteine	104-120	signal transducer and activator of transcription 3	Mus musculus	28-33
35296207-7	2022	I/R-induced upregulation of STAT3 phosphorylation and ZIP2 expression was reversed by the ROS scavenger N-acetylcysteine (NAC) and the NOX inhibitor diphenyleneiodonium (DPI).	Acetylcysteine	122-125	signal transducer and activator of transcription 3	Mus musculus	28-33
35296207-9	2022	Both NAC and DPI prevented upregulation of STAT3 phosphorylation and ZIP2 expression induced by overexpression of p67phox, whereas the STAT3 inhibitor stattic abrogated upregulation ZIP2 expression, indicating that the increase of p67phox at reperfusion is an upstream signaling event responsible for ZIP2 upregulation via STAT3.	Acetylcysteine	5-8	signal transducer and activator of transcription 3	Mus musculus	43-48
35296207-9	2022	Both NAC and DPI prevented upregulation of STAT3 phosphorylation and ZIP2 expression induced by overexpression of p67phox, whereas the STAT3 inhibitor stattic abrogated upregulation ZIP2 expression, indicating that the increase of p67phox at reperfusion is an upstream signaling event responsible for ZIP2 upregulation via STAT3.	Acetylcysteine	5-8	signal transducer and activator of transcription 3	Mus musculus	323-328
3518737-3	1986	Following addition of 59.6mM N-acetylcysteine, the amidolytic activity of leukocyte elastase was decreased by 55.3% and that of porcine pancreatic elastase by 57.0%.	Acetylcysteine	29-45	elastase, neutrophil expressed	Homo sapiens	74-92
6580492-3	1983	Group I received placebo 1 hour before doxorubicin administration; group II received acetylcysteine (N-acetyl-L-cysteine) (Nac) 1 hour before doxorubicin.	Acetylcysteine	101-120	nucleus accumbens associated 1	Homo sapiens	123-129
33661545-0	2021	Association of heat shock protein A2 expression and sperm quality after N-acetyl-cysteine supplementation in astheno-terato-zoospermic infertile men.	Acetylcysteine	72-89	heat shock protein family A (Hsp70) member 2	Homo sapiens	15-36
33661545-2	2021	The present study has aimed to investigate the effects of N-acetyl-cysteine (NAC) supplementation on expression of heat shock protein A2 (HSPA2).	Acetylcysteine	58-75	heat shock protein family A (Hsp70) member 2	Homo sapiens	115-136
33661545-2	2021	The present study has aimed to investigate the effects of N-acetyl-cysteine (NAC) supplementation on expression of heat shock protein A2 (HSPA2).	Acetylcysteine	58-75	heat shock protein family A (Hsp70) member 2	Homo sapiens	138-143
33661545-2	2021	The present study has aimed to investigate the effects of N-acetyl-cysteine (NAC) supplementation on expression of heat shock protein A2 (HSPA2).	Acetylcysteine	77-80	heat shock protein family A (Hsp70) member 2	Homo sapiens	115-136
33661545-2	2021	The present study has aimed to investigate the effects of N-acetyl-cysteine (NAC) supplementation on expression of heat shock protein A2 (HSPA2).	Acetylcysteine	77-80	heat shock protein family A (Hsp70) member 2	Homo sapiens	138-143
33661545-3	2021	In this study in continuation of previous study, semen samples from 50 astheno-terato-zoospermic men who have received NAC (600 mg/day) orally for three months were evaluated for expression HSPA2 using RT-PCR, and Western blot analysis.	Acetylcysteine	119-122	heat shock protein family A (Hsp70) member 2	Homo sapiens	190-195
33661545-6	2021	In addition to improved sperm parameters and aforementioned functional parameters, the presented results revealed the significant increase in relative expression levels of HSPA2 was obtained after using NAC treatment (p < .05).	Acetylcysteine	203-206	heat shock protein family A (Hsp70) member 2	Homo sapiens	172-177
2597169-6	1989	Inhibition of renal cysteine-S-conjugate beta-lyase by aminooxyacetic acid alleviated the cytotoxicity of both the cysteine-S-conjugates and the mercapturic acids of the four haloethylenes.	Acetylcysteine	145-162	kynurenine aminotransferase 1	Rattus norvegicus	20-51
552659-2	1979	Although many authors agree with the opinion that some of these drugs, above all aerosols of acetylcysteine at convenient dosages, provided they are associated with beta 2-sympathomimetics, may be useful in the treatment of bronchial obstruction due to inspissated mucus in excess in the lumens, many specialists remain reluctant concerning the activity of mucolytics given by mouth.	Acetylcysteine	93-107	potassium calcium-activated channel subfamily M regulatory beta subunit 2	Homo sapiens	165-171
33404763-9	2021	RESULTS: Five-millimolar NAC promoted the highest LPS-treated APC proliferation.	Acetylcysteine	25-28	APC regulator of WNT signaling pathway	Homo sapiens	62-65
33404763-12	2021	Ten-minute NAC treatment downregulated the IL-6 and TNF-alpha expression, whereas the expression of Bcl-2/Bax and Mfn-2/Drp-1 ratios was upregulated at 6 h. CONCLUSIONS: Under the LPS-induced inflammatory condition, NAC stimulated APC survival and decreased inflammation.	Acetylcysteine	11-14	APC regulator of WNT signaling pathway	Homo sapiens	231-234
34006821-8	2021	Elimination of oxidative stress by Acetylcysteine, also called N-acetyl cysteine (NAC), downregulated autophagy and alleviated HG-stimulated apoptosis and senescence, while activation of the AMPK signaling pathway by AICAR not only upregulated autophagy but also alleviated HG-stimulated apoptosis and senescence.	Acetylcysteine	35-49	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	191-195
34006821-8	2021	Elimination of oxidative stress by Acetylcysteine, also called N-acetyl cysteine (NAC), downregulated autophagy and alleviated HG-stimulated apoptosis and senescence, while activation of the AMPK signaling pathway by AICAR not only upregulated autophagy but also alleviated HG-stimulated apoptosis and senescence.	Acetylcysteine	35-49	5-aminoimidazole-4-carboxamide ribonucleotide formyltransferase/IMP cyclohydrolase	Homo sapiens	217-222
34006821-8	2021	Elimination of oxidative stress by Acetylcysteine, also called N-acetyl cysteine (NAC), downregulated autophagy and alleviated HG-stimulated apoptosis and senescence, while activation of the AMPK signaling pathway by AICAR not only upregulated autophagy but also alleviated HG-stimulated apoptosis and senescence.	Acetylcysteine	63-80	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	191-195
34006821-8	2021	Elimination of oxidative stress by Acetylcysteine, also called N-acetyl cysteine (NAC), downregulated autophagy and alleviated HG-stimulated apoptosis and senescence, while activation of the AMPK signaling pathway by AICAR not only upregulated autophagy but also alleviated HG-stimulated apoptosis and senescence.	Acetylcysteine	63-80	5-aminoimidazole-4-carboxamide ribonucleotide formyltransferase/IMP cyclohydrolase	Homo sapiens	217-222
34006821-8	2021	Elimination of oxidative stress by Acetylcysteine, also called N-acetyl cysteine (NAC), downregulated autophagy and alleviated HG-stimulated apoptosis and senescence, while activation of the AMPK signaling pathway by AICAR not only upregulated autophagy but also alleviated HG-stimulated apoptosis and senescence.	Acetylcysteine	82-85	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	191-195
34006821-8	2021	Elimination of oxidative stress by Acetylcysteine, also called N-acetyl cysteine (NAC), downregulated autophagy and alleviated HG-stimulated apoptosis and senescence, while activation of the AMPK signaling pathway by AICAR not only upregulated autophagy but also alleviated HG-stimulated apoptosis and senescence.	Acetylcysteine	82-85	5-aminoimidazole-4-carboxamide ribonucleotide formyltransferase/IMP cyclohydrolase	Homo sapiens	217-222
33661545-8	2021	NAC may directly or indecently impose its beneficial effect through increased expression of HSPA2, which plays a potential role in proper folding of element needed to counteract stress condition in infertile individuals.	Acetylcysteine	0-3	heat shock protein family A (Hsp70) member 2	Homo sapiens	92-97
32291602-8	2021	Further in vitro studies show that CD21 (20 muM) strongly enhanced the Msr1 mRNA and MSR1 protein levers in RAW264.7 cells and PRX1 internalization in cellular lysosomes, which were significantly reversed by N-acetylcysteine treatment.	Acetylcysteine	208-224	macrophage scavenger receptor 1	Mus musculus	85-89
33991932-6	2021	Also, N-acetyl cysteine (NAC, effective antioxidant and free radical scavenger) pretreatment inhibited the production of intracellular ROS, significantly suppressed Cr (VI)-induced oxidative stress, lipid accumulation, decreased G6P and GLUT2, and improved impaired glucose tolerance and glucose and insulin intolerance caused by Cr (VI) in mice.	Acetylcysteine	6-23	solute carrier family 2 (facilitated glucose transporter), member 2	Mus musculus	237-242
33247942-13	2021	In all NAC treatment groups, levels of serum IL-6, neuronal apoptosis and brain NFkB, nNOS, Caspase 3, TNF-alpha, IL-6 and IL-1beta protein levels were significantly reduced compared to NEC group.	Acetylcysteine	7-10	caspase 3	Rattus norvegicus	92-101
33247942-14	2021	The most pronounced decrease was demonstrated within the NAC-NEC-NAC group CONCLUSIONS: NAC treatment can attenuate newborn inflammatory response syndrome and decrease offspring brain neuro apoptosis and inflammation in a rat model of NEC by inhibition of NFkB, nNOS and Caspase 3 pathways.	Acetylcysteine	57-60	caspase 3	Rattus norvegicus	271-280
33946939-6	2021	The benefit of NAC was related to the modulation of signaling proteins in the AMPK-SIRT3-SOD2 axis.	Acetylcysteine	15-18	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	78-82
33946939-6	2021	The benefit of NAC was related to the modulation of signaling proteins in the AMPK-SIRT3-SOD2 axis.	Acetylcysteine	15-18	superoxide dismutase 2	Homo sapiens	89-93
33640978-5	2021	Synergistic rescue occurred only with glucose, nicotinic acid, and N-acetylcysteine (Glu + NA + NAC), yielding improved mitochondrial membrane potential that reflects integrated respiratory chain function, without exacerbating oxidative stress and while reducing mitochondrial stress (UPRmt) and improving intermediary metabolic disruptions at the levels of the transcriptome, steady-state metabolites, and intermediary metabolic flux.	Acetylcysteine	67-83	melanocyte inducing transcription factor a	Danio rerio	96-99
34004559-6	2021	N-acetyl-L-cysteine (NAC) counteracted the effects of RCN2 on pyroptosis (all p < 0.01).	Acetylcysteine	0-19	reticulocalbin 2	Homo sapiens	54-58
34004559-6	2021	N-acetyl-L-cysteine (NAC) counteracted the effects of RCN2 on pyroptosis (all p < 0.01).	Acetylcysteine	21-24	reticulocalbin 2	Homo sapiens	54-58
33991932-6	2021	Also, N-acetyl cysteine (NAC, effective antioxidant and free radical scavenger) pretreatment inhibited the production of intracellular ROS, significantly suppressed Cr (VI)-induced oxidative stress, lipid accumulation, decreased G6P and GLUT2, and improved impaired glucose tolerance and glucose and insulin intolerance caused by Cr (VI) in mice.	Acetylcysteine	25-28	solute carrier family 2 (facilitated glucose transporter), member 2	Mus musculus	237-242
34016350-6	2021	In addition, NAC attenuated the activity of the Nf-kappaB pathway activated by heat stress and decreased the expression of the proinflammatory cytokines IL-6, IL-18, TNF-alpha, IKK, and IFN-gamma.	Acetylcysteine	13-16	lipopolysaccharide induced TNF factor	Gallus gallus	166-175
33945789-0	2021	Perineuronal net abnormalities in Slc13a4+/- mice are rescued by postnatal administration of N-acetylcysteine.	Acetylcysteine	93-109	solute carrier family 13 (sodium/sulfate symporters), member 4	Mus musculus	34-41
33945789-7	2021	Finally, we reveal that postnatal administration of N-acetylcysteine prevented PNN abnormalities from manifesting in Slc13a4+/- adult animals.	Acetylcysteine	52-68	solute carrier family 13 (sodium/sulfate symporters), member 4	Mus musculus	117-124
33919218-7	2021	Treating C2C12 cells with antioxidant N-acetylcysteine also promoted osteoblast differentiation, and upregulated Runx2/Osterix/Dlx5, while ROS generator antimycin A treatment performed the opposite.	Acetylcysteine	38-54	distal-less homeobox 5	Mus musculus	127-131
34016350-7	2021	In addition, NAC treatment regulated the expression of HO-1, GSH, SOD2 and PRDX3 by regulating the activity of Nrf2 at different time points to resist oxidative stress caused by heat exposure.	Acetylcysteine	13-16	heme oxygenase 1	Gallus gallus	55-59
33930758-6	2021	Interestingly, CQ-induced DSBs and cell death caused by CQ/LBH combination were largely abolished by the ROS scavenger N-Acetylcysteine, revealing the critical role of DSB generation in CQ/LBH-induced lethality.	Acetylcysteine	119-135	LBH regulator of WNT signaling pathway	Homo sapiens	189-192
33930758-6	2021	Interestingly, CQ-induced DSBs and cell death caused by CQ/LBH combination were largely abolished by the ROS scavenger N-Acetylcysteine, revealing the critical role of DSB generation in CQ/LBH-induced lethality.	Acetylcysteine	119-135	LBH regulator of WNT signaling pathway	Homo sapiens	59-62
33882750-8	2021	Treated rats with N-acetylcysteine (N-AC) and granulocyte colony stimulating factor (G-CSF) showed a decrease in serum levels of ALT, AST and LDH, while the level of ALP in the G-CSF group was still high.	Acetylcysteine	18-34	colony stimulating factor 3	Rattus norvegicus	177-182
33882750-8	2021	Treated rats with N-acetylcysteine (N-AC) and granulocyte colony stimulating factor (G-CSF) showed a decrease in serum levels of ALT, AST and LDH, while the level of ALP in the G-CSF group was still high.	Acetylcysteine	36-40	colony stimulating factor 3	Rattus norvegicus	177-182
33592258-12	2021	N-acetylcysteine (NAC) reduced the level of phosphorylated p38-MAPK and the production of intracellular ROS and inhibited apoptosis.	Acetylcysteine	0-16	mitogen activated protein kinase 14	Rattus norvegicus	59-67
33592258-12	2021	N-acetylcysteine (NAC) reduced the level of phosphorylated p38-MAPK and the production of intracellular ROS and inhibited apoptosis.	Acetylcysteine	18-21	mitogen activated protein kinase 14	Rattus norvegicus	59-67
33632046-8	2021	The antioxidant N-acetyl cysteine (NAC) also showed similar effects on JNK and NF-kappaB-P65 phosphorylation and inflammatory cytokines (p < .00).	Acetylcysteine	16-33	RELA proto-oncogene, NF-kB subunit	Homo sapiens	79-92
33921050-9	2021	NAC treatment upregulated ATG-5 (p < 0.0001), beclin-1 (p < 0.0001) and LC3-I to LC3-II (p < 0.0001) conversion, which was inhibited in the DA treatment group.	Acetylcysteine	0-3	autophagy related 5	Mus musculus	26-31
33632046-8	2021	The antioxidant N-acetyl cysteine (NAC) also showed similar effects on JNK and NF-kappaB-P65 phosphorylation and inflammatory cytokines (p < .00).	Acetylcysteine	35-38	RELA proto-oncogene, NF-kB subunit	Homo sapiens	79-92
33758187-0	2021	NAC blocks Cystatin C amyloid complex aggregation in a cell system and in skin of HCCAA patients.	Acetylcysteine	0-3	cystatin C	Homo sapiens	11-21
33545736-10	2021	N-Acetyl cysteine (NAC), a ROS scavenger, markedly abolished H2O2-stimulated PI3K/Akt/GSK3beta signaling, caspase-3 activation, and phosphatidylserine exposure.	Acetylcysteine	0-17	glycogen synthase kinase 3 alpha	Homo sapiens	86-94
33545736-10	2021	N-Acetyl cysteine (NAC), a ROS scavenger, markedly abolished H2O2-stimulated PI3K/Akt/GSK3beta signaling, caspase-3 activation, and phosphatidylserine exposure.	Acetylcysteine	19-22	glycogen synthase kinase 3 alpha	Homo sapiens	86-94
33486763-6	2021	Treatment of patients with high dose N-acetylcysteine (NAC) plus glyceryl trinitrate rapidly increased platelet responsiveness to SNP and decreased plasma syndecan-1 concentrations.	Acetylcysteine	37-53	syndecan 1	Homo sapiens	155-165
33139125-5	2021	Herein, we report the therapeutic effects of dietary therapy, cysteamine, and NAC in two siblings with ECHS1D, including their clinical, neuroradiological, and chemical aspects.	Acetylcysteine	78-81	enoyl-CoA hydratase, short chain 1	Homo sapiens	103-109
33574492-5	2021	However, with N-acetylcysteine treatment, the level of oxidative stress was decreased, accompanied by significant increases in antioxidant enzyme activities and the mRNA levels of SOD, CAT, GSTCD, and GSTO1.	Acetylcysteine	14-30	catalase	Pelodiscus sinensis	185-188
33574492-5	2021	However, with N-acetylcysteine treatment, the level of oxidative stress was decreased, accompanied by significant increases in antioxidant enzyme activities and the mRNA levels of SOD, CAT, GSTCD, and GSTO1.	Acetylcysteine	14-30	glutathione S-transferase C-terminal domain-containing protein	Pelodiscus sinensis	190-195
33563887-10	2021	When DUOX1-overexpressing cells were treated with the ROS inhibitor N-acetyl-L-cysteine (NAC), the protein levels that were increased by DUOX1 overexpression were reversed.	Acetylcysteine	68-87	dual oxidase 1	Homo sapiens	5-10
33563887-10	2021	When DUOX1-overexpressing cells were treated with the ROS inhibitor N-acetyl-L-cysteine (NAC), the protein levels that were increased by DUOX1 overexpression were reversed.	Acetylcysteine	68-87	dual oxidase 1	Homo sapiens	137-142
33563887-10	2021	When DUOX1-overexpressing cells were treated with the ROS inhibitor N-acetyl-L-cysteine (NAC), the protein levels that were increased by DUOX1 overexpression were reversed.	Acetylcysteine	89-92	dual oxidase 1	Homo sapiens	5-10
33563887-10	2021	When DUOX1-overexpressing cells were treated with the ROS inhibitor N-acetyl-L-cysteine (NAC), the protein levels that were increased by DUOX1 overexpression were reversed.	Acetylcysteine	89-92	dual oxidase 1	Homo sapiens	137-142
33504419-12	2021	While ROS scavenger N-acetyl-L-cysteine (NAC) inhibited the silica-induced release of ROS, and then inhibited the expression of ABC protein and Wnt/beta-catenin signal activity.	Acetylcysteine	20-39	Wnt family member 3A	Homo sapiens	144-147
33504419-12	2021	While ROS scavenger N-acetyl-L-cysteine (NAC) inhibited the silica-induced release of ROS, and then inhibited the expression of ABC protein and Wnt/beta-catenin signal activity.	Acetylcysteine	41-44	Wnt family member 3A	Homo sapiens	144-147
33486763-6	2021	Treatment of patients with high dose N-acetylcysteine (NAC) plus glyceryl trinitrate rapidly increased platelet responsiveness to SNP and decreased plasma syndecan-1 concentrations.	Acetylcysteine	55-58	syndecan 1	Homo sapiens	155-165
33574693-13	2021	Moreover, IRD targeted pyruvate kinase isozyme type M2 (PKM2) and suppressed its downstream p-JAK1, p-STAT1, p-STAT3, p-p65, iNOS, and COX2, which could be abolished by PKM2 agonist DASA-58 and antioxidant N-acetyl-L-cysteine, but partly be reversed by NF-kappaB activator CUT129 and JAK1 activator RO8191.	Acetylcysteine	206-225	pyruvate kinase, muscle	Mus musculus	23-54
32515291-5	2021	Following the combined treatment with piperlongumine and 10 mM N-acetyl-L-cysteine (NAC), intracellular ROS and cell viability returned to normal levels, and the expression of LC3B-II decreased to the predose level.	Acetylcysteine	63-82	microtubule associated protein 1 light chain 3 beta	Homo sapiens	176-180
33574693-13	2021	Moreover, IRD targeted pyruvate kinase isozyme type M2 (PKM2) and suppressed its downstream p-JAK1, p-STAT1, p-STAT3, p-p65, iNOS, and COX2, which could be abolished by PKM2 agonist DASA-58 and antioxidant N-acetyl-L-cysteine, but partly be reversed by NF-kappaB activator CUT129 and JAK1 activator RO8191.	Acetylcysteine	206-225	pyruvate kinase, muscle	Mus musculus	56-60
33613826-8	2021	Additionally, dosing with N-acetylcysteine (NAC) effectively mitigated bone loss and normalized expression of ALP, Runx2, and OPN.	Acetylcysteine	26-42	secreted phosphoprotein 1	Mus musculus	126-129
32515291-5	2021	Following the combined treatment with piperlongumine and 10 mM N-acetyl-L-cysteine (NAC), intracellular ROS and cell viability returned to normal levels, and the expression of LC3B-II decreased to the predose level.	Acetylcysteine	84-87	microtubule associated protein 1 light chain 3 beta	Homo sapiens	176-180
33613826-8	2021	Additionally, dosing with N-acetylcysteine (NAC) effectively mitigated bone loss and normalized expression of ALP, Runx2, and OPN.	Acetylcysteine	44-47	secreted phosphoprotein 1	Mus musculus	126-129
33740178-9	2022	NAC treatments significantly decreased the expression of c-myc, and Ask-1 in rats exposed to single or continuous Cd.	Acetylcysteine	0-3	MYC proto-oncogene, bHLH transcription factor	Rattus norvegicus	57-62
33188856-7	2021	The genes (ApoE/TET1/TIMP2/TIMP3) suppressed by Cd were further suppressed by hydroquinone (HQ; a reactive oxygen species [ROS] producer), whereas N-acetyl-L-cysteine (NAC; a ROS scavenger) prevented the suppression of their expression by HQ.	Acetylcysteine	168-171	TIMP metallopeptidase inhibitor 3	Rattus norvegicus	27-32
33515593-6	2021	This is supported by the evidence that using ROS scavenger N-acetyl cysteine (NAC) significantly alleviated Bort-activated mTORC1 pathway.	Acetylcysteine	59-76	CREB regulated transcription coactivator 1	Mus musculus	123-129
33035499-7	2020	In striatum and cortex, NAC prevented glial cells activation (GFAP and Iba-1), decreased NGF, Bcl-2 and NeuN, the increase of lipid peroxidation and PARP induced by GA in both ages.	Acetylcysteine	24-27	RNA binding protein, fox-1 homolog (C. elegans) 3	Mus musculus	104-108
33615065-0	2021	A Systematic Review of the Effect of N-Acetylcysteine on Serum Creatinine and Cystatin C Measurements.	Acetylcysteine	37-53	cystatin C	Homo sapiens	78-88
33515593-6	2021	This is supported by the evidence that using ROS scavenger N-acetyl cysteine (NAC) significantly alleviated Bort-activated mTORC1 pathway.	Acetylcysteine	78-81	CREB regulated transcription coactivator 1	Mus musculus	123-129
33615065-7	2021	The secondary outcome was a change in cystatin C after NAC administration.	Acetylcysteine	55-58	cystatin C	Homo sapiens	38-48
33689540-5	2021	Conversely, NAC/DTT in MetS recovered RyR2/SERCA2a function, improving SCaTs and CaS frequency, but unexpectedly decreasing CaW propagation.	Acetylcysteine	12-15	ryanodine receptor 2	Rattus norvegicus	38-42
32030632-5	2020	We further found that the pre-treatment with N-acetylcysteine, a widely used ROS scavenger, and the over-expression of antioxidant NRF2 protein, both significantly reduced arsenite-induced oxidative stress in arsenite-treated HBE cells, and the linc-ROR over-expression was also inhibited, suggesting that oxidative stress is a key factor for the increase of linc-ROR in arsenite-treated HBE cells.	Acetylcysteine	45-61	long intergenic non-protein coding RNA, regulator of reprogramming	Homo sapiens	245-253
32030632-5	2020	We further found that the pre-treatment with N-acetylcysteine, a widely used ROS scavenger, and the over-expression of antioxidant NRF2 protein, both significantly reduced arsenite-induced oxidative stress in arsenite-treated HBE cells, and the linc-ROR over-expression was also inhibited, suggesting that oxidative stress is a key factor for the increase of linc-ROR in arsenite-treated HBE cells.	Acetylcysteine	45-61	long intergenic non-protein coding RNA, regulator of reprogramming	Homo sapiens	359-367
33564095-7	2021	When N-acetyl-L-cysteine was given from 6 weeks of age, DEN-administered Mcl-1Deltahep mice had reduced oxidative stress and suppressed tumorigenesis in the liver but showed no changes in hepatocyte apoptosis or proliferation.	Acetylcysteine	5-24	myeloid cell leukemia sequence 1	Mus musculus	73-78
33231124-10	2020	Downregulation of SENP3 expression was observed in HAECs cultured with high glucose levels using the free radical scavenger N-acetyl-L-cysteine or NOX4 siRNA.	Acetylcysteine	124-143	SUMO/sentrin specific peptidase 3	Mus musculus	18-23
33522955-12	2021	Moreover, low levels of ROS induced by N-acetylcysteine (NAC) which is an antioxidant inhibited the cell proliferation, migration, and invasion abilities mediated by FOXC1 overexpression, whereas high levels of ROS induced by L-Buthionine-sulfoximine (BSO) rescued the suppression results mediated by FOXC1 knockdown.	Acetylcysteine	39-55	forkhead box C1	Homo sapiens	166-171
32960947-11	2020	Furthermore, two anti-oxidant species from NBA, N-acetylcysteine and vitamin B6, diminished the induction of Npy in the mHypoA-59 cells, demonstrating these supplements can counteract BPA-induced dysregulation in certain subpopulations.	Acetylcysteine	48-64	neuropeptide Y	Mus musculus	109-112
33522955-12	2021	Moreover, low levels of ROS induced by N-acetylcysteine (NAC) which is an antioxidant inhibited the cell proliferation, migration, and invasion abilities mediated by FOXC1 overexpression, whereas high levels of ROS induced by L-Buthionine-sulfoximine (BSO) rescued the suppression results mediated by FOXC1 knockdown.	Acetylcysteine	39-55	forkhead box C1	Homo sapiens	301-306
33121166-6	2020	Interestingly, intracellular reactive oxygen species (ROS) levels were significantly increased by iron in 12Z cells, and N-acetyl-L-cysteine significantly reduced iron-induced migration and MMP-2/-9 expression.	Acetylcysteine	121-140	matrix metallopeptidase 2	Homo sapiens	190-198
33522955-12	2021	Moreover, low levels of ROS induced by N-acetylcysteine (NAC) which is an antioxidant inhibited the cell proliferation, migration, and invasion abilities mediated by FOXC1 overexpression, whereas high levels of ROS induced by L-Buthionine-sulfoximine (BSO) rescued the suppression results mediated by FOXC1 knockdown.	Acetylcysteine	57-60	forkhead box C1	Homo sapiens	166-171
33522955-12	2021	Moreover, low levels of ROS induced by N-acetylcysteine (NAC) which is an antioxidant inhibited the cell proliferation, migration, and invasion abilities mediated by FOXC1 overexpression, whereas high levels of ROS induced by L-Buthionine-sulfoximine (BSO) rescued the suppression results mediated by FOXC1 knockdown.	Acetylcysteine	57-60	forkhead box C1	Homo sapiens	301-306
33302164-9	2021	Low-dose NAC increased CCDN1 and decreased CASP3 and CASP8 mRNA levels (P < 0.05), whereas high-dose NAC decreased CDK4 and CCDN1 and increased CASP3 mRNA levels (P < 0.05).	Acetylcysteine	9-12	caspase 8	Homo sapiens	53-58
32744307-0	2020	A Drosophila model of Friedreich Ataxia with CRISPR/Cas9 insertion of GAA repeats in the frataxin gene reveals in vivo protection by N-acetyl cysteine.	Acetylcysteine	133-150	frataxin	Drosophila melanogaster	89-97
32744307-10	2020	Finally, in a candidate drug screening, we observed that N-acetyl cysteine improved the survival, locomotor function, resistance to oxidative stress and aconitase activity of frataxin-deficient flies.	Acetylcysteine	57-74	frataxin	Homo sapiens	175-183
33302164-9	2021	Low-dose NAC increased CCDN1 and decreased CASP3 and CASP8 mRNA levels (P < 0.05), whereas high-dose NAC decreased CDK4 and CCDN1 and increased CASP3 mRNA levels (P < 0.05).	Acetylcysteine	101-104	cyclin dependent kinase 4	Homo sapiens	115-119
33478072-6	2021	The antioxidant NAC enhanced the antitumor activity of ADI-PEG 20 and strengthened its ICD-associated features including the secretion of high mobility group box 1 (HMGB1) and adenosine triphosphate (ATP).	Acetylcysteine	16-19	high mobility group box 1	Mus musculus	138-163
31880198-8	2020	In conclusion, our research reveals a novel molecular mechanism that oxidative modification at Cys292 and Cys361 sites regulates ATG4B function, which modulates autophagy.Abbreviations: Air-ox: air-oxidation; ATG4B: autophagy related 4B cysteine peptidase; BCNU: 1,3-bis(2-chloroethyl)-1-nitrosourea; CBB: Coomassie Brilliant Blue; CM: complete medium; CQ: chloroquine; DTT: dithiothreitol; GSH: reduced glutathione; GSNO: S-nitrosoglutathione; GSSG: oxidized glutathione; HMW: high molecular weight; H2O2: hydrogen peroxide; NAC: N-acetyl-L-cysteine; NEM: N-ethylmaleimide; PE: phosphatidylethanolamine; PTM: post-translational modification; ROS, reactive oxygen species; WT: wild type.	Acetylcysteine	531-550	autophagy related 4B cysteine peptidase	Homo sapiens	129-134
31880198-8	2020	In conclusion, our research reveals a novel molecular mechanism that oxidative modification at Cys292 and Cys361 sites regulates ATG4B function, which modulates autophagy.Abbreviations: Air-ox: air-oxidation; ATG4B: autophagy related 4B cysteine peptidase; BCNU: 1,3-bis(2-chloroethyl)-1-nitrosourea; CBB: Coomassie Brilliant Blue; CM: complete medium; CQ: chloroquine; DTT: dithiothreitol; GSH: reduced glutathione; GSNO: S-nitrosoglutathione; GSSG: oxidized glutathione; HMW: high molecular weight; H2O2: hydrogen peroxide; NAC: N-acetyl-L-cysteine; NEM: N-ethylmaleimide; PE: phosphatidylethanolamine; PTM: post-translational modification; ROS, reactive oxygen species; WT: wild type.	Acetylcysteine	531-550	autophagy related 4B cysteine peptidase	Homo sapiens	209-214
32599978-13	2020	In vitro, NAC treatment significantly reduced the expression of NRF2, LC3B, p62, and Beclin-1 in keratinocytes compared with that after radiation treatment.	Acetylcysteine	10-13	KH RNA binding domain containing, signal transduction associated 1	Rattus norvegicus	76-79
33478072-6	2021	The antioxidant NAC enhanced the antitumor activity of ADI-PEG 20 and strengthened its ICD-associated features including the secretion of high mobility group box 1 (HMGB1) and adenosine triphosphate (ATP).	Acetylcysteine	16-19	high mobility group box 1	Mus musculus	165-170
32599978-13	2020	In vitro, NAC treatment significantly reduced the expression of NRF2, LC3B, p62, and Beclin-1 in keratinocytes compared with that after radiation treatment.	Acetylcysteine	10-13	beclin 1	Rattus norvegicus	85-93
32871518-9	2020	Importantly, the anti-apoptotic property of NAC could be attributed to inactivation of MAPK signaling molecules; p38 and JNK, and enhancement of the ovarian vascular endothelial growth factor (VEGF) expression.	Acetylcysteine	44-47	mitogen activated protein kinase 14	Rattus norvegicus	113-116
33290259-9	2020	The ROS inhibitor N-acetylcysteine abrogated the suppression of LOX-1+ PMN-MDSCs on T cell activation.	Acetylcysteine	18-34	oxidized low density lipoprotein receptor 1	Homo sapiens	64-69
32627147-6	2020	PM exposure promoted P. aeruginosa invasion into BEAS-2B cells through ROS-mediated PI3K pathway which enhanced the expression of PAFR, which could be alleviated by treatment with NAC, LY294002, and BAY 11-7082.	Acetylcysteine	180-183	platelet activating factor receptor	Homo sapiens	130-134
32813131-0	2020	Invited Response on: Impact of N-Acetylcysteine on Autologous Fat Graft-The Consideration of Blood Concentration.	Acetylcysteine	31-47	FAT atypical cadherin 1	Homo sapiens	62-65
32619679-14	2020	Furthermore, data from treatment of reactive oxygen species inhibitor N-acetyl-L-cysteine or NOXs inhibitor diphenyleneiodonium in fructose-exposed HepG2 cells showed that fructose enhanced NOX1, NOX2 and NOX4 expression to increase reactive oxygen species generation, causing oxidative stress and inflammation, more importantly, these disturbances were significantly attenuated by magnesium isoglycyrrhizinate.	Acetylcysteine	70-89	NADPH oxidase 1	Homo sapiens	190-194
32619679-14	2020	Furthermore, data from treatment of reactive oxygen species inhibitor N-acetyl-L-cysteine or NOXs inhibitor diphenyleneiodonium in fructose-exposed HepG2 cells showed that fructose enhanced NOX1, NOX2 and NOX4 expression to increase reactive oxygen species generation, causing oxidative stress and inflammation, more importantly, these disturbances were significantly attenuated by magnesium isoglycyrrhizinate.	Acetylcysteine	70-89	NADPH oxidase 4	Homo sapiens	205-209
32098455-11	2020	Conclusions: CLDN18 plays a role in the pathogenesis of asthma and NAC diminishes airway inflammation and responsiveness by modulating CLDN18 expression.	Acetylcysteine	67-70	claudin 18	Homo sapiens	135-141
33218094-7	2020	Both patients made a full recovery following antimicrobial therapy with rifampicin, azithromycin, and pradofloxacin (plus N-acetyl cysteine in cat 2).	Acetylcysteine	122-139	solute carrier family 7 member 2	Homo sapiens	143-148
32720162-7	2020	Treating the cells with an ROS scavenger, N-acetyl cysteine (NAC), led to AMPK inactivation and apoptosis inhibition, allowing the recovery of cell health.	Acetylcysteine	61-64	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	74-78
32545880-11	2020	Meanwhile, NAC pretreatment also blocked the phosphorylation of ERK1/2 and p38 induced by NEFA, and the nucleation of Nrf2 and p53, suggesting that ROS plays a crucial role in regulating the NEFA-induced apoptosis of GCs.	Acetylcysteine	11-14	mitogen-activated protein kinase 3	Bos taurus	64-70
32526845-5	2020	In the group treated with NAC, reductions in inflammatory infiltration; AST (aspartate aminotransferase), nitrite, and TBARS levels; GPx (gutathione peroxidase) activity; cytokines synthesis; and number of apoptotic cells were observed while the GR (glutathione reductase) activity was increased.	Acetylcysteine	26-29	glutathione reductase	Mus musculus	246-248
32526845-5	2020	In the group treated with NAC, reductions in inflammatory infiltration; AST (aspartate aminotransferase), nitrite, and TBARS levels; GPx (gutathione peroxidase) activity; cytokines synthesis; and number of apoptotic cells were observed while the GR (glutathione reductase) activity was increased.	Acetylcysteine	26-29	glutathione reductase	Mus musculus	250-271
32454937-9	2020	The Western blot analysis suggested that Zerumbone activated the NF-kappaB p65, which was partly inhibited by NAC treatment.	Acetylcysteine	110-113	RELA proto-oncogene, NF-kB subunit	Homo sapiens	65-78
32188759-8	2020	The endoplasmic reticulum stress response in the TLR9/RP105-stimulated cells was higher in IgG+ than in IgG- cells and was reduced by NAC in IgG+ cells only.	Acetylcysteine	134-137	toll like receptor 9	Homo sapiens	49-53
32205843-9	2020	Furthermore, treatment with N-acetyl-cysteine, a reactive oxygen species (ROS) scavenger, attenuated iron overload-induced hippocampal damage by inhibiting ROS production, ER-stress, and mitochondrial fission in iron-loaded Prx5-/- mice.	Acetylcysteine	28-45	peroxiredoxin 5	Mus musculus	224-228
31984795-13	2020	The antioxidants polyethylene glycol-catalase, ammonium pyrrolidithiocarbamate, and N-acetylcysteine significantly blocked the high glucose-induced increase of I-mfa protein.	Acetylcysteine	84-100	MyoD family inhibitor	Homo sapiens	160-165
31894323-12	2020	H2O2 significantly increased the intracellular ROS levels and miR-335-5p expression, whereas N-acetyl-cysteine pretreatment prior to H2O2 treatment reversed the increases in miR-335-5p expression.	Acetylcysteine	93-110	microRNA 335	Homo sapiens	174-181
32127147-6	2020	Western blot analysis revealed a downregulation of Beclin-1 protein in both the NAC and CAT groups (p < 0.05) while ELISA revealed significantly lower levels of ROS in the NAC and CAT groups (p < 0.05).	Acetylcysteine	80-83	beclin 1	Rattus norvegicus	51-59
32127147-7	2020	CONCLUSION: The antioxidants NAC and CAT significantly reduced levels of the autophagy marker LC3 and caused levels of Beclin-1 to significantly decrease.	Acetylcysteine	29-32	beclin 1	Rattus norvegicus	119-127
31631367-15	2020	Combination of NAC with DEX obtained a maximum effect on decreasing Galectin-9/Tim-3 expression.	Acetylcysteine	15-18	hepatitis A virus cellular receptor 2	Mus musculus	79-84
31812668-4	2020	We demonstrate that mutant p53 induces MnSOD expression, which is recovered by the ROS scavenger N-acetyl-l-cysteine.	Acetylcysteine	97-116	superoxide dismutase 2	Homo sapiens	39-44
31699387-6	2020	Caspase-3 inhibition assay revealed that compounds 6a, 6b and 6d weaken caspase-3 expression to an extent higher than NAC (1.063, 0.430, 0.731 and 1.115, respectively).	Acetylcysteine	118-121	caspase 3	Rattus norvegicus	0-9
31699387-7	2020	Docking studies with caspase-3 revealed that most of the tested compounds showed good binding with the enzyme especially for compound 6d make several interactions better than that of the reference NAC.	Acetylcysteine	197-200	caspase 3	Rattus norvegicus	21-30
31493144-14	2019	Importantly, we found that activation of the p38 and JNK signaling pathways prompted by PL and oxaliplatin was also reversed by NAC pretreatment.	Acetylcysteine	128-131	mitogen-activated protein kinase 14	Mus musculus	45-48
30676497-6	2019	NAC ameliorated the gentamicin-induced decreases in the levels of autophagy-related proteins, such as LC3 (microtubule-associated protein 1 light chain 3), PINK1 (phosphatase and tensin homologue deleted on chromosome10-induced kinase 1), phospho-parkin, AMBRA1 (activatingmolecule in Beclin 1-regulated autophagy), p62/SQSTM1 (sequestosome protein 1), and polyubiquitinated protein aggregates.	Acetylcysteine	0-3	autophagy and beclin 1 regulator 1	Sus scrofa	255-261
31890447-4	2019	Some papers have demonstrated that N-acetylcysteine may have a role in non-acetaminophen induced acute liver failure (NAI-ALF).	Acetylcysteine	35-51	afamin	Homo sapiens	122-125
31890447-15	2019	Treatment with intravenous N-acetylcysteine was initiated for non-acetaminophen induced acute liver failure (NAI-ALF) and resulted in a dramatic improvement in transaminases before discharge.	Acetylcysteine	27-43	afamin	Homo sapiens	113-116
29735977-8	2019	Exogenous administration of N-Acetyl-L-cysteine (NAC), a small molecular inhibitor of ROS, remarkably suppressed caspase-1 p20 expression and IL-1beta and IL-18 production in livers of Tim-3 KO mice, thus significantly reducing the severity of steatohepatitis induced by MCD.	Acetylcysteine	28-47	caspase 1	Mus musculus	113-122
29735977-8	2019	Exogenous administration of N-Acetyl-L-cysteine (NAC), a small molecular inhibitor of ROS, remarkably suppressed caspase-1 p20 expression and IL-1beta and IL-18 production in livers of Tim-3 KO mice, thus significantly reducing the severity of steatohepatitis induced by MCD.	Acetylcysteine	28-47	interleukin 18	Mus musculus	155-160
29735977-8	2019	Exogenous administration of N-Acetyl-L-cysteine (NAC), a small molecular inhibitor of ROS, remarkably suppressed caspase-1 p20 expression and IL-1beta and IL-18 production in livers of Tim-3 KO mice, thus significantly reducing the severity of steatohepatitis induced by MCD.	Acetylcysteine	28-47	hepatitis A virus cellular receptor 2	Mus musculus	185-190
29735977-8	2019	Exogenous administration of N-Acetyl-L-cysteine (NAC), a small molecular inhibitor of ROS, remarkably suppressed caspase-1 p20 expression and IL-1beta and IL-18 production in livers of Tim-3 KO mice, thus significantly reducing the severity of steatohepatitis induced by MCD.	Acetylcysteine	49-52	caspase 1	Mus musculus	113-122
29735977-8	2019	Exogenous administration of N-Acetyl-L-cysteine (NAC), a small molecular inhibitor of ROS, remarkably suppressed caspase-1 p20 expression and IL-1beta and IL-18 production in livers of Tim-3 KO mice, thus significantly reducing the severity of steatohepatitis induced by MCD.	Acetylcysteine	49-52	interleukin 18	Mus musculus	155-160
29735977-8	2019	Exogenous administration of N-Acetyl-L-cysteine (NAC), a small molecular inhibitor of ROS, remarkably suppressed caspase-1 p20 expression and IL-1beta and IL-18 production in livers of Tim-3 KO mice, thus significantly reducing the severity of steatohepatitis induced by MCD.	Acetylcysteine	49-52	hepatitis A virus cellular receptor 2	Mus musculus	185-190
31545445-10	2019	However, pretreatment of HUVECs with NAC significantly attenuated the increase in the expression of inflammatory factors and the level of phosphorylated p65; this indicated that NAC prevented the activation of the NF-kappaB signaling pathway.	Acetylcysteine	178-181	RELA proto-oncogene, NF-kB subunit	Homo sapiens	153-156
32041914-9	2019	RESULTS: HsCRP, MPO, and Gal-3 levels between NAC and control groups at admission were not significantly different; while intergroup differences after 72 h of NAC supplementation were significant (p values of HsCRP, MPO, and Gal-3 levels were 0.0001, 0.001, and 0.017, respectively).	Acetylcysteine	159-162	galectin 3	Homo sapiens	225-230
32041914-10	2019	Furthermore, in the NAC group, HsCRP, MPO, and Gal-3 levels at 72 h after treatment were significantly different from the corresponding levels at admission (p values: 0.0001, 0.0001, and 0.0001, respectively); the control group did not show these differences.	Acetylcysteine	20-23	galectin 3	Homo sapiens	47-52
32041914-11	2019	There were also significant intergroup differences between the NAC and control groups regarding HsCRP, MPO, and Gal-3 levels (p values: 0.011, 0.022, and 0.014, respectively).	Acetylcysteine	63-66	galectin 3	Homo sapiens	112-117
32041914-12	2019	CONCLUSION: oral supplementation of 600 mg NAC every 8 h for 72 h can reduce HsCRP, MPO, and Gal-3 levels in AMI patients receiving fibrinolytic therapy.	Acetylcysteine	43-46	galectin 3	Homo sapiens	93-98
31392607-9	2019	NAC reduced the levels of TNS, MDA, and caspase-3 expression, but increased the levels of renal tissue GSH.	Acetylcysteine	0-3	caspase 3	Rattus norvegicus	40-49
30982974-11	2019	Furthermore, ROS inhibitor N-acetyl-L-cysteine (NAC) also suppressed BaP co-exposure-induced expression of epithelial TSLP, IL-33, and IL-25.	Acetylcysteine	27-46	thymic stromal lymphopoietin	Mus musculus	118-122
30982974-11	2019	Furthermore, ROS inhibitor N-acetyl-L-cysteine (NAC) also suppressed BaP co-exposure-induced expression of epithelial TSLP, IL-33, and IL-25.	Acetylcysteine	27-46	interleukin 25	Mus musculus	135-140
30982974-11	2019	Furthermore, ROS inhibitor N-acetyl-L-cysteine (NAC) also suppressed BaP co-exposure-induced expression of epithelial TSLP, IL-33, and IL-25.	Acetylcysteine	48-51	thymic stromal lymphopoietin	Mus musculus	118-122
30982974-11	2019	Furthermore, ROS inhibitor N-acetyl-L-cysteine (NAC) also suppressed BaP co-exposure-induced expression of epithelial TSLP, IL-33, and IL-25.	Acetylcysteine	48-51	interleukin 25	Mus musculus	135-140
31158660-6	2019	FD exposure impaired vasorelaxation in response to bradykinin and activated the local angiotensin system (LAS), which was inhibited by treatment with the antioxidant N-acetyl cysteine (NAC) and angiotensin II receptor type 1 (AT1) antagonist losartan (LOS).	Acetylcysteine	166-183	angiotensin II receptor type 1	Homo sapiens	226-229
31447555-5	2019	NAC can effectively mitigate iron-induced oxidative injury of cardiomyocytes, evidenced by reduced production of MDA, 8-iso-PGF2alpha, and 8-OHDG and maintained concentrations of SOD, CAT, GSH-Px, and GSH in ELISA and biochemical tests; downregulated expression of CHOP, GRP78, p62, and LC3-II proteins in Western Blot, and less cardiomyocytes apoptosis in flow cytometric analysis.	Acetylcysteine	0-3	KH RNA binding domain containing, signal transduction associated 1	Rattus norvegicus	278-281
31229567-8	2019	Pretreatment with N-acetyl-L-cysteine (NAC), a ROS scavenger and antioxidant, suppressed maduramicin-induced inhibition of PP5 and activation of JNK as well as apoptosis.	Acetylcysteine	18-37	protein phosphatase 5, catalytic subunit	Mus musculus	123-126
31229567-8	2019	Pretreatment with N-acetyl-L-cysteine (NAC), a ROS scavenger and antioxidant, suppressed maduramicin-induced inhibition of PP5 and activation of JNK as well as apoptosis.	Acetylcysteine	39-42	protein phosphatase 5, catalytic subunit	Mus musculus	123-126
31071510-8	2019	Moreover, NAC (N-acetylcysteine), a potent ROS scavenger, obviously suppressed apoptosis induced by UCP2 silencing, which suggests that the increased ROS levels were associated with tubular epithelial cell apoptosis induced by UCP2 silencing.	Acetylcysteine	10-13	uncoupling protein 2	Homo sapiens	100-104
31071510-8	2019	Moreover, NAC (N-acetylcysteine), a potent ROS scavenger, obviously suppressed apoptosis induced by UCP2 silencing, which suggests that the increased ROS levels were associated with tubular epithelial cell apoptosis induced by UCP2 silencing.	Acetylcysteine	10-13	uncoupling protein 2	Homo sapiens	227-231
31071510-8	2019	Moreover, NAC (N-acetylcysteine), a potent ROS scavenger, obviously suppressed apoptosis induced by UCP2 silencing, which suggests that the increased ROS levels were associated with tubular epithelial cell apoptosis induced by UCP2 silencing.	Acetylcysteine	15-31	uncoupling protein 2	Homo sapiens	100-104
31071510-8	2019	Moreover, NAC (N-acetylcysteine), a potent ROS scavenger, obviously suppressed apoptosis induced by UCP2 silencing, which suggests that the increased ROS levels were associated with tubular epithelial cell apoptosis induced by UCP2 silencing.	Acetylcysteine	15-31	uncoupling protein 2	Homo sapiens	227-231
31115495-5	2019	In addition, LIUS-DDP significantly increased intracellular reactive oxygen species (ROS) levels in vitro, and the upregulation of miR-34a induced by LIUS-DDP was reversed by the ROS scavenger N-acetylcysteine, suggesting that LIUS upregulates the expression of miR-34a via production of ROS.	Acetylcysteine	193-209	microRNA 34a	Homo sapiens	131-138
31115495-5	2019	In addition, LIUS-DDP significantly increased intracellular reactive oxygen species (ROS) levels in vitro, and the upregulation of miR-34a induced by LIUS-DDP was reversed by the ROS scavenger N-acetylcysteine, suggesting that LIUS upregulates the expression of miR-34a via production of ROS.	Acetylcysteine	193-209	microRNA 34a	Homo sapiens	262-269
31075539-7	2019	N-acetyl-cysteine inhibited the effect of DISC1, suggesting that DISC1 affects translation in response to oxidative stress.	Acetylcysteine	0-17	DISC1 scaffold protein	Homo sapiens	42-47
31075539-7	2019	N-acetyl-cysteine inhibited the effect of DISC1, suggesting that DISC1 affects translation in response to oxidative stress.	Acetylcysteine	0-17	DISC1 scaffold protein	Homo sapiens	65-70
30862482-8	2019	Furthermore, overexpression of MRPL35 or treatment of cells with the ROS scavenger, N-acetyl cysteine, abrogated ROS production, cell cycle arrest, and apoptosis in vitro.	Acetylcysteine	84-101	mitochondrial ribosomal protein L35	Mus musculus	31-37
30956169-0	2019	Postnatal N-acetylcysteine administration rescues impaired social behaviors and neurogenesis in Slc13a4 haploinsufficient mice.	Acetylcysteine	10-26	solute carrier family 13 (sodium/sulfate symporters), member 4	Mus musculus	96-103
30956169-9	2019	Furthermore, administration of N-acetylcysteine (NAC) within postnatal window P14-P30 prevents the onset of phenotypes in adult Slc13a4+/- mice.	Acetylcysteine	31-47	solute carrier family 13 (sodium/sulfate symporters), member 4	Mus musculus	128-135
30956169-9	2019	Furthermore, administration of N-acetylcysteine (NAC) within postnatal window P14-P30 prevents the onset of phenotypes in adult Slc13a4+/- mice.	Acetylcysteine	49-52	solute carrier family 13 (sodium/sulfate symporters), member 4	Mus musculus	128-135
30896878-6	2019	Mechanistically, CsA treatment increased reactive oxygen species (ROS) generation, and the intracellular ROS scavenger N-acetyl-cysteine (NAC) attenuated CsA-induced cell proliferation as well as the activation of Akt/Cyclin D1 signaling.	Acetylcysteine	119-136	cyclin D1	Homo sapiens	218-227
30896878-6	2019	Mechanistically, CsA treatment increased reactive oxygen species (ROS) generation, and the intracellular ROS scavenger N-acetyl-cysteine (NAC) attenuated CsA-induced cell proliferation as well as the activation of Akt/Cyclin D1 signaling.	Acetylcysteine	138-141	cyclin D1	Homo sapiens	218-227
30979951-6	2019	Inflammatory dynamic networks, and in particular HMGB1 connectivity, were associated with the use of NAC in the context of APAPo.	Acetylcysteine	101-104	high mobility group box 1	Mus musculus	49-54
30979951-9	2019	HC HMGB1 may thus coordinate a pro-inflammatory program in PALF non-survivors (which is antagonized by NAC), while driving an anti-inflammatory/repair program in survivors.	Acetylcysteine	103-106	high mobility group box 1	Mus musculus	3-8
31679953-1	2021	BACKGROUND: Bromelain (Brom) and Acetylcysteine (Ac) have synergistic activity resulting in dissolution of tumour-produced mucin both in vitro and in vivo.	Acetylcysteine	33-47	LOC100508689	Homo sapiens	123-128
31679953-1	2021	BACKGROUND: Bromelain (Brom) and Acetylcysteine (Ac) have synergistic activity resulting in dissolution of tumour-produced mucin both in vitro and in vivo.	Acetylcysteine	33-35	LOC100508689	Homo sapiens	123-128
33426071-11	2020	The cellular expression levels of ZO-1, Occludin, and Claudin-4, which were lowered by hyperoxia, were increased by NAC.	Acetylcysteine	116-119	occludin	Homo sapiens	40-48
32958257-5	2020	The mechanism of NAC reversing PM2.5-mediated action may be related to its anti-oxidant and anti-inflammatory effects, which may provide some new insights for the prevention of AR exacerbated by exposure to PM2.5.	Acetylcysteine	17-20	ferredoxin reductase	Rattus norvegicus	177-179
32696164-0	2020	Impact of N-Acetylcysteine on Autologous Fat Graft: The Consideration of Blood Concentration.	Acetylcysteine	10-26	FAT atypical cadherin 1	Homo sapiens	41-44
33469619-3	2020	The patient was treated with five days of N-acetyl cysteine to which he responded, with his alanine aminotransferase improving from 5,599 to 652 and international normalised ratio from 5.0 to 0.9.	Acetylcysteine	42-59	glutamic--pyruvic transaminase	Homo sapiens	92-116
33208818-6	2020	AMPK agonist Epi determined direct effects on the alpha1-AR, metformin was used as an activator for AMPK, while buthionine sulphoximine (BSO) and N-acetyl cysteine (NAC) assessed GSH inhibition and supplementation respectively.	Acetylcysteine	165-168	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	0-4
33201734-6	2021	Administration of NAC or melatonin significantly improved the lipid parameters, gonadal hormones, TNFalpha level, sperm count and abnormal morphology, oxidant/antioxidant system and the absolute testicular and epididymal mass with an enhancement of testicular architecture, AR expression and apoptosis as compared to that in the obese group.	Acetylcysteine	18-21	ferredoxin reductase	Rattus norvegicus	274-276
33139577-4	2020	As a result, Akt3-expressing cells activate the DNA damage response pathway, express high levels of p53 and its direct transcriptional target miR-34, and exhibit a proliferation defect, which is rescued by the antioxidant N-acetylcysteine.	Acetylcysteine	222-238	microRNA 34a	Homo sapiens	142-148
32549180-7	2020	N-Acetyl cysteine (NAC) administration completely suppressed ER stress as well as caspase-3 activity.	Acetylcysteine	0-17	caspase 3	Rattus norvegicus	82-91
32549180-7	2020	N-Acetyl cysteine (NAC) administration completely suppressed ER stress as well as caspase-3 activity.	Acetylcysteine	19-22	caspase 3	Rattus norvegicus	82-91
32683294-8	2020	Reduced expression of occludin mRNA and protein induced by As2O3 was entirely restored with NAC and resveratrol.	Acetylcysteine	92-95	occludin	Homo sapiens	22-30
32438104-4	2020	RESULTS: Pretreatment of NAC significantly alleviated pathologic damage of kidney tissues in septic rats; decreased the levels of serum creatinine, blood urea nitrogen, plasma neutrophil gelatinase-associated lipocalin, and kidney injury molecule-1; and reduced the expression of tumor necrosis factor a, interleukin [IL]-1beta, IL-6, and IL-8.	Acetylcysteine	25-28	lipocalin 2	Rattus norvegicus	176-218
32438104-6	2020	Moreover, pretreatment of NAC reduced the number of apoptosis in kidney tissues induced by CLP, decreased the mRNA levels of caspase-3, caspase-9, cytochrome c, and poly ADP-ribose polymerase, and increased mitochondrial membrane activity in renal cortical cells (complex I/II/III/IV).	Acetylcysteine	26-29	caspase 3	Rattus norvegicus	125-134
32961891-10	2020	Besides, the potentiating effect of beta-glucan on pulmonary chemoreflex responses was significantly attenuated by N-acetyl-L-cysteine (a ROS scavenger), HC-030031 (a TRPA1 antagonist), and Laminarin (a Dectin-1 antagonist).	Acetylcysteine	115-134	C-type lectin domain containing 7A	Rattus norvegicus	203-211
32512010-7	2020	Pre-treatment of N-acetyl-l-cysteine (NAC) or ERK1/2 or phosphoinositide3-kinase (PI3-K)/Akt inhibitors in RGC-5 cells significantly reduced the HG-induced IRF3 expression and declined the expression of neurodegenerative markers.	Acetylcysteine	17-36	interferon regulatory factor 3	Mus musculus	156-160
32512010-7	2020	Pre-treatment of N-acetyl-l-cysteine (NAC) or ERK1/2 or phosphoinositide3-kinase (PI3-K)/Akt inhibitors in RGC-5 cells significantly reduced the HG-induced IRF3 expression and declined the expression of neurodegenerative markers.	Acetylcysteine	38-41	interferon regulatory factor 3	Mus musculus	156-160
32574682-2	2020	This study analyzed the role of peroxisome proliferator-activated receptor (PPAR)-gamma on HPA axis hyperactivity induced by N-acetyl-cysteine (NAC).	Acetylcysteine	125-142	peroxisome proliferator activated receptor gamma	Mus musculus	32-87
32574682-2	2020	This study analyzed the role of peroxisome proliferator-activated receptor (PPAR)-gamma on HPA axis hyperactivity induced by N-acetyl-cysteine (NAC).	Acetylcysteine	144-147	peroxisome proliferator activated receptor gamma	Mus musculus	32-87
32574682-8	2020	NAC treatment reduces the expression of PPARgamma in the adrenals, but rosiglitazone did not restore the expression of this cytoprotective gene.	Acetylcysteine	0-3	peroxisome proliferator activated receptor gamma	Mus musculus	40-49
32848711-7	2020	Treatment with N-acetylcysteine (NAC; an ROS scavenger) or Z-VAD-FMK (a caspase inhibitor) significantly attenuated TMEM230-induced apoptosis in both cultured cells and primary neurons.	Acetylcysteine	15-31	transmembrane protein 230	Homo sapiens	116-123
32848711-7	2020	Treatment with N-acetylcysteine (NAC; an ROS scavenger) or Z-VAD-FMK (a caspase inhibitor) significantly attenuated TMEM230-induced apoptosis in both cultured cells and primary neurons.	Acetylcysteine	33-36	transmembrane protein 230	Homo sapiens	116-123
32753716-5	2020	This potentiation was eliminated by the competitive antagonist AMG-21629, the NADPH oxidase assembly inhibitor apocynin, and the reactive oxygen species (ROS) scavenger N-acetylcysteine, suggesting that ROS contributes to magnetogenetic TRPV1 activation.	Acetylcysteine	169-185	transient receptor potential cation channel subfamily V member 1	Homo sapiens	237-242
32722598-7	2020	Treatment of cancer cell lines with the antioxidant N-acetylcysteine reduces the extent of membrane dysfunction and the expression of both CHOP-DR5 and miR-425-PTEN axes, attenuating PAM/TRAIL-induced cancer cell apoptosis.	Acetylcysteine	52-68	microRNA 425	Homo sapiens	152-159
32658869-7	2020	Decrease of mtROS with N-acetyl-L-cysteine attenuated the activation of JNK and the increase of SOD2 transcription.	Acetylcysteine	23-42	superoxide dismutase 2	Homo sapiens	96-100
32647651-7	2020	15d-PGJ2-mediated inhibition of IKKbeta and nuclear translocation of phospho-p65 was blocked by NAC treatment.	Acetylcysteine	96-99	RELA proto-oncogene, NF-kB subunit	Homo sapiens	77-80
32321806-9	2020	Treatment of PCV2-infected cells with ethyl pyruvate or N-acetylcysteine downregulated PCV2-induced ROS production, suppressed nucleocytoplasmic HMGB1 translocation, and decreased PCV2 replication.	Acetylcysteine	56-72	high mobility group box 1	Homo sapiens	145-150
31465111-13	2020	Finally, it was shown that N-acetyl-cysteine (NAC) could reduce MMP-9/2 activities and attenuate CIPN effectively and safely.	Acetylcysteine	27-44	matrix metallopeptidase 9	Mus musculus	64-69
31465111-13	2020	Finally, it was shown that N-acetyl-cysteine (NAC) could reduce MMP-9/2 activities and attenuate CIPN effectively and safely.	Acetylcysteine	46-49	matrix metallopeptidase 9	Mus musculus	64-69
31465111-15	2020	Direct inhibition of MMP-9 by NAC may be a potential therapeutic regimen for CIPN treatment.	Acetylcysteine	30-33	matrix metallopeptidase 9	Mus musculus	21-26
32509139-11	2020	Treatment with N-acetylcysteine (NAC), a classic ROS scavenger, could suppress ROS production and P38 MAPK activation.	Acetylcysteine	15-31	mitogen-activated protein kinase 14	Mus musculus	98-106
32509139-11	2020	Treatment with N-acetylcysteine (NAC), a classic ROS scavenger, could suppress ROS production and P38 MAPK activation.	Acetylcysteine	33-36	mitogen-activated protein kinase 14	Mus musculus	98-106
30917096-0	2019	Development of near-infrared region luminescent N-acetyl-L-cysteine-coated Ag2S quantum dots with differential therapeutic effect.	Acetylcysteine	48-67	angiotensin II receptor type 1	Homo sapiens	75-79
30917096-2	2019	We developed NAC-coated Ag2S (NAC-Ag2S) quantum dot (QD) as an optical imaging and therapeutic agent.	Acetylcysteine	13-16	angiotensin II receptor type 1	Homo sapiens	24-28
30917096-2	2019	We developed NAC-coated Ag2S (NAC-Ag2S) quantum dot (QD) as an optical imaging and therapeutic agent.	Acetylcysteine	30-33	angiotensin II receptor type 1	Homo sapiens	24-28
30917096-5	2019	RESULTS: NAC-Ag2S QDs have strong emission, that is tunable between 748 and 840 nm, and are stable in biologically relevant media.	Acetylcysteine	9-12	angiotensin II receptor type 1	Homo sapiens	13-17
30614543-9	2019	Moreover, high levels of reactive oxygen species (ROS) were detected in sRBC-DCs, and treatment with N-acetylcysteine simultaneously decreased the lymph node-homing ability of DCs and phosphorylation of RhoA, ROCK1, and cortactin.	Acetylcysteine	101-117	ras homolog family member A	Mus musculus	203-207
30614543-9	2019	Moreover, high levels of reactive oxygen species (ROS) were detected in sRBC-DCs, and treatment with N-acetylcysteine simultaneously decreased the lymph node-homing ability of DCs and phosphorylation of RhoA, ROCK1, and cortactin.	Acetylcysteine	101-117	Rho-associated coiled-coil containing protein kinase 1	Mus musculus	209-214
32179647-6	2020	We also show that N-acetylcysteine, a widely-used antioxidant, is a poor substrate for MPST and is unlikely to function as a thiophilic acceptor.	Acetylcysteine	18-34	mercaptopyruvate sulfurtransferase	Homo sapiens	87-91
33262689-0	2020	N-Acetylcysteine Rescues Hippocampal Oxidative Stress-Induced Neuronal Injury via Suppression of p38/JNK Signaling in Depressed Rats.	Acetylcysteine	0-16	mitogen activated protein kinase 14	Rattus norvegicus	97-100
31796366-5	2020	Under in vitro conditions, BPA was glutathionylated by GSH, which was further catalyzed by GST to cysteine and N-acetylcysteine conjugates.	Acetylcysteine	111-127	glutathione S-transferase	Solanum lycopersicum	91-94
31669540-11	2020	N-acetyl-l-cysteine treatment attenuated the 15-keto PGE2-induced phosphorylation of GSK3beta, transcriptional activity of Nrf2, and subsequently HO-1 expression.	Acetylcysteine	0-19	glycogen synthase kinase 3 alpha	Homo sapiens	85-93
33268712-6	2020	Together, the results of this study suggest that renal interstitial fibrosis induced by UUO was ameliorated by NAC via several mechanisms including increased glutathione peroxidase activity, reduced phosphorylation of ERK1/2, and reduced expression of TNF-alpha and type III collagen mRNAs.	Acetylcysteine	111-114	mitogen-activated protein kinase 3	Mus musculus	218-224
30764601-7	2019	GPR120 knockdown reduced the expression of ER stress response genes, similar to the case for the pre-treatment of the cells with N-acetyl-L-cysteine (NAC), an ROS scavenger, or 2-APB.	Acetylcysteine	129-148	free fatty acid receptor 4	Homo sapiens	0-6
30764601-7	2019	GPR120 knockdown reduced the expression of ER stress response genes, similar to the case for the pre-treatment of the cells with N-acetyl-L-cysteine (NAC), an ROS scavenger, or 2-APB.	Acetylcysteine	150-153	free fatty acid receptor 4	Homo sapiens	0-6
30926903-5	2019	FX11 treatment and LDHA knockdown suppressed migration and invasion through ROS generation, but this was partially reversed by the antioxidant N-acetylcysteine (NAC).	Acetylcysteine	143-159	lactate dehydrogenase A	Mus musculus	19-23
30926903-5	2019	FX11 treatment and LDHA knockdown suppressed migration and invasion through ROS generation, but this was partially reversed by the antioxidant N-acetylcysteine (NAC).	Acetylcysteine	161-164	lactate dehydrogenase A	Mus musculus	19-23
32239424-5	2020	NAC was administered in a 3-mug/kg IV dose in a 24-h infusion to 70 patients when any alanine aminotransferase (ALT) or gamma-glutamyl transferase (GGT) values reached three times the normal levels.	Acetylcysteine	0-3	glutamic--pyruvic transaminase	Homo sapiens	86-110
31049140-11	2019	Phosphorylated ASK1 and p38 levels were significantly higher in the 1000 nM dexamethasone group, which NAC or DPI markedly attenuated.	Acetylcysteine	103-106	mitogen-activated protein kinase 14	Mus musculus	24-27
30742845-10	2019	N-Acetyl-cysteine and SB203580 pretreatment essentially abolished arsenic-induced phosphorylation of p38 and reversed arsenic-induced increased osteoclast differentiation in Nrf2 deficiency.	Acetylcysteine	0-17	mitogen-activated protein kinase 14	Mus musculus	101-104
30633982-9	2019	Simultaneously, NAC pretreatment downregulated XBP1 splicing, reduced JNK phosphorylation and further blocked cleavage of caspase-3, all these might contribute to the inhibition of testicular cell apoptosis.	Acetylcysteine	16-19	caspase 3	Rattus norvegicus	122-131
31722253-10	2020	NAC also inhibited increased MMP-9 activity after global brain ischemia.	Acetylcysteine	0-3	matrix metallopeptidase 9	Mus musculus	29-34
31722253-11	2020	NAC increased laminin and NeuN expression and inhibited increases in TUNEL-positive cells, all in the hippocampus.	Acetylcysteine	0-3	RNA binding protein, fox-1 homolog (C. elegans) 3	Mus musculus	26-30
31722253-12	2020	These results suggest that NAC reduces hippocampal neuronal damage following transient global ischemia, potentially via reductions in MMP-9 activity.	Acetylcysteine	27-30	matrix metallopeptidase 9	Mus musculus	134-139
33133334-6	2020	Methods: AR murine model was established using OVA and administrated intranasally with resveratrol or N-acetylcysteine (NAC).	Acetylcysteine	102-118	ferredoxin reductase	Mus musculus	9-11
31921893-7	2019	The effect of ET1 on miR-29 and TGFbeta expression/secretion was antagonized by N-acetyl-cysteine, a reactive oxygen species scavenger.	Acetylcysteine	80-97	transforming growth factor alpha	Homo sapiens	32-39
30700808-6	2019	In vitro, NAC pre-treatment significantly reduced TNF-alpha and NF-kappaB, TNF-alpha, IFN-gamma, and IL-6 expression in LPS-induced IPEC-J2 cells.	Acetylcysteine	10-13	tumor necrosis factor	Sus scrofa	50-59
30700808-6	2019	In vitro, NAC pre-treatment significantly reduced TNF-alpha and NF-kappaB, TNF-alpha, IFN-gamma, and IL-6 expression in LPS-induced IPEC-J2 cells.	Acetylcysteine	10-13	tumor necrosis factor	Sus scrofa	75-84
30700808-6	2019	In vitro, NAC pre-treatment significantly reduced TNF-alpha and NF-kappaB, TNF-alpha, IFN-gamma, and IL-6 expression in LPS-induced IPEC-J2 cells.	Acetylcysteine	10-13	interferon gamma	Sus scrofa	86-95
31817202-7	2019	Inhibition experiments with NAC and pharmacological inhibitors demonstrated that NaVO3-induced IL-6 production is signaled by ROS-triggered p38-mediated NF-kappaB-dependent pathways.	Acetylcysteine	28-31	mitogen-activated protein kinase 14	Mus musculus	140-143
33133334-6	2020	Methods: AR murine model was established using OVA and administrated intranasally with resveratrol or N-acetylcysteine (NAC).	Acetylcysteine	120-123	ferredoxin reductase	Mus musculus	9-11
31752383-11	2019	Furthermore, NAC could alleviate p53 and the p53 upregulated modulator of apoptosis (PUMA) expression induced by TRAIL and ASH.	Acetylcysteine	13-16	BCL2 binding component 3	Homo sapiens	85-89
30700808-6	2019	In vitro, NAC pre-treatment significantly reduced TNF-alpha and NF-kappaB, TNF-alpha, IFN-gamma, and IL-6 expression in LPS-induced IPEC-J2 cells.	Acetylcysteine	10-13	interleukin 6	Sus scrofa	101-105
33123307-8	2020	ROS induced by iron overload promote necroptosis via a positive feedback mechanism, as on the one hand N-acetylcysteine attenuates the upregulation of RIPK1 and RIPK3 and phosphorylation of RIPK1, RIPK3, and MLKL and on the other hand Nec-1, siRIPK1, or siRIPK3 reduced ROS generation.	Acetylcysteine	103-119	mixed lineage kinase domain like pseudokinase	Homo sapiens	208-212
30606241-12	2019	Meanwhile, NAC had a decreasing effect on the mRNA and protein levels of its downstream targets Hes1 and Hey1.	Acetylcysteine	11-14	hes family bHLH transcription factor 1	Homo sapiens	96-100
30362123-6	2019	Moreover, the participation of oxidative stress is supported by the antioxidant action of N-acetylcysteine (NAC), which significantly protects XP-V cells from UVA light, even in the presence of the ATR inhibitor.	Acetylcysteine	90-106	DNA polymerase eta	Homo sapiens	143-147
30362123-6	2019	Moreover, the participation of oxidative stress is supported by the antioxidant action of N-acetylcysteine (NAC), which significantly protects XP-V cells from UVA light, even in the presence of the ATR inhibitor.	Acetylcysteine	108-111	DNA polymerase eta	Homo sapiens	143-147
31521246-8	2019	Accumulation of an autophagy substrate p62/SQSTM1 in monomeric p62 and polyubiquitinated (polyUb)-p62 forms, was suppressed upon N-acetylcysteine treatment Cd-exposed Raw264.7 cells, indicating an impairment of autophagic degradation during oxidative stress.	Acetylcysteine	129-145	sequestosome 1	Mus musculus	39-42
31521246-8	2019	Accumulation of an autophagy substrate p62/SQSTM1 in monomeric p62 and polyubiquitinated (polyUb)-p62 forms, was suppressed upon N-acetylcysteine treatment Cd-exposed Raw264.7 cells, indicating an impairment of autophagic degradation during oxidative stress.	Acetylcysteine	129-145	sequestosome 1	Mus musculus	43-49
31521246-8	2019	Accumulation of an autophagy substrate p62/SQSTM1 in monomeric p62 and polyubiquitinated (polyUb)-p62 forms, was suppressed upon N-acetylcysteine treatment Cd-exposed Raw264.7 cells, indicating an impairment of autophagic degradation during oxidative stress.	Acetylcysteine	129-145	sequestosome 1	Mus musculus	63-66
31521246-8	2019	Accumulation of an autophagy substrate p62/SQSTM1 in monomeric p62 and polyubiquitinated (polyUb)-p62 forms, was suppressed upon N-acetylcysteine treatment Cd-exposed Raw264.7 cells, indicating an impairment of autophagic degradation during oxidative stress.	Acetylcysteine	129-145	sequestosome 1	Mus musculus	63-66
31419475-6	2019	Importantly, TCE exposure resulted in the activation of hepatic inflammasome (NLRP3 and caspase-1) and up-regulation of pro-inflammatory cytokine IL-1beta, and these changes were attenuated by NAC supplementation.	Acetylcysteine	193-196	caspase 1	Mus musculus	88-97
30538807-10	2018	Treatment with N-acetyl-L-cysteine (NAC) reduced endothelial dysfunctions mediated by siALDH2, indicating that oxidative stress downstream to siALDH2 plays an instrumental role.	Acetylcysteine	15-34	neuronally altered carbohydrate	Drosophila melanogaster	36-39
32439580-9	2020	Specifically, the decreased expression of TFE3 was closely related to the disruption of reactive oxygen species (ROS) homeostasis, which could be prevented by inhibiting intracellular ROS with N-acetyl cysteine (NAC).	Acetylcysteine	193-210	transcription factor binding to IGHM enhancer 3	Homo sapiens	42-46
30247156-8	2018	Treatment with rapamycin and the antioxidant N-acetylcysteine rescued Tsc1-cKO hair cells from injury in vivo.	Acetylcysteine	45-61	TSC complex subunit 1	Mus musculus	70-74
31392779-5	2019	Caspase activation is dependent on ROS as shown by the ability of CGs to generate ROS and the ROS-N-acetylcysteine (NAC) relationship, which inhibits apoptosis during cotreatment by preventing the formation of caspase-8 and -3.	Acetylcysteine	98-114	caspase 8	Homo sapiens	210-226
31545445-10	2019	However, pretreatment of HUVECs with NAC significantly attenuated the increase in the expression of inflammatory factors and the level of phosphorylated p65; this indicated that NAC prevented the activation of the NF-kappaB signaling pathway.	Acetylcysteine	37-40	RELA proto-oncogene, NF-kB subunit	Homo sapiens	153-156
32439580-9	2020	Specifically, the decreased expression of TFE3 was closely related to the disruption of reactive oxygen species (ROS) homeostasis, which could be prevented by inhibiting intracellular ROS with N-acetyl cysteine (NAC).	Acetylcysteine	212-215	transcription factor binding to IGHM enhancer 3	Homo sapiens	42-46
32339879-7	2020	Furthermore, N-acetylcysteine was applied as an enhancer for ATP synthesis, which reversed the downregulation of ATP5F, NDUF, and COX7A, and consequently alleviated the elevation of RELA, CAPN1, and RIP3.	Acetylcysteine	13-29	RELA proto-oncogene, NF-kB subunit	Homo sapiens	182-186
30139658-9	2018	RESULTS: We identified a number of novel genes, including Regulator of calcineurin 1 (Rcan1) and Sestrin 2 (Sesn2) and demonstrated that they are induced by oxidative stress, by stimulation with H2O2 and by inhibiting caerulein stimulated expression with the antioxidant N-acetylcysteine.	Acetylcysteine	271-287	regulator of calcineurin 1	Mus musculus	58-84
32640348-4	2020	Furthermore, RT-qPCR and immunofluorescence assay results indicated that NAC restored the expression of Gclc, reduced the expression of ATF4, JNK and Caspase-12, and decreased the expression of eNOS and IGF-1, in the placenta.	Acetylcysteine	73-76	caspase 12	Mus musculus	150-160
30139658-9	2018	RESULTS: We identified a number of novel genes, including Regulator of calcineurin 1 (Rcan1) and Sestrin 2 (Sesn2) and demonstrated that they are induced by oxidative stress, by stimulation with H2O2 and by inhibiting caerulein stimulated expression with the antioxidant N-acetylcysteine.	Acetylcysteine	271-287	regulator of calcineurin 1	Mus musculus	86-91
29894800-10	2018	In addition, SiO2-NPs generated reactive oxygen species (ROS) and treatment of N-acetyl cysteine (NAC) attenuated the phosphorylation of JAK2, Src, Akt and STAT3, as well as the expression of COX-2 in SiO2-NPs-treated HaCaT cells.	Acetylcysteine	79-96	Janus kinase 2	Homo sapiens	137-141
29894800-10	2018	In addition, SiO2-NPs generated reactive oxygen species (ROS) and treatment of N-acetyl cysteine (NAC) attenuated the phosphorylation of JAK2, Src, Akt and STAT3, as well as the expression of COX-2 in SiO2-NPs-treated HaCaT cells.	Acetylcysteine	98-101	Janus kinase 2	Homo sapiens	137-141
31454652-10	2019	Pretreatment with the antioxidant N-acetyl-L-cysteine prevented SFN-induced apoptosis in CL1-0 cells and production of gammaH2AX in both CL1-0 and CL1-5 cells.	Acetylcysteine	34-53	adhesion G protein-coupled receptor L3	Homo sapiens	147-152
31432125-13	2019	The antioxidant N-acetylcysteine was identified to antagonize 2,5-HD-stimulated cleaved-caspase-3 and Bax upregulation, and Bcl-2 downregulation.	Acetylcysteine	16-32	caspase 3	Rattus norvegicus	88-97
32640348-4	2020	Furthermore, RT-qPCR and immunofluorescence assay results indicated that NAC restored the expression of Gclc, reduced the expression of ATF4, JNK and Caspase-12, and decreased the expression of eNOS and IGF-1, in the placenta.	Acetylcysteine	73-76	insulin-like growth factor 1	Mus musculus	203-208
32736702-5	2020	TGF-beta1 treatment increased reactive oxygen species (ROS) via NOX4 upregulation, which acts downstream of ERK and mTORC1, as the ROS scavenger N-acetylcysteine and a pan-NADPH oxidase (NOX) inhibitor DPI dissipated excess ROS generation.	Acetylcysteine	145-161	NADPH oxidase 4	Homo sapiens	64-68
32736702-5	2020	TGF-beta1 treatment increased reactive oxygen species (ROS) via NOX4 upregulation, which acts downstream of ERK and mTORC1, as the ROS scavenger N-acetylcysteine and a pan-NADPH oxidase (NOX) inhibitor DPI dissipated excess ROS generation.	Acetylcysteine	145-161	CREB regulated transcription coactivator 1	Mus musculus	116-122
31382676-0	2019	N-Acetylcysteine Serves as Substrate of 3-Mercaptopyruvate Sulfurtransferase and Stimulates Sulfide Metabolism in Colon Cancer Cells.	Acetylcysteine	0-16	mercaptopyruvate sulfurtransferase	Homo sapiens	40-76
30232291-6	2018	Upon ACT, NAC-generated Tscm cells established long-term memory in vivo and exerted more potent antitumor immunity in a xenogeneic model when redirected with CD19-specific CAR, highlighting the translational relevance of NAC as a simple and inexpensive method to improve ACT.	Acetylcysteine	10-13	CD19 molecule	Homo sapiens	158-162
32574682-0	2020	Activation of PPARgamma reduces N-acetyl-cysteine -induced hypercorticoidism by down-regulating MC2R expression into adrenal glands.	Acetylcysteine	32-49	peroxisome proliferator activated receptor gamma	Mus musculus	14-23
29960031-6	2018	ROS scavenger N-acetyl cysteine abrogated the effects of XTT on ERK/p38 MAPK activation and JAK2/STAT3 inhibition, and rescued HCC cells from XTT-induced apoptosis.	Acetylcysteine	14-31	Janus kinase 2	Homo sapiens	92-96
30180452-9	2018	Co-treatment with NAC, an antioxidant, inhibited hIAPP-induced ROS generation, and the expression of LC3-II/LC3-I and p-AMPK in the INS-1 cells (all P&lt;0.05).	Acetylcysteine	18-21	islet amyloid polypeptide	Homo sapiens	49-54
31254666-6	2019	In addition to attenuating an abnormal pro-inflammatory response and limiting oxidative damage, NAC could inhibit lipid accumulation by targeting adipogenic transcription factors such as peroxisome proliferator-activated receptor gamma (PPARgamma) and CCAAT/enhancer binding protein beta (C/EBPbeta), and improve insulin sensitivity through augmenting phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT) pathway.	Acetylcysteine	96-99	CCAAT enhancer binding protein beta	Homo sapiens	252-287
31254666-6	2019	In addition to attenuating an abnormal pro-inflammatory response and limiting oxidative damage, NAC could inhibit lipid accumulation by targeting adipogenic transcription factors such as peroxisome proliferator-activated receptor gamma (PPARgamma) and CCAAT/enhancer binding protein beta (C/EBPbeta), and improve insulin sensitivity through augmenting phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT) pathway.	Acetylcysteine	96-99	CCAAT enhancer binding protein beta	Homo sapiens	289-298
31273057-12	2019	We also found the down-regulation of oxidising enzymes (NOX2, iNOS, SOD2, and XO) after NAC treatment.	Acetylcysteine	88-91	cytochrome b-245, beta polypeptide	Mus musculus	56-60
32707767-6	2020	The CPA-induced CSE upregulation, as well as bladder pain was prevented by HMGB1 inactivation, inhibition of HMGB1 release from macrophages, antagonists of RAGE or P2X4/P2X7 receptors, and N-acetylcysteine, an antioxidant.	Acetylcysteine	189-205	cystathionase (cystathionine gamma-lyase)	Mus musculus	16-19
31172724-4	2019	RESULTS: In A549 cells, the levels of reactive oxygen species (ROS) and thymic stromal lymphopoietin (TSLP) were significantly increased by GCE treatment, but were suppressed by PAR2-antagonist (PAR2-ant) or N-acetylcysteine (NAC) treatment.	Acetylcysteine	208-224	thymic stromal lymphopoietin	Mus musculus	72-100
30082742-8	2018	In ascidian spermatozoa, the NAC supplementation decreased external pH, which in turn brought to a pHi lowering.	Acetylcysteine	29-32	glucose-6-phosphate isomerase	Homo sapiens	99-102
32720162-7	2020	Treating the cells with an ROS scavenger, N-acetyl cysteine (NAC), led to AMPK inactivation and apoptosis inhibition, allowing the recovery of cell health.	Acetylcysteine	42-59	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	74-78
29715464-15	2018	Antioxidant N-acetylcysteine abrogated the elevated UCP1 expression and reversed some inflammatory genes induced by SAT1 activation.	Acetylcysteine	12-28	uncoupling protein 1 (mitochondrial, proton carrier)	Mus musculus	52-56
31051153-10	2019	NAC enhanced the protective efficacy of ATR and 2-PAM in most parameters, without any appreciable protection in iNOS and c-fos expression.	Acetylcysteine	0-3	peptidylglycine alpha-amidating monooxygenase	Mus musculus	50-53
29715464-15	2018	Antioxidant N-acetylcysteine abrogated the elevated UCP1 expression and reversed some inflammatory genes induced by SAT1 activation.	Acetylcysteine	12-28	spermidine/spermine N1-acetyl transferase 1	Mus musculus	116-120
32361974-5	2020	The presence of NAC antagonized the ROS production, expressions of IRE1alpha and p-IRE1alpha; however, STF-083010 could decrease the expression levels of GRP78, XBP1, NF-kappaB, and p-NF-kappaB and attenuate IL-1beta, IL-6, TNF-alpha, VCAM-1, and ET-1 release induced by endosulfan.	Acetylcysteine	16-19	endoplasmic reticulum to nucleus signaling 1	Homo sapiens	67-76
32361974-5	2020	The presence of NAC antagonized the ROS production, expressions of IRE1alpha and p-IRE1alpha; however, STF-083010 could decrease the expression levels of GRP78, XBP1, NF-kappaB, and p-NF-kappaB and attenuate IL-1beta, IL-6, TNF-alpha, VCAM-1, and ET-1 release induced by endosulfan.	Acetylcysteine	16-19	endoplasmic reticulum to nucleus signaling 1	Homo sapiens	83-92
31099374-6	2019	In addition, PaH-PDT markedly increased the generation of intracellular ROS, which can be suppressed using the ROS scavenger N-acetylcysteine (NAC).	Acetylcysteine	125-141	phenylalanine hydroxylase	Homo sapiens	13-20
31099374-6	2019	In addition, PaH-PDT markedly increased the generation of intracellular ROS, which can be suppressed using the ROS scavenger N-acetylcysteine (NAC).	Acetylcysteine	143-146	phenylalanine hydroxylase	Homo sapiens	13-20
32433928-7	2020	Moreover, the levels of CREB, miR-630 expression, and double-strand breaks (DSBs) were attenuated by 5 mM N-acetyl-L-cysteine (NAC) pretreatment, indicating that reactive oxygen species (ROS)-dependent CREB-miR-630 was involved in DSB repair.	Acetylcysteine	106-125	microRNA 630	Homo sapiens	30-37
29513566-7	2018	Interestingly, antioxidant treatments such as N-acetylcysteine and TEMPOL, but not catalase, blocked the clinorotation-mediated activation of ERK1/2.	Acetylcysteine	46-62	mitogen activated protein kinase 3	Rattus norvegicus	142-148
30664687-6	2019	Treatment with antioxidant N-acetyl cysteine phenocopied loss of Klf9 including suppression of melanocytic hyperplasia.	Acetylcysteine	27-44	Kruppel-like factor 9	Mus musculus	65-69
32433928-7	2020	Moreover, the levels of CREB, miR-630 expression, and double-strand breaks (DSBs) were attenuated by 5 mM N-acetyl-L-cysteine (NAC) pretreatment, indicating that reactive oxygen species (ROS)-dependent CREB-miR-630 was involved in DSB repair.	Acetylcysteine	106-125	microRNA 630	Homo sapiens	207-214
29794203-9	2018	Although guaifenesin is used widely, its effectiveness is unclear, whereas N-acetylcysteine currently has strong evidence supporting a decreased risk of COPD exacerbations.	Acetylcysteine	75-91	COPD	Homo sapiens	153-157
32433928-7	2020	Moreover, the levels of CREB, miR-630 expression, and double-strand breaks (DSBs) were attenuated by 5 mM N-acetyl-L-cysteine (NAC) pretreatment, indicating that reactive oxygen species (ROS)-dependent CREB-miR-630 was involved in DSB repair.	Acetylcysteine	127-130	microRNA 630	Homo sapiens	30-37
32433928-7	2020	Moreover, the levels of CREB, miR-630 expression, and double-strand breaks (DSBs) were attenuated by 5 mM N-acetyl-L-cysteine (NAC) pretreatment, indicating that reactive oxygen species (ROS)-dependent CREB-miR-630 was involved in DSB repair.	Acetylcysteine	127-130	microRNA 630	Homo sapiens	207-214
31114231-7	2019	The ROS scavenger N-acetylcysteine was used for treatment of BCPAP-SIRT6, and the same measurements as described above were detected again.	Acetylcysteine	18-34	sirtuin 6	Homo sapiens	61-72
31837856-8	2020	Incidentally, both CH and NAC attenuated the EOM-induced changes in the mRNA expression of genes involved in cardiac development (nkx2.5, sox9b), oxidative stress (nrf2a, nrf2b, gstp1, gstp2, sod2, ho1, cat) and apoptosis (p53, bax).	Acetylcysteine	26-29	nfe2 like bZIP transcription factor 2b	Danio rerio	171-176
29928571-6	2018	Moreover, levels of the inflammatory markers thioredoxin-interacting protein and prostaglandin-endoperoxide synthase 2 were upregulated under l-Ser-depleted conditions; this was suppressed by the addition of N-acetyl-l-cysteine.	Acetylcysteine	208-227	prostaglandin-endoperoxide synthase 2	Mus musculus	81-118
32450865-10	2020	In the unfolded protein response (UPR) pathway, the expression of ECHS1, HSP60, and HSP70 was decreased in the HFD group (p < 0.05) and rescued by NAC therapy.	Acetylcysteine	147-150	enoyl Coenzyme A hydratase, short chain, 1, mitochondrial	Mus musculus	66-71
32432106-8	2020	In addition, suppressing ROS production by N-acetyl-L-cysteine down-regulated the number of intracellular autophagosomes and the expression of Beclin-1, ATG5, and cytokines IL-1beta, IL-6, and TNF-alpha.	Acetylcysteine	43-62	beclin-1	Ovis aries	143-151
29292841-9	2018	Meanwhile, N-acetylcysteine (NAC) significantly attenuated the HMGB1-mediated pro-inflammatory cytokines release.	Acetylcysteine	11-27	high mobility group box 1	Mus musculus	63-68
30956032-9	2019	Pretreatment with N-acetylcysteine (NAC) abrogate the difference between HI and LIUVA radiation on fibroblasts in terms of intracellular ROS, JNK phosphorylation, MMP-1 expression and type I collagen expression.	Acetylcysteine	18-34	matrix metallopeptidase 13	Mus musculus	163-168
30956032-9	2019	Pretreatment with N-acetylcysteine (NAC) abrogate the difference between HI and LIUVA radiation on fibroblasts in terms of intracellular ROS, JNK phosphorylation, MMP-1 expression and type I collagen expression.	Acetylcysteine	36-39	matrix metallopeptidase 13	Mus musculus	163-168
29292841-9	2018	Meanwhile, N-acetylcysteine (NAC) significantly attenuated the HMGB1-mediated pro-inflammatory cytokines release.	Acetylcysteine	29-32	high mobility group box 1	Mus musculus	63-68
30948926-5	2019	Secondly, the influence of ROS content on the activity of the JNK1/Sirt1/FoxO3a signaling pathway was explored through the application of NAC, sp600125 (a JNK1 inhibitor), and nicotinamide (a Sirt1 inhibitor).	Acetylcysteine	138-141	forkhead box O3	Rattus norvegicus	73-79
30496017-9	2019	Expressions of Brca2, Xpc, Mlh3, Rad51, Xrcc2, Hus1, Rad9a, Cdkn1a, Gadd45a which are the DNA-repair genes were found to be significantly higher in NAC + ALC + IR group than those in individual treatment of ALC or NAC.	Acetylcysteine	214-217	XPC complex subunit, DNA damage recognition and repair factor	Homo sapiens	22-25
30496017-9	2019	Expressions of Brca2, Xpc, Mlh3, Rad51, Xrcc2, Hus1, Rad9a, Cdkn1a, Gadd45a which are the DNA-repair genes were found to be significantly higher in NAC + ALC + IR group than those in individual treatment of ALC or NAC.	Acetylcysteine	214-217	RAD9 checkpoint clamp component A	Homo sapiens	53-58
32432106-8	2020	In addition, suppressing ROS production by N-acetyl-L-cysteine down-regulated the number of intracellular autophagosomes and the expression of Beclin-1, ATG5, and cytokines IL-1beta, IL-6, and TNF-alpha.	Acetylcysteine	43-62	interleukin-1 alpha	Ovis aries	173-181
32568258-6	2020	N-acetylcysteine increased the number of immune cells and decreased TNF-alpha production after cyclophosphamide injection and decreased TNF-alpha, IFN-gamma, NF-kappaB, and IL-8 expression and increased IL-10 expression in peripheral blood mononuclear cells.	Acetylcysteine	0-16	tumor necrosis factor	Sus scrofa	68-77
29429900-5	2018	We provide evidence suggesting the possibility that sulfane sulfur species produced by 3-mercaptopyruvate sulfurtransferase and sulfide:quinone oxidoreductase are the actual mediators of the immediate antioxidative and cytoprotective effects provided by NAC.	Acetylcysteine	254-257	mercaptopyruvate sulfurtransferase	Homo sapiens	87-123
32568258-6	2020	N-acetylcysteine increased the number of immune cells and decreased TNF-alpha production after cyclophosphamide injection and decreased TNF-alpha, IFN-gamma, NF-kappaB, and IL-8 expression and increased IL-10 expression in peripheral blood mononuclear cells.	Acetylcysteine	0-16	tumor necrosis factor	Sus scrofa	136-145
32568258-6	2020	N-acetylcysteine increased the number of immune cells and decreased TNF-alpha production after cyclophosphamide injection and decreased TNF-alpha, IFN-gamma, NF-kappaB, and IL-8 expression and increased IL-10 expression in peripheral blood mononuclear cells.	Acetylcysteine	0-16	interferon gamma	Sus scrofa	147-156
32568258-6	2020	N-acetylcysteine increased the number of immune cells and decreased TNF-alpha production after cyclophosphamide injection and decreased TNF-alpha, IFN-gamma, NF-kappaB, and IL-8 expression and increased IL-10 expression in peripheral blood mononuclear cells.	Acetylcysteine	0-16	C-X-C motif chemokine ligand 8	Sus scrofa	173-177
30717309-9	2019	Furthermore, TP4-induced cytotoxicity, oxidative stress, phosphorylation of p38, and DNA damage were all attenuated by the mitochondrial-targeted reactive oxygen species (ROS) scavenger MitoTEMPO, or the reactive oxygen species scavenger N-acetyl-L-cysteine.	Acetylcysteine	238-257	moronecidin	Oreochromis niloticus	13-16
32313093-8	2020	The addition of NAC and miR-200c inhibitor had an opposite impact on the expression of miR-200c and ZEB1, thus hindered the effects of UTMD on MDA231 cells EMT.	Acetylcysteine	16-19	microRNA 200c	Homo sapiens	87-95
30289994-9	2019	N-acetylcysteine combined with sildenafil decreased MMP-2 and MMP-9 activity and NO consumption and inhibited apoptosis of pulmonary arterial endothelial cells.	Acetylcysteine	0-16	matrix metalloproteinase-9	Oryctolagus cuniculus	62-67
31088037-5	2019	Both, Fyn activation and the GCDC-induced Ntcp retrieval from the plasma membrane were sensitive to the NADPH oxidase inhibitor apocynin, the antioxidant N-acetylcysteine and the Src family kinase inhibitors SU6656 and PP-2, whereas PP-2 did not inhibit GCDC-induced Yes activation.	Acetylcysteine	154-170	FYN proto-oncogene, Src family tyrosine kinase	Rattus norvegicus	6-9
31088037-5	2019	Both, Fyn activation and the GCDC-induced Ntcp retrieval from the plasma membrane were sensitive to the NADPH oxidase inhibitor apocynin, the antioxidant N-acetylcysteine and the Src family kinase inhibitors SU6656 and PP-2, whereas PP-2 did not inhibit GCDC-induced Yes activation.	Acetylcysteine	154-170	solute carrier family 10 member 1	Rattus norvegicus	42-46
30387809-4	2019	The results revealed that NAC pretreatment increased cell viability and inhibited the activation of caspase-3, -8 and -9 during hydrogen peroxide (H2O2)-induced oxidative stress in H9c2 cells.	Acetylcysteine	26-29	caspase 3	Rattus norvegicus	100-120
29395036-4	2018	The control with N-acetyl cysteine of the oxidative status in FVIII-deficient mice, a model of severe hemophilia A, reduced the immune response to exogenous FVIII.	Acetylcysteine	17-34	coagulation factor VIII	Mus musculus	62-67
29395036-4	2018	The control with N-acetyl cysteine of the oxidative status in FVIII-deficient mice, a model of severe hemophilia A, reduced the immune response to exogenous FVIII.	Acetylcysteine	17-34	coagulation factor VIII	Mus musculus	157-162
29353375-4	2018	A dual inhibitor of the biosynthetic enzymes for H2S, cystathionine beta-synthase (CBS) and cystathionine gamma-lyase (CSE), amino-oxyacetic acid (AOA; 3 mM) reversed the inhibitory responses caused by GYY 4137, L-cysteine and N-acetylcysteine on K+-evoked [3H]D-aspartate release.	Acetylcysteine	227-243	cystathionine beta-synthase	Bos taurus	54-81
31068539-9	2019	Pretreatment of cells with ROS scavenger N-acetyl cysteine (NAC) abrogated the stimulatory effect of TiO2-NPs on p65, p50, and COX-2 expression.	Acetylcysteine	41-58	RELA proto-oncogene, NF-kB subunit	Homo sapiens	113-116
31068539-9	2019	Pretreatment of cells with ROS scavenger N-acetyl cysteine (NAC) abrogated the stimulatory effect of TiO2-NPs on p65, p50, and COX-2 expression.	Acetylcysteine	60-63	RELA proto-oncogene, NF-kB subunit	Homo sapiens	113-116
32316268-8	2020	SIN-1 (500 muM, a generator nitric oxide, superoxide and peroxynitrite), which facilitates the cystine-cysteine shuttle mediated by xCT (a glutamate/cystein:cystine/NAC antiporter), did not affect basal GSH concentration in WT and P2X7R knockout (KO) mice.	Acetylcysteine	165-168	mitogen-activated protein kinase associated protein 1	Mus musculus	0-5
32316268-8	2020	SIN-1 (500 muM, a generator nitric oxide, superoxide and peroxynitrite), which facilitates the cystine-cysteine shuttle mediated by xCT (a glutamate/cystein:cystine/NAC antiporter), did not affect basal GSH concentration in WT and P2X7R knockout (KO) mice.	Acetylcysteine	165-168	solute carrier family 7 (cationic amino acid transporter, y+ system), member 11	Mus musculus	132-135
32316268-9	2020	However, SIN-1 effectively reduced the efficacy of NAC in GSH synthesis in WT mice, but not in P2X7R KO mice.	Acetylcysteine	51-54	mitogen-activated protein kinase associated protein 1	Mus musculus	9-14
31168028-8	2019	The antioxidant N-acetylcysteine reduced the expression of phosphorylated ATM and H2AX, and the ATM inhibitor, caffeine, inhibited p53 activation.	Acetylcysteine	16-32	H2A.X variant histone	Homo sapiens	82-86
32084513-8	2020	Addition of reducing reagents (dithiothreitol, glutathione and N-acetyl cysteine) led to a partial recovery of CatS activity following incubation with CSE, hydrogen peroxide and peroxynitrite.	Acetylcysteine	63-80	cathepsin S	Felis catus	111-115
30315841-8	2019	Interestingly, NAC supplementation not only attenuated elevated 8-OHdG, PARP-1, caspase-3, cleaved caspase-9, and Bax, but also the TCE-mediated autoimmune response supported by significantly reduced serum anti-ssDNA antibodies.	Acetylcysteine	15-18	caspase 9	Mus musculus	99-108
29378951-2	2018	Here we show that holo-Lcn2 (Lcn2-siderophore-iron, 1:3:1) increases mitochondrial reactive oxygen species (ROS) generation and attenuates mitochondrial oxidative phosphorylation in adult rat primary cardiomyocytes in a manner blocked by N-acetyl-cysteine or the mitochondria-specific antioxidant SkQ1.	Acetylcysteine	238-255	lipocalin 2	Rattus norvegicus	23-27
29378951-2	2018	Here we show that holo-Lcn2 (Lcn2-siderophore-iron, 1:3:1) increases mitochondrial reactive oxygen species (ROS) generation and attenuates mitochondrial oxidative phosphorylation in adult rat primary cardiomyocytes in a manner blocked by N-acetyl-cysteine or the mitochondria-specific antioxidant SkQ1.	Acetylcysteine	238-255	lipocalin 2	Rattus norvegicus	29-33
29422061-12	2018	Among patients with available genetic data, a marginally higher proportion of ANA positive patients (p = 0.08) carried the rs3750920 (TOLLIP) genotype previously shown to predict favorable outcome in NAC exposed patients.	Acetylcysteine	200-203	toll interacting protein	Homo sapiens	134-140
30504734-12	2018	Moreover, palmitate administration overcame the antioxidant effect of 3 mM N-acetylcysteine to significantly inhibit apoptosis, DNA fragmentation, and caspase-3 activity.	Acetylcysteine	75-91	caspase 3	Rattus norvegicus	151-160
32040762-0	2020	Activation of MIP-2 and MCP-5 Expression in Methylmercury-Exposed Mice and Their Suppression by N-Acetyl-L-Cysteine.	Acetylcysteine	96-115	chymase 1, mast cell	Mus musculus	24-29
32040762-8	2020	NAC significantly suppressed MeHg-induced IL-6 and MIP-2 expressions in the serum (p &lt; 0.05 for both), and slightly reduced MCP-5 expression in the cerebrum.	Acetylcysteine	0-3	chymase 1, mast cell	Mus musculus	127-132
31697963-11	2020	Equally, administration of n-acetylcysteine to fasted WT mice prevented HFD-dependent learning impairment and caspase-1 activation in the BLp.	Acetylcysteine	27-43	caspase 1	Mus musculus	110-119
29425508-4	2018	l-BAIBA was as or more protective than estrogen or N-acetyl cysteine, signaling through the Mas-Related G Protein-Coupled Receptor Type D (MRGPRD) to prevent the breakdown of mitochondria due to ROS.	Acetylcysteine	51-68	MAS-related GPR, member D	Mus musculus	92-137
29425508-4	2018	l-BAIBA was as or more protective than estrogen or N-acetyl cysteine, signaling through the Mas-Related G Protein-Coupled Receptor Type D (MRGPRD) to prevent the breakdown of mitochondria due to ROS.	Acetylcysteine	51-68	MAS-related GPR, member D	Mus musculus	139-145
30241048-8	2018	Furthermore, Cd(NO3)2-induced apoptosis, caspases activities, mitochondrial dysfunction, and ROS generation were reduced by N-acetyl-l-cysteine (NAC).	Acetylcysteine	124-143	caspase 9	Mus musculus	41-49
30873870-8	2019	Moreover, after pretreatment with N-acetyl-cysteine, Shikonin increased the production of reactive oxygen species that are involved in regulating ER stress-mediated apoptosis and p38-activated autophagy, as evidenced by the reversion of cell viability and apoptosis and a decrease in p-eIF2alpha, CHOP, p-p38, LC3B-II, and Beclin 1 levels.	Acetylcysteine	34-51	microtubule associated protein 1 light chain 3 beta	Homo sapiens	310-314
30241048-8	2018	Furthermore, Cd(NO3)2-induced apoptosis, caspases activities, mitochondrial dysfunction, and ROS generation were reduced by N-acetyl-l-cysteine (NAC).	Acetylcysteine	145-148	caspase 9	Mus musculus	41-49
31539536-7	2019	Moreover, the antioxidant, N-acetylcysteine (NAC), significantly attenuates oxidative stress levels and dendritic spine deficiencies resulting from COX-2 overexpression; and, suppression of oxidative stress by NAC also significantly ameliorates depressive behaviors in rats.	Acetylcysteine	27-43	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	148-153
30141055-7	2018	Pulsed continuous arterial spin labelling was used to assess the effects of NAC on resting cerebral blood flow (rCBF) in the same regions.	Acetylcysteine	76-79	CCAAT/enhancer binding protein zeta	Rattus norvegicus	112-116
29459829-7	2018	In the presence of either an antioxidant (N-acetylcysteine, NAC) or diphenylene iodonium (DPI), PTTH-stimulated JNK phosphorylation was blocked.	Acetylcysteine	42-58	prothoracicotropic hormone	Bombyx mori	96-100
29459829-7	2018	In the presence of either an antioxidant (N-acetylcysteine, NAC) or diphenylene iodonium (DPI), PTTH-stimulated JNK phosphorylation was blocked.	Acetylcysteine	42-58	c-Jun NH2-terminal kinase	Bombyx mori	112-115
29459829-7	2018	In the presence of either an antioxidant (N-acetylcysteine, NAC) or diphenylene iodonium (DPI), PTTH-stimulated JNK phosphorylation was blocked.	Acetylcysteine	60-63	prothoracicotropic hormone	Bombyx mori	96-100
29459829-7	2018	In the presence of either an antioxidant (N-acetylcysteine, NAC) or diphenylene iodonium (DPI), PTTH-stimulated JNK phosphorylation was blocked.	Acetylcysteine	60-63	c-Jun NH2-terminal kinase	Bombyx mori	112-115
28898446-7	2018	In diethylnitrosamine (DEN)-treated primary hepatocytes, NAC and Trolox alleviated DNA damage by activating ataxia-telangiectasia mutated (ATM)/ATM and Rad3-related (ATR) for DNA repair whereas SS-31 and Mito-Q aggravated damage by inactivating them.	Acetylcysteine	57-60	ataxia telangiectasia mutated	Mus musculus	139-142
28898446-7	2018	In diethylnitrosamine (DEN)-treated primary hepatocytes, NAC and Trolox alleviated DNA damage by activating ataxia-telangiectasia mutated (ATM)/ATM and Rad3-related (ATR) for DNA repair whereas SS-31 and Mito-Q aggravated damage by inactivating them.	Acetylcysteine	57-60	ataxia telangiectasia mutated	Mus musculus	144-147
28898446-9	2018	Localization of ATM between mitochondria and nuclei was altered after NAC and SS-31 treatment.	Acetylcysteine	70-73	ataxia telangiectasia mutated	Mus musculus	16-19
30187952-10	2018	Moreover, N-acetyl-cysteine, an reactive oxygen species (ROS) scavenger, abrogated the effects of ivermectin on TFE3-dependent autophagy.	Acetylcysteine	10-27	transcription factor binding to IGHM enhancer 3	Homo sapiens	112-116
31539536-7	2019	Moreover, the antioxidant, N-acetylcysteine (NAC), significantly attenuates oxidative stress levels and dendritic spine deficiencies resulting from COX-2 overexpression; and, suppression of oxidative stress by NAC also significantly ameliorates depressive behaviors in rats.	Acetylcysteine	45-48	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	148-153
29935984-6	2018	Furthermore, the capacity of NAC to ameliorate acute toluene-induced deficits in object recognition and social interaction was blocked by the xCT inhibitor (S)-4-carboxyphenylglycine and the mGluR2/3 antagonist LY341495.	Acetylcysteine	29-32	solute carrier family 7 (cationic amino acid transporter, y+ system), member 11	Mus musculus	142-145
29258000-7	2018	Treatment of RAW264.7 cells with OMF increased the intracellular level of reactive oxygen species (ROS) and the phosphorylation levels of p38 mitogen-activated protein kinase (MAPK); co-treatment with the antioxidant N-acetyl-cysteine (NAC) blocked this OMF-induced p38 MAPK phosphorylation.	Acetylcysteine	217-234	mitogen-activated protein kinase 14	Mus musculus	138-141
29258000-7	2018	Treatment of RAW264.7 cells with OMF increased the intracellular level of reactive oxygen species (ROS) and the phosphorylation levels of p38 mitogen-activated protein kinase (MAPK); co-treatment with the antioxidant N-acetyl-cysteine (NAC) blocked this OMF-induced p38 MAPK phosphorylation.	Acetylcysteine	217-234	mitogen-activated protein kinase 14	Mus musculus	266-269
29258000-7	2018	Treatment of RAW264.7 cells with OMF increased the intracellular level of reactive oxygen species (ROS) and the phosphorylation levels of p38 mitogen-activated protein kinase (MAPK); co-treatment with the antioxidant N-acetyl-cysteine (NAC) blocked this OMF-induced p38 MAPK phosphorylation.	Acetylcysteine	236-239	mitogen-activated protein kinase 14	Mus musculus	138-141
31890447-16	2019	Evidence suggests that there is a beneficial role for N-acetylcysteine in the management of NAI-ALF.	Acetylcysteine	54-70	afamin	Homo sapiens	96-99
29258000-8	2018	Moreover, NAC, or SB203580 (a p38 MAPK inhibitor), blocked the OMF-induced nuclear translocation of Nrf2 and HO-1 expression, suggesting that OMF induces HO-1 expression by activating Nrf2 through the p38 MAPK pathway.	Acetylcysteine	10-13	mitogen-activated protein kinase 14	Mus musculus	201-209
29207099-7	2018	Compared with the controls, serum NGAL levels were high in UUO+iohexol rats 1 day following injection and 3 weeks after obstruction relief, but UUO+iohexol+NAC rats exhibited lower serum NGAL levels compared with UUO+iohexol rats (all P&lt;0.05).	Acetylcysteine	156-159	lipocalin 2	Rattus norvegicus	187-191
30103798-11	2018	CONCLUSION: Taken together with the finding that ablation of FOS-induced intestinal ROS using NAC decreased peroxynitrite production as well as PA phagocytic activity of AMs and protein expression of CRP-ductin, IL-17, Reg3beta, and RELMbeta in the intestinal mucosa, we conclude that commensal microflora plays a key role in stimulating lung immunity.	Acetylcysteine	94-97	resistin like beta	Mus musculus	233-241
30011295-6	2018	Pre-treatment with the antioxidant, N-acetylcysteine, prevented the actions of arecoline on cell viability, G2/M growth arrest, reactive oxygen species (ROS) production, and the levels of CDK1, p21, p27, p53, cyclin B1, and phospho-AMPK proteins.	Acetylcysteine	36-52	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	232-236
31754457-7	2019	Interestingly, superoxide scavengers N-acetylcysteine (NAC) and Tempol, chemicals that reduce oxidative stress, were able to recover liver phenotypes, indicating that mTORC1 hyperactivation induced liver damage mainly through oxidative stress pathways.	Acetylcysteine	37-53	CREB regulated transcription coactivator 1	Mus musculus	167-173
29602802-5	2018	Furthermore, we measured radioresistance by clonogenic survival assay after treatment with autophagy inhibitor (Chloroquine) and ROS inhibitor (N-acetyl-l-cysteine) in SMAD4-depleted pancreatic cancer cells.	Acetylcysteine	144-163	SMAD family member 4	Homo sapiens	168-173
29552311-8	2018	On the other hand, expression plasmid of SIRT1, N-acetyl cysteine or SP600125 (JNK specific inhibitor) abolished the effect of miR-29b on oxaliplatin-treated OR-SW480.	Acetylcysteine	48-65	microRNA 29b-1	Homo sapiens	127-134
31754457-7	2019	Interestingly, superoxide scavengers N-acetylcysteine (NAC) and Tempol, chemicals that reduce oxidative stress, were able to recover liver phenotypes, indicating that mTORC1 hyperactivation induced liver damage mainly through oxidative stress pathways.	Acetylcysteine	55-58	CREB regulated transcription coactivator 1	Mus musculus	167-173
29222055-8	2018	Pre-incubation of cells with antioxidant N-acetyl-l-cysteine (NAC) or resveratrol improved cell survival, accompanied by decreased LC3-II expression and increased expression level of p62, suggesting a down regulation of autophagy flux.	Acetylcysteine	41-60	KH RNA binding domain containing, signal transduction associated 1	Rattus norvegicus	183-186
31542488-9	2019	Furthermore, N-acetyl-L-cysteine (NAC), a widely accepted ROS scavenger, efficiently reversed DAC-induced apoptosis by inhibiting ROS generation (***P < 0.00051) in mitochondria and restoring mitochondrial membrane potential.	Acetylcysteine	13-32	arylacetamide deacetylase	Homo sapiens	94-97
29222055-8	2018	Pre-incubation of cells with antioxidant N-acetyl-l-cysteine (NAC) or resveratrol improved cell survival, accompanied by decreased LC3-II expression and increased expression level of p62, suggesting a down regulation of autophagy flux.	Acetylcysteine	62-65	KH RNA binding domain containing, signal transduction associated 1	Rattus norvegicus	183-186
29620169-13	2018	Furthermore, the ROS scavenger N-acetylcysteine also suppressed hypoxia inducible factor 1alpha and HES1 expression in breast cancer cells during hypoxia, but hydrogen peroxide (H2O2) levels were increased.	Acetylcysteine	31-47	hes family bHLH transcription factor 1	Homo sapiens	100-104
29522769-7	2018	Finally, NAC-treated MSG rats retained normal liver glucokinase and fructokinase activities, and Srebp1c, Fas and Gpat (lipogenic genes) expression levels.	Acetylcysteine	9-12	glucokinase	Rattus norvegicus	52-63
29522769-7	2018	Finally, NAC-treated MSG rats retained normal liver glucokinase and fructokinase activities, and Srebp1c, Fas and Gpat (lipogenic genes) expression levels.	Acetylcysteine	9-12	sterol regulatory element binding transcription factor 1	Rattus norvegicus	97-104
29642488-6	2018	These caspases and PARP activations were suppressed by N-acetylcysteine (NAC) pretreatment.	Acetylcysteine	55-71	caspase 8	Homo sapiens	6-14
29642488-6	2018	These caspases and PARP activations were suppressed by N-acetylcysteine (NAC) pretreatment.	Acetylcysteine	73-76	caspase 8	Homo sapiens	6-14
31542488-9	2019	Furthermore, N-acetyl-L-cysteine (NAC), a widely accepted ROS scavenger, efficiently reversed DAC-induced apoptosis by inhibiting ROS generation (***P < 0.00051) in mitochondria and restoring mitochondrial membrane potential.	Acetylcysteine	34-37	arylacetamide deacetylase	Homo sapiens	94-97
30788945-8	2018	Compared with TCP group, serum levels of TNF-alpha, IL-1beta and IL-6, and osteolysis area were decreased markedly in NAC group (P&lt;0.05), serum level of T-AOC and SOD activity were increased obviously in NAC group (P&lt;0.05), and GRP78 expression, the ratio of p-PERK/PERK and p-eIF2alpha/eIF2alpha were obviously down-regulated.	Acetylcysteine	118-121	eukaryotic translation initiation factor 2A	Mus musculus	283-292
29130363-11	2018	Administration of N-acetyl-l-cysteine, a ROS scavenger, to atg5-cKO mice rescued the glomerular phenotypes.	Acetylcysteine	18-37	autophagy related 5	Mus musculus	59-63
31390228-6	2019	Selective angiotensin II type 1 receptor (AT1R) blocker losartan suppressed ROS production and ROS scavenger N-Acetyl-L-cysteine (NAC) prevented p38 MAPK phosphorylation.	Acetylcysteine	109-128	angiotensin II receptor type 1	Homo sapiens	10-40
30788945-8	2018	Compared with TCP group, serum levels of TNF-alpha, IL-1beta and IL-6, and osteolysis area were decreased markedly in NAC group (P&lt;0.05), serum level of T-AOC and SOD activity were increased obviously in NAC group (P&lt;0.05), and GRP78 expression, the ratio of p-PERK/PERK and p-eIF2alpha/eIF2alpha were obviously down-regulated.	Acetylcysteine	118-121	eukaryotic translation initiation factor 2A	Mus musculus	293-302
31401317-4	2019	Importantly, NAC attenuated Cisplatin-induced placental apoptosis through down-regulation of Fas and Caspase-3 genes expression.	Acetylcysteine	13-16	caspase 3	Rattus norvegicus	101-110
29396562-3	2018	Elevated production of reactive oxygen species (ROS) in COX 4I1 deficient fibroblasts was detected in cells grown in glucose free medium and normalized by ascorbate or N-acetylcysteine supplementation.	Acetylcysteine	168-184	cytochrome c oxidase subunit 4I1	Homo sapiens	56-63
30041247-10	2018	RESULTS: oxLDL induced HMGB-1 translocation and secretion in a dose- and time-dependent manner, which was inhibited by NAC.	Acetylcysteine	119-122	high mobility group box 1	Mus musculus	23-29
29327381-16	2018	N-Acetyl-cysteine or tempol prevented the decreases in the LC3 II/I ratio and Beclin1 and Atg5 expression and attenuated the increases in LV wall thickness, myocyte diameter and brain natriuretic peptide expression in AAC rats.	Acetylcysteine	0-17	beclin 1	Rattus norvegicus	78-85
28644049-10	2018	Seven of 34 patients receiving N-acetylcysteine (NAC) within 8 h had alanine aminotransferase (ALT) above reference range.	Acetylcysteine	31-47	glutamic--pyruvic transaminase	Homo sapiens	69-93
31401317-6	2019	The protective role of NAC, on the other hand, was characterized by attenuation of Fas and Caspase-3 genes- mediated apoptosis.	Acetylcysteine	23-26	caspase 3	Rattus norvegicus	91-100
28644049-10	2018	Seven of 34 patients receiving N-acetylcysteine (NAC) within 8 h had alanine aminotransferase (ALT) above reference range.	Acetylcysteine	49-52	glutamic--pyruvic transaminase	Homo sapiens	69-93
31569917-9	2019	Regarding biochemical markers, NAC and verapamil significantly decreased serum nitric oxide synthase, C-reactive protein, and cyclooxygenase- 2 levels compared to the edema control value.	Acetylcysteine	31-34	prostaglandin-endoperoxide synthase 2	Rattus norvegicus	126-143
31533227-9	2019	In addition, both reactive oxygen species (ROS) scavenger N-acetyl-L-cysteine (NAC) and VAC abolished HG-evoked dephosphorylation of AMPK and eNOS, increased miRNA-34a expression, and decreased NO production.	Acetylcysteine	58-77	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	133-137
30345869-11	2018	Distinct N-terminal cysteine and lysine residues seemed to mediate gating of TRPA1, although the electrophile scavenger N-acetyl-L-cysteine did not prevent its activation by etomidate.	Acetylcysteine	120-139	transient receptor potential cation channel subfamily A member 1	Homo sapiens	77-82
29451469-0	2018	Evaluation of the warming sensation, acceptability, and local tolerability of an acetylcysteine oral solution containing the flavoring agent IFF flavor 316282 in the treatment of productive cough : .	Acetylcysteine	81-95	interferon beta 1	Homo sapiens	141-144
29451469-1	2018	OBJECTIVE: This open-label study sought to evaluate the warming sensation produced by IFF flavor 316282 in an acetylcysteine oral solution in subjects with productive cough.	Acetylcysteine	110-124	interferon beta 1	Homo sapiens	86-89
29451469-2	2018	MATERIALS: 2% ace-tylcysteine oral solution (200 mg per 10 mL) containing IFF flavor 316282.	Acetylcysteine	14-29	interferon beta 1	Homo sapiens	74-77
29451469-10	2018	CONCLUSION: The addition of IFF flavor 316282 to a 2% acetylcysteine oral solution produced a warming sensation with rapid onset and relatively short duration, which the majority of subjects found acceptable.	Acetylcysteine	54-68	interferon beta 1	Homo sapiens	28-31
29288670-10	2018	Notably, reducing ROS production by its scavenger, N-acetyl cysteine (NAC), could down-regulate p-AMPK levels, while up-regulate the phosphorylated mechanistic target of rapamycin (p-mTOR) expressions, accompanied with the restored cell viability, as well as the reduced apoptosis and autophagy in Bri-treated liver cancer cells.	Acetylcysteine	51-68	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	98-102
31533227-9	2019	In addition, both reactive oxygen species (ROS) scavenger N-acetyl-L-cysteine (NAC) and VAC abolished HG-evoked dephosphorylation of AMPK and eNOS, increased miRNA-34a expression, and decreased NO production.	Acetylcysteine	58-77	microRNA 34a	Homo sapiens	158-167
29288670-10	2018	Notably, reducing ROS production by its scavenger, N-acetyl cysteine (NAC), could down-regulate p-AMPK levels, while up-regulate the phosphorylated mechanistic target of rapamycin (p-mTOR) expressions, accompanied with the restored cell viability, as well as the reduced apoptosis and autophagy in Bri-treated liver cancer cells.	Acetylcysteine	70-73	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	98-102
28866821-7	2017	The expression of GSR, SOD1, and SOD2 were variable in peripheral blood mononuclear cells treated with lipopolysaccharide but were consistently upregulated when co-incubated with the antioxidant, N-acetyl cysteine.	Acetylcysteine	196-213	superoxide dismutase [Cu-Zn]	Bos taurus	23-27
31533227-9	2019	In addition, both reactive oxygen species (ROS) scavenger N-acetyl-L-cysteine (NAC) and VAC abolished HG-evoked dephosphorylation of AMPK and eNOS, increased miRNA-34a expression, and decreased NO production.	Acetylcysteine	79-82	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	133-137
28866821-7	2017	The expression of GSR, SOD1, and SOD2 were variable in peripheral blood mononuclear cells treated with lipopolysaccharide but were consistently upregulated when co-incubated with the antioxidant, N-acetyl cysteine.	Acetylcysteine	196-213	superoxide dismutase 2, mitochondrial	Bos taurus	33-37
31533227-9	2019	In addition, both reactive oxygen species (ROS) scavenger N-acetyl-L-cysteine (NAC) and VAC abolished HG-evoked dephosphorylation of AMPK and eNOS, increased miRNA-34a expression, and decreased NO production.	Acetylcysteine	79-82	microRNA 34a	Homo sapiens	158-167
29329563-8	2018	Pretreating A549 cells with N-acetyl cysteine (NAC), an antioxidant, attenuated O-PMs-induced ROS generation, the phosphorylation of the mentioned kinases, and the expression of ICAM-1.	Acetylcysteine	28-45	intercellular adhesion molecule 1	Mus musculus	178-184
30861304-6	2019	The release of TGF-alpha induced by Si50 (200 microg/mL) was significantly reduced by NAC, but not by DPI nor siRNA against NADPH oxidase DUOX-1 (siDUOX-1).	Acetylcysteine	86-89	transforming growth factor alpha	Homo sapiens	15-24
29329563-8	2018	Pretreating A549 cells with N-acetyl cysteine (NAC), an antioxidant, attenuated O-PMs-induced ROS generation, the phosphorylation of the mentioned kinases, and the expression of ICAM-1.	Acetylcysteine	47-50	intercellular adhesion molecule 1	Mus musculus	178-184
30755039-7	2019	NAC significantly reduced the glutamate-induced cell death, apoptosis, Ca2+ influx, caspase-3/7 activity, and intracellular ROS production (p &lt; 0.001).	Acetylcysteine	0-3	caspase 3	Rattus norvegicus	84-93
28504001-12	2018	Moreover, mutant strains in ABC transporters Pdr5, Yor1, Bpt1 or Pdr15, were more sensitive to DCF; while mutant strains in Pdr5, Vmr1 or Pdr12 were more sensitive to NAC/DCF interaction.	Acetylcysteine	167-170	ATP-binding cassette transporter YOR1	Saccharomyces cerevisiae S288C	51-55
28504001-12	2018	Moreover, mutant strains in ABC transporters Pdr5, Yor1, Bpt1 or Pdr15, were more sensitive to DCF; while mutant strains in Pdr5, Vmr1 or Pdr12 were more sensitive to NAC/DCF interaction.	Acetylcysteine	167-170	ATP-binding cassette bilirubin transporter BPT1	Saccharomyces cerevisiae S288C	57-61
28892098-10	2017	NAC rescued the ts-Src MDCK cells from ROS-induced apoptosis without upregulation of survivin resulting in a situation resembling untransformed MDCK cells in 3D environment and E-cadherin delineating the lateral cell walls.	Acetylcysteine	0-3	SRC proto-oncogene, non-receptor tyrosine kinase	Canis lupus familiaris	19-22
28892098-10	2017	NAC rescued the ts-Src MDCK cells from ROS-induced apoptosis without upregulation of survivin resulting in a situation resembling untransformed MDCK cells in 3D environment and E-cadherin delineating the lateral cell walls.	Acetylcysteine	0-3	cadherin 1	Canis lupus familiaris	177-187
29250183-7	2017	Furthermore, reactive oxygen species (ROS)-mediated ER stress/AMPK apoptotic signaling pathway in Amp-treated colon cancer cells were markedly inhibited by treatment with N-acetyl-L-cysteine, a ROS scavenger.	Acetylcysteine	171-190	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	62-66
31173782-0	2019	Amelioration of fenitrothion induced oxidative DNA damage and inactivation of caspase-3 in the brain and spleen tissues of male rats by N-acetylcysteine.	Acetylcysteine	136-152	caspase 3	Rattus norvegicus	78-87
28986255-7	2017	Analysis of mTORC2, the complex responsible for phosphorylating Akt at S473, reveals increased cysteine oxidation of Rictor in Prdx3 KD cells that can be rescued with NAC.	Acetylcysteine	167-170	CREB regulated transcription coactivator 2	Mus musculus	12-18
28840582-3	2017	This study examined whether N-acetylcysteine (NAC), a precursor of the anti-oxidant glutathione, attenuates the increase in Cys-DA production during MAO inhibition.	Acetylcysteine	28-44	monoamine oxidase A	Rattus norvegicus	149-152
28840582-3	2017	This study examined whether N-acetylcysteine (NAC), a precursor of the anti-oxidant glutathione, attenuates the increase in Cys-DA production during MAO inhibition.	Acetylcysteine	46-49	monoamine oxidase A	Rattus norvegicus	149-152
28840582-7	2017	NAC therefore mitigates the increase in spontaneous oxidation of dopamine during MAO inhibition.	Acetylcysteine	0-3	monoamine oxidase A	Rattus norvegicus	81-84
29049376-7	2017	In HDF and HGF, TGFbeta1 induces CCN2, CCN1, endothelin-1 and alpha-smooth muscle actin (SMA) in a fashion sensitive to NAC.	Acetylcysteine	120-123	hepatocyte growth factor	Homo sapiens	11-14
29049376-7	2017	In HDF and HGF, TGFbeta1 induces CCN2, CCN1, endothelin-1 and alpha-smooth muscle actin (SMA) in a fashion sensitive to NAC.	Acetylcysteine	120-123	cellular communication network factor 2	Homo sapiens	33-37
29049376-10	2017	NAC and DPI impaired the ability of TGFbeta1 to induce protein expression of CCN2 and alpha-SMA in HDF and HGF.	Acetylcysteine	0-3	cellular communication network factor 2	Homo sapiens	77-81
29049376-10	2017	NAC and DPI impaired the ability of TGFbeta1 to induce protein expression of CCN2 and alpha-SMA in HDF and HGF.	Acetylcysteine	0-3	hepatocyte growth factor	Homo sapiens	107-110
28941500-8	2017	Thus, we propose that AGA patients might benefit from the use of N-acetyl-cysteine or other antioxidants as a supplement to currently available or emerging AGA therapies such as finasteride, minoxidil, and PGD2 receptor blockers.	Acetylcysteine	65-82	prostaglandin D2 receptor	Homo sapiens	206-219
28936177-8	2017	Moreover, pretreating Ca9-22 cells with N-acetylcysteine (NAC) rescued WFA-induced selective killing, apoptosis, G2/M arrest, oxidative stress, and DNA damage.	Acetylcysteine	40-56	carbonic anhydrase 9	Homo sapiens	22-25
28936177-8	2017	Moreover, pretreating Ca9-22 cells with N-acetylcysteine (NAC) rescued WFA-induced selective killing, apoptosis, G2/M arrest, oxidative stress, and DNA damage.	Acetylcysteine	58-61	carbonic anhydrase 9	Homo sapiens	22-25
28814068-5	2017	The expression levels of the NLRP3-inflammasome and caspase-1 were upregulated in RAW 264.7 cells by stimulation with CSE and DEPs and were inhibited by NAC.	Acetylcysteine	153-156	caspase 1	Mus musculus	52-61
28487393-9	2017	RESULTS: We demonstrated that intravenous NAC administration promotes lysis of arterial thrombi that are resistant to conventional approaches such as recombinant tissue-type plasminogen activator, direct thrombin inhibitors, and antiplatelet treatments.	Acetylcysteine	42-45	plasminogen activator, tissue	Mus musculus	162-195
28678840-9	2017	Treatment of ob/ob mice with N-acetylcysteine (NAC) in vivo or addition of NAC in vitro to HG-treated smooth muscle reversed the effect of glucose on the expression of miR-133a and RhoA, Rho kinase activity and muscle contraction.	Acetylcysteine	29-45	ras homolog family member A	Mus musculus	181-185
28678840-9	2017	Treatment of ob/ob mice with N-acetylcysteine (NAC) in vivo or addition of NAC in vitro to HG-treated smooth muscle reversed the effect of glucose on the expression of miR-133a and RhoA, Rho kinase activity and muscle contraction.	Acetylcysteine	47-50	ras homolog family member A	Mus musculus	181-185
28678840-9	2017	Treatment of ob/ob mice with N-acetylcysteine (NAC) in vivo or addition of NAC in vitro to HG-treated smooth muscle reversed the effect of glucose on the expression of miR-133a and RhoA, Rho kinase activity and muscle contraction.	Acetylcysteine	75-78	ras homolog family member A	Mus musculus	181-185
28499986-10	2017	The increase in AChE activity and decrease in pTrkB and MnSOD levels caused by STZ in the cerebral cortex and hippocampus, were prevented by the NAC and PHY treatments.	Acetylcysteine	145-148	acetylcholinesterase	Mus musculus	16-20
28499986-12	2017	In conclusion, NAC treatment prevented the cognitive impairment induced by STZ, normalizing the AChE activity and rescuing the synaptic plasticity loss.	Acetylcysteine	15-18	acetylcholinesterase	Mus musculus	96-100
28487945-3	2017	Nox4 and the Notch pathway were inhibited by N-acetylcysteine (NAC), diphenylene iodonium (DPI) or gamma-secretase inhibitor (DAPT).	Acetylcysteine	45-61	NADPH oxidase 4	Homo sapiens	0-4
28487945-3	2017	Nox4 and the Notch pathway were inhibited by N-acetylcysteine (NAC), diphenylene iodonium (DPI) or gamma-secretase inhibitor (DAPT).	Acetylcysteine	63-66	NADPH oxidase 4	Homo sapiens	0-4
28487945-10	2017	Inhibition of Nox4 by NAC and DPI inhibited the Notch signaling pathway and ROS generation, which prevented HKC cell apoptosis.	Acetylcysteine	22-25	NADPH oxidase 4	Homo sapiens	14-18
28915583-7	2017	In the MUC4-positive JIMT1-tumors, the NAC-trastuzumab combination resulted in improved tumor-growth control compared to trastuzumab alone; with smaller tumor volume/weight, lower 18F-FDG uptake, lower %Ki67 and pAkt-expression.	Acetylcysteine	39-42	mucin 4, cell surface associated	Homo sapiens	7-11
28915583-8	2017	NAC reduced MUC4-expression, but did not affect HER2-expression or the trastuzumab-sensitivity of the MUC4-negative SKBr3-tumors.	Acetylcysteine	0-3	mucin 4, cell surface associated	Homo sapiens	12-16
28915583-9	2017	These findings suggest that improving HER2-accessibility by reducing MUC4-masking with the mucolytic drug NAC, results in a higher anti-tumor effect of trastuzumab.	Acetylcysteine	106-109	mucin 4, cell surface associated	Homo sapiens	69-73
28202395-6	2017	Our data also show that HG-induced AP1 activation and Srx expression were almost abolished by JNK inhibitor and N-acetylcysteine (NAC).	Acetylcysteine	112-128	Jun proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	35-38
28202395-6	2017	Our data also show that HG-induced AP1 activation and Srx expression were almost abolished by JNK inhibitor and N-acetylcysteine (NAC).	Acetylcysteine	130-133	Jun proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	35-38
28063998-9	2017	Furthermore, N-acetyl-cysteine (NAC), a ROS scavenger, abrogated the effects of brazilin on the NF-kappaB p65-dependent autophagy.	Acetylcysteine	13-30	RELA proto-oncogene, NF-kB subunit	Homo sapiens	106-109
28063998-9	2017	Furthermore, N-acetyl-cysteine (NAC), a ROS scavenger, abrogated the effects of brazilin on the NF-kappaB p65-dependent autophagy.	Acetylcysteine	32-35	RELA proto-oncogene, NF-kB subunit	Homo sapiens	106-109
28115645-9	2017	Mitigation of mucin induction by cotreatment of cultures with N-acetylcysteine suggests that oxidative stress contributes to mucus hypersecretion.	Acetylcysteine	62-78	LOC100508689	Homo sapiens	14-19
27238838-6	2017	The ROS inhibitor N-acetyl-l-cysteine rescued cells from Foxp3-expression-induced senescence.	Acetylcysteine	18-37	forkhead box P3	Homo sapiens	57-62
28075404-16	2017	NAC pre-treatment enhanced the amount of cell surface thiols and prevented their reduction due to treatment with AOPP.	Acetylcysteine	0-3	peroxiredoxin 5	Mus musculus	113-117
28075404-17	2017	Both ROS production and RAW264.7 differentiation into DC-like cells induced by HSA-AOPP were reduced by NAC.	Acetylcysteine	104-107	peroxiredoxin 5	Mus musculus	83-87
27777014-5	2016	The induction of HO-1 by 7-O-galloylquercetin was significantly suppressed by N-acetyl-l-cysteine and SB203580, indicating the involvement of reactive oxygen species and p38 mitogen-activated protein kinase activity, respectively.	Acetylcysteine	78-97	mitogen-activated protein kinase 14	Mus musculus	170-173
27687210-10	2016	In wild-type cells, the antioxidant N-acetylcysteine blocked CoCl2- and DFO-induced AMPK and autophagy activation, but not endoplasmic reticulum stress induced by CoCl2.	Acetylcysteine	36-52	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	84-88
27671340-11	2016	NAC supplementation dampened the accumulation of NGAL or L-FABP, hyaluronic acid, and nitric oxide in kidney tissue (p &lt; 0.01).	Acetylcysteine	0-3	lipocalin 2	Rattus norvegicus	49-53
26808296-7	2016	Pre-treatment of AGS cells with N-acetylcysteine, a well-known reactive oxygen species (ROS) scavenger, attenuated the H. pylori-induced activation of Erk, its binding to Snail promoter, inactivation of GSK-3beta, and accumulation of Snail.	Acetylcysteine	32-48	glycogen synthase kinase 3 beta	Homo sapiens	203-212
27840125-7	2016	We found that the pre-incubation with N-Acetyl-l-Cysteine (a quinone reductase inducer) or Deferoxamine (an iron chelator) prevents the generation of ROS, restores the autophagy degradation of mHtt and preserves the cell viability in SH-SY5Y cells expressing the polyQ Htt and exposed to DA.	Acetylcysteine	38-57	huntingtin	Homo sapiens	194-197
27721085-7	2016	N-Acetyl-L-cysteine significantly inhibited the activation of MEK1/2, ERK1/2, p38 MAPK, and Nrf2.	Acetylcysteine	0-19	mitogen activated protein kinase kinase 1	Rattus norvegicus	62-68
27721085-7	2016	N-Acetyl-L-cysteine significantly inhibited the activation of MEK1/2, ERK1/2, p38 MAPK, and Nrf2.	Acetylcysteine	0-19	mitogen activated protein kinase 3	Rattus norvegicus	70-76
27721085-7	2016	N-Acetyl-L-cysteine significantly inhibited the activation of MEK1/2, ERK1/2, p38 MAPK, and Nrf2.	Acetylcysteine	0-19	mitogen activated protein kinase 14	Rattus norvegicus	78-81
27477353-9	2016	Furthermore, our results showed that antioxidant N-acetyl-L-cysteine (NAC) significantly inhibited CS-induced recruitment of TLR4 into lipid rafts as well as IL-8 production.	Acetylcysteine	70-73	chemokine (C-X-C motif) ligand 15	Mus musculus	158-162
27427516-4	2016	The purpose of this study was to determine the role of ROS generating processes in affecting both the intracellular localization of the inhibitor of apoptosis protein survivin and its subsequent effect on radiation response in the presence or absence of the anti-oxidant N-acetyl-L-cysteine (NAC).	Acetylcysteine	271-290	baculoviral IAP repeat-containing 5	Mus musculus	167-175
27427516-4	2016	The purpose of this study was to determine the role of ROS generating processes in affecting both the intracellular localization of the inhibitor of apoptosis protein survivin and its subsequent effect on radiation response in the presence or absence of the anti-oxidant N-acetyl-L-cysteine (NAC).	Acetylcysteine	292-295	baculoviral IAP repeat-containing 5	Mus musculus	167-175
27427516-14	2016	Exposure of SA-NH and FSa tumor cells to 10mM NAC inhibited the ability of 5mGy and Emodin to induce intracellular translocation of survivin and the corresponding altered adaptive survival response.	Acetylcysteine	46-49	baculoviral IAP repeat-containing 5	Mus musculus	132-140
27557522-6	2016	In addition, Ca2+ levels and the expression of the Ca2+ channels, RyR1, SERCA, CACNA1S, TRPC1, and TRPC3 were recovered to normal levels by N-acetyl-L-cysteine (NAC) treatment compared with SelW knockdown cells.	Acetylcysteine	140-159	transient receptor potential cation channel subfamily C member 3	Gallus gallus	99-104
27557522-6	2016	In addition, Ca2+ levels and the expression of the Ca2+ channels, RyR1, SERCA, CACNA1S, TRPC1, and TRPC3 were recovered to normal levels by N-acetyl-L-cysteine (NAC) treatment compared with SelW knockdown cells.	Acetylcysteine	161-164	transient receptor potential cation channel subfamily C member 3	Gallus gallus	99-104
27328773-5	2016	Increased LC3 processing upon knockdown of RPIA can be reversed by treatment with the antioxidant N-acetyl cysteine.	Acetylcysteine	98-115	ribose 5-phosphate isomerase A	Homo sapiens	43-47
27339892-8	2016	In this study, we show that extracellular TGase activity increased when the ROS level in HPT or APC cells was reduced after NAC treatment.	Acetylcysteine	124-127	Transglutaminase	Drosophila melanogaster	42-47
29698950-8	2018	However, the mice treated with TSLP- and neutrophil-neutralizing antibodies and ROS and glucocorticoid receptor inhibitors (N-acetyl-L-cysteine [NAC] and RU-486, respectively) experienced an improvement.	Acetylcysteine	124-143	thymic stromal lymphopoietin	Mus musculus	31-35
29066618-8	2017	Restoration of OXPHOS Complex I inhibitor-induced miR-663 expression by N-acetylcysteine suggested that reactive oxygen species (ROS) play a key role in epigenetic regulation of miR-663.	Acetylcysteine	72-88	microRNA 663a	Homo sapiens	50-57
29066618-8	2017	Restoration of OXPHOS Complex I inhibitor-induced miR-663 expression by N-acetylcysteine suggested that reactive oxygen species (ROS) play a key role in epigenetic regulation of miR-663.	Acetylcysteine	72-88	microRNA 663a	Homo sapiens	178-185
29435131-5	2018	The expression of HIF-1alpha and YAP1 was concomitantly decreased by PD-L1 silencing or by ROS scavenger treatment (N-acetylcysteine, NAC); however, a ROS inducer treatment (pyocyanin) completely reversed the decreased expression of both genes in EGFR-mutated and -wild-type (WT) NSCLC cells.	Acetylcysteine	116-132	Yes1 associated transcriptional regulator	Homo sapiens	33-37
28864499-9	2017	Further examination of microtubule-independent steps of the pathway revealed that Jak2/STAT5B activation by growth hormone was prevented by DAS and NAC.	Acetylcysteine	148-151	signal transducer and activator of transcription 5B	Homo sapiens	87-93
29106990-10	2017	N-Acetylcysteine, a ROS scavenger, protected the cells from LED light-induced cellular damage, with rescued cell viability and restored mRNA expression of IGF-1 and TNF-alpha.	Acetylcysteine	0-16	insulin-like growth factor 1	Mus musculus	155-160
29296199-8	2017	Further studies showed that N-acetyl cysteine blocked JNK and p38 phosphorylation, suggesting that ROS were upstream activators of JNK and p38.	Acetylcysteine	28-45	mitogen-activated protein kinase 14	Mus musculus	62-65
29296199-8	2017	Further studies showed that N-acetyl cysteine blocked JNK and p38 phosphorylation, suggesting that ROS were upstream activators of JNK and p38.	Acetylcysteine	28-45	mitogen-activated protein kinase 14	Mus musculus	139-142
27670786-2	2017	We have previously demonstrated that treatment with the antioxidant N-acetylcysteine (NAC) inhibits cellular triglyceride (Tg) accumulation as well as total cellular monoamine oxidase A (MAOA) expression in 3T3-L1 mature adipocytes (Calzadilla et al., Redox Rep. 2013;210-218).	Acetylcysteine	68-84	monoamine oxidase A	Mus musculus	166-185
28848050-7	2017	Similarly, combined N-acetyl-l-cysteine and catalase treatment also suppressed VDAC1-induced redistribution of Parkin.	Acetylcysteine	20-39	voltage dependent anion channel 1	Homo sapiens	79-84
28858636-9	2017	OS and senescence caused the translocation of HMGB1 and cffTF from AECs" nuclei to cytoplasm compared to untreated cells, which was inhibited by antioxidant N-acetyl cysteine (NAC).	Acetylcysteine	157-174	high mobility group box 1	Homo sapiens	46-51
28858636-9	2017	OS and senescence caused the translocation of HMGB1 and cffTF from AECs" nuclei to cytoplasm compared to untreated cells, which was inhibited by antioxidant N-acetyl cysteine (NAC).	Acetylcysteine	176-179	high mobility group box 1	Homo sapiens	46-51
29089150-6	2017	HMGB1 release by UVB was significantly reduced by hemin, N-acetyl-cysteine and DPI (NADPH oxidase inhibitor).	Acetylcysteine	57-74	high mobility group box 1	Homo sapiens	0-5
28288879-7	2017	The oxidative stress associated with d-galactosamine (Gal) or buthionine sulfoximine (BSO) treatments induces BHMT nuclear translocation, an effect that is prevented by administration of N-acetylcysteine (NAC) and glutathione ethyl ester (EGSH), respectively.	Acetylcysteine	187-203	betaine--homocysteine S-methyltransferase	Homo sapiens	110-114
28288879-7	2017	The oxidative stress associated with d-galactosamine (Gal) or buthionine sulfoximine (BSO) treatments induces BHMT nuclear translocation, an effect that is prevented by administration of N-acetylcysteine (NAC) and glutathione ethyl ester (EGSH), respectively.	Acetylcysteine	205-208	betaine--homocysteine S-methyltransferase	Homo sapiens	110-114
28388573-6	2017	What is more, when detect the function of alphaMSH in ROS-induced apoptosis, similar inhibitory trend was found with the oxidative stress inhibitor N-acetyl-L-cysteine (NAC) in ROS-induced adipocyte apoptosis and this trend is alphaMSH receptor melanocortin 5 receptor (MC5R) depended, while an opposite trend was found between alphaMSH and Foxo1, which is a known positive regulator of adipocyte apoptosis.	Acetylcysteine	169-172	pro-opiomelanocortin-alpha	Mus musculus	42-50
28388573-6	2017	What is more, when detect the function of alphaMSH in ROS-induced apoptosis, similar inhibitory trend was found with the oxidative stress inhibitor N-acetyl-L-cysteine (NAC) in ROS-induced adipocyte apoptosis and this trend is alphaMSH receptor melanocortin 5 receptor (MC5R) depended, while an opposite trend was found between alphaMSH and Foxo1, which is a known positive regulator of adipocyte apoptosis.	Acetylcysteine	169-172	pro-opiomelanocortin-alpha	Mus musculus	227-235
28388573-6	2017	What is more, when detect the function of alphaMSH in ROS-induced apoptosis, similar inhibitory trend was found with the oxidative stress inhibitor N-acetyl-L-cysteine (NAC) in ROS-induced adipocyte apoptosis and this trend is alphaMSH receptor melanocortin 5 receptor (MC5R) depended, while an opposite trend was found between alphaMSH and Foxo1, which is a known positive regulator of adipocyte apoptosis.	Acetylcysteine	169-172	melanocortin 5 receptor	Mus musculus	245-268
28388573-6	2017	What is more, when detect the function of alphaMSH in ROS-induced apoptosis, similar inhibitory trend was found with the oxidative stress inhibitor N-acetyl-L-cysteine (NAC) in ROS-induced adipocyte apoptosis and this trend is alphaMSH receptor melanocortin 5 receptor (MC5R) depended, while an opposite trend was found between alphaMSH and Foxo1, which is a known positive regulator of adipocyte apoptosis.	Acetylcysteine	169-172	melanocortin 5 receptor	Mus musculus	270-274
28388573-6	2017	What is more, when detect the function of alphaMSH in ROS-induced apoptosis, similar inhibitory trend was found with the oxidative stress inhibitor N-acetyl-L-cysteine (NAC) in ROS-induced adipocyte apoptosis and this trend is alphaMSH receptor melanocortin 5 receptor (MC5R) depended, while an opposite trend was found between alphaMSH and Foxo1, which is a known positive regulator of adipocyte apoptosis.	Acetylcysteine	169-172	pro-opiomelanocortin-alpha	Mus musculus	227-235
30263604-4	2017	NAC further increased the lifespan of age-1 and clk-1 mutants, which have increased lifespan owing to reduced insulin/IGF-1-like signaling and mitochondrial function, respectively.	Acetylcysteine	0-3	5-demethoxyubiquinone hydroxylase, mitochondrial	Caenorhabditis elegans	48-53
28695042-10	2017	Analysis of autophagy showed that NAC inhibited basic autophagy flux of PC12 cells, as evidenced by a decrease in LC3-II level and an increase in p62 expression.	Acetylcysteine	34-37	KH RNA binding domain containing, signal transduction associated 1	Rattus norvegicus	146-149
28604588-8	2017	The antioxidants N-acetyl-l-cysteine and Trolox attenuated DHA-induced activation of PKCdelta, phosphorylation of Nrf2, and and its target protein expression.	Acetylcysteine	17-36	protein kinase C delta	Homo sapiens	85-93
28915583-0	2017	N-Acetylcysteine breaks resistance to trastuzumab caused by MUC4 overexpression in human HER2 positive BC-bearing nude mice monitored by 89Zr-Trastuzumab and 18F-FDG PET imaging.	Acetylcysteine	0-16	mucin 4, cell surface associated	Homo sapiens	60-64
28915583-3	2017	Previously, we demonstrated an increase of Zirconium-89-radiolabeled-trastuzumab (89Zr-Trastuzumab) accumulation when MUC4-overexpressing BC-cells were challenged with the mucolytic drug N-Acetylcysteine (NAC).	Acetylcysteine	187-203	mucin 4, cell surface associated	Homo sapiens	118-122
28915583-3	2017	Previously, we demonstrated an increase of Zirconium-89-radiolabeled-trastuzumab (89Zr-Trastuzumab) accumulation when MUC4-overexpressing BC-cells were challenged with the mucolytic drug N-Acetylcysteine (NAC).	Acetylcysteine	205-208	mucin 4, cell surface associated	Homo sapiens	118-122
28088003-9	2017	Acetylcysteine-stabilized polymers exhibited an optimum cross-linked structure, with free thiol groups ensuring polymer-mucin interactions, resulting in the best mucoadhesive properties.	Acetylcysteine	0-14	LOC100508689	Homo sapiens	120-125
28274308-7	2017	Then, T-butyl-4 (BHA), N-acetylcysteine (NAC) and coenzyme Q10 (CoQ10) were used separately to block the ROS and the expression of LC3B in Pg-LPS-treated HGFs was tested by Western blotting.	Acetylcysteine	23-39	microtubule associated protein 1 light chain 3 beta	Homo sapiens	131-135
28274308-7	2017	Then, T-butyl-4 (BHA), N-acetylcysteine (NAC) and coenzyme Q10 (CoQ10) were used separately to block the ROS and the expression of LC3B in Pg-LPS-treated HGFs was tested by Western blotting.	Acetylcysteine	41-44	microtubule associated protein 1 light chain 3 beta	Homo sapiens	131-135
28225868-1	2017	We determined the effect of N-acetylcysteine (NAC) on the expression of the phosphorylated p38 (p-p38) protein and superoxide anion generation (SAG), two important players in the processing of neuropathic pain, in the lumbosacral spinal cord of rats with chronic constriction injury (CCI)-induced neuropathic pain.	Acetylcysteine	28-44	mitogen activated protein kinase 14	Rattus norvegicus	91-94
28225868-1	2017	We determined the effect of N-acetylcysteine (NAC) on the expression of the phosphorylated p38 (p-p38) protein and superoxide anion generation (SAG), two important players in the processing of neuropathic pain, in the lumbosacral spinal cord of rats with chronic constriction injury (CCI)-induced neuropathic pain.	Acetylcysteine	28-44	mitogen activated protein kinase 14	Rattus norvegicus	98-101
28225868-1	2017	We determined the effect of N-acetylcysteine (NAC) on the expression of the phosphorylated p38 (p-p38) protein and superoxide anion generation (SAG), two important players in the processing of neuropathic pain, in the lumbosacral spinal cord of rats with chronic constriction injury (CCI)-induced neuropathic pain.	Acetylcysteine	46-49	mitogen activated protein kinase 14	Rattus norvegicus	91-94
28225868-1	2017	We determined the effect of N-acetylcysteine (NAC) on the expression of the phosphorylated p38 (p-p38) protein and superoxide anion generation (SAG), two important players in the processing of neuropathic pain, in the lumbosacral spinal cord of rats with chronic constriction injury (CCI)-induced neuropathic pain.	Acetylcysteine	46-49	mitogen activated protein kinase 14	Rattus norvegicus	98-101
28225868-8	2017	NAC induced a downregulation in p-p38 expression at all time-points evaluated, but did not reverse the increased SAG induced by CCI.	Acetylcysteine	0-3	mitogen activated protein kinase 14	Rattus norvegicus	34-37
28225868-9	2017	Since p-p38 is a mediator in neuropathic pain and/or nerve regeneration, modulation of this protein may play a role in NAC-induced effects in CCI rats.	Acetylcysteine	119-122	mitogen activated protein kinase 14	Rattus norvegicus	8-11
28451559-13	2017	The NAC modulated the NaAsO2 associated alterations of CAT and SOD2 mRNA levels, therefore, the NaAsO2 might act through inducing reactive oxygen species.	Acetylcysteine	4-7	superoxide dismutase 2	Homo sapiens	63-67
28107387-5	2017	Confocal microscopy and cell viability analyses showed that treatment with an antioxidant N-acetylcysteine or a specific inhibitor of iNOS 1400W significantly prevented the increased apoptosis of neuro-2A cells by HIV-1 Tat or gp120 protein, demonstrating the causal role of HIV-1 mediated nitroxidative stress and protein nitration in promoting neuronal cell death.	Acetylcysteine	90-106	Envelope surface glycoprotein gp160, precursor	Human immunodeficiency virus 1	227-232
29456784-7	2017	In addition, acrolein-induced toxicity in idh2 shRNA-transfected LLC cells and in idh2 knockout mice was ameliorated by the antioxidant, N-acetylcysteine, through attenuation of oxidative stress resulting from idh2 deficiency.	Acetylcysteine	137-153	isocitrate dehydrogenase 2 (NADP+), mitochondrial	Mus musculus	82-86
29456784-7	2017	In addition, acrolein-induced toxicity in idh2 shRNA-transfected LLC cells and in idh2 knockout mice was ameliorated by the antioxidant, N-acetylcysteine, through attenuation of oxidative stress resulting from idh2 deficiency.	Acetylcysteine	137-153	isocitrate dehydrogenase 2 (NADP+), mitochondrial	Mus musculus	82-86
28193016-3	2016	The probe is successfully used for studying the biochemical transformation of N-acetylcysteine, a commonly prescribed Cys supplement drug to Cys by aminoacylase-1 (ACY-1), an important and endogenous mammalian enzyme.	Acetylcysteine	78-94	aminoacylase 1	Homo sapiens	148-162
28193016-3	2016	The probe is successfully used for studying the biochemical transformation of N-acetylcysteine, a commonly prescribed Cys supplement drug to Cys by aminoacylase-1 (ACY-1), an important and endogenous mammalian enzyme.	Acetylcysteine	78-94	aminoacylase 1	Homo sapiens	164-169
26822174-6	2016	Antioxidant N-acetyl-L-cysteine (NAC) and c-Jun NH2-terminal kinase (JNK) inhibitor SP600125 inhibited PEITC-induced DR4 and DR5 expression.	Acetylcysteine	12-31	TNF receptor superfamily member 10a	Homo sapiens	117-120
26822174-6	2016	Antioxidant N-acetyl-L-cysteine (NAC) and c-Jun NH2-terminal kinase (JNK) inhibitor SP600125 inhibited PEITC-induced DR4 and DR5 expression.	Acetylcysteine	33-36	TNF receptor superfamily member 10a	Homo sapiens	117-120
27812954-6	2016	Targeting mTORC1 over-activation with N-acetylcysteine, rapamycin, and rapalogs provides an opportunity to supplant current therapies with severe side effect profiles such as prednisone or cyclophosphamide.	Acetylcysteine	38-54	CREB regulated transcription coactivator 1	Mus musculus	10-16
27235905-8	2016	NAC also decreased malonaldehyde (MDA) in liver, increased glutathione S-transferase (GST) activity in plasma, up-regulated mRNA expression of Superoxide dismutase (SOD) and GPx in liver and headkidney.	Acetylcysteine	0-3	glutathione S-transferase	Oreochromis niloticus	59-84
27235905-8	2016	NAC also decreased malonaldehyde (MDA) in liver, increased glutathione S-transferase (GST) activity in plasma, up-regulated mRNA expression of Superoxide dismutase (SOD) and GPx in liver and headkidney.	Acetylcysteine	0-3	glutathione S-transferase	Oreochromis niloticus	86-89
27235905-10	2016	Immune ability only enhanced by the supplementation of NAC through increased interleukin-1beta (IL-1beta) mRNA expression.	Acetylcysteine	55-58	interleukin-1 beta	Oreochromis niloticus	77-94
27235905-10	2016	Immune ability only enhanced by the supplementation of NAC through increased interleukin-1beta (IL-1beta) mRNA expression.	Acetylcysteine	55-58	interleukin-1 beta	Oreochromis niloticus	96-104
27600005-12	2016	Compared with the control group, the CXCL10 expression in the CIH group and the CIH+NAC group was increased (both P&lt;0.01).	Acetylcysteine	84-87	C-X-C motif chemokine ligand 10	Rattus norvegicus	37-43
27600005-13	2016	The CXCL10 expression in the CIH+NAC group was down-regulated compared with that in the CIH group (P&lt;0.01).	Acetylcysteine	33-36	C-X-C motif chemokine ligand 10	Rattus norvegicus	4-10
27364593-5	2016	Pretreatment with lipid raft disruptor (Methyl-beta-cyclodextrin, MbetaCD) and oxidative stress inhibitor (N-acetyl-L-cysteine, NAC) slightly rescued the viability of cells damaged by C12-HSL exposure, while the paraoxonase 2 (PON2) inhibitor (Triazolo[4,3-a]quinolone, TQ416) significantly affected recovering cells viability and mucin secretion.	Acetylcysteine	107-126	LOC100508689	Homo sapiens	331-336
27825965-4	2016	The effects of K27 were significantly reversed by ectopic expression of Srx or antioxidant N-acetyl cysteine.	Acetylcysteine	91-108	keratin 27	Homo sapiens	15-18
27081862-7	2016	The treatment of H9c2 cells with N-acetyl-L-cysteine (NAC), a scavenger of ROS, prior to DOX exposure, also markedly increased the phosphorylation of Akt and FoxO3a which was inhibited by DOX alone.	Acetylcysteine	33-52	forkhead box O3	Rattus norvegicus	158-164
30954547-8	2019	Moreover, the antioxidant N-acetyl-l-cysteine increased cell viability, GLP-1 expressions and the mTOR signaling pathway-related proteins, and inhibited the ROS production.	Acetylcysteine	26-45	glucagon	Mus musculus	72-77
27081862-7	2016	The treatment of H9c2 cells with N-acetyl-L-cysteine (NAC), a scavenger of ROS, prior to DOX exposure, also markedly increased the phosphorylation of Akt and FoxO3a which was inhibited by DOX alone.	Acetylcysteine	54-57	forkhead box O3	Rattus norvegicus	158-164
27103440-8	2016	ROS scavengers (N-acetylcysteine and MnTBAP), but not AMPKalpha shRNAs, largely inhibited prostate cancer cell necrosis and cytotoxicity by AICAR.	Acetylcysteine	16-32	5-aminoimidazole-4-carboxamide ribonucleotide formyltransferase/IMP cyclohydrolase	Homo sapiens	140-145
27989750-6	2016	We further demonstrate that the radical scavenger N-acetyl-L-cysteine reverts hnRNPA2/B1 and PKM2 inhibition by genipin indicating a role for reactive oxygen species in the metabolic reprogramming of cancer cells mediated by UCP2.	Acetylcysteine	50-69	uncoupling protein 2	Homo sapiens	225-229
27474782-11	2016	CONCLUSION: This is the first report describing the generation of a partly humanized HMGB1-neutralizing antibody with validated therapeutic efficacy and with a prolonged therapeutic window, as compared to NAC, in APAP-ALI.	Acetylcysteine	205-208	high mobility group box 1	Mus musculus	85-90
27477353-9	2016	Furthermore, our results showed that antioxidant N-acetyl-L-cysteine (NAC) significantly inhibited CS-induced recruitment of TLR4 into lipid rafts as well as IL-8 production.	Acetylcysteine	49-68	chemokine (C-X-C motif) ligand 15	Mus musculus	158-162
30511398-7	2019	Furthermore, Mad-induced reactive oxygen species (ROS) activated PTEN and inactivated Akt-Erk1/2 contributing to cell death, as N-acetyl- L-cysteine ameliorated the event.	Acetylcysteine	128-148	mitogen activated protein kinase 3	Rattus norvegicus	90-96
27457783-10	2016	NAC and selective inhibitors of CYP2B6 and CYP3A4 significantly reduced TMP covalent binding.	Acetylcysteine	0-3	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	32-38
31248223-7	2019	The mitochondria-mediated cell death induced by frugoside was inhibited by the overexpression of Srx and antioxidants, such as N-acetyl cysteine and diphenyleneiodonium.	Acetylcysteine	127-144	sulfiredoxin 1	Homo sapiens	97-100
27253772-6	2016	A recent pharmacogenetic analysis of patients enrolled in an IPF clinical trial identified a variant within TOLLIP to be associated with differential response to N-acetylcysteine therapy.	Acetylcysteine	162-178	toll interacting protein	Homo sapiens	108-114
27576730-9	2016	NOX4 knockdown and N-acetylcysteine (NAC) treatment illustrated that NOX4-derived ROS generation was critical for TGF-beta-induced SMAD phosphorylation and myofibroblast differentiation.	Acetylcysteine	19-35	NADPH oxidase 4	Homo sapiens	69-73
29756048-8	2016	The antioxidants N-acetyl cysteine and vitamin C lowered the alcohol-induced elevation of ROS and blunted the alcohol-mediated induction of CYP2A5.	Acetylcysteine	17-34	cytochrome P450, family 2, subfamily a, polypeptide 5	Mus musculus	140-146
26919956-9	2016	CONCLUSIONS: N-Acetyl-l-cysteine can lower the incidence rate of infection-associated preterm labor by prohibiting the activation of the protein AP-1/MCP-1 and decreasing the expression of NF-kappaBp65 and TNF-alpha in the pregnant tissues of premature mice to reduce the inflammatory reactions.	Acetylcysteine	13-32	jun proto-oncogene	Mus musculus	145-149
27576730-9	2016	NOX4 knockdown and N-acetylcysteine (NAC) treatment illustrated that NOX4-derived ROS generation was critical for TGF-beta-induced SMAD phosphorylation and myofibroblast differentiation.	Acetylcysteine	37-40	NADPH oxidase 4	Homo sapiens	69-73
31148586-8	2019	NAC inhibited the induction and nuclear localization of phospho-Smad2 protein in bladder tissues and the upregulation of genes related to fibrosis, such as Tgfb2, Tgfb3, Smad2, Smad3, Cxcl10, and Card10.	Acetylcysteine	0-3	C-X-C motif chemokine ligand 10	Rattus norvegicus	184-190
30849338-7	2019	The reverse effect of NAC on LC3beta expression revealed the ROS-responsibility in autophagy regulation of CKD myopathy.	Acetylcysteine	22-25	microtubule-associated protein 1 light chain 3 beta	Mus musculus	29-36
27351177-8	2016	NAC restored ERK1/2.	Acetylcysteine	0-3	mitogen activated protein kinase 3	Rattus norvegicus	13-19
30684762-7	2019	Among those genes, N-acetyl-L-cysteine (NAC) treatment blocked the H2S-triggered expression of FOS and IL8.	Acetylcysteine	19-38	interleukin 8-like 2	Gallus gallus	103-106
27444019-6	2016	Interestingly, antioxidant N-acetyl cysteine treatment in mice starting at age of 5 mo improved lung function and prevented emphysema development in Hhip(+/-) mice, suggesting that N-acetyl cysteine treatment limits the progression of age-related emphysema in Hhip(+/-) mice.	Acetylcysteine	27-44	Hedgehog-interacting protein	Mus musculus	149-153
30684762-7	2019	Among those genes, N-acetyl-L-cysteine (NAC) treatment blocked the H2S-triggered expression of FOS and IL8.	Acetylcysteine	40-43	interleukin 8-like 2	Gallus gallus	103-106
27444019-6	2016	Interestingly, antioxidant N-acetyl cysteine treatment in mice starting at age of 5 mo improved lung function and prevented emphysema development in Hhip(+/-) mice, suggesting that N-acetyl cysteine treatment limits the progression of age-related emphysema in Hhip(+/-) mice.	Acetylcysteine	27-44	Hedgehog-interacting protein	Mus musculus	260-264
30652495-12	2019	The antioxidant N-acetylcysteine prevents CSE-induced miR-29b downregulation and BRD4 and IL-8 upregulation.	Acetylcysteine	16-32	microRNA 29b-1	Homo sapiens	54-61
27444019-6	2016	Interestingly, antioxidant N-acetyl cysteine treatment in mice starting at age of 5 mo improved lung function and prevented emphysema development in Hhip(+/-) mice, suggesting that N-acetyl cysteine treatment limits the progression of age-related emphysema in Hhip(+/-) mice.	Acetylcysteine	181-198	Hedgehog-interacting protein	Mus musculus	149-153
27444019-6	2016	Interestingly, antioxidant N-acetyl cysteine treatment in mice starting at age of 5 mo improved lung function and prevented emphysema development in Hhip(+/-) mice, suggesting that N-acetyl cysteine treatment limits the progression of age-related emphysema in Hhip(+/-) mice.	Acetylcysteine	181-198	Hedgehog-interacting protein	Mus musculus	260-264
27288489-7	2016	Moreover, adiponectin-upregulated cPLA2 and COX-2 expression was significantly abrogated by ROS scavenger (N-acetylcysteine) or the inhibitors of NADPH oxidase (apocynin), mitochondrial complex I (rotenone), PKC (Ro31-8220, Go-6976, and rottlerin), and p300 (garcinol).	Acetylcysteine	107-123	E1A binding protein p300	Homo sapiens	253-257
26851769-5	2016	NAC 50mg/kg/d administered 1h after initiation of hypothermia significantly decreased iNOS expression and caspase 3 activation in the injured hemisphere versus hypothermia alone.	Acetylcysteine	0-3	caspase 3	Rattus norvegicus	106-115
26783539-7	2016	N-Acetylcysteine but not sevo-postC decreased myocardial FoxO1 while sevo-postC but not N-Acetylcysteine significantly increased myocardiac adiponectin in diabetic rats.	Acetylcysteine	0-16	forkhead box O1	Rattus norvegicus	57-62
30917096-8	2019	NAC-Ag2S reduces reactive oxygen species (ROS) but causes cell death via DNA damage and apoptosis.	Acetylcysteine	0-3	angiotensin II receptor type 1	Homo sapiens	4-8
26671656-0	2016	N-acetyl-L-cysteine increases MnSOD activity and enhances the recruitment of quiescent human fibroblasts to the proliferation cycle during wound healing.	Acetylcysteine	0-19	superoxide dismutase 2	Homo sapiens	30-35
28105252-7	2016	Furthermore, we demonstrated that contrast exposure resulted in Trx1 downregulation and increased ASK1/p38 MAPK phosphorylation, which could be reversed by NACA and NAC.	Acetylcysteine	156-159	mitogen activated protein kinase 14	Rattus norvegicus	103-106
30917096-9	2019	CONCLUSION: NAC-Ag2S QDs are stable and strong signal-generating theranostic agents offering selective therapeutic effects.	Acetylcysteine	12-15	angiotensin II receptor type 1	Homo sapiens	16-20
27272863-0	2016	Utility of Bromelain and N-Acetylcysteine in Treatment of Peritoneal Dissemination of Gastrointestinal Mucin-Producing Malignancies.	Acetylcysteine	25-41	LOC100508689	Homo sapiens	103-108
30496017-9	2019	Expressions of Brca2, Xpc, Mlh3, Rad51, Xrcc2, Hus1, Rad9a, Cdkn1a, Gadd45a which are the DNA-repair genes were found to be significantly higher in NAC + ALC + IR group than those in individual treatment of ALC or NAC.	Acetylcysteine	148-151	XPC complex subunit, DNA damage recognition and repair factor	Homo sapiens	22-25
27010086-8	2016	With NAC pretreatment, ROS increases were prevented, cells were rescued from apoptosis, and both MMP and caspase-3 activity returned to normal levels.	Acetylcysteine	5-8	caspase 3	Rattus norvegicus	105-114
30496017-9	2019	Expressions of Brca2, Xpc, Mlh3, Rad51, Xrcc2, Hus1, Rad9a, Cdkn1a, Gadd45a which are the DNA-repair genes were found to be significantly higher in NAC + ALC + IR group than those in individual treatment of ALC or NAC.	Acetylcysteine	148-151	RAD9 checkpoint clamp component A	Homo sapiens	53-58
27162476-6	2016	Meanwhile, the observed increases in nuclear NF-kappaB, NOX4, p47(phox), and COX2 expression were attenuated by treatment with Bay 117082, N-acetyl-l-cysteine (NAC), or RSV.	Acetylcysteine	139-158	NADPH oxidase 4	Mus musculus	56-60
26331942-7	2015	MEASUREMENTS AND MAIN RESULTS: Significant interaction was observed between N-acetylcysteine (NAC) therapy and rs3750920 within TOLLIP (P interaction = 0.001).	Acetylcysteine	76-92	toll interacting protein	Homo sapiens	128-134
26331942-7	2015	MEASUREMENTS AND MAIN RESULTS: Significant interaction was observed between N-acetylcysteine (NAC) therapy and rs3750920 within TOLLIP (P interaction = 0.001).	Acetylcysteine	94-97	toll interacting protein	Homo sapiens	128-134
27162476-6	2016	Meanwhile, the observed increases in nuclear NF-kappaB, NOX4, p47(phox), and COX2 expression were attenuated by treatment with Bay 117082, N-acetyl-l-cysteine (NAC), or RSV.	Acetylcysteine	139-158	cytochrome c oxidase II, mitochondrial	Mus musculus	77-81
26331942-10	2015	CONCLUSIONS: NAC may be an efficacious therapy for individuals with IPF with an rs3750920 (TOLLIP) TT genotype, but it was associated with a trend toward harm in those with a CC genotype.	Acetylcysteine	13-16	toll interacting protein	Homo sapiens	91-97
27162476-6	2016	Meanwhile, the observed increases in nuclear NF-kappaB, NOX4, p47(phox), and COX2 expression were attenuated by treatment with Bay 117082, N-acetyl-l-cysteine (NAC), or RSV.	Acetylcysteine	160-163	NADPH oxidase 4	Mus musculus	56-60
30496017-9	2019	Expressions of Brca2, Xpc, Mlh3, Rad51, Xrcc2, Hus1, Rad9a, Cdkn1a, Gadd45a which are the DNA-repair genes were found to be significantly higher in NAC + ALC + IR group than those in individual treatment of ALC or NAC.	Acetylcysteine	148-151	growth arrest and DNA damage inducible alpha	Homo sapiens	68-75
27162476-6	2016	Meanwhile, the observed increases in nuclear NF-kappaB, NOX4, p47(phox), and COX2 expression were attenuated by treatment with Bay 117082, N-acetyl-l-cysteine (NAC), or RSV.	Acetylcysteine	160-163	cytochrome c oxidase II, mitochondrial	Mus musculus	77-81
26184564-4	2015	Previously, we demonstrated that N-acetyl cysteine (NAC) pretreatment up-regulates DUSP4 expression in endothelial cells, regulating p38 and ERK1/2 activities, and thus providing a protective effect against oxidative stress.	Acetylcysteine	33-50	mitogen-activated protein kinase 14	Mus musculus	133-136
30581001-7	2019	Furthermore, enhanced cytotoxicity of L-OHP by DAC was cancelled with the presence of N-acetyl-l-cysteine, a ROS scavenger.	Acetylcysteine	86-105	arylacetamide deacetylase	Homo sapiens	47-50
26184564-4	2015	Previously, we demonstrated that N-acetyl cysteine (NAC) pretreatment up-regulates DUSP4 expression in endothelial cells, regulating p38 and ERK1/2 activities, and thus providing a protective effect against oxidative stress.	Acetylcysteine	33-50	mitogen-activated protein kinase 3	Mus musculus	141-147
26184564-4	2015	Previously, we demonstrated that N-acetyl cysteine (NAC) pretreatment up-regulates DUSP4 expression in endothelial cells, regulating p38 and ERK1/2 activities, and thus providing a protective effect against oxidative stress.	Acetylcysteine	52-55	mitogen-activated protein kinase 14	Mus musculus	133-136
26184564-4	2015	Previously, we demonstrated that N-acetyl cysteine (NAC) pretreatment up-regulates DUSP4 expression in endothelial cells, regulating p38 and ERK1/2 activities, and thus providing a protective effect against oxidative stress.	Acetylcysteine	52-55	mitogen-activated protein kinase 3	Mus musculus	141-147
26964642-7	2016	Interestingly, reductions in ROS generation and apoptosis, and upregulation of miR-223 were found in ADSCs treated with antioxidants NAC and AAP.	Acetylcysteine	133-136	microRNA 223	Homo sapiens	79-86
26964642-11	2016	These results indicate that NAC and AAP suppress AGE-HSA-induced apoptosis of ADSCs, possibly through downregulation of miR-223.	Acetylcysteine	28-31	microRNA 223	Homo sapiens	120-127
26497050-5	2015	In addition, the expression levels of MMP-2 and MMP-9 were inhibited by NAC, IAA-94 and SB203580.	Acetylcysteine	72-75	matrix metallopeptidase 2	Homo sapiens	38-43
30696468-11	2019	Attenuation of ROS production with N-acetylcysteine abolishes AK4-induced invasion potential under hypoxia.	Acetylcysteine	35-51	adenylate kinase 4	Homo sapiens	62-65
26747500-6	2016	Furthermore, the levels of IGF-1R and EGFR proteins and not of PDGFR were also enhanced in VSMCs from SHRs, which were attenuated significantly by NAC, DPI, and PP2.	Acetylcysteine	147-150	insulin-like growth factor 1 receptor	Rattus norvegicus	27-33
26747500-7	2016	In addition, NAC, DPI, and PP2 also attenuated the enhanced phosphorylation of IGF-1R, PDGFR, EGFR, c-Src, and EKR1/2 in VSMCs from SHRs.	Acetylcysteine	13-16	insulin-like growth factor 1 receptor	Rattus norvegicus	79-85
26291957-6	2016	Treating RAW264.7 cells with 7-MCPA increased the intracellular level of reactive oxygen species (ROS) and the phosphorylation level of p38 mitogen-activated protein kinase (MAPK); however, co-treatment with the antioxidant N-acetyl-cysteine (NAC) blocked 7-MCPA-induced p38 MAPK phosphorylation.	Acetylcysteine	224-241	mitogen-activated protein kinase 14	Mus musculus	136-139
26599235-7	2015	Importantly, pre-incubation with antioxidants including N-acetylcysteine (NAC) and vitamin C, respectively, resulted in significant attenuation of the induction of CTGF in GO orbital fibroblasts in response to H2O2 (p = 0.004 and 0.015, respectively).	Acetylcysteine	56-72	cellular communication network factor 2	Homo sapiens	164-168
26599235-7	2015	Importantly, pre-incubation with antioxidants including N-acetylcysteine (NAC) and vitamin C, respectively, resulted in significant attenuation of the induction of CTGF in GO orbital fibroblasts in response to H2O2 (p = 0.004 and 0.015, respectively).	Acetylcysteine	74-77	cellular communication network factor 2	Homo sapiens	164-168
26291957-6	2016	Treating RAW264.7 cells with 7-MCPA increased the intracellular level of reactive oxygen species (ROS) and the phosphorylation level of p38 mitogen-activated protein kinase (MAPK); however, co-treatment with the antioxidant N-acetyl-cysteine (NAC) blocked 7-MCPA-induced p38 MAPK phosphorylation.	Acetylcysteine	243-246	mitogen-activated protein kinase 14	Mus musculus	136-139
30574085-7	2018	Rats fed with NAC for 3-weeks prior to AbetaOs injections displayed comparable redox potential, RyR2 and Arc protein contents, similar ERK1/2 phosphorylation and RyR2 single channel activation by Ca2+ as saline-injected (control) rats.	Acetylcysteine	14-17	ryanodine receptor 2	Rattus norvegicus	96-100
30574085-7	2018	Rats fed with NAC for 3-weeks prior to AbetaOs injections displayed comparable redox potential, RyR2 and Arc protein contents, similar ERK1/2 phosphorylation and RyR2 single channel activation by Ca2+ as saline-injected (control) rats.	Acetylcysteine	14-17	mitogen activated protein kinase 3	Rattus norvegicus	135-141
26547530-13	2015	Meantime, knockdown of caspase-2, pretreatment with Z-VAD-fmk or NAC (N-Acety-L-Cysteine) efficiently inhibited the autophagy induced by DHTS.	Acetylcysteine	70-88	caspase 2	Mus musculus	23-32
30574085-7	2018	Rats fed with NAC for 3-weeks prior to AbetaOs injections displayed comparable redox potential, RyR2 and Arc protein contents, similar ERK1/2 phosphorylation and RyR2 single channel activation by Ca2+ as saline-injected (control) rats.	Acetylcysteine	14-17	ryanodine receptor 2	Rattus norvegicus	162-166
26783013-8	2016	The combinatorial effects of adenanthin and VD3 were shown to be associated with the ROS-CCAAT-enhancer-binding protein (C/EBP)beta axis, since N-acetylcysteine, a ROS scavenger, was able to abrogate the differentiation-enhancing effects of adenanthin, and the knockdown of C/EBPbeta also inhibited the combinatorial effects of adenanthin and VD3.	Acetylcysteine	144-160	CCAAT enhancer binding protein beta	Homo sapiens	121-131
26783013-8	2016	The combinatorial effects of adenanthin and VD3 were shown to be associated with the ROS-CCAAT-enhancer-binding protein (C/EBP)beta axis, since N-acetylcysteine, a ROS scavenger, was able to abrogate the differentiation-enhancing effects of adenanthin, and the knockdown of C/EBPbeta also inhibited the combinatorial effects of adenanthin and VD3.	Acetylcysteine	144-160	CCAAT enhancer binding protein beta	Homo sapiens	274-283
30241048-9	2018	These results indicated that Cd(NO3)2-induced neuronal apoptosis was reduced by NAC via intrinsic apoptotic caspase cascade activities and their up-stream factors, including mitochondrial dysfunction and ROS generation.	Acetylcysteine	80-83	caspase 9	Mus musculus	108-115
26474283-4	2015	This response leads to G2/M cell cycle arrest and induces a senescent-like phenotype accompanied by enlargement of cells and increased senescence-associated beta-galactosidase activity, which are abrogated by N-acetyl cysteine (NAC) pre-treatment.	Acetylcysteine	209-226	galactosidase beta 1	Homo sapiens	157-175
26850138-4	2016	The shift of subcellular OATP2A1 was abolished in the presence of anti-oxidant N-acetyl-L-cysteine or an inhibitor of protein kinase C, which evokes exocytosis.	Acetylcysteine	79-98	solute carrier organic anion transporter family member 2A1	Homo sapiens	25-32
26474283-4	2015	This response leads to G2/M cell cycle arrest and induces a senescent-like phenotype accompanied by enlargement of cells and increased senescence-associated beta-galactosidase activity, which are abrogated by N-acetyl cysteine (NAC) pre-treatment.	Acetylcysteine	228-231	galactosidase beta 1	Homo sapiens	157-175
30194941-14	2018	NAC prevented the increases in LC3 II protein, LC3 scores, Beclin1, Atg12 and ERK activity in AAC rats.	Acetylcysteine	0-3	annexin A3	Rattus norvegicus	31-34
25199686-8	2015	Endosulfan-induced Akt/MAPK pathways and COX-2 expression were attenuated by DPI, a specific NOX inhibitor, and the ROS scavenger N-acetylcysteine.	Acetylcysteine	130-146	cytochrome c oxidase II, mitochondrial	Mus musculus	41-46
27003169-6	2016	Furthermore, NAC blocked the decrease of B-cell lymphoma 2/Bcl-2 associated X protein (Bcl-2/Bax) ratio, release of cytochrome c, cleavage of caspase-3 and poly(ADP-ribose) polymerase (PARP), and nuclear translocation of apoptosis-inducing factor (AIF) and endonuclease G (Endo G).	Acetylcysteine	13-16	caspase 3	Rattus norvegicus	142-151
30194941-14	2018	NAC prevented the increases in LC3 II protein, LC3 scores, Beclin1, Atg12 and ERK activity in AAC rats.	Acetylcysteine	0-3	annexin A3	Rattus norvegicus	47-50
30194941-14	2018	NAC prevented the increases in LC3 II protein, LC3 scores, Beclin1, Atg12 and ERK activity in AAC rats.	Acetylcysteine	0-3	beclin 1	Rattus norvegicus	59-66
30056058-6	2018	AGEs significantly increased DPP-4 expression and soluble DPP-4 production by tubular cells, the latter of which was attenuated by RAGE-aptamer or an anti-oxidant, N-acetylcysteine.	Acetylcysteine	164-180	dipeptidylpeptidase 4	Rattus norvegicus	29-34
26878792-8	2016	Interestingly, the in vivo antioxidant therapy with N-acetylcysteine abolished the CLA-induced rise of body metabolism and liver UCP expression and activity, while the in vitro antioxidant treatment with catalase mitigated the CLA-dependent UCP-2 expression in hepatocytes; these findings suggest the participation of an oxidative-dependent pathway.	Acetylcysteine	52-68	uncoupling protein 1 (mitochondrial, proton carrier)	Mus musculus	129-132
27184952-9	2016	High-mobility group box 1 (HMGB1) was rapidly released and associated with TLR4 after TNF-alpha stimulation with a peak at 5 min, which was prevented by N-acetylcysteine, an antioxidant.	Acetylcysteine	153-169	high mobility group box 1	Homo sapiens	0-25
27184952-9	2016	High-mobility group box 1 (HMGB1) was rapidly released and associated with TLR4 after TNF-alpha stimulation with a peak at 5 min, which was prevented by N-acetylcysteine, an antioxidant.	Acetylcysteine	153-169	high mobility group box 1	Homo sapiens	27-32
26474608-4	2015	In addition, reactive oxygen species (ROS) inhibitor (N-acetylcysteine, NAC) was added to test its effect on the action of TGF-beta1.	Acetylcysteine	54-70	transforming growth factor, beta 1	Mus musculus	123-132
26341012-11	2015	Plumbagin, and the GR inhibitor sodium arsenite all increased intracellular reactive oxygen species (ROS) levels and this increase was significantly attenuated by pretreatment with the ROS scavenger N-acetyl-cysteine (NAC) in HepG2 cells.	Acetylcysteine	199-216	glutathione-disulfide reductase	Homo sapiens	19-21
26341012-11	2015	Plumbagin, and the GR inhibitor sodium arsenite all increased intracellular reactive oxygen species (ROS) levels and this increase was significantly attenuated by pretreatment with the ROS scavenger N-acetyl-cysteine (NAC) in HepG2 cells.	Acetylcysteine	218-221	glutathione-disulfide reductase	Homo sapiens	19-21
30056058-6	2018	AGEs significantly increased DPP-4 expression and soluble DPP-4 production by tubular cells, the latter of which was attenuated by RAGE-aptamer or an anti-oxidant, N-acetylcysteine.	Acetylcysteine	164-180	dipeptidylpeptidase 4	Rattus norvegicus	58-63
26622517-9	2015	Pretreatment of H9c2 cells with N-acetyl-L-cysteine (NAC), a scavenger of ROS, prior to exposure to DOX dramatically increased the phosphorylation of FoxO3a and led to a marked reduction in Prx III expression in the H9c2 cells.	Acetylcysteine	32-51	forkhead box O3	Rattus norvegicus	150-156
26622517-9	2015	Pretreatment of H9c2 cells with N-acetyl-L-cysteine (NAC), a scavenger of ROS, prior to exposure to DOX dramatically increased the phosphorylation of FoxO3a and led to a marked reduction in Prx III expression in the H9c2 cells.	Acetylcysteine	53-56	forkhead box O3	Rattus norvegicus	150-156
26798412-5	2016	However, inhibition of oxidative stress with N-acetylcysteine (NAC) partially inhibited the induction of HMGB-1 induced by AGEs.	Acetylcysteine	45-61	high mobility group box 1	Mus musculus	105-111
26798412-5	2016	However, inhibition of oxidative stress with N-acetylcysteine (NAC) partially inhibited the induction of HMGB-1 induced by AGEs.	Acetylcysteine	63-66	high mobility group box 1	Mus musculus	105-111
30037311-9	2018	NAC administration decreased the mRNA levels of both iNOS and NOX4 with a concomitant increase in Gpx1 expression.	Acetylcysteine	0-3	NADPH oxidase 4	Homo sapiens	62-66
26472193-8	2015	Mice deficient in NADPH oxidase 4 had markedly increased susceptibility to acetaminophen-induced hepatic injury which could be corrected by administration of N-acetyl cysteine.	Acetylcysteine	158-175	NADPH oxidase 4	Mus musculus	18-33
25998424-6	2015	Both resveratrol and NAC partially restored DeltaPsim and ROS levels and prevented GAG release and cell loss and normalized SOD1 and SOD2 protein expression.	Acetylcysteine	21-24	superoxide dismutase 1	Equus caballus	124-128
25953698-9	2015	GSH or NAC treatment inhibited DMF-induced JNK, p38, and ERK activation in CT26 cells.	Acetylcysteine	7-10	mitogen-activated protein kinase 14	Mus musculus	48-51
26431905-10	2015	NAC decreased fluoride-induced ROS generation and attenuated JNK and c-Jun phosphorylation.	Acetylcysteine	0-3	jun proto-oncogene	Mus musculus	69-74
30132044-8	2018	In addition, CYP2E1 inhibitors and the antioxidant, N-acetylcysteine, also attenuated gamma-H2AX generation following exposure to 2,4-DMA.	Acetylcysteine	52-68	H2A.X variant histone	Homo sapiens	86-96
27352350-5	2015	In addition, physcion provoked the generation of reactive oxygen species (ROS) in SGC-7901 cells, while the antioxidant N-acetyl cysteine almost completely blocked physcion-induced AMPK activation and apoptosis.	Acetylcysteine	120-137	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	181-185
25649257-8	2015	The antioxidant N-acetylcysteine (NAC) increased UBE1L protein levels, while pro-oxidants such as hydrogen peroxide and tert-butyl hydroperoxide (tBHP) decreased UBE1L protein levels, indicating that the intracellular redox status is associated with UBE1L expression.	Acetylcysteine	16-32	ubiquitin like modifier activating enzyme 7	Homo sapiens	49-54
30114659-7	2018	The antioxidant N-acetyl-L-cysteine (NAC) can significantly reduce TiO2-NPs-induced ERS characterized by the down-regulation of GRP78 and cleaved caspase-12 levels, which indicates that oxidative stress is participated in TiO2-NPs-induced ERS.	Acetylcysteine	16-35	caspase 12	Mus musculus	146-156
25649257-8	2015	The antioxidant N-acetylcysteine (NAC) increased UBE1L protein levels, while pro-oxidants such as hydrogen peroxide and tert-butyl hydroperoxide (tBHP) decreased UBE1L protein levels, indicating that the intracellular redox status is associated with UBE1L expression.	Acetylcysteine	34-37	ubiquitin like modifier activating enzyme 7	Homo sapiens	49-54
25058850-4	2015	AZM significantly upregulated NLRC1 and NLRC2 while NAC upregulated only NLRC2 receptor expression in CF cells.	Acetylcysteine	52-55	nucleotide binding oligomerization domain containing 2	Homo sapiens	73-78
26436698-0	2015	Depletion of mucin in mucin-producing human gastrointestinal carcinoma: Results from in vitro and in vivo studies with bromelain and N-acetylcysteine.	Acetylcysteine	133-149	LOC100508689	Homo sapiens	13-18
26436698-7	2015	Our results suggest that a combination of BR and NAC with dual effects on growth and mucin products of mucin-expressing tumor cells is a promising candidate towards the development of novel approaches to gastrointestinal malignancies with the involvement of mucin pathology.	Acetylcysteine	49-52	LOC100508689	Homo sapiens	85-90
30114659-7	2018	The antioxidant N-acetyl-L-cysteine (NAC) can significantly reduce TiO2-NPs-induced ERS characterized by the down-regulation of GRP78 and cleaved caspase-12 levels, which indicates that oxidative stress is participated in TiO2-NPs-induced ERS.	Acetylcysteine	37-40	caspase 12	Mus musculus	146-156
26436698-7	2015	Our results suggest that a combination of BR and NAC with dual effects on growth and mucin products of mucin-expressing tumor cells is a promising candidate towards the development of novel approaches to gastrointestinal malignancies with the involvement of mucin pathology.	Acetylcysteine	49-52	LOC100508689	Homo sapiens	103-108
26436698-7	2015	Our results suggest that a combination of BR and NAC with dual effects on growth and mucin products of mucin-expressing tumor cells is a promising candidate towards the development of novel approaches to gastrointestinal malignancies with the involvement of mucin pathology.	Acetylcysteine	49-52	LOC100508689	Homo sapiens	103-108
30166062-10	2018	Antioxidants, such as N-acetyl-l-cysteine and quercetin, markedly inhibited the nuclear-to-cytoplasmic translocation of HMGB1 and its release into the extracellular milieu.	Acetylcysteine	22-41	high mobility group box 1	Homo sapiens	120-125
26134131-6	2015	In addition, pretreatment of H9c2 cells with N-acetyl-L-cysteine, a scavenger of reactive oxygen species (ROS) prior to exposure to DOX, markedly decreased the expression of CRT.	Acetylcysteine	45-64	calreticulin	Rattus norvegicus	174-177
25753204-3	2015	We found that TAK1 was activated by Dex in both osteocytic MLO-Y4 and osteoblastic OB-6 cells, which was prevented by two known anti-oxidants N-acetylcysteine (NAC) and ebselen.	Acetylcysteine	142-158	mitogen-activated protein kinase kinase kinase 7	Mus musculus	14-18
25753204-3	2015	We found that TAK1 was activated by Dex in both osteocytic MLO-Y4 and osteoblastic OB-6 cells, which was prevented by two known anti-oxidants N-acetylcysteine (NAC) and ebselen.	Acetylcysteine	160-163	mitogen-activated protein kinase kinase kinase 7	Mus musculus	14-18
30021379-8	2018	Further experiments indicated that NLRP3-ASC pathway was activated by reactive oxygen species (ROS), since ROS scavenger of N-acetyl-cysteine (NAC) prevented, which was further reduced by PepE addition.	Acetylcysteine	124-141	steroid sulfatase	Mus musculus	41-44
25915766-7	2015	Similar to cell proliferation, GSH, NAC and L-cysteine but not D-cysteine, completely restored the processing of caspase-8 and caspase-3 to their respective subunits in z-FA-FMK-treated activated T cells.	Acetylcysteine	36-39	caspase 8	Homo sapiens	113-122
27551466-5	2015	Suppression of ERK activity and addition of N-acetyl-cysteine inhibited VacA-dependent increase in Cx43 and LC3-II.	Acetylcysteine	44-61	gap junction protein alpha 1	Homo sapiens	99-103
30021379-8	2018	Further experiments indicated that NLRP3-ASC pathway was activated by reactive oxygen species (ROS), since ROS scavenger of N-acetyl-cysteine (NAC) prevented, which was further reduced by PepE addition.	Acetylcysteine	124-141	peptidase E	Homo sapiens	188-192
32262475-7	2015	Moreover, the autophagy activated by TEGDMA occurred via the AMPK/mTOR pathway, which could be abrogated by NAC pretreatment.	Acetylcysteine	108-111	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	61-65
25665792-7	2015	Surprisingly, at 32 weeks, despite no tumor formation in the WT mice, all Cygb(-/-) mice developed liver cancer, which was ameliorated by N-acetyl cysteine treatment.	Acetylcysteine	138-155	cytoglobin	Mus musculus	74-78
30021379-8	2018	Further experiments indicated that NLRP3-ASC pathway was activated by reactive oxygen species (ROS), since ROS scavenger of N-acetyl-cysteine (NAC) prevented, which was further reduced by PepE addition.	Acetylcysteine	143-146	steroid sulfatase	Mus musculus	41-44
30021379-8	2018	Further experiments indicated that NLRP3-ASC pathway was activated by reactive oxygen species (ROS), since ROS scavenger of N-acetyl-cysteine (NAC) prevented, which was further reduced by PepE addition.	Acetylcysteine	143-146	peptidase E	Homo sapiens	188-192
25315005-9	2015	Treatment of mice with the antioxidant N-acetylcysteine diminishes PGC-1alpha variation observed among the iron diets, suggesting that iron is acting through reactive oxygen species signaling.	Acetylcysteine	39-55	peroxisome proliferative activated receptor, gamma, coactivator 1 alpha	Mus musculus	67-77
29935984-2	2018	N-acetylcysteine (NAC) is capable of reversing the psychotomimetic effects of PCP via activation of cystine-glutamate antiporters (xCT).	Acetylcysteine	0-16	solute carrier family 7 (cationic amino acid transporter, y+ system), member 11	Mus musculus	131-134
25858686-9	2015	N-acetylcysteine and phosphoinositide 3-kinase (PI3K) inhibitor restored the inhibitory effects of Th2 cytokines over RV-16-induced activation of IRF3.	Acetylcysteine	0-16	interferon regulatory factor 3	Homo sapiens	146-150
29935984-2	2018	N-acetylcysteine (NAC) is capable of reversing the psychotomimetic effects of PCP via activation of cystine-glutamate antiporters (xCT).	Acetylcysteine	18-21	solute carrier family 7 (cationic amino acid transporter, y+ system), member 11	Mus musculus	131-134
29935984-6	2018	Furthermore, the capacity of NAC to ameliorate acute toluene-induced deficits in object recognition and social interaction was blocked by the xCT inhibitor (S)-4-carboxyphenylglycine and the mGluR2/3 antagonist LY341495.	Acetylcysteine	29-32	glutamate receptor, ionotropic, AMPA2 (alpha 2)	Mus musculus	191-197
29935984-7	2018	These results indicate that NAC could prevent toluene-induced reward facilitation and behavioral disturbances and its beneficial effects, at least for cognitive function and social interaction, are associated with activation of the xCT and mGluR2/3.	Acetylcysteine	28-31	solute carrier family 7 (cationic amino acid transporter, y+ system), member 11	Mus musculus	232-235
25155888-6	2015	Treatment with CoCl2 resulted in an increased intracellular ROS generation, which is inhibited by dieckol or N-acetyl cysteine (NAC, a ROS scavenger), and p38 MAPK phosphorylation, which is also blocked by dieckol or NAC.	Acetylcysteine	217-220	mitogen-activated protein kinase 14	Mus musculus	155-158
30106373-5	2018	Using the ROS scavenger, N-Acetyl-Cysteine (NAC), in primary cultures we show that a physiological increase in ROS is required for satellite cells to exit the cell cycle and initiate differentiation through the redox activation of p38alpha MAP kinase.	Acetylcysteine	25-42	mitogen-activated protein kinase 14	Mus musculus	231-239
25155888-10	2015	Similar to the effect of dieckol, NAC also blocked CoCl2-induced COX-2 expression.	Acetylcysteine	34-37	cytochrome c oxidase II, mitochondrial	Mus musculus	65-70
25769956-7	2015	Pretreatment with the ROS inhibitor N-acetylcysteine abrogated the phosphorylation of p38 and JNK induced by high glucose.	Acetylcysteine	36-52	mitogen activated protein kinase 14	Rattus norvegicus	86-89
30106373-5	2018	Using the ROS scavenger, N-Acetyl-Cysteine (NAC), in primary cultures we show that a physiological increase in ROS is required for satellite cells to exit the cell cycle and initiate differentiation through the redox activation of p38alpha MAP kinase.	Acetylcysteine	44-47	mitogen-activated protein kinase 14	Mus musculus	231-239
29775111-11	2018	Hepatic Mmd-2 expression was downregulated in the control group while remaining stable or exhibiting elevated levels in the TAM or NAC groups.	Acetylcysteine	131-134	monocyte to macrophage differentiation-associated 2	Mus musculus	8-13
25721293-8	2015	SFN induced increase in MICA/MICB expression as well as increased susceptibility to NK cell mediated killing was abrogated by N-acetyl cysteine in A549 and MDA-MB-231 cells suggesting a ROS mediated mechanism.	Acetylcysteine	126-143	MHC class I polypeptide-related sequence A	Homo sapiens	24-28
24142891-8	2015	Furthermore, pretreatment with the antioxidants, N-acetylcysteine and vitamin C, significantly decreased MC-LR-induced ROS generation and effectively attenuated p38-MAPK activation as well as tau hyperphosphorylation.	Acetylcysteine	49-65	mitogen activated protein kinase 14	Rattus norvegicus	161-164
25749517-7	2015	NAC pre-treatment reversed inhibition of mTORC1 targets, demonstrating a ROS-dependent mechanism.	Acetylcysteine	0-3	CREB regulated transcription coactivator 1	Mus musculus	41-47
25849069-13	2015	CSE inhibited virus-mediated BAFF induction in a dose-dependent manner in BEAS-2B cells, while this inhibition of BAFF by CSE was prevented by pretreatment with the antioxidant N-acetylcysteine.	Acetylcysteine	177-193	TNF superfamily member 13b	Homo sapiens	29-33
30012208-7	2018	Pretreatment of ARPE-19 cells with NAC or 3-MA under high glucose stress resulted in a marked reduction in the expression levels of PINK1, BNIP3L and LC3-II (p &lt; 0.05).	Acetylcysteine	35-38	BCL2 interacting protein 3 like	Homo sapiens	139-145
25849069-13	2015	CSE inhibited virus-mediated BAFF induction in a dose-dependent manner in BEAS-2B cells, while this inhibition of BAFF by CSE was prevented by pretreatment with the antioxidant N-acetylcysteine.	Acetylcysteine	177-193	TNF superfamily member 13b	Homo sapiens	114-118
24612076-10	2015	We hypothesized that the increased reinstatement after inhibiting NAC induction of GLT-1 resulted from increased extracellular glutamate, and show that augmented reinstatement is prevented by blocking mGluR5.	Acetylcysteine	66-69	glutamate receptor, ionotropic, kainate 1	Mus musculus	201-207
25666878-0	2015	N-acetyl cysteine reduces oxidative toxicity, apoptosis, and calcium entry through TRPV1 channels in the neutrophils of patients with polycystic ovary syndrome.	Acetylcysteine	0-17	transient receptor potential cation channel subfamily V member 1	Homo sapiens	83-88
25666878-3	2015	We aimed to investigate the effects of NAC on apoptosis, oxidative stress, and Ca(2+) entry through transient receptor potential vanilloid 1 (TRPV1) and TRP melastatin 2 (TRPM2) channels in neutrophils from patients with PCOS.	Acetylcysteine	39-42	transient receptor potential cation channel subfamily V member 1	Homo sapiens	100-140
25666878-3	2015	We aimed to investigate the effects of NAC on apoptosis, oxidative stress, and Ca(2+) entry through transient receptor potential vanilloid 1 (TRPV1) and TRP melastatin 2 (TRPM2) channels in neutrophils from patients with PCOS.	Acetylcysteine	39-42	transient receptor potential cation channel subfamily V member 1	Homo sapiens	142-147
25666878-10	2015	In conclusion, NAC reduced oxidative stress, apoptosis, cytokine levels, and Ca(2+) entry through TRPV1 channel, which provide supportive evidence that oxidative stress and TRPV1 channel plays a key role in etiology of PCOS.	Acetylcysteine	15-18	transient receptor potential cation channel subfamily V member 1	Homo sapiens	98-103
25666878-10	2015	In conclusion, NAC reduced oxidative stress, apoptosis, cytokine levels, and Ca(2+) entry through TRPV1 channel, which provide supportive evidence that oxidative stress and TRPV1 channel plays a key role in etiology of PCOS.	Acetylcysteine	15-18	transient receptor potential cation channel subfamily V member 1	Homo sapiens	173-178
25147052-5	2015	Antioxidants MCI-186 and N-acetyl cysteine prevented E-FABP"s induction in expression by PAM-LTx, while tert-butyl hydroperoxide increased ROS and E-FABP expression.	Acetylcysteine	25-42	fatty acid binding protein 5	Rattus norvegicus	53-59
25096910-6	2014	We found that treatment with CAY10598 generated reactive oxygen species (ROS) and pretreatment of cells with N-acetyl cysteine rescued cells from apoptosis by abrogating the inhibitory effect of CAY10598 on the activation of JAK2/STAT3 signaling.	Acetylcysteine	109-126	Janus kinase 2	Homo sapiens	225-229
25256574-3	2015	We hypothesized that the reducing agent N-acetylcysteine (NAC), a well-tolerated drug used widely in clinical practice to treat acetaminophen overdose, would reduce disulfide bond formation, and inhibit mutant IL7R-mediated oncogenic signalling.	Acetylcysteine	40-56	interleukin 7 receptor	Homo sapiens	210-214
25256574-3	2015	We hypothesized that the reducing agent N-acetylcysteine (NAC), a well-tolerated drug used widely in clinical practice to treat acetaminophen overdose, would reduce disulfide bond formation, and inhibit mutant IL7R-mediated oncogenic signalling.	Acetylcysteine	58-61	interleukin 7 receptor	Homo sapiens	210-214
29410271-8	2018	In addition, a ROS scavenger N-acetyl-l-cysteine (NAC) down-regulated the protein level of p-p38, p-JNK and Prdx1, and H9c2 cell apoptosis.	Acetylcysteine	29-48	mitogen activated protein kinase 14	Rattus norvegicus	93-96
25256574-4	2015	We found that treatment with NAC disrupted IL7R homodimerization in IL7R-mutant DND-41 cells as assessed by non-reducing Western blot, as well as in a luciferase complementation assay.	Acetylcysteine	29-32	interleukin 7 receptor	Homo sapiens	43-47
25256574-4	2015	We found that treatment with NAC disrupted IL7R homodimerization in IL7R-mutant DND-41 cells as assessed by non-reducing Western blot, as well as in a luciferase complementation assay.	Acetylcysteine	29-32	interleukin 7 receptor	Homo sapiens	68-72
25256574-5	2015	NAC led to STAT5 dephosphorylation and cell apoptosis at clinically achievable concentrations in DND-41 cells, and Ba/F3 cells transformed by an IL7R-mutant construct containing a cysteine insertion.	Acetylcysteine	0-3	interleukin 7 receptor	Mus musculus	145-149
25256574-8	2015	Thus, targeting leukaemogenic IL7R homodimerization with NAC offers a potentially effective and feasible therapeutic strategy that warrants testing in patients with T-ALL.	Acetylcysteine	57-60	interleukin 7 receptor	Homo sapiens	30-34
24718901-8	2014	WA demonstrated induction of N-acetyl-L-cysteine-repressible oxidative stress as measured directly and through a subsequent heat shock response with HSP32 and HSP70 upregulation and decreased HSF1.	Acetylcysteine	29-48	heat shock transcription factor 1	Homo sapiens	192-196
24085626-6	2014	CoCl2-induced increase of Bax/Bcl-2 ratio and Caspase-3 expression was attenuated by RA, NAC and SB203580 (p38MAPK inhibitor).	Acetylcysteine	89-92	caspase 3	Rattus norvegicus	46-55
29410271-8	2018	In addition, a ROS scavenger N-acetyl-l-cysteine (NAC) down-regulated the protein level of p-p38, p-JNK and Prdx1, and H9c2 cell apoptosis.	Acetylcysteine	50-53	mitogen activated protein kinase 14	Rattus norvegicus	93-96
24085626-9	2014	Similar to the effect of RA, both NAC and NS-398 (COX-2 inhibitor) blocked CoCl2-induced COX-2 expression and PGE2 secretion.	Acetylcysteine	34-37	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	50-55
24085626-9	2014	Similar to the effect of RA, both NAC and NS-398 (COX-2 inhibitor) blocked CoCl2-induced COX-2 expression and PGE2 secretion.	Acetylcysteine	34-37	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	89-94
25896065-9	2015	High-mobility group box-1 (HMGB-1), an endogenous activator of TLR4, rapidly increased in TLR4 immunoprecipitates upon high glucose stimulation, and this association was reduced by N-acetylcysteine, an antioxidant.	Acetylcysteine	181-197	high mobility group box 1	Homo sapiens	0-25
25896065-9	2015	High-mobility group box-1 (HMGB-1), an endogenous activator of TLR4, rapidly increased in TLR4 immunoprecipitates upon high glucose stimulation, and this association was reduced by N-acetylcysteine, an antioxidant.	Acetylcysteine	181-197	high mobility group box 1	Homo sapiens	27-33
29736011-8	2018	S-nitrosylation of sGC was increased (P &lt; 0.05) after BCNI, and it was prevented (P &lt; 0.05) by NAC treatment.	Acetylcysteine	101-104	guanylate cyclase 1 soluble subunit alpha 1	Rattus norvegicus	19-22
24795232-7	2014	The induction of HO-1 by R-scy was inhibited by pretreatment with an antioxidant, N-acetyl-cysteine (NAC), as well as SB203580 and LY294002, inhibitors for p38 MAPK and PI3K/Akt, respectively.	Acetylcysteine	101-104	mitogen-activated protein kinase 14	Mus musculus	156-164
29620243-6	2018	Furthermore, knockdown of Prx V protein expression with a lentivirus significantly enhanced HT22 cell apoptosis mediated by glutamate, which was reversed by inhibition of ROS with N-acetyl-L-cysteine.	Acetylcysteine	180-199	peroxiredoxin 5	Mus musculus	26-31
24987341-10	2014	The effects of NAC on social interaction and anxiety-like behavior in the VPA-exposed offspring were blocked after intra-amygdala infusion of mGluR2/3 antagonist LY341495.	Acetylcysteine	15-18	glutamate receptor, ionotropic, AMPA2 (alpha 2)	Mus musculus	142-148
24987341-13	2014	These results provide the first evidence that the disruption of social interaction and enhanced presynaptic excitatory transmission in VPA-exposed offspring could be rescued by NAC, which depends on the activation of mGluR2/3.	Acetylcysteine	177-180	glutamate receptor, ionotropic, AMPA2 (alpha 2)	Mus musculus	217-223
27031525-6	2015	Treatment with antioxidant N-acetyl cysteine restored oxLDL-induced p38 phosphorylation to basal levels.	Acetylcysteine	27-44	mitogen-activated protein kinase 14	Mus musculus	68-71
29656300-10	2018	N-acetyl-L-cysteine (NAC) partially attenuated SIX1 siRNA-induced ROS level increases, and autophagy inhibitor 3-MA notably enhanced SIX1 siRNA-induced cell apoptosis.	Acetylcysteine	0-19	SIX homeobox 1	Homo sapiens	47-51
25398325-11	2014	Restoration of pre-TCR expression or treatment of RhoA-deficient mice with a ROS scavenger N-acetylcysteine partially restored thymocyte development.	Acetylcysteine	91-107	ras homolog family member A	Mus musculus	50-54
25398951-6	2014	RESULTS: The greatest increase in 0- to 8-hour postexposure concentrations of mercapturic acids from baseline was MHBMA-3 (parent, 1,3-butadiene; 2.1-fold), then CNEMA (acrylonitrile; 1.7-fold), PMA (benzene; 1.6-fold), MMA (methylating agents; 1.6-fold), and HEMA (ethylene oxide; 1.3-fold).	Acetylcysteine	78-95	glutamyl-tRNA reductase 1, chloroplastic-like	Nicotiana tabacum	260-264
24727104-9	2014	In addition, calpain 1 staining and creatinine were significantly lower in the CM+GSPE group compared to the CM+NAC group.	Acetylcysteine	112-115	calpain 1	Rattus norvegicus	13-22
28770700-10	2018	Interestingly, FasL-induced RIP1/3 binding was significantly suppressed by the antioxidants Trolox and N-acetyl cysteine (NAC), suggesting the involvement of reactive oxygen species (ROS) in FasL-induced necroptotic cellular processes.	Acetylcysteine	103-120	Fas ligand (TNF superfamily, member 6)	Mus musculus	15-19
25193743-9	2014	Interestingly, inhibition of ROS with N-acetylcysteine abrogated Akt/Gsk-3beta activation and the LA-induced cytoprotection following SNP stimulation.	Acetylcysteine	38-54	glycogen synthase kinase 3 beta	Rattus norvegicus	69-78
25386077-7	2014	In addition, NAC treatment significantly reduced caspase-3 activity and apoptosis after reperfusion, which correlated with the protein expression of Bcl-2 and Bcl-xl.	Acetylcysteine	13-16	BCL2-like 1	Mus musculus	159-165
24412703-7	2014	Blocking ROS generation using the antioxidant N-acetyl-l-cysteine abolished the apoptosis and caspase-3 activities induced by POMC gene delivery and hypoxia.	Acetylcysteine	46-65	pro-opiomelanocortin-alpha	Mus musculus	126-130
28770700-10	2018	Interestingly, FasL-induced RIP1/3 binding was significantly suppressed by the antioxidants Trolox and N-acetyl cysteine (NAC), suggesting the involvement of reactive oxygen species (ROS) in FasL-induced necroptotic cellular processes.	Acetylcysteine	103-120	Fas ligand (TNF superfamily, member 6)	Mus musculus	191-195
28770700-10	2018	Interestingly, FasL-induced RIP1/3 binding was significantly suppressed by the antioxidants Trolox and N-acetyl cysteine (NAC), suggesting the involvement of reactive oxygen species (ROS) in FasL-induced necroptotic cellular processes.	Acetylcysteine	122-125	Fas ligand (TNF superfamily, member 6)	Mus musculus	15-19
28770700-10	2018	Interestingly, FasL-induced RIP1/3 binding was significantly suppressed by the antioxidants Trolox and N-acetyl cysteine (NAC), suggesting the involvement of reactive oxygen species (ROS) in FasL-induced necroptotic cellular processes.	Acetylcysteine	122-125	Fas ligand (TNF superfamily, member 6)	Mus musculus	191-195
25151118-9	2014	We observed that N-acetylcysteine reduced (i) Syk activation, (ii) band 3 clusterization, (iii) HSP27 membrane association, and (iv) erythroid microparticle release, resulting in increased Prx2(-/-) mouse red cell survival.	Acetylcysteine	17-33	peroxiredoxin 2	Mus musculus	189-193
24063596-9	2014	Leptin expression was suppressed by AngII receptor blockers, an ROS scavenger [NAC (N-acetylcysteine)], an ERK (extracellular-signal-regulated kinase) pathway inhibitor (PD98059) and ERK siRNA.	Acetylcysteine	79-82	leptin	Rattus norvegicus	0-6
29622768-6	2018	The ROS scavenger N-acetyl-L-cysteine, a PLD effector phosphatidic acid and a possible CK2 activator spermidine attenuated the lifespan shortening and age-related biomarkers triggered by pld-1 knockdown.	Acetylcysteine	18-37	Phospholipase	Caenorhabditis elegans	187-190
24063596-9	2014	Leptin expression was suppressed by AngII receptor blockers, an ROS scavenger [NAC (N-acetylcysteine)], an ERK (extracellular-signal-regulated kinase) pathway inhibitor (PD98059) and ERK siRNA.	Acetylcysteine	84-100	leptin	Rattus norvegicus	0-6
25063220-3	2014	Treatment with Ang IIinduced RANKL expression in a dose- and time-dependent manner in osteoblasts, which was attenuated by pre-treatment with an AT1 receptor antagonist (olmesartan), ROS scavenger (N-acetylcysteine, NAC), or the ERK inhibitor (U0126), but not with AT2R antagonist (PD123319).	Acetylcysteine	198-214	angiogenin, ribonuclease, RNase A family, 5	Mus musculus	15-18
29587772-5	2018	In addition, the effect of antioxidant, N-acetylcysteine (NAC) in the expression of IL-33 was compared between HBECs from healthy subjects and those from COPD patients.	Acetylcysteine	40-56	interleukin 33	Homo sapiens	84-89
25333278-7	2014	However, Antioxidant N-acetylcysteine (NAC) treatment inhibited MMP2 expression and activity, and partially reversed cell apoptosis and insulin secretion dysfunction induced by AGE.	Acetylcysteine	21-37	matrix metallopeptidase 2	Rattus norvegicus	64-68
25333278-7	2014	However, Antioxidant N-acetylcysteine (NAC) treatment inhibited MMP2 expression and activity, and partially reversed cell apoptosis and insulin secretion dysfunction induced by AGE.	Acetylcysteine	39-42	matrix metallopeptidase 2	Rattus norvegicus	64-68
24361123-10	2014	Inhibitors of reactive oxygen species (N-acetyl-l-cysteine) blocked l-arginine-induced DNA damage, necrosis, apoptosis, release of nucleosomes, and activation of nuclear factor kappaB in pancreatic tissues and acinar cells from Pdx1-Cre; HMGB1(flox/flox) and control mice.	Acetylcysteine	39-58	pancreatic and duodenal homeobox 1	Mus musculus	228-232
24361123-10	2014	Inhibitors of reactive oxygen species (N-acetyl-l-cysteine) blocked l-arginine-induced DNA damage, necrosis, apoptosis, release of nucleosomes, and activation of nuclear factor kappaB in pancreatic tissues and acinar cells from Pdx1-Cre; HMGB1(flox/flox) and control mice.	Acetylcysteine	39-58	high mobility group box 1	Mus musculus	238-243
24449419-9	2014	N-acetylcysteine, a glutathione (GSH) precursor, blocked Cd2+-evoked PTEN degradation as well as Akt phosphorylation.	Acetylcysteine	0-16	CD2 antigen	Mus musculus	57-60
24365793-0	2014	Does intravenous or oral high-dose N-acetylcysteine in addition to saline prevent contrast-induced nephropathy assessed by cystatin C?	Acetylcysteine	35-51	cystatin C	Homo sapiens	123-133
29587772-5	2018	In addition, the effect of antioxidant, N-acetylcysteine (NAC) in the expression of IL-33 was compared between HBECs from healthy subjects and those from COPD patients.	Acetylcysteine	58-61	interleukin 33	Homo sapiens	84-89
29587772-6	2018	RESULTS: Treatment with H2O2 significantly potentiated IL-33 expression in NCI-H292 cells, and the potentiation was reversed by NAC treatment.	Acetylcysteine	128-131	interleukin 33	Homo sapiens	55-60
29587772-9	2018	In HBECs from healthy subjects, H2O2-potentiated IL-33 expression and its reversal by NAC was also confirmed.	Acetylcysteine	86-89	interleukin 33	Homo sapiens	49-54
24838627-7	2014	Moreover, treatment with the thiol group donor N-acetylcysteine completely blocked PRIMA-1-induced apoptosis and reinforced the hypothesis that thiol modifications are important for PRIMA-1 biological activity.	Acetylcysteine	47-63	proline rich membrane anchor 1	Homo sapiens	83-90
29587772-10	2018	Under the condition without H2O2-stimulation, treatment with NAC significantly decreased the expression of IL-33 in HBECs from COPD patients, but not in those from healthy subjects.	Acetylcysteine	61-64	interleukin 33	Homo sapiens	107-112
24838627-7	2014	Moreover, treatment with the thiol group donor N-acetylcysteine completely blocked PRIMA-1-induced apoptosis and reinforced the hypothesis that thiol modifications are important for PRIMA-1 biological activity.	Acetylcysteine	47-63	proline rich membrane anchor 1	Homo sapiens	182-189
24105017-4	2014	RESULTS: In patients who received NAC, the serum levels of matrix metalloproteinase (MMP)-9 and MMP-2 after 72 h were significantly lower than those in the placebo group (p = 0.014 and p = 0.045, respectively).	Acetylcysteine	34-37	matrix metallopeptidase 2	Homo sapiens	96-101
24872003-1	2014	OBJECTIVE: The objective of this study was to evaluate the effects of potential renoprotective interventions such as the administration of N-acetylcysteine (NAC; antioxidant) and furosemide (diuretic) on intrarenal oxygenation as evaluated by blood oxygen level-dependent (BOLD) magnetic resonance imaging (MRI) in combination with urinary neutrophil gelatinase-associated lipocalin (NGAL) measurements.	Acetylcysteine	139-155	lipocalin 2	Rattus norvegicus	340-382
29353042-12	2018	The expressions of autophagy- and cell cycle arrest-related molecules, as well as mTORC1 were also reversed by N-acetyl-l-cysteine (NAC) in GA-treated cells.	Acetylcysteine	111-130	CREB regulated transcription coactivator 1	Mus musculus	82-88
24872003-1	2014	OBJECTIVE: The objective of this study was to evaluate the effects of potential renoprotective interventions such as the administration of N-acetylcysteine (NAC; antioxidant) and furosemide (diuretic) on intrarenal oxygenation as evaluated by blood oxygen level-dependent (BOLD) magnetic resonance imaging (MRI) in combination with urinary neutrophil gelatinase-associated lipocalin (NGAL) measurements.	Acetylcysteine	139-155	lipocalin 2	Rattus norvegicus	384-388
24872003-11	2014	Urinary NGAL showed little to no increase in R2* after administration of iodixanol in the rats pretreated with furosemide but demonstrated significant increase in the rats pretreated with NAC or placebo (P &lt; 0.05).	Acetylcysteine	188-191	lipocalin 2	Rattus norvegicus	8-12
25078973-7	2014	Pre-treatment with N-acetyl-l-cysteine (NAC), significantly inhibited the SP-A and SP-B mediated apoptosis, suggesting a vital role of ROS involved in the lethality of both agents.	Acetylcysteine	19-38	surfactant protein A1	Homo sapiens	74-78
24105017-8	2014	CONCLUSION: NAC can be beneficial in preventing early remodeling by reducing the level of MMP-2 and MMP-9.	Acetylcysteine	12-15	matrix metallopeptidase 2	Homo sapiens	90-95
24486459-5	2014	Notably, NAC and GSH abolished the LPS-induced expression of iNOS and Cox-2 in BV2 microglial cells by inhibiting NF-kappaB activity.	Acetylcysteine	9-12	prostaglandin-endoperoxide synthase 2	Mus musculus	70-75
24470519-7	2014	These effects were p38-dependent and reversed in vivo by treatment of hypercholesterolemic mice with antioxidant N-acetylcysteine.	Acetylcysteine	113-129	mitogen-activated protein kinase 14	Mus musculus	19-22
25078973-7	2014	Pre-treatment with N-acetyl-l-cysteine (NAC), significantly inhibited the SP-A and SP-B mediated apoptosis, suggesting a vital role of ROS involved in the lethality of both agents.	Acetylcysteine	19-38	surfactant protein B	Homo sapiens	83-87
25078973-7	2014	Pre-treatment with N-acetyl-l-cysteine (NAC), significantly inhibited the SP-A and SP-B mediated apoptosis, suggesting a vital role of ROS involved in the lethality of both agents.	Acetylcysteine	40-43	surfactant protein A1	Homo sapiens	74-78
25078973-7	2014	Pre-treatment with N-acetyl-l-cysteine (NAC), significantly inhibited the SP-A and SP-B mediated apoptosis, suggesting a vital role of ROS involved in the lethality of both agents.	Acetylcysteine	40-43	surfactant protein B	Homo sapiens	83-87
25002534-5	2014	However, pretreatment with N-acetylcysteine or diphenylene iodonium significantly reduced the OC differentiation, as well as the ROS accumulation and NF-kappaB activation, that were enhanced by TRP14 depletion.	Acetylcysteine	27-43	thioredoxin domain containing 17	Mus musculus	194-199
24180497-3	2014	Preincubation with the general antioxidants tempol (superoxide dismutase mimic) and N-acetyl cysteine (NAC) or the mitochondria-specific antioxidants mito-tempol and SS31 significantly decreased the rates of long-lived protein degradation and LC3B flux and blocked the induction of autophagy-related gene expression.	Acetylcysteine	84-101	microtubule-associated protein 1 light chain 3 beta	Mus musculus	243-247
29137484-8	2018	In H9C2 cardiomyocytes, under a basal condition, NAC or tempol increased the ratio of LC3 II/I proteins and reduced LC3 II autophagic flux.	Acetylcysteine	49-52	annexin A3	Rattus norvegicus	86-89
24180497-3	2014	Preincubation with the general antioxidants tempol (superoxide dismutase mimic) and N-acetyl cysteine (NAC) or the mitochondria-specific antioxidants mito-tempol and SS31 significantly decreased the rates of long-lived protein degradation and LC3B flux and blocked the induction of autophagy-related gene expression.	Acetylcysteine	103-106	microtubule-associated protein 1 light chain 3 beta	Mus musculus	243-247
24180497-7	2014	NAC significantly decreased basal LC3B autophagic flux in skeletal muscles of mice.	Acetylcysteine	0-3	microtubule-associated protein 1 light chain 3 beta	Mus musculus	34-38
25202081-8	2014	Pre-treatment with N-acetylcysteine blocked loss of MMP, caused increase of Bcl-2-associated X protein (Bax)/B-cell lymphoma 2 (Bcl-2) ratio, caspase-8 activation, and apoptosis induced by equol.	Acetylcysteine	19-35	caspase 8	Homo sapiens	142-151
29137484-8	2018	In H9C2 cardiomyocytes, under a basal condition, NAC or tempol increased the ratio of LC3 II/I proteins and reduced LC3 II autophagic flux.	Acetylcysteine	49-52	annexin A3	Rattus norvegicus	116-119
29137484-9	2018	Under nutrient deprivation, NAC increased the LC3 II/I ratio and reduced LC3 II autophagic flux.	Acetylcysteine	28-31	annexin A3	Rattus norvegicus	46-49
29137484-9	2018	Under nutrient deprivation, NAC increased the LC3 II/I ratio and reduced LC3 II autophagic flux.	Acetylcysteine	28-31	annexin A3	Rattus norvegicus	73-76
29137484-10	2018	In vivo studies in rats, NAC treatment increased the LC3 II/I ratio and p-Akt protein expression in myocardium.	Acetylcysteine	25-28	annexin A3	Rattus norvegicus	53-56
29269267-4	2018	This effect was also supported by the finding that treatment with N-acetylcysteine dampened the complex II stimulation, SDHA subunit tyrosine phosphorylation, and levels of antioxidant enzymes.	Acetylcysteine	66-82	succinate dehydrogenase complex flavoprotein subunit A	Homo sapiens	120-124
25246272-3	2014	The antioxidant N-acetylcysteine decreased GSK3beta phosphorylation and poly(ADP-ribose) polymerase cleavage induced by 4HPR, As2O3, and PEITC, implicating oxidative stress in these effects.	Acetylcysteine	16-32	glycogen synthase kinase 3 beta	Homo sapiens	43-51
24270669-6	2014	As well, PES treatment caused HSP70, BiP and p53 to accumulate in the detergent-insoluble fraction, and this too was prevented by NAC.	Acetylcysteine	130-133	cellular tumor antigen p53	Oncorhynchus mykiss	45-48
25197166-7	2014	N-acetylcysteine significantly reduced ROS levels and KLF5 and NF-kappaB translocation in nuclear extracts.	Acetylcysteine	0-16	Kruppel like factor 5	Homo sapiens	54-58
25197166-8	2014	Therefore, N-acetylcysteine pretreatment before LPS exposure reduces ROS, downregulates KLF5 expression, and subsequently reduces inflammatory responses by scavenging ROS.	Acetylcysteine	11-27	Kruppel like factor 5	Homo sapiens	88-92
24842665-4	2014	Therefore, we tested the effects of Se and NAC administration on apoptosis, oxidative stress, and Ca(2+) influx through TRPV1 channel activations in the hippocampus of TBI-induced rats.	Acetylcysteine	43-46	transient receptor potential cation channel, subfamily V, member 1	Rattus norvegicus	120-125
29593120-6	2018	Furthermore, sulforaphane provoked the generation of intracellular ROS; especially when ROS production was blocked by antioxidant N-acetylcysteine, both AMPK activation and growth inhibition by sulforaphane were completely abolished.	Acetylcysteine	130-146	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	153-157
24842665-11	2014	In conclusion, we observed that NAC and Se have protective effects on oxidative stress, apoptosis, and Ca(2+) entry via TRPV1 channel activation in the hippocampus of this TBI model, but the effect of NAC appears to be much greater than that of Se.	Acetylcysteine	32-35	transient receptor potential cation channel, subfamily V, member 1	Rattus norvegicus	120-125
24836981-14	2014	NAC also down-regulated both increases in NLRP3, ASC, caspase-1 and IL-1beta mRNA levels, along with their immunostaining.	Acetylcysteine	0-3	steroid sulfatase	Mus musculus	49-52
24836981-14	2014	NAC also down-regulated both increases in NLRP3, ASC, caspase-1 and IL-1beta mRNA levels, along with their immunostaining.	Acetylcysteine	0-3	caspase 1	Mus musculus	54-63
23475579-5	2014	Overexpression of anti-oxidant enzymes superoxide dismutase 1 (SOD1), SOD2, and catalase, or pretreatment with the pharmacological inhibitor N-acetylcysteine (NAC) significantly attenuated both pso-mediated ROS generation and pso-mediated growth inhibition in CaP cells.	Acetylcysteine	141-157	superoxide dismutase 2	Homo sapiens	70-74
25711080-1	2014	We have shown that antioxidant N-acetylcysteine (NAC, 2-10 mM) quickly (for 2 hours) and completely inactivates the activity of matrix metalloproteinases (gelatinases MMP-2 and MMP-9, and collagenases MMP-1 and MMP-8) secreted by transformed mouse fibroblasts 3T3-SV40 into the medium.	Acetylcysteine	31-47	matrix metallopeptidase 9	Mus musculus	177-182
25711080-1	2014	We have shown that antioxidant N-acetylcysteine (NAC, 2-10 mM) quickly (for 2 hours) and completely inactivates the activity of matrix metalloproteinases (gelatinases MMP-2 and MMP-9, and collagenases MMP-1 and MMP-8) secreted by transformed mouse fibroblasts 3T3-SV40 into the medium.	Acetylcysteine	31-47	matrix metallopeptidase 13	Mus musculus	201-206
25176089-6	2014	NAC treatment obviously alleviated intestinal damages induced by CPB, decreased the levels of intestinal MDA, TNF-alpha, IL-6 and serum DAO and increased activity of SOD, GSH, and GSH-Px in the intestines.	Acetylcysteine	0-3	amine oxidase, copper containing 1	Rattus norvegicus	136-139
25711080-1	2014	We have shown that antioxidant N-acetylcysteine (NAC, 2-10 mM) quickly (for 2 hours) and completely inactivates the activity of matrix metalloproteinases (gelatinases MMP-2 and MMP-9, and collagenases MMP-1 and MMP-8) secreted by transformed mouse fibroblasts 3T3-SV40 into the medium.	Acetylcysteine	49-52	matrix metallopeptidase 9	Mus musculus	177-182
28421532-9	2018	MMP-8 was inhibited directly using a MMP-8I (5 mg/kg) and indirectly by reducing neutrophil infiltration with sivelestat sodium (50 mg/kg) or using the antioxidant N-acetyl-L-cysteine (100 mg/kg).	Acetylcysteine	164-183	matrix metallopeptidase 8	Rattus norvegicus	0-5
25711080-1	2014	We have shown that antioxidant N-acetylcysteine (NAC, 2-10 mM) quickly (for 2 hours) and completely inactivates the activity of matrix metalloproteinases (gelatinases MMP-2 and MMP-9, and collagenases MMP-1 and MMP-8) secreted by transformed mouse fibroblasts 3T3-SV40 into the medium.	Acetylcysteine	49-52	matrix metallopeptidase 13	Mus musculus	201-206
25711080-3	2014	Besides inhibitory effect, NAC decreased MMP-1 and MMP-9 (but not MMP-2) production in the cell medium.	Acetylcysteine	27-30	matrix metallopeptidase 13	Mus musculus	41-46
25711080-3	2014	Besides inhibitory effect, NAC decreased MMP-1 and MMP-9 (but not MMP-2) production in the cell medium.	Acetylcysteine	27-30	matrix metallopeptidase 9	Mus musculus	51-56
23770845-6	2013	We show that the mechanism by which GW9662 treatment causes a reduction in ALDH-positive population cells is partially due to ROS, as it can be rescued by treatment with N-acetyl-cysteine.	Acetylcysteine	170-187	aldehyde dehydrogenase family 3, subfamily A1	Mus musculus	75-79
24534112-2	2014	The effect of NAC has been associated with facilitating the activity of cystine-glutamate antiporters on glial cells concomitant with the release of non-vesicular glutamate, which mainly stimulates the presynaptic metabotropic glutamate receptor subtype 2 receptors (mGluR2).	Acetylcysteine	14-17	glutamate receptor, ionotropic, AMPA2 (alpha 2)	Mus musculus	267-273
24578384-14	2014	However, pretreatment with N-acetyl-l-cysteine, a reactive oxygen species scavenger, suppressed CTRP3-induced extracellular signal-regulated kinase 1/2 phosphorylation.	Acetylcysteine	27-46	mitogen activated protein kinase 3	Rattus norvegicus	110-149
24519543-2	2014	N-acetylcysteine (NAC) and selenium (Se) display neuroprotective activities mediated at least in part by their antioxidant and anti-inflammatory properties although there is no report on oxidative stress, antioxidant vitamin, interleukin-1 beta (IL)-1beta and IL-4 levels in brain and blood of TBI-induced rats.	Acetylcysteine	0-16	interleukin 4	Rattus norvegicus	260-264
24519543-2	2014	N-acetylcysteine (NAC) and selenium (Se) display neuroprotective activities mediated at least in part by their antioxidant and anti-inflammatory properties although there is no report on oxidative stress, antioxidant vitamin, interleukin-1 beta (IL)-1beta and IL-4 levels in brain and blood of TBI-induced rats.	Acetylcysteine	18-21	interleukin 4	Rattus norvegicus	260-264
24533448-10	2014	Furthermore, pregestational diabetes increased ROS, impaired cell proliferation, and altered Gata4, Gata5 and Vegf-a expression in the fetal heart of diabetic offspring, which were all prevented by NAC treatment.	Acetylcysteine	198-201	GATA binding protein 5	Mus musculus	100-105
23975535-10	2013	NAC protected against MDMA-induced cell death and the up -regulation of Bax and Caspase-3, in addition to the down-regulation of Bcl-2.	Acetylcysteine	0-3	caspase 3	Rattus norvegicus	80-89
29328400-6	2018	Nacetylcysteine, a Nox4 inhibitor, was demonstrated to inhibit ROS generation, suppress VCAM-1 and ICAM-1 protein expression, and decrease oxidative stress and inflammation in HK-2 cells following overexpression of miR-146a.	Acetylcysteine	0-15	NADPH oxidase 4	Homo sapiens	19-23
24157283-8	2014	NAC and the specific JNK inhibitor (SP600125) and ERK1/2 inhibitor (PD98059) abrogated iAs-induced cell cytotoxicity, caspase-3/-7 activity, and JNK and ERK1/2 activation.	Acetylcysteine	0-3	mitogen-activated protein kinase 3	Mus musculus	153-159
29440671-6	2018	However, administration of expectorant N-acetylcysteine removed the mucus and rescued the PspA-specific nasal IgA response.	Acetylcysteine	39-55	surfactant associated protein A1	Mus musculus	90-94
24713665-10	2014	The expression levels of NF-kappaB-regulated inflammatory cytokines, namely TNF-alpha, IL-6 and IL-1beta, were markedly increased after BHBA treatment, while significantly decreased after NAC treatment.	Acetylcysteine	188-191	interferon beta-2	Bos taurus	87-91
24713665-10	2014	The expression levels of NF-kappaB-regulated inflammatory cytokines, namely TNF-alpha, IL-6 and IL-1beta, were markedly increased after BHBA treatment, while significantly decreased after NAC treatment.	Acetylcysteine	188-191	interleukin 1 beta	Bos taurus	96-104
23978445-6	2013	Pretreatment with an anti-oxidant (N-acetyl cysteine) or a selective inhibitor of NADPH oxidase (diphenyleneiodonium chloride (DPI)) prevented ethanol-induced MMP-12 expression.	Acetylcysteine	35-52	matrix metallopeptidase 12	Mus musculus	159-165
24008628-4	2013	Here, we observed that cross-linking of CD80 and CD86 in EBV-transformed B cells induced apoptosis through caspase-dependent release of apoptosis-related molecules, cytochrome c and apoptosis-inducing factor (AIF) from mitochondria, because Z-VAD-fmk (N-benzyloxycarbonyl-Val-Ala-Asp-fluoromethylketone) and N-acetylcysteine (NAC) blocked apoptosis and disruption of mitochondria.	Acetylcysteine	326-329	CD80 molecule	Homo sapiens	40-44
24008628-4	2013	Here, we observed that cross-linking of CD80 and CD86 in EBV-transformed B cells induced apoptosis through caspase-dependent release of apoptosis-related molecules, cytochrome c and apoptosis-inducing factor (AIF) from mitochondria, because Z-VAD-fmk (N-benzyloxycarbonyl-Val-Ala-Asp-fluoromethylketone) and N-acetylcysteine (NAC) blocked apoptosis and disruption of mitochondria.	Acetylcysteine	326-329	CD86 molecule	Homo sapiens	49-53
27558879-0	2018	mGluR2/3 mediates short-term control of nicotine-seeking by acute systemic N-acetylcysteine.	Acetylcysteine	75-91	glutamate receptor, ionotropic, AMPA2 (alpha 2)	Mus musculus	0-6
23850346-10	2013	Moreover, the results of reactive oxygen species (ROS) scavenging by N-acetyl cysteine (NAC) indicated that ROS were required in the Nox4-mediated upregulation of ADAM17 expression.	Acetylcysteine	69-86	NADPH oxidase 4	Homo sapiens	133-137
23850346-10	2013	Moreover, the results of reactive oxygen species (ROS) scavenging by N-acetyl cysteine (NAC) indicated that ROS were required in the Nox4-mediated upregulation of ADAM17 expression.	Acetylcysteine	88-91	NADPH oxidase 4	Homo sapiens	133-137
24162829-4	2014	GA activated calcium/calmodulin-dependent protein kinase II (CaMKII), c-Jun N-terminal kinase (JNK) and P38; but these activating effects were attenuated by pretreatment with N-acetyl-L-cysteine, a ROS inhibitor.	Acetylcysteine	175-194	mitogen activated protein kinase 14	Rattus norvegicus	104-107
23433350-8	2014	In first and the second moments, latent MMP-2 was significantly elevated in the eyes treated with NAC and CS (P &lt; 0.001).	Acetylcysteine	98-101	matrix metallopeptidase 2	Rattus norvegicus	40-45
27558879-3	2018	Restoring basal concentrations of extracellular Glu, thereby increasing tonic activation of the presynaptic group II metabotropic Glu receptors (mGluR2/3) with N-acetylcysteine (N-AC), might offer a valid therapeutic approach for maintaining smoking abstinence.	Acetylcysteine	160-176	glutamate receptor, ionotropic, AMPA2 (alpha 2)	Mus musculus	145-151
24397138-14	2013	CONCLUSION: NAC can relieve ischemia reperfusion injury in rats" heart transplantation by improving myocardial SOD content, and reducing active Caspase-3 activity and AI, which has a protective effect on myocardial cell of donor heart.	Acetylcysteine	12-15	caspase 3	Rattus norvegicus	144-169
27558879-3	2018	Restoring basal concentrations of extracellular Glu, thereby increasing tonic activation of the presynaptic group II metabotropic Glu receptors (mGluR2/3) with N-acetylcysteine (N-AC), might offer a valid therapeutic approach for maintaining smoking abstinence.	Acetylcysteine	178-182	glutamate receptor, ionotropic, AMPA2 (alpha 2)	Mus musculus	145-151
27558879-11	2018	Blocking mGluR2/3 with the selective antagonist LY341495, 1 mg/kg i.p., completely prevented the antirelapse activity of N-AC.	Acetylcysteine	121-125	glutamate receptor, ionotropic, AMPA2 (alpha 2)	Mus musculus	9-15
27558879-12	2018	The finding that N-AC prevents cue-induced nicotine-seeking by stimulating mGluR2/3 might indicate a therapeutic opportunity for acute cue-controlled nicotine-seeking.	Acetylcysteine	17-21	glutamate receptor, ionotropic, AMPA2 (alpha 2)	Mus musculus	75-81
23109061-8	2013	Treatment with N-acetylcysteine and deferoxamine prevented both the memory deficit and the increase in the BDNF levels induced by BCAA administration.	Acetylcysteine	15-31	AT-rich interaction domain 4B	Rattus norvegicus	130-134
24358342-9	2013	Antioxidant n-acetyl cysteine (NAC) significantly inhibited salinomycin-induced AMPK activation and autophagy induction.	Acetylcysteine	12-29	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	80-84
24358342-9	2013	Antioxidant n-acetyl cysteine (NAC) significantly inhibited salinomycin-induced AMPK activation and autophagy induction.	Acetylcysteine	31-34	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	80-84
28992480-5	2018	However, ROS inhibitor N-acetyl-l-cysteine (NAC) reduced IL-1beta and IL-18 release to 45 pg mL-1 and 108 pg mL-1.	Acetylcysteine	23-42	interleukin 18	Mus musculus	70-75
24015194-0	2013	Both PKA and Epac pathways mediate N-acetylcysteine-induced Connexin43 preservation in rats with myocardial infarction.	Acetylcysteine	35-51	Rap guanine nucleotide exchange factor 3	Rattus norvegicus	13-17
24015194-10	2013	In an ex vivo study, enhanced connexin43 levels afforded by N-acetylcysteine were partially blocked by either H-89 (a PKA inhibitor) or brefeldin A (an Epac-signaling inhibitor) and completely blocked when H-89 and brefeldin A were given in combination.	Acetylcysteine	60-76	Rap guanine nucleotide exchange factor 3	Rattus norvegicus	152-156
28992480-5	2018	However, ROS inhibitor N-acetyl-l-cysteine (NAC) reduced IL-1beta and IL-18 release to 45 pg mL-1 and 108 pg mL-1.	Acetylcysteine	44-47	interleukin 18	Mus musculus	70-75
24113378-7	2013	Furthermore, knocking down hBVR induced a marked increase in the levels of intracellular reactive oxygen species under hypoxic conditions, and the chemosensitizing effect of hBVR depletion was reversed by pretreatment with the antioxidant N-acetylcysteine.	Acetylcysteine	239-255	biliverdin reductase A	Homo sapiens	27-31
29115375-6	2018	The levels of intracellular ROS and gamma-H2AX were decreased by the ROS scavenger (N-acetylcysteine), and ROS levels were also markedly reduced by STAT5 inhibitor (SH-4-54).	Acetylcysteine	84-100	H2A.X variant histone	Homo sapiens	36-46
24113378-7	2013	Furthermore, knocking down hBVR induced a marked increase in the levels of intracellular reactive oxygen species under hypoxic conditions, and the chemosensitizing effect of hBVR depletion was reversed by pretreatment with the antioxidant N-acetylcysteine.	Acetylcysteine	239-255	biliverdin reductase A	Homo sapiens	174-178
23666878-9	2013	OPG-induced apoptosis was abolished by the ROS scavenger N-acetylcysteine and the NOX inhibitor diphenyleniodonium.	Acetylcysteine	57-73	TNF receptor superfamily member 11b	Homo sapiens	0-3
29106395-10	2018	Moreover, N-acetyl-L-cysteine (NAC)-mediated inhibition of ROS suppressed cell injury led by Nox4 overexpression, indicating Nox4-mediated ROS generation may be the key mediator in cisplatin-induced nephrotoxicity.	Acetylcysteine	10-29	NADPH oxidase 4	Mus musculus	93-97
24036416-8	2013	At the impact site, MINO plus NAC attenuated CD68-expressing phagocytic microglia without altering neutrophil infiltration or astrocyte activation.	Acetylcysteine	30-33	Cd68 molecule	Rattus norvegicus	45-49
24036416-10	2013	In the corpus callosum, MINO plus NAC decreased CD68 expression yet increased overall microglial activation as measured by Iba-1.	Acetylcysteine	34-37	Cd68 molecule	Rattus norvegicus	48-52
23948373-8	2013	Following treatment with the antioxidant NAC, cybrid B4 cells showed significantly reduced insulin-induced phosphorylation of P38 and increased GLUT1/GLUT4 translocation to the cell membrane, suggesting that NAC may divert insulin signaling from pro-inflammation to glucose uptake.	Acetylcysteine	41-44	solute carrier family 2 member 4	Homo sapiens	150-155
23948373-8	2013	Following treatment with the antioxidant NAC, cybrid B4 cells showed significantly reduced insulin-induced phosphorylation of P38 and increased GLUT1/GLUT4 translocation to the cell membrane, suggesting that NAC may divert insulin signaling from pro-inflammation to glucose uptake.	Acetylcysteine	208-211	solute carrier family 2 member 4	Homo sapiens	150-155
29106395-10	2018	Moreover, N-acetyl-L-cysteine (NAC)-mediated inhibition of ROS suppressed cell injury led by Nox4 overexpression, indicating Nox4-mediated ROS generation may be the key mediator in cisplatin-induced nephrotoxicity.	Acetylcysteine	10-29	NADPH oxidase 4	Mus musculus	125-129
29106395-10	2018	Moreover, N-acetyl-L-cysteine (NAC)-mediated inhibition of ROS suppressed cell injury led by Nox4 overexpression, indicating Nox4-mediated ROS generation may be the key mediator in cisplatin-induced nephrotoxicity.	Acetylcysteine	31-34	NADPH oxidase 4	Mus musculus	93-97
29106395-10	2018	Moreover, N-acetyl-L-cysteine (NAC)-mediated inhibition of ROS suppressed cell injury led by Nox4 overexpression, indicating Nox4-mediated ROS generation may be the key mediator in cisplatin-induced nephrotoxicity.	Acetylcysteine	31-34	NADPH oxidase 4	Mus musculus	125-129
29115506-6	2018	The results of the present study ndicated that Ang II upregulated MCP-1 expression in osteoblasts, which was mitigated by agonists of the AT1R, including olmesartan, a ROS scavenger N-acetylcysteine (NAC), ammonium pyrrolidinethiocarbamate (PDTC) and nuclear factor (NF)-kappaB, but not by the Ang II type 2 receptor antagonist, PD123319.	Acetylcysteine	182-198	angiogenin	Homo sapiens	47-50
29115506-6	2018	The results of the present study ndicated that Ang II upregulated MCP-1 expression in osteoblasts, which was mitigated by agonists of the AT1R, including olmesartan, a ROS scavenger N-acetylcysteine (NAC), ammonium pyrrolidinethiocarbamate (PDTC) and nuclear factor (NF)-kappaB, but not by the Ang II type 2 receptor antagonist, PD123319.	Acetylcysteine	182-198	angiotensin II receptor type 1	Homo sapiens	138-142
23583676-6	2013	In contrast, treatment with the thiol-based antioxidant N-acetylcysteine promoted the relocalization of Tms to cortical actin microfilaments and partially rescued the migration defects associated with attenuated LDHA expression.	Acetylcysteine	56-72	lactate dehydrogenase A	Mus musculus	212-216
23708739-5	2013	TOP mRNA and protein were also consistently up-regulated by shear, events which could be completely prevented by pre-treatment of cells with either N-acetylcysteine, superoxide dismutase, or catalase, confirming ROS involvement.	Acetylcysteine	148-164	thimet oligopeptidase 1	Homo sapiens	0-3
29115506-6	2018	The results of the present study ndicated that Ang II upregulated MCP-1 expression in osteoblasts, which was mitigated by agonists of the AT1R, including olmesartan, a ROS scavenger N-acetylcysteine (NAC), ammonium pyrrolidinethiocarbamate (PDTC) and nuclear factor (NF)-kappaB, but not by the Ang II type 2 receptor antagonist, PD123319.	Acetylcysteine	200-203	angiogenin	Homo sapiens	47-50
23867003-8	2013	NAC induced p53 and reduced p65 protein expression through activation of PPARalpha.	Acetylcysteine	0-3	RELA proto-oncogene, NF-kB subunit	Homo sapiens	28-31
23867003-9	2013	Silencing of p53 and overexpression of p65 blocked the effect of NAC on PDK1 promoter activity and protein expression.	Acetylcysteine	65-68	RELA proto-oncogene, NF-kB subunit	Homo sapiens	39-42
29115506-6	2018	The results of the present study ndicated that Ang II upregulated MCP-1 expression in osteoblasts, which was mitigated by agonists of the AT1R, including olmesartan, a ROS scavenger N-acetylcysteine (NAC), ammonium pyrrolidinethiocarbamate (PDTC) and nuclear factor (NF)-kappaB, but not by the Ang II type 2 receptor antagonist, PD123319.	Acetylcysteine	200-203	angiotensin II receptor type 1	Homo sapiens	138-142
23867003-10	2013	CONCLUSION: Our results show that NAC inhibits PDK1 expression through PPARalpha-mediated induction of p53 and inhibition of p65 protein expression.	Acetylcysteine	34-37	RELA proto-oncogene, NF-kB subunit	Homo sapiens	125-128
24086766-7	2013	Additionally, although the ROS scavenger N-acetyl-l-cysteine abrogated 5-HT-induced PDGFbeta and TrkB receptor transactivation, it was unable to prevent 5-HT-induced ERK1/2 phosphorylation.	Acetylcysteine	41-60	neurotrophic receptor tyrosine kinase 2	Homo sapiens	97-101
28864499-8	2017	Somewhat surprisingly, both DAS and NAC prevented impaired STAT5B nuclear translocation.	Acetylcysteine	36-39	signal transducer and activator of transcription 5B	Homo sapiens	59-65
23660334-4	2013	However, the quenching of ROS generation by N-acetyl-l-cysteine, a scavenger of ROS, reversed the sanguinarine-induced apoptosis effects via inhibition of the MMP collapse, tBid expression, and activation of caspases.	Acetylcysteine	44-63	caspase 8	Homo sapiens	208-216
28864499-9	2017	Further examination of microtubule-independent steps of the pathway revealed that Jak2/STAT5B activation by growth hormone was prevented by DAS and NAC.	Acetylcysteine	148-151	Janus kinase 2	Homo sapiens	82-86
23825130-11	2013	Importantly a significant reduction in cortisol production was demonstrated with AAAS knockdown, which was partially reversed with N-acetylcysteine treatment.	Acetylcysteine	131-147	aladin WD repeat nucleoporin	Homo sapiens	81-85
29160844-6	2017	Aco2 activity in the striatum of R6/2 mice could be restored by the anti-oxidant, N-acetyl-l-cysteine, supporting that decreased Aco2 activity in HD is probably caused by increased oxidative damage.	Acetylcysteine	82-101	aconitase 2, mitochondrial	Mus musculus	0-4
23669236-14	2013	However, our results demonstrated that NAC treatment induced an increase in CD69 expression on unstimulated CD8(+) T lymphocytes obtained from HTLV-1 infected individuals, healthy donors and HTLV carriers.	Acetylcysteine	39-42	CD69 molecule	Homo sapiens	76-80
24015194-12	2013	These findings suggest that N-acetylcysteine protects ventricular arrhythmias by attenuating reduced connexin43 expression and function via both PKA- and Epac-dependent pathways, which converge through the inactivation of glycogen synthase kinase-3beta.	Acetylcysteine	28-44	Rap guanine nucleotide exchange factor 3	Rattus norvegicus	154-158
24015194-12	2013	These findings suggest that N-acetylcysteine protects ventricular arrhythmias by attenuating reduced connexin43 expression and function via both PKA- and Epac-dependent pathways, which converge through the inactivation of glycogen synthase kinase-3beta.	Acetylcysteine	28-44	glycogen synthase kinase 3 beta	Rattus norvegicus	222-252
23080342-7	2013	Moreover, the anti-oxidant N-acetyl-l-cysteine prevented p38 phosphorylation, showing that p38 activation is triggered by an oxidative stress.	Acetylcysteine	27-46	mitogen-activated protein kinase 14	Mus musculus	57-60
23080342-7	2013	Moreover, the anti-oxidant N-acetyl-l-cysteine prevented p38 phosphorylation, showing that p38 activation is triggered by an oxidative stress.	Acetylcysteine	27-46	mitogen-activated protein kinase 14	Mus musculus	91-94
23307410-8	2013	The role of COX-2 appeared to be 2-fold and its expression was divergently modulated by NAC.	Acetylcysteine	88-91	prostaglandin-endoperoxide synthase 2	Rattus norvegicus	12-17
23065916-8	2013	After one month of NAC both p50-p50/p50-p65 dimers were significantly reduced (P&lt;.004 and .006).	Acetylcysteine	19-22	RELA proto-oncogene, NF-kB subunit	Homo sapiens	40-43
29160844-6	2017	Aco2 activity in the striatum of R6/2 mice could be restored by the anti-oxidant, N-acetyl-l-cysteine, supporting that decreased Aco2 activity in HD is probably caused by increased oxidative damage.	Acetylcysteine	82-101	aconitase 2, mitochondrial	Mus musculus	129-133
28543759-7	2017	Interestingly, AGG-dependent p73 expression was found to be regulated by ROS, which was reversed by NAC treatment.	Acetylcysteine	100-103	tumor protein p73	Homo sapiens	29-32
22212518-0	2013	N-acetylcysteine in preventing contrast-induced nephropathy assessed by cystatin C.	Acetylcysteine	0-16	cystatin C	Homo sapiens	72-82
22212518-3	2013	We investigated NAC for the prevention of CIN by monitoring creatinine and cystatin C.	Acetylcysteine	16-19	cystatin C	Homo sapiens	75-85
22212518-8	2013	RESULTS: The incidence of cystatin C-based CIN was 28.5% (n = 14) in NAC and 23.4% (n = 15) in control group (p = 0.663) and serum creatinine-based CIN was 12.2% (n = 6) in NAC and 17.2% (n = 11) in control group (P= 0.468).	Acetylcysteine	69-72	cystatin C	Homo sapiens	26-36
23500899-8	2013	Lowering the serum homocysteine level by a simultaneous supplementation with N-acetylcysteine improved OPG and FOXO1 expression and partially antagonized RANKL and proresorptive cytokine synthesis in the bone milieu.	Acetylcysteine	77-93	forkhead box O1	Rattus norvegicus	111-116
23500899-8	2013	Lowering the serum homocysteine level by a simultaneous supplementation with N-acetylcysteine improved OPG and FOXO1 expression and partially antagonized RANKL and proresorptive cytokine synthesis in the bone milieu.	Acetylcysteine	77-93	TNF superfamily member 11	Rattus norvegicus	154-159
28840582-0	2017	N-Acetylcysteine Prevents the Increase in Spontaneous Oxidation of Dopamine During Monoamine Oxidase Inhibition in PC12 Cells.	Acetylcysteine	0-16	monoamine oxidase A	Rattus norvegicus	83-100
23353834-7	2013	Treatment of TR-rPCT1 with NAC or an inhibition of TXNIP by AzaS or siTXNIP3 each reduces HG-induced ROS, caspase-3 activation and DNA damage demonstrating that TXNIP up-regulation under chronic hyperglycemia is critically involved in cellular oxidative stress, DNA damage and retinal pericyte apoptosis.	Acetylcysteine	27-30	caspase 3	Rattus norvegicus	106-115
28753455-7	2017	Moreover, DATS provoked intracellular ROS generation and the loss of mitochondrial membrane potential, and in particular, when ROS production was blocked by antioxidant N-acety-l-cysteine, both AMPK activation and growth inhibition by DATS were completely abolished.	Acetylcysteine	169-187	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	194-198
23434081-4	2013	AAP (0.125-1.0mM) and NAC (0.0625-1.0mM) down-regulate the expression of cytokines and inhibit NF-kappaB p65 protein transfer from the cytoplasm to the nucleus in vitro.	Acetylcysteine	22-25	RELA proto-oncogene, NF-kB subunit	Homo sapiens	105-108
23407882-7	2013	Both NAC and DPI suppressed indoxyl sulfate-induced expression of NF-kappaB p65 and CREB.	Acetylcysteine	5-8	RELA proto-oncogene, NF-kB subunit	Homo sapiens	76-79
23407882-10	2013	Indoxyl sulfate induced the expression of NOX4 in proximal tubular cells, which was suppressed by NAC, DPI, NF-kappaB inhibitors, NF-kappaB p65 siRNA, and CREB siRNA.	Acetylcysteine	98-101	NADPH oxidase 4	Homo sapiens	42-46
23353715-8	2013	Moreover, NAC inhibited the Cd-induced phosphorylation of testicular eukaryotic translation initiation factor 2alpha (eIF2alpha), a downstream target of the double-stranded RNA-activated kinase-like ER kinase (PERK) pathway.	Acetylcysteine	10-13	eukaryotic translation initiation factor 2A	Mus musculus	69-116
23353715-8	2013	Moreover, NAC inhibited the Cd-induced phosphorylation of testicular eukaryotic translation initiation factor 2alpha (eIF2alpha), a downstream target of the double-stranded RNA-activated kinase-like ER kinase (PERK) pathway.	Acetylcysteine	10-13	eukaryotic translation initiation factor 2A	Mus musculus	118-127
23708970-9	2013	NAC inhibited the magnolol-mediated induction of ROS generation and suppression of PECAM expression.	Acetylcysteine	0-3	platelet/endothelial cell adhesion molecule 1	Mus musculus	83-88
23708127-7	2013	Demonstrating the role of ROS, pretreatment of A549 cells with the antioxidant N-acetylcysteine (NAC) followed by MB-PDT resulted in increased cell viability and reduced proteolytic cleavage of PARP.	Acetylcysteine	79-95	collagen type XI alpha 2 chain	Homo sapiens	194-198
23708127-7	2013	Demonstrating the role of ROS, pretreatment of A549 cells with the antioxidant N-acetylcysteine (NAC) followed by MB-PDT resulted in increased cell viability and reduced proteolytic cleavage of PARP.	Acetylcysteine	97-100	collagen type XI alpha 2 chain	Homo sapiens	194-198
23922799-8	2013	Furthermore, the addition of N-acetyl cysteine (NAC), a reactive oxygen species (ROS) scavenger, significantly decreased the effect of low temperature on mitigating cardia bifida in s1pr2(as10) embryos.	Acetylcysteine	29-46	sphingosine-1-phosphate receptor 2	Danio rerio	182-187
23922799-8	2013	Furthermore, the addition of N-acetyl cysteine (NAC), a reactive oxygen species (ROS) scavenger, significantly decreased the effect of low temperature on mitigating cardia bifida in s1pr2(as10) embryos.	Acetylcysteine	48-51	sphingosine-1-phosphate receptor 2	Danio rerio	182-187
23525857-4	2013	3T3-L1 and C3H/10T 1/2-clone 8 cells showed increased B cell activating factor expression upon exposure to hydrogen peroxide, and these changes were inhibited by treatment with the antioxidant N-acetyl-cysteine.	Acetylcysteine	193-210	tumor necrosis factor (ligand) superfamily, member 13b	Mus musculus	54-78
28554049-7	2017	In addition, DSS-induced colitis is ameliorated by an antioxidant N-acetylcysteine (NAC) through attenuation of oxidative stress, resulting from deficiency of the IDH2 gene.	Acetylcysteine	66-82	isocitrate dehydrogenase 2 (NADP+), mitochondrial	Mus musculus	163-167
23525857-6	2013	In addition, serum BAFF levels in high fat diet-fed mice were reduced by N-acetyl-cysteine treatment.	Acetylcysteine	73-90	tumor necrosis factor (ligand) superfamily, member 13b	Mus musculus	19-23
23660503-10	2013	Alcohol-induced and H2O2-induced increases in intestinal cell CLOCK and PER2 were significantly inhibited by treatment with NAC.	Acetylcysteine	124-127	clock circadian regulator	Homo sapiens	62-67
28554049-7	2017	In addition, DSS-induced colitis is ameliorated by an antioxidant N-acetylcysteine (NAC) through attenuation of oxidative stress, resulting from deficiency of the IDH2 gene.	Acetylcysteine	84-87	isocitrate dehydrogenase 2 (NADP+), mitochondrial	Mus musculus	163-167
23124986-9	2013	The antioxidant, N-acetylcysteine (NAC), significantly prevented the production of ROS, the reduction of DeltaPsim, the release of cytochrome c and the activation of caspase-3.	Acetylcysteine	17-33	caspase 3	Rattus norvegicus	166-175
28715154-7	2017	It is revealed that 3 h after the introduction of LPS, levels of reactive oxygen species in the kidney were significantly increased, and the injection of the antioxidant N-acetylcysteine afforded protection from AKI, evaluated by urine KIM-1 and NGAL levels.	Acetylcysteine	170-186	lipocalin 2	Rattus norvegicus	246-250
23124986-9	2013	The antioxidant, N-acetylcysteine (NAC), significantly prevented the production of ROS, the reduction of DeltaPsim, the release of cytochrome c and the activation of caspase-3.	Acetylcysteine	35-38	caspase 3	Rattus norvegicus	166-175
24489592-7	2013	Andrographolide significantly induced reactive oxygen species (ROS) formation, p53 activation, Bax, and active caspase-3 expression, and these phenomena were suppressed by pretreating the cells with N-acetyl-L-cysteine, a ROS scavenger, or diphenylene iodonium, a nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (Nox) inhibitor.	Acetylcysteine	199-218	caspase 3	Rattus norvegicus	111-120
23271497-7	2013	NAC treatment, increasing this ratio, reduced MMP-2 secretion and exhibited a direct effect on the secreted MMP-2 activity.	Acetylcysteine	0-3	matrix metallopeptidase 2	Homo sapiens	46-51
23271497-7	2013	NAC treatment, increasing this ratio, reduced MMP-2 secretion and exhibited a direct effect on the secreted MMP-2 activity.	Acetylcysteine	0-3	matrix metallopeptidase 2	Homo sapiens	108-113
23271497-8	2013	In NAC-treated and TNFalpha-stimulated ISEMFs of CD patients" MMP-2 activity were restored to physiological value.	Acetylcysteine	3-6	matrix metallopeptidase 2	Homo sapiens	62-67
28852176-6	2017	S17 robustly induced generation of ROS with Keap/Nrf2 pathway activated and the application of ROS scavenger N-acetyl cysteine (NAC) completely blocked these effects by S17 in MGC803 cells.	Acetylcysteine	109-126	sperm associated antigen 5	Mus musculus	169-172
23570668-5	2013	High glucose levels also increased the generation of ROS; inhibition of ROS activity by N-acetyl-l-cysteine attenuated the high glucose-induced increase in TRPC6 expression and Ca(2+) influx.	Acetylcysteine	88-107	transient receptor potential cation channel subfamily C member 6	Homo sapiens	156-161
23108103-6	2013	Occludin glycation and ZO-1 disruption were prevented by N-acetylcysteine (NAC).	Acetylcysteine	57-73	occludin	Rattus norvegicus	0-8
23108103-6	2013	Occludin glycation and ZO-1 disruption were prevented by N-acetylcysteine (NAC).	Acetylcysteine	75-78	occludin	Rattus norvegicus	0-8
28852176-6	2017	S17 robustly induced generation of ROS with Keap/Nrf2 pathway activated and the application of ROS scavenger N-acetyl cysteine (NAC) completely blocked these effects by S17 in MGC803 cells.	Acetylcysteine	128-131	sperm associated antigen 5	Mus musculus	169-172
23091297-6	2012	Finally, reactive oxygen species scavenging by N-acetyl cysteine or stabilization of hypoxia signaling by knockdown of the von-Hippel-Lindau (VHL) protein led to reversal of the effects of Meis1 deletion.	Acetylcysteine	47-64	Meis homeobox 1	Mus musculus	189-194
28106298-8	2017	Inhibiting as well as silencing of IP3 R receptor also resulted in increase in ROS production which was abolished after pretreatment with N-acetyl cysteine.	Acetylcysteine	138-155	inositol 1,4,5-trisphosphate receptor type 3	Homo sapiens	35-40
23271287-12	2012	The elevated ROS was strongly associated with the activation of JNK and ERK1/2 signal pathways after MPP(+) exposure, since the pretreatment of NAC significantly reduced the upregulation of p-JNK and p-ERK1/2.	Acetylcysteine	144-147	mitogen activated protein kinase 3	Rattus norvegicus	72-78
23271287-12	2012	The elevated ROS was strongly associated with the activation of JNK and ERK1/2 signal pathways after MPP(+) exposure, since the pretreatment of NAC significantly reduced the upregulation of p-JNK and p-ERK1/2.	Acetylcysteine	144-147	mitogen activated protein kinase 3	Rattus norvegicus	202-208
23485152-4	2013	Hcy-induced COX-2 expression was attenuated not only by the calcium chelators, EGTA and BAPTA-AM, but also by an antioxidant, N-acetylcysteine.	Acetylcysteine	126-142	cytochrome c oxidase II, mitochondrial	Mus musculus	12-17
23658858-13	2013	Treatments produced no or minor effects on the activities of antioxidant enzymes catalase, glutathione peroxidase and glutathione reductase, whereas the activity of the thioredoxin reductase was decreased in the brain and increased the liver of the animals in the groups receiving TeAsp or TeAsp plus NAC.	Acetylcysteine	301-304	peroxiredoxin 2	Mus musculus	169-190
23434081-10	2013	AAP or NAC treated alone could reduce the NF-kappaB p65 concentration ratio.	Acetylcysteine	7-10	RELA proto-oncogene, NF-kB subunit	Homo sapiens	52-55
28106298-9	2017	Its role in autophagy was confirmed through decrease in the levels of LC3 II after pretreatment with IP3 R inhibitor and N acetyl cysteine.Moreover, inhibiting as well as silencing IP3 R-induced cell death in MCF-7 cells was attenuated by autophagic inhibitors (Bafilomycin A1 or 3-Methyladeneine).	Acetylcysteine	121-138	inositol 1,4,5-trisphosphate receptor type 3	Homo sapiens	181-186
23434081-13	2013	The NF-kappaB p65 concentration ratio had significantly reduced (P&lt;0.05) when AAP and NAC were used in combination.	Acetylcysteine	89-92	RELA proto-oncogene, NF-kB subunit	Homo sapiens	14-17
28769771-7	2017	Furthermore, since pretreatment of n-acetyl-l-cysteine (NAC), a powerful antioxidant amino acid, could attenuate the elevated levels of MMP-9, p-p38, p-ERK2 and p-JNK1/2 in 2-CE exposed astrocytes, activation of MAPK signal pathways in 2-CE exposed astrocytes could be mediated partially by reactive oxygen species (ROS), which was most likely generated in the metabolism of 2-CE.	Acetylcysteine	35-54	mitogen activated protein kinase 14	Rattus norvegicus	145-148
23011098-7	2013	In addition, inhibition of ROS with N-acetyl-L-cysteine or diphenyleneiodonium significantly reduced the activated levels of caspase-1.	Acetylcysteine	36-55	caspase 1	Mus musculus	125-134
22990675-5	2012	We demonstrated that N-acetylcysteine (NAC) is a novel allosteric chaperone for GAA.	Acetylcysteine	21-37	alpha glucosidase	Homo sapiens	80-83
22990675-5	2012	We demonstrated that N-acetylcysteine (NAC) is a novel allosteric chaperone for GAA.	Acetylcysteine	39-42	alpha glucosidase	Homo sapiens	80-83
22990675-7	2012	A computational analysis of NAC-GAA interactions confirmed that NAC does not interact with GAA catalytic domain.	Acetylcysteine	28-31	alpha glucosidase	Homo sapiens	32-35
22990675-7	2012	A computational analysis of NAC-GAA interactions confirmed that NAC does not interact with GAA catalytic domain.	Acetylcysteine	64-67	alpha glucosidase	Homo sapiens	32-35
22990675-8	2012	NAC enhanced the residual activity of mutated GAA in cultured PD fibroblasts and in COS7 cells overexpressing mutated GAA.	Acetylcysteine	0-3	alpha glucosidase	Homo sapiens	46-49
22990675-8	2012	NAC enhanced the residual activity of mutated GAA in cultured PD fibroblasts and in COS7 cells overexpressing mutated GAA.	Acetylcysteine	0-3	alpha glucosidase	Homo sapiens	118-121
28769771-7	2017	Furthermore, since pretreatment of n-acetyl-l-cysteine (NAC), a powerful antioxidant amino acid, could attenuate the elevated levels of MMP-9, p-p38, p-ERK2 and p-JNK1/2 in 2-CE exposed astrocytes, activation of MAPK signal pathways in 2-CE exposed astrocytes could be mediated partially by reactive oxygen species (ROS), which was most likely generated in the metabolism of 2-CE.	Acetylcysteine	35-54	mitogen activated protein kinase 1	Rattus norvegicus	152-156
22618532-7	2012	NAC-mediated neuroprotection was attributed to the direct scavenging of reactive oxygen species and was mediated by targeting the hypoxia-inducible factor-1alpha pathway via the BNIP3 and PI3K/Akt/mTOR pathways.	Acetylcysteine	0-3	BCL2/adenovirus E1B interacting protein 3	Mus musculus	178-183
22665050-9	2013	In addition, treatment with N-acetyl-L-cysteine, a reactive oxygen species (ROS) scavenger, suppressed the induction of beclin-1 and LC3 II, implying that the differential SVCT-2 protein-dependent L-ascorbate uptake was attributable to intracellular ROS induced by L-ascorbate, subsequently leading to autophagy.	Acetylcysteine	28-47	solute carrier family 23 member 2	Homo sapiens	172-178
28769771-7	2017	Furthermore, since pretreatment of n-acetyl-l-cysteine (NAC), a powerful antioxidant amino acid, could attenuate the elevated levels of MMP-9, p-p38, p-ERK2 and p-JNK1/2 in 2-CE exposed astrocytes, activation of MAPK signal pathways in 2-CE exposed astrocytes could be mediated partially by reactive oxygen species (ROS), which was most likely generated in the metabolism of 2-CE.	Acetylcysteine	35-54	mitogen activated protein kinase 3	Rattus norvegicus	212-216
23083489-7	2013	These effects on PDI were mimicked by exogenous 4-HNE and prevented by the carbonyl-scavengers N-acetylcysteine and pyridoxamine, which reduced CHOP expression and toxicity by oxLDLs.	Acetylcysteine	95-111	prolyl 4-hydroxylase subunit beta	Homo sapiens	17-20
28769771-7	2017	Furthermore, since pretreatment of n-acetyl-l-cysteine (NAC), a powerful antioxidant amino acid, could attenuate the elevated levels of MMP-9, p-p38, p-ERK2 and p-JNK1/2 in 2-CE exposed astrocytes, activation of MAPK signal pathways in 2-CE exposed astrocytes could be mediated partially by reactive oxygen species (ROS), which was most likely generated in the metabolism of 2-CE.	Acetylcysteine	56-59	mitogen activated protein kinase 14	Rattus norvegicus	145-148
23268108-7	2013	We showed that NF-kappaB inhibitor N-acetyl-L-cysteine (NAC) effectively attenuates the expression of LPS-stimulated iNOS, COX-2 and TNF-alpha.	Acetylcysteine	35-54	prostaglandin-endoperoxide synthase 2	Mus musculus	123-128
23268108-7	2013	We showed that NF-kappaB inhibitor N-acetyl-L-cysteine (NAC) effectively attenuates the expression of LPS-stimulated iNOS, COX-2 and TNF-alpha.	Acetylcysteine	56-59	prostaglandin-endoperoxide synthase 2	Mus musculus	123-128
28769771-7	2017	Furthermore, since pretreatment of n-acetyl-l-cysteine (NAC), a powerful antioxidant amino acid, could attenuate the elevated levels of MMP-9, p-p38, p-ERK2 and p-JNK1/2 in 2-CE exposed astrocytes, activation of MAPK signal pathways in 2-CE exposed astrocytes could be mediated partially by reactive oxygen species (ROS), which was most likely generated in the metabolism of 2-CE.	Acetylcysteine	56-59	mitogen activated protein kinase 1	Rattus norvegicus	152-156
22672579-12	2012	Surprisingly, rapamycin decreased lifespan in sod1 mutant but not wild-type males fed the standard, HS-LP, and low-calorie diets, whereas antioxidant N-acetylcysteine only increased lifespan in sod1 mutant males fed the HS-LP diet, when compared to diet-matched controls.	Acetylcysteine	150-166	Superoxide dismutase 1	Drosophila melanogaster	194-198
28769771-7	2017	Furthermore, since pretreatment of n-acetyl-l-cysteine (NAC), a powerful antioxidant amino acid, could attenuate the elevated levels of MMP-9, p-p38, p-ERK2 and p-JNK1/2 in 2-CE exposed astrocytes, activation of MAPK signal pathways in 2-CE exposed astrocytes could be mediated partially by reactive oxygen species (ROS), which was most likely generated in the metabolism of 2-CE.	Acetylcysteine	56-59	mitogen activated protein kinase 3	Rattus norvegicus	212-216
28363602-10	2017	Nox1 upregulation was inhibited by actinomycin D (ACD), an inhibitor of transcription, by inhibition of NF-kappaB, a known Nox1 transcriptional regulator and by N-acetyl cysteine (NAC) and MitoTEMPO, suggesting that NF-kappaB and mitochondrial ROS mediate zinc effects.	Acetylcysteine	161-178	NADPH oxidase 1	Homo sapiens	0-4
22700867-8	2012	Moreover, the antioxidant, N-acetyl-L-cysteine (NAC), significantly reduced HIF-1alpha, ERK-1,2 phosphorylation, and CCL2 protein levels that were synergistically increased by the combination of PDGF and NiNPs.	Acetylcysteine	27-46	mitogen activated protein kinase 3	Rattus norvegicus	88-95
22700867-8	2012	Moreover, the antioxidant, N-acetyl-L-cysteine (NAC), significantly reduced HIF-1alpha, ERK-1,2 phosphorylation, and CCL2 protein levels that were synergistically increased by the combination of PDGF and NiNPs.	Acetylcysteine	48-51	mitogen activated protein kinase 3	Rattus norvegicus	88-95
23147562-0	2013	NTPDase and 5"-nucleotidase activities from synaptosomes and platelets of rats exposed to cadmium and treated with N-acetylcysteine.	Acetylcysteine	115-131	5' nucleotidase, ecto	Rattus norvegicus	12-27
23147562-5	2013	In relation to hippocampus synaptosomes, no differences on the NTPDase and 5"-nucleotidase activities of Cd-poisoned rats were observed and only the 5"-nucleotidase activity was increased by the administration of NAC per se.	Acetylcysteine	213-216	5' nucleotidase, ecto	Rattus norvegicus	149-164
23175375-7	2013	In addition, NAC inhibited KSHV infection-induced translocation of alphaVbeta3 integrin into lipid rafts, actin-dependent membrane perturbations, such as blebs, observed during macropinocytosis, and activation of the signal molecules ephrin-A2 receptor, FAK, Src, and Rac1.	Acetylcysteine	13-16	ephrin A2	Homo sapiens	234-243
23175375-7	2013	In addition, NAC inhibited KSHV infection-induced translocation of alphaVbeta3 integrin into lipid rafts, actin-dependent membrane perturbations, such as blebs, observed during macropinocytosis, and activation of the signal molecules ephrin-A2 receptor, FAK, Src, and Rac1.	Acetylcysteine	13-16	protein tyrosine kinase 2	Homo sapiens	254-257
28363602-10	2017	Nox1 upregulation was inhibited by actinomycin D (ACD), an inhibitor of transcription, by inhibition of NF-kappaB, a known Nox1 transcriptional regulator and by N-acetyl cysteine (NAC) and MitoTEMPO, suggesting that NF-kappaB and mitochondrial ROS mediate zinc effects.	Acetylcysteine	180-183	NADPH oxidase 1	Homo sapiens	0-4
23103613-9	2013	Pretreatment with NAC and specific p38-MAPK inhibitor (SB203580), but not JNK inhibitor (SP600125) effectively abrogated the phosphorylation of p38-MAPK and attenuated the apoptotic signals (including: decrease in cytotoxicity, caspase-3/-7 activation, the cytosolic cytochrome c release, and the reversed alteration of Bcl-2 and Bax mRNA) in CA-treated Neuro-2a cells.	Acetylcysteine	18-21	mitogen-activated protein kinase 14	Mus musculus	144-147
23723006-9	2013	Notably, normalization of cardiac function and oxidant/antioxidant level after N-acetylcysteine (NAC)-treatment of diabetic rats resulted with a significant restoration in the expression levels of miR-499, miR-1, miR-133a, and miR-133b in the myocardium.	Acetylcysteine	79-95	microRNA 499a	Rattus norvegicus	197-204
23723006-9	2013	Notably, normalization of cardiac function and oxidant/antioxidant level after N-acetylcysteine (NAC)-treatment of diabetic rats resulted with a significant restoration in the expression levels of miR-499, miR-1, miR-133a, and miR-133b in the myocardium.	Acetylcysteine	79-95	microRNA 1	Rattus norvegicus	206-211
23723006-9	2013	Notably, normalization of cardiac function and oxidant/antioxidant level after N-acetylcysteine (NAC)-treatment of diabetic rats resulted with a significant restoration in the expression levels of miR-499, miR-1, miR-133a, and miR-133b in the myocardium.	Acetylcysteine	79-95	microRNA 133a-1	Rattus norvegicus	213-221
22796440-5	2012	Administration of N-acetyl-L-cysteine, an antioxidant, in the drinking water improved these protein expressions in the skin of Flg(ft) mice.	Acetylcysteine	18-37	filaggrin	Mus musculus	127-130
22798682-5	2012	IEX-1 deficiency-facilitated Th17 cell differentiation was mediated by the increased formation of reactive oxygen species (ROS) at mitochondria following T cell activation, as suggested by marked inhibition of Th17 induction with ROS scavenger N-acetylcysteine or mitoquinone, a specific inhibitor for mitochondrial ROS production.	Acetylcysteine	244-260	immediate early response 3	Mus musculus	0-5
23723006-9	2013	Notably, normalization of cardiac function and oxidant/antioxidant level after N-acetylcysteine (NAC)-treatment of diabetic rats resulted with a significant restoration in the expression levels of miR-499, miR-1, miR-133a, and miR-133b in the myocardium.	Acetylcysteine	97-100	microRNA 499a	Rattus norvegicus	197-204
28560439-12	2017	Pretreatment with NAC abrogated the inhibitory effect of ISL on activation of STAT3 and blocked the cleavage of caspase-9, -7 and -3, and that of PARP in Caki cells.	Acetylcysteine	18-21	collagen type XI alpha 2 chain	Homo sapiens	146-150
23723006-9	2013	Notably, normalization of cardiac function and oxidant/antioxidant level after N-acetylcysteine (NAC)-treatment of diabetic rats resulted with a significant restoration in the expression levels of miR-499, miR-1, miR-133a, and miR-133b in the myocardium.	Acetylcysteine	97-100	microRNA 1	Rattus norvegicus	206-211
23723006-9	2013	Notably, normalization of cardiac function and oxidant/antioxidant level after N-acetylcysteine (NAC)-treatment of diabetic rats resulted with a significant restoration in the expression levels of miR-499, miR-1, miR-133a, and miR-133b in the myocardium.	Acetylcysteine	97-100	microRNA 133a-1	Rattus norvegicus	213-221
23723006-11	2013	Junctin but not triadin is markedly overexpressed in diabetic cardiomyocytes while its level was normalized in NAC-treated diabetics.	Acetylcysteine	111-114	aspartate-beta-hydroxylase	Rattus norvegicus	0-7
28205121-2	2017	We aimed to study the value of intravenous NAC in reducing liver transplantation and mortality in NAI-ALF.	Acetylcysteine	43-46	afamin	Homo sapiens	102-105
24096134-10	2013	Inhibition of Hsp70/Hsc70 activity with VER 155008 attenuated the protection afforded by N-acetyl cysteine in a dose-responsive manner.	Acetylcysteine	89-106	heat shock protein 8	Mus musculus	20-25
23577223-4	2013	The results of western blot showed that NAC preincubation affected Cd-activated MAPK pathways, p38 and ERK phosphorylation.	Acetylcysteine	40-43	mitogen activated protein kinase 14	Rattus norvegicus	95-98
22870983-4	2012	Addition of N-acetylcysteine, a precursor of the intracellular antioxidant glutathione, suppressed the BSO-mediated upregulation of BMP2 and FGF2.	Acetylcysteine	12-28	bone morphogenetic protein 2	Rattus norvegicus	132-136
22870983-4	2012	Addition of N-acetylcysteine, a precursor of the intracellular antioxidant glutathione, suppressed the BSO-mediated upregulation of BMP2 and FGF2.	Acetylcysteine	12-28	fibroblast growth factor 2	Rattus norvegicus	141-145
23085521-3	2012	Embryonic fibroblasts from xCT-deficient mice fail to survive unless a cysteine precursor, N-acetylcysteine, is present.	Acetylcysteine	91-107	solute carrier family 7 (cationic amino acid transporter, y+ system), member 11	Mus musculus	27-30
28205121-15	2017	CONCLUSIONS: When administered on admission, intravenous NAC caused a reduction in NAI-ALF mortality and need for transplantation.	Acetylcysteine	57-60	afamin	Homo sapiens	87-90
23007278-8	2012	Pretreatment with the c-Jun N-terminal kinase (JNK) inhibitor SP600125 and the reactive oxygen species (ROS) scavenger N-acetylcysteine reduced the SVT and TRAIL-induced upregulation of DR4 and DR5 expression, expression of the apoptosis related protein such as caspase-3 and-9, as well as cell growth inhibitory effects.	Acetylcysteine	119-135	TNF receptor superfamily member 10a	Homo sapiens	186-189
22349737-3	2012	Mercapturic acids thus formed (S-substitued-N-acetyl-l-cysteines) may be accumulated in the kidney and either excreted in the urine or desacetylated by Acylase 1 (ACY1) to yield cysteine S-conjugates.	Acetylcysteine	0-17	aminoacylase 1	Homo sapiens	152-161
22349737-3	2012	Mercapturic acids thus formed (S-substitued-N-acetyl-l-cysteines) may be accumulated in the kidney and either excreted in the urine or desacetylated by Acylase 1 (ACY1) to yield cysteine S-conjugates.	Acetylcysteine	0-17	aminoacylase 1	Homo sapiens	163-167
28400474-5	2017	Moreover, we show that the reactive oxygen species (ROS) scavenger N-acetyl cysteine boosts Th17 cell differentiation in a MINK1-dependent manner and exacerbates the severity of EAE.	Acetylcysteine	67-84	misshapen like kinase 1	Homo sapiens	123-128
22349737-3	2012	Mercapturic acids thus formed (S-substitued-N-acetyl-l-cysteines) may be accumulated in the kidney and either excreted in the urine or desacetylated by Acylase 1 (ACY1) to yield cysteine S-conjugates.	Acetylcysteine	44-64	aminoacylase 1	Homo sapiens	152-161
22349737-3	2012	Mercapturic acids thus formed (S-substitued-N-acetyl-l-cysteines) may be accumulated in the kidney and either excreted in the urine or desacetylated by Acylase 1 (ACY1) to yield cysteine S-conjugates.	Acetylcysteine	44-64	aminoacylase 1	Homo sapiens	163-167
22349737-4	2012	To be toxic, the N-acetyl-l-cysteine-S-conjugates first have to undergo deacetylation by ACY 1.	Acetylcysteine	17-38	aminoacylase 1	Homo sapiens	89-94
22932892-6	2012	The H(2)O(2)-mediated hepcidin induction requires STAT3 phosphorylation and is effectively blocked by siRNA-mediated STAT3 silencing, overexpression of SOCS3 (suppressor of cytokine signaling 3), and antioxidants such as N-acetylcysteine.	Acetylcysteine	221-237	suppressor of cytokine signaling 3	Homo sapiens	152-157
27706903-6	2017	Standard of care, N-acetylcysteine and, to a lesser extent, tauroursodeoxycholic treatment were associated with significantly lower transaminase levels, hepatocyte death, unfolded protein response activation, oxidative stress markers, caspase 1 expression and NLRP3 levels.	Acetylcysteine	18-34	caspase 1	Mus musculus	235-244
22549432-10	2012	NAC increased Deltapsim (P = 0.0001) in all T cells, profoundly reduced mTOR activity (P = 0.0009), enhanced apoptosis (P = 0.0004), reversed expansion of CD4-CD8- T cells (mean +- SEM 1.35 +- 0.12-fold change; P = 0.008), stimulated FoxP3 expression in CD4+CD25+ T cells (P = 0.045), and reduced anti-DNA production (P = 0.049).	Acetylcysteine	0-3	forkhead box P3	Homo sapiens	234-239
27706903-7	2017	Importantly, the combination of N-acetylcysteine and tauroursodeoxycholic acid improved serum transaminase levels, reduced histopathological liver damage, UPR-activated CHOP, oxidative stress, caspase 1 expression, NLRP3 levels, IL-1beta levels and the expression of pro-inflammatory cytokines and this to a greater extend than N-acetylcysteine alone.	Acetylcysteine	32-48	caspase 1	Mus musculus	193-202
22714038-5	2012	Importantly, N-acetyl cysteine (NAC) treatment effectively blocked apoptosis via the caspase-9 and caspase-3 pathways while NAC attenuated the inhibition of mitochondrial complex I activity as well as the oxidative metabolism of dopamine (DA).	Acetylcysteine	13-30	caspase 3	Rattus norvegicus	99-108
22714038-5	2012	Importantly, N-acetyl cysteine (NAC) treatment effectively blocked apoptosis via the caspase-9 and caspase-3 pathways while NAC attenuated the inhibition of mitochondrial complex I activity as well as the oxidative metabolism of dopamine (DA).	Acetylcysteine	32-35	caspase 3	Rattus norvegicus	99-108
21953860-6	2012	Pretreatment with antioxidant N-acetyl-L-cysteine, apoptosis signal-regulating kinase 1 inhibitor thioredoxin, and c-Jun NH(2) -terminal kinase inhibitor SP600125 significantly reduced thrombin-induced CCN2 synthesis.	Acetylcysteine	30-49	cellular communication network factor 2	Homo sapiens	202-206
22428706-7	2012	Remarkably, co-administration of antioxidants, such as N-acetylcysteine, ebselen or diphenylene iodonium chloride, drastically reduced PDGF-BB-induced CSE expression.	Acetylcysteine	55-71	cystathionine gamma-lyase	Rattus norvegicus	151-154
28382174-7	2017	Consistently, overexpression of SLC3A1 enhanced tumorigenesis of breast cancer cells, whereas blocking SLC3A1 either with specific siRNA or SLC3A1 specific inhibitor sulfasalazine suppressed tumor growth and also abolished dietary NAC-promoted tumor growth.	Acetylcysteine	231-234	solute carrier family 3 member 1	Homo sapiens	103-109
22336129-10	2012	The administration of NAC increased GSH, attenuated ROS, cytokines, MPO, JNK, pAKT and caspase-3 and lung permeability associated with decreased activation of nuclear factor-kappaB.	Acetylcysteine	22-25	caspase 3	Rattus norvegicus	87-96
22552773-8	2012	Antioxidants (N-acetyl-cysteine and vitamin C), which blocked oxidative stress induced by chronic ethanol in WT mice and acute ethanol in Cyp2e1  (-/-)   KI mice, also blunted the induction of CYP2A5 and Nrf2 by ethanol but not the induction of CYP2E1 by ethanol.	Acetylcysteine	14-31	cytochrome P450, family 2, subfamily a, polypeptide 5	Mus musculus	193-199
22231145-9	2012	RESULTS: IL-1beta-induced cPLA2 expression was mediated through NOX activation/ROS production, which was attenuated by N-acetylcysteine (NAC; a scavenger of ROS), the inhibitors of NOX (diphenyleneiodonium chloride and apocynin), MEK-1/2 (U0126), and JNK-1/2 (SP600125), transfection with the respective siRNAs, and the overexpression of HO-1 in RASFs.	Acetylcysteine	119-135	phospholipase A2, group IVA (cytosolic, calcium-dependent)	Mus musculus	26-31
22231145-9	2012	RESULTS: IL-1beta-induced cPLA2 expression was mediated through NOX activation/ROS production, which was attenuated by N-acetylcysteine (NAC; a scavenger of ROS), the inhibitors of NOX (diphenyleneiodonium chloride and apocynin), MEK-1/2 (U0126), and JNK-1/2 (SP600125), transfection with the respective siRNAs, and the overexpression of HO-1 in RASFs.	Acetylcysteine	119-135	mitogen-activated protein kinase kinase 1	Mus musculus	230-237
22231145-9	2012	RESULTS: IL-1beta-induced cPLA2 expression was mediated through NOX activation/ROS production, which was attenuated by N-acetylcysteine (NAC; a scavenger of ROS), the inhibitors of NOX (diphenyleneiodonium chloride and apocynin), MEK-1/2 (U0126), and JNK-1/2 (SP600125), transfection with the respective siRNAs, and the overexpression of HO-1 in RASFs.	Acetylcysteine	137-140	phospholipase A2, group IVA (cytosolic, calcium-dependent)	Mus musculus	26-31
22042537-11	2012	N-acetyl cysteine, an anti-oxidant, reduced the expression of miR-21 and miR-29b in C. parvum-treated WT mice (p &lt; 0.005) as compared with control C. parvum-treated mice.	Acetylcysteine	0-17	microRNA 21a	Mus musculus	62-68
22522044-11	2012	Treatment of infected animals with anti-oxidants alpha-lipoic acid and N-acetylcysteine and HO inhibitor stannous protoporphyrin (SnPPIX) showed only selective beneficial effects on HO-1 and COX-2 expression in the liver and spleen and serum levels of KC and MCP-1.	Acetylcysteine	71-87	cytochrome c oxidase II, mitochondrial	Mus musculus	191-196
22231145-9	2012	RESULTS: IL-1beta-induced cPLA2 expression was mediated through NOX activation/ROS production, which was attenuated by N-acetylcysteine (NAC; a scavenger of ROS), the inhibitors of NOX (diphenyleneiodonium chloride and apocynin), MEK-1/2 (U0126), and JNK-1/2 (SP600125), transfection with the respective siRNAs, and the overexpression of HO-1 in RASFs.	Acetylcysteine	137-140	mitogen-activated protein kinase kinase 1	Mus musculus	230-237
28382174-7	2017	Consistently, overexpression of SLC3A1 enhanced tumorigenesis of breast cancer cells, whereas blocking SLC3A1 either with specific siRNA or SLC3A1 specific inhibitor sulfasalazine suppressed tumor growth and also abolished dietary NAC-promoted tumor growth.	Acetylcysteine	231-234	solute carrier family 3 member 1	Homo sapiens	103-109
22497815-5	2012	Treatments of N-acetylcysteine and glutathione markedly reduced protein levels of both NFAT5 and Hsp72.	Acetylcysteine	14-30	nuclear factor of activated T cells 5	Homo sapiens	87-92
28382174-8	2017	Collectively, our data demonstrate that SLC3A1 promotes cysteine uptake and determines cellular response to antioxidant N-acetylcysteine, suggesting SLC3A1 is a potential therapeutic target for breast cancer.	Acetylcysteine	120-136	solute carrier family 3 member 1	Homo sapiens	40-46
22294162-5	2012	N-acetylcysteine, a reactive oxygen species scavenger, not only blocked the oridonin-induced increase in hydrogen peroxide and glutathione depletion, but also blocked apoptosis and senescence induced by oridonin, as evidenced by the decrease in Annexin V and senescence-associated beta-galactosidase- positive cells and the inhibition of oridonin-induced upregulation of p53 and p16 and downregulation of c-Myc.	Acetylcysteine	0-16	galactosidase beta 1	Homo sapiens	281-299
28382174-8	2017	Collectively, our data demonstrate that SLC3A1 promotes cysteine uptake and determines cellular response to antioxidant N-acetylcysteine, suggesting SLC3A1 is a potential therapeutic target for breast cancer.	Acetylcysteine	120-136	solute carrier family 3 member 1	Homo sapiens	149-155
22166790-5	2012	Pre-treatment with antioxidant vitamin E or N-acetylcysteine (NAC) completely abolished the I6-induced generation of ROS, loss of MMP, release of cytochrome c, activation of caspase-9 and caspase-3, and cleavage of PARP.	Acetylcysteine	44-60	caspase 3	Rattus norvegicus	188-197
22166790-5	2012	Pre-treatment with antioxidant vitamin E or N-acetylcysteine (NAC) completely abolished the I6-induced generation of ROS, loss of MMP, release of cytochrome c, activation of caspase-9 and caspase-3, and cleavage of PARP.	Acetylcysteine	62-65	caspase 3	Rattus norvegicus	188-197
22537850-12	2012	In addition, hBAFF activity stimulated by PMA/IOM was reduced by N-acetyl-cysteine (NAC), a well-known ROS scavenger.	Acetylcysteine	65-82	TNF superfamily member 13b	Homo sapiens	13-18
22537850-12	2012	In addition, hBAFF activity stimulated by PMA/IOM was reduced by N-acetyl-cysteine (NAC), a well-known ROS scavenger.	Acetylcysteine	84-87	TNF superfamily member 13b	Homo sapiens	13-18
28000869-7	2017	Conversely, N-acetylcysteine inhibited the activation of JNK and p38 MAPK, thus suggesting that the AOPPs-induced activation of JNK/p38 MAPK is reactive oxygen species (ROS)-dependent.	Acetylcysteine	12-28	mitogen-activated protein kinase 14	Mus musculus	65-73
22137594-7	2012	In slices, a low concentration of NAC reduced the amplitude of evoked glutamatergic synaptic currents in the NAcore in an mGluR2/3-dependent manner, while high doses of NAC increased amplitude in an mGluR5-dependent manner.	Acetylcysteine	34-37	glutamate receptor, ionotropic, AMPA2 (alpha 2)	Mus musculus	122-128
22137594-7	2012	In slices, a low concentration of NAC reduced the amplitude of evoked glutamatergic synaptic currents in the NAcore in an mGluR2/3-dependent manner, while high doses of NAC increased amplitude in an mGluR5-dependent manner.	Acetylcysteine	34-37	glutamate receptor, ionotropic, kainate 1	Mus musculus	199-205
22137594-7	2012	In slices, a low concentration of NAC reduced the amplitude of evoked glutamatergic synaptic currents in the NAcore in an mGluR2/3-dependent manner, while high doses of NAC increased amplitude in an mGluR5-dependent manner.	Acetylcysteine	169-172	glutamate receptor, ionotropic, kainate 1	Mus musculus	199-205
22137594-9	2012	Finally, we showed that by blocking mGluR5 the inhibition of cocaine seeking by NAC was potentiated.	Acetylcysteine	80-83	glutamate receptor, ionotropic, kainate 1	Mus musculus	36-42
22137594-10	2012	CONCLUSIONS: The effect of NAC on relapse to cocaine seeking depends on the balance between stimulating mGluR2/3 and mGluR5 in the NAcore, and the efficacy of NAC can be improved by simultaneously inhibiting mGluR5.	Acetylcysteine	27-30	glutamate receptor, ionotropic, kainate 1	Mus musculus	117-123
22137594-10	2012	CONCLUSIONS: The effect of NAC on relapse to cocaine seeking depends on the balance between stimulating mGluR2/3 and mGluR5 in the NAcore, and the efficacy of NAC can be improved by simultaneously inhibiting mGluR5.	Acetylcysteine	27-30	glutamate receptor, ionotropic, kainate 1	Mus musculus	208-214
22137594-10	2012	CONCLUSIONS: The effect of NAC on relapse to cocaine seeking depends on the balance between stimulating mGluR2/3 and mGluR5 in the NAcore, and the efficacy of NAC can be improved by simultaneously inhibiting mGluR5.	Acetylcysteine	159-162	glutamate receptor, ionotropic, kainate 1	Mus musculus	117-123
22137594-10	2012	CONCLUSIONS: The effect of NAC on relapse to cocaine seeking depends on the balance between stimulating mGluR2/3 and mGluR5 in the NAcore, and the efficacy of NAC can be improved by simultaneously inhibiting mGluR5.	Acetylcysteine	159-162	glutamate receptor, ionotropic, kainate 1	Mus musculus	208-214
22065336-5	2012	Furthermore, both triptolide and NAC inhibited activation of c-jun NH2-terminal kinases (JNK) and mitogen-activated protein kinase p38 (p38), phosphorylation of inhibitor of nuclear factor-kappa B (IkappaB) and activation of nuclear factor-kappaB (NF-kappaB).	Acetylcysteine	33-36	mitogen-activated protein kinase 14	Mus musculus	131-134
22065336-5	2012	Furthermore, both triptolide and NAC inhibited activation of c-jun NH2-terminal kinases (JNK) and mitogen-activated protein kinase p38 (p38), phosphorylation of inhibitor of nuclear factor-kappa B (IkappaB) and activation of nuclear factor-kappaB (NF-kappaB).	Acetylcysteine	33-36	mitogen-activated protein kinase 14	Mus musculus	136-139
22316545-1	2012	OBJECTIVE: To investigate the effect of N-acetylcysteine (NAC) on apoptosis of pneumocytes and expression of caspase-3 during lung ischemia/reperfusion injury (LIRI) in rats, and to explore the possible role of NAC in pneumocyte apoptosis.	Acetylcysteine	40-56	caspase 3	Rattus norvegicus	109-118
22316545-12	2012	CONCLUSION: During early period of LIRI, caspase-3 was significantly deregulated by NAC, therefore the cellular apoptosis was inhibited, thus protecting lung tissue from LIRI.	Acetylcysteine	84-87	caspase 3	Rattus norvegicus	41-50
22078209-0	2012	Modulation of CD40-activated B lymphocytes by N-acetylcysteine involves decreased phosphorylation of STAT3.	Acetylcysteine	46-62	CD40 molecule	Homo sapiens	14-18
22078209-4	2012	Then, by treatments with two well-known antioxidants, N-acetylcysteine (NAC) and Trolox, we further investigate the influence of REDOX fluctuation in CD40-activated B lymphocyte homeostasis in long term culture (13 days).	Acetylcysteine	72-75	CD40 molecule	Homo sapiens	150-154
22078209-6	2012	The NAC-induced homoaggregation phenotype is paralleled with increased expressions of CD54, CD11a, CD27 and CD38.	Acetylcysteine	4-7	integrin subunit alpha L	Homo sapiens	92-97
28000869-7	2017	Conversely, N-acetylcysteine inhibited the activation of JNK and p38 MAPK, thus suggesting that the AOPPs-induced activation of JNK/p38 MAPK is reactive oxygen species (ROS)-dependent.	Acetylcysteine	12-28	mitogen-activated protein kinase 14	Mus musculus	65-68
21934138-9	2011	Increased oxidative stress and urothelial cell hyperplasia with evidence of activated p44/42 MAPK (ERK1/2) and cyclin D1 were found in the DMA(V) and NAC (high dose) cotreated group.	Acetylcysteine	150-153	mitogen activated protein kinase 3	Rattus norvegicus	86-89
28054986-7	2017	Moreover, blockage of ROS production by using the ROS inhibitor N-acetyl-l-cysteine totally reversed SFN-mediated down-regulation of JAK2/Src-STAT3 signaling activation and the subsequent effects on apoptosis by blocking the induction of apoptosis-related genes in GBM cells.	Acetylcysteine	64-83	Janus kinase 2	Homo sapiens	133-137
22440610-3	2012	PhB-induced apoptosis was significantly inhibited by N-acetyl-l-cysteine, but not by catalase, indicating that ROS generation occurred intracellularly, and by SP600125 and AG490, specific inhibitors of JNK and IFN-gamma signaling, respectively, confirming their roles in the apoptotic pathway.	Acetylcysteine	53-72	prohibitin 1	Homo sapiens	0-3
22389501-6	2012	Phorbol myristate acetate, a known stimulator of NF-kappaB, increased the levels of GRK5 in myocytes whereas treatment of cells with N-acetyl cysteine, a known inhibitor of NF-kappaB, or with SC 514, an inhibitor of IkappaB kinase 2 decreased GRK5.	Acetylcysteine	133-150	G protein-coupled receptor kinase 5	Mus musculus	84-88
21954051-0	2011	Proteomic analysis of brain proteins in APP/PS-1 human double mutant knock-in mice with increasing amyloid beta-peptide deposition: insights into the effects of in vivo treatment with N-acetylcysteine as a potential therapeutic intervention in mild cognitive impairment and Alzheimer"s disease.	Acetylcysteine	184-200	presenilin 1	Homo sapiens	44-48
26278389-7	2017	The antioxidants N-acetyl cysteine and vitamin C lowered the alcohol elevation of ROS and blunted the alcohol induction of CYP2A5, but not CYP2E1, suggesting ROS play a novel role in the crosstalk between CYP2E1 and CYP2A5.	Acetylcysteine	17-34	cytochrome P450, family 2, subfamily a, polypeptide 5	Mus musculus	123-129
21441382-8	2011	Furthermore, CO-dependent induction of LC3B expression was inhibited by N-acetyl-L-cysteine and the mitochondria-targeting antioxidant, Mito-TEMPO.	Acetylcysteine	72-91	microtubule associated protein 1 light chain 3 beta	Homo sapiens	39-43
22418739-9	2012	We conclude that oxidative stress is an important pathophysiological mechanism in RYR1-related myopathies and that N-acetylcysteine is a successful treatment modality ex vivo and in a vertebrate disease model.	Acetylcysteine	115-131	ryanodine receptor 1a (skeletal)	Danio rerio	82-86
26278389-7	2017	The antioxidants N-acetyl cysteine and vitamin C lowered the alcohol elevation of ROS and blunted the alcohol induction of CYP2A5, but not CYP2E1, suggesting ROS play a novel role in the crosstalk between CYP2E1 and CYP2A5.	Acetylcysteine	17-34	cytochrome P450, family 2, subfamily a, polypeptide 5	Mus musculus	216-222
21913995-11	2012	Toxicity by CYP2B6 was abolished with the reactive oxygen species scavenger N-acetylcysteine.	Acetylcysteine	76-92	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	12-18
27959381-8	2017	Furthermore, the nobiletin-induced VASP phosphorylation was surprisingly reversed by the intracellular antioxidant, N-acetylcysteine (NAC), but not by the inhibitor of NADPH oxidase, diphenyleneiodonium chloride (DPI).	Acetylcysteine	116-132	vasodilator stimulated phosphoprotein	Homo sapiens	35-39
22420031-9	2012	NAC prevented the reduction in DNA synthesis and the marked increase in caspase-3 immunoreactivity.	Acetylcysteine	0-3	caspase 3	Rattus norvegicus	72-81
21827635-6	2012	Nuclear factor-kappaB p65 phosphorylation was unaffected by exercise; however, it was reduced in NAC at fatigue by 14% (P &lt; 0.05) compared with pre-infusion.	Acetylcysteine	97-100	RELA proto-oncogene, NF-kB subunit	Homo sapiens	22-25
27959381-8	2017	Furthermore, the nobiletin-induced VASP phosphorylation was surprisingly reversed by the intracellular antioxidant, N-acetylcysteine (NAC), but not by the inhibitor of NADPH oxidase, diphenyleneiodonium chloride (DPI).	Acetylcysteine	134-137	vasodilator stimulated phosphoprotein	Homo sapiens	35-39
22134701-5	2012	Exposure of H9c2 cells to CoCl(2) or hydrogen peroxide (H(2)O(2)) upregulated expression of phosphorylated (p) ERK1/2, which was reduced by pretreatment with NaHS or N-acetyl-L-cysteine, a ROS scavenger.	Acetylcysteine	166-185	mitogen activated protein kinase 3	Rattus norvegicus	111-117
27959381-9	2017	It was surprising to observe the differential effects of nobiletin and NAC on VASP phosphorylation in human platelets, since they both have been reported to have antioxidant properties.	Acetylcysteine	71-74	vasodilator stimulated phosphoprotein	Homo sapiens	78-82
28004071-8	2016	Administration of NAC could attenuate the alveolar wall structure damage induced by O3 exposure and reduce the amount of infiltrated inflammatory cells, total and differential leukocyte counts (P &lt; 0.05), as well as the IL-6, IL-8 (P &lt; 0.01) and MDA release (P &lt; 0.05).	Acetylcysteine	18-21	chemokine (C-X-C motif) ligand 15	Mus musculus	229-233
22227002-5	2012	In addition, social isolation-induced increase in calpain activity and p25/p35 ratio concomitant with decrease in membrane-associated p35 and p35/Cdk5 activity was normalized by NAC.	Acetylcysteine	178-181	cyclin-dependent kinase 5, regulatory subunit 1 (p35)	Mus musculus	71-74
22227002-5	2012	In addition, social isolation-induced increase in calpain activity and p25/p35 ratio concomitant with decrease in membrane-associated p35 and p35/Cdk5 activity was normalized by NAC.	Acetylcysteine	178-181	cyclin-dependent kinase 5, regulatory subunit 1 (p35)	Mus musculus	75-78
28004071-9	2016	Western blotting results showed that the O3 exposure up-regulated the p38 MAPK and NF-kappaB p65 protein expression in the lung tissue of mice (P &lt; 0.05), which could be alleviated by NAC (P &lt; 0.05).	Acetylcysteine	187-190	mitogen-activated protein kinase 14	Mus musculus	70-78
22227002-5	2012	In addition, social isolation-induced increase in calpain activity and p25/p35 ratio concomitant with decrease in membrane-associated p35 and p35/Cdk5 activity was normalized by NAC.	Acetylcysteine	178-181	cyclin-dependent kinase 5, regulatory subunit 1 (p35)	Mus musculus	134-137
22227002-5	2012	In addition, social isolation-induced increase in calpain activity and p25/p35 ratio concomitant with decrease in membrane-associated p35 and p35/Cdk5 activity was normalized by NAC.	Acetylcysteine	178-181	cyclin-dependent kinase 5, regulatory subunit 1 (p35)	Mus musculus	134-137
28004071-11	2016	The beneficial effect of NAC might be related with the p38 MAPK and NF-kappaB p65 signal pathway.	Acetylcysteine	25-28	mitogen-activated protein kinase 14	Mus musculus	55-63
22227002-6	2012	NAC pretreatment also reversed isolation-induced decrease in GluR1 Ser831 phosphorylation, surface expression of AMPARs and p35-GluR1-CaMKII interactions.	Acetylcysteine	0-3	glutamate receptor, ionotropic, AMPA1 (alpha 1)	Mus musculus	61-66
22227002-6	2012	NAC pretreatment also reversed isolation-induced decrease in GluR1 Ser831 phosphorylation, surface expression of AMPARs and p35-GluR1-CaMKII interactions.	Acetylcysteine	0-3	glutamate receptor, ionotropic, AMPA1 (alpha 1)	Mus musculus	113-119
28081748-8	2016	Inhibition of ROS generation by NAC resulted in a significant reduction of HVJ-E-induced Erk1/2, JNK, and p38 MAPK activation.	Acetylcysteine	32-35	mitogen-activated protein kinase 3	Mus musculus	89-95
22227002-6	2012	NAC pretreatment also reversed isolation-induced decrease in GluR1 Ser831 phosphorylation, surface expression of AMPARs and p35-GluR1-CaMKII interactions.	Acetylcysteine	0-3	cyclin-dependent kinase 5, regulatory subunit 1 (p35)	Mus musculus	124-127
22227002-6	2012	NAC pretreatment also reversed isolation-induced decrease in GluR1 Ser831 phosphorylation, surface expression of AMPARs and p35-GluR1-CaMKII interactions.	Acetylcysteine	0-3	glutamate receptor, ionotropic, AMPA1 (alpha 1)	Mus musculus	128-133
28081748-8	2016	Inhibition of ROS generation by NAC resulted in a significant reduction of HVJ-E-induced Erk1/2, JNK, and p38 MAPK activation.	Acetylcysteine	32-35	mitogen-activated protein kinase 14	Mus musculus	106-109
22227002-7	2012	These results suggest that NAC decreases gamma-secretase activity resulting in the attenuation of Abeta production, calpain activity and conversion of p35 to p25 which stabilized p35-GluR1-CaMKII interactions and restored GluR1 and GluR2 surface expression.	Acetylcysteine	27-30	cyclin-dependent kinase 5, regulatory subunit 1 (p35)	Mus musculus	151-154
22227002-7	2012	These results suggest that NAC decreases gamma-secretase activity resulting in the attenuation of Abeta production, calpain activity and conversion of p35 to p25 which stabilized p35-GluR1-CaMKII interactions and restored GluR1 and GluR2 surface expression.	Acetylcysteine	27-30	cyclin-dependent kinase 5, regulatory subunit 1 (p35)	Mus musculus	158-161
27932980-8	2016	We found that pretreatment with NAC, DPI, or APO also attenuated the TNF-alpha-stimulated IKKalpha/beta and NF-kappaB p65 phosphorylation, NF-kappaB (p65) translocation, and NF-kappaB promoter activity in HPAEpiCs.	Acetylcysteine	32-35	RELA proto-oncogene, NF-kB subunit	Homo sapiens	118-121
22227002-7	2012	These results suggest that NAC decreases gamma-secretase activity resulting in the attenuation of Abeta production, calpain activity and conversion of p35 to p25 which stabilized p35-GluR1-CaMKII interactions and restored GluR1 and GluR2 surface expression.	Acetylcysteine	27-30	cyclin-dependent kinase 5, regulatory subunit 1 (p35)	Mus musculus	179-182
22227002-7	2012	These results suggest that NAC decreases gamma-secretase activity resulting in the attenuation of Abeta production, calpain activity and conversion of p35 to p25 which stabilized p35-GluR1-CaMKII interactions and restored GluR1 and GluR2 surface expression.	Acetylcysteine	27-30	glutamate receptor, ionotropic, AMPA1 (alpha 1)	Mus musculus	183-188
22227002-7	2012	These results suggest that NAC decreases gamma-secretase activity resulting in the attenuation of Abeta production, calpain activity and conversion of p35 to p25 which stabilized p35-GluR1-CaMKII interactions and restored GluR1 and GluR2 surface expression.	Acetylcysteine	27-30	glutamate receptor, ionotropic, AMPA1 (alpha 1)	Mus musculus	222-227
27932980-8	2016	We found that pretreatment with NAC, DPI, or APO also attenuated the TNF-alpha-stimulated IKKalpha/beta and NF-kappaB p65 phosphorylation, NF-kappaB (p65) translocation, and NF-kappaB promoter activity in HPAEpiCs.	Acetylcysteine	32-35	RELA proto-oncogene, NF-kB subunit	Homo sapiens	150-153
22227002-7	2012	These results suggest that NAC decreases gamma-secretase activity resulting in the attenuation of Abeta production, calpain activity and conversion of p35 to p25 which stabilized p35-GluR1-CaMKII interactions and restored GluR1 and GluR2 surface expression.	Acetylcysteine	27-30	glutamate receptor, ionotropic, AMPA2 (alpha 2)	Mus musculus	232-237
27457113-12	2016	However, melatonin and N-acetylcysteine reprogrammed the renin-angiotensin system and arachidonic acid pathway differentially.	Acetylcysteine	23-39	renin	Rattus norvegicus	57-62
22096246-5	2012	Thrombus formation was then initiated by the binding of platelet GPIbalpha to endothelial VWF in our model, and this effect was inhibited by the ROS scavenger N-acetylcysteine.	Acetylcysteine	159-175	glycoprotein 1b, alpha polypeptide	Mus musculus	65-74
26320741-5	2016	LPS and Pam3csk4 also induced IRAK1/4-, ERK- and ROS-dependent activation of activator protein-1 (AP-1), IL-1beta transcription, and IL-1beta processing because significant inhibition in AP-1 activity, IL-1beta transcription, Pro- and mature IL-beta expression, and caspase-1 activity was observed with PD98059, U0126, DPI, NAC, an IRAK1/4 inhibitor, tanshinone IIa, and IRAK1 siRNA treatment.	Acetylcysteine	324-327	interleukin 1 receptor associated kinase 1	Homo sapiens	30-35
22085843-9	2012	Furthermore, Cu(2+)/PDTC complex was capable of increasing the phosphorylations of ERK1/2 and JNK, and its upstream kinase MEK1/2 and MKK4, which could be reversed by NAC.	Acetylcysteine	167-170	mitogen activated protein kinase 3	Rattus norvegicus	83-89
22085843-9	2012	Furthermore, Cu(2+)/PDTC complex was capable of increasing the phosphorylations of ERK1/2 and JNK, and its upstream kinase MEK1/2 and MKK4, which could be reversed by NAC.	Acetylcysteine	167-170	mitogen activated protein kinase kinase 1	Rattus norvegicus	123-129
21902453-6	2012	The antioxidants, N-acetyl L-cysteine (NAC) and 4,5-dihydroxy-1,3-benzenedisulfonic acid (Tiron), both suppressed myogenesis and Prx-2 expression.	Acetylcysteine	18-37	peroxiredoxin 2	Mus musculus	129-134
27572503-12	2016	Curcumin and NAC were able to inhibit H2O2-induced ROS production, reduce the migration and invasion, and decrease the expression of MMP-2 and MMP-9 in pancreatic cancer cells.	Acetylcysteine	13-16	matrix metallopeptidase 2	Homo sapiens	133-138
21902453-6	2012	The antioxidants, N-acetyl L-cysteine (NAC) and 4,5-dihydroxy-1,3-benzenedisulfonic acid (Tiron), both suppressed myogenesis and Prx-2 expression.	Acetylcysteine	39-42	peroxiredoxin 2	Mus musculus	129-134
21928347-8	2012	Furthermore, these effects were regulated by redox conditions since antioxidant N-acetylcysteine abolished the HO-1/HMGB1/caspase-3 axis.	Acetylcysteine	80-96	high mobility group box 1	Mus musculus	116-121
27854233-6	2016	In contrast, N-acetyl-cysteine had a beneficial effect on mitochondrial translation in TRMU and MTO1 deficient fibroblasts.	Acetylcysteine	13-30	mitochondrial tRNA translation optimization 1	Homo sapiens	96-100
27075430-7	2016	The administration of NAC blocked the maturation of interleukin-1beta, which is a critical substrate of MMPs, and markedly suppressed the neuronal activation induced by CCI, including inhibiting the phosphorylation of protein kinase Cgamma, NMDAR1, and mitogen-activated protein kinases.	Acetylcysteine	22-25	matrix metallopeptidase 2	Rattus norvegicus	104-108
27075430-7	2016	The administration of NAC blocked the maturation of interleukin-1beta, which is a critical substrate of MMPs, and markedly suppressed the neuronal activation induced by CCI, including inhibiting the phosphorylation of protein kinase Cgamma, NMDAR1, and mitogen-activated protein kinases.	Acetylcysteine	22-25	glutamate ionotropic receptor NMDA type subunit 1	Rattus norvegicus	241-247
27087133-2	2016	Recently we reported that the N-acetylcysteine (NAC) decreases brain acetylcholinesterase (AChE) activity in vitro.	Acetylcysteine	30-46	acetylcholinesterase	Mus musculus	91-95
21856376-0	2012	Differential modulation of apoptotic gene expression by N-acetyl-L-cysteine in Leydig cells stimulated persistently with hCG in vivo.	Acetylcysteine	56-75	hypertrichosis 2 (generalised, congenital)	Homo sapiens	121-124
21856376-1	2012	The present study was designed to investigate the molecular mechanisms of NAC (150 mg/kg bw twice/week) action in vivo under repeated hCG (100 IU/rat/day) stimulation to adult rats.	Acetylcysteine	74-77	hypertrichosis 2 (generalised, congenital)	Homo sapiens	134-137
27087133-2	2016	Recently we reported that the N-acetylcysteine (NAC) decreases brain acetylcholinesterase (AChE) activity in vitro.	Acetylcysteine	48-51	acetylcholinesterase	Mus musculus	91-95
21856376-2	2012	Leydig cell refractoriness led to a significant decline in serum testosterone and intracellular cAMP by day 30 of chronic hCG intervention which improved significantly following NAC co-administration.	Acetylcysteine	178-181	hypertrichosis 2 (generalised, congenital)	Homo sapiens	122-125
27087133-12	2016	Brain cortex and hippocampus AChE and hippocampus BChE activities increase induced by STZ were also prevented by NAC treatment.	Acetylcysteine	113-116	acetylcholinesterase	Mus musculus	29-33
27106530-5	2016	NAC and Ac-DEVD-CHO partially reversed CuE-induced cleavage of caspase-3, caspase-7, and PARP.	Acetylcysteine	0-3	collagen type XI alpha 2 chain	Homo sapiens	89-93
27106530-8	2016	CuE-triggered protein expression of p-AKT, p-mTOR, Beclin-1, and p-ULK1 was partially reversed by NAC pretreatment.	Acetylcysteine	98-101	unc-51 like autophagy activating kinase 1	Homo sapiens	67-71
27322250-9	2016	Further, pretreatment with antioxidant N-acetylcysteine (NAC) effectively abrogated cypermethrin-induced cell cytotoxicity, G1 cell cycle arrest, DNA damage, PARP activity, and JNK and ERK1/2 activation.	Acetylcysteine	39-55	mitogen-activated protein kinase 3	Mus musculus	185-191
22033125-11	2012	The antioxidant N-acetylcysteine (NAC) protected cells from TEGDMA-induced cell death, and inhibited the activation of ERK1/2, p38 and JNK by TEGDMA.	Acetylcysteine	16-32	mitogen-activated protein kinase 3	Mus musculus	119-125
22033125-11	2012	The antioxidant N-acetylcysteine (NAC) protected cells from TEGDMA-induced cell death, and inhibited the activation of ERK1/2, p38 and JNK by TEGDMA.	Acetylcysteine	16-32	mitogen-activated protein kinase 14	Mus musculus	127-130
22033125-11	2012	The antioxidant N-acetylcysteine (NAC) protected cells from TEGDMA-induced cell death, and inhibited the activation of ERK1/2, p38 and JNK by TEGDMA.	Acetylcysteine	34-37	mitogen-activated protein kinase 3	Mus musculus	119-125
22033125-11	2012	The antioxidant N-acetylcysteine (NAC) protected cells from TEGDMA-induced cell death, and inhibited the activation of ERK1/2, p38 and JNK by TEGDMA.	Acetylcysteine	34-37	mitogen-activated protein kinase 14	Mus musculus	127-130
21806545-13	2012	The gel shift and promoter activity assay showed that Ang II increased AP-1 (activator protein-1)-binding activity and leptin promoter activity, while SP600125, NAC and atorvastatin inhibited the AP-1-binding activity and leptin promoter activity induced by Ang II.	Acetylcysteine	161-164	angiogenin	Homo sapiens	258-261
27322250-9	2016	Further, pretreatment with antioxidant N-acetylcysteine (NAC) effectively abrogated cypermethrin-induced cell cytotoxicity, G1 cell cycle arrest, DNA damage, PARP activity, and JNK and ERK1/2 activation.	Acetylcysteine	57-60	mitogen-activated protein kinase 3	Mus musculus	185-191
21806545-15	2012	Ang II significantly increased secretion of leptin from human VSMCs, and addition of SP600125, atorvastatin and NAC before Ang II stimulation almost completely inhibited the leptin secretion induced by Ang II.	Acetylcysteine	112-115	angiogenin	Homo sapiens	0-3
26152521-9	2016	Pretreatment of cells with ROS scavenger N-acetyl cysteine abrogated the inhibitory effect of CA on the JAK2-STAT3/Src-STAT3 signaling and rescued cells from CA-induced apoptosis by blocking the induction of p53 and the cleavage of caspase-3 and PARP in HCT116 cells.	Acetylcysteine	41-58	Janus kinase 2	Homo sapiens	104-108
26152521-9	2016	Pretreatment of cells with ROS scavenger N-acetyl cysteine abrogated the inhibitory effect of CA on the JAK2-STAT3/Src-STAT3 signaling and rescued cells from CA-induced apoptosis by blocking the induction of p53 and the cleavage of caspase-3 and PARP in HCT116 cells.	Acetylcysteine	41-58	collagen type XI alpha 2 chain	Homo sapiens	246-250
27102435-4	2016	HeLa cells treated with NAC exhibited a time- and concentration-dependent decrease in Notch3 levels and its downstream effectors Hes1 and HRT1 in a manner independent of f-secretase or glutathione.	Acetylcysteine	24-27	hes family bHLH transcription factor 1	Homo sapiens	129-133
23284930-7	2012	Supplementation with NAC prevented the HF diet-induced reductions in GSH and GSH/2GSSG in soleus, but did not prevent the loss of Ad response in either muscle.	Acetylcysteine	21-24	GS homeobox 2	Rattus norvegicus	77-82
22701695-9	2012	The free radical scavenger N-acetyl-cysteine (NAC) was able to completely suppress cell death induced by jacaranone as it blocked Akt downregulation, p38 MAPK activation as well as upregulation of proapoptotic Bax.	Acetylcysteine	27-44	mitogen-activated protein kinase 14	Mus musculus	150-153
27107686-12	2016	Finally, treatment of TrxR2 deficiency cells with N-acetylcysteine (NAC) inhibited mitochondrial ROS production and chondrocyte apoptosis.	Acetylcysteine	50-66	thioredoxin reductase 2	Mus musculus	22-27
22701695-9	2012	The free radical scavenger N-acetyl-cysteine (NAC) was able to completely suppress cell death induced by jacaranone as it blocked Akt downregulation, p38 MAPK activation as well as upregulation of proapoptotic Bax.	Acetylcysteine	46-49	mitogen-activated protein kinase 14	Mus musculus	150-153
21934138-9	2011	Increased oxidative stress and urothelial cell hyperplasia with evidence of activated p44/42 MAPK (ERK1/2) and cyclin D1 were found in the DMA(V) and NAC (high dose) cotreated group.	Acetylcysteine	150-153	mitogen activated protein kinase 3	Rattus norvegicus	99-105
21934138-10	2011	These results suggest that cotreatment with NAC enhanced DMA(V)-induced urinary bladder injury and that the effects may be mediated by excess oxidative stress and ERK signaling.	Acetylcysteine	44-47	mitogen activated protein kinase 3	Rattus norvegicus	163-166
21453200-7	2011	INNOVATION: Treating Abcd1(-) mice with the antioxidants N-acetylcysteine and alpha-lipoic acid (LA) prevents protein oxidation; preserves NADH, NADPH, ATP, and GSH levels; and normalizes pyruvate kinase activity, which implies that oxidative stress provoked by VLCFA results in bioenergetic dysfunction, at a presymptomatic stage.	Acetylcysteine	57-73	2,4-dienoyl CoA reductase 1, mitochondrial	Mus musculus	145-150
27107686-12	2016	Finally, treatment of TrxR2 deficiency cells with N-acetylcysteine (NAC) inhibited mitochondrial ROS production and chondrocyte apoptosis.	Acetylcysteine	68-71	thioredoxin reductase 2	Mus musculus	22-27
27107686-13	2016	NAC also prevented chondrogenic differentiation of TrxR2 deficiency cells by suppression of ECM gene expression, GAGs accumulation and mineralization, as well as attenuation of Akt signaling.	Acetylcysteine	0-3	thioredoxin reductase 2	Mus musculus	51-56
21849471-7	2011	Blocking ROS activity using the ROS scavenger N-acetylcysteine abrogated MT1-MMP-mediated increase in cell migration and invasion.	Acetylcysteine	46-62	matrix metallopeptidase 14	Homo sapiens	73-80
26825874-10	2016	Additionally, both apocynin and NAC completely prevented the decreased MHC, decreased myotube diameter, and increased MuRF-1 induced by TGF-beta.	Acetylcysteine	32-35	transforming growth factor, beta 1	Mus musculus	136-144
21642840-6	2011	Treatment with N-acetyl-L-cysteine, a thiol-containing antioxidant completely blocked combined treatment-induced Bax translocation as well as DR5 upregulation.	Acetylcysteine	15-34	tumor necrosis factor receptor superfamily, member 10b	Mus musculus	142-145
21810225-10	2011	The initiation of the AA pathway due to MAF02 particle exposure was demonstrated to depend on the formation of ROS since the presence of the antioxidant N-acetyl-cysteine (NAC) prevented the MAF02-mediated enhancement of free AA, the subsequent conversion to PGE2/TXB2 via the induction of COX-2 and the ERK1/2 and JNK1/2 phosphorylation.	Acetylcysteine	153-170	mitochondrial Cytochrome c oxidase subunit II	Drosophila melanogaster	290-295
26825874-13	2016	Additionally, the administration of NAC to mice prevented all atrophic effects and the increase in ROS induced by TGF-beta in the tibialis anterior.	Acetylcysteine	36-39	transforming growth factor, beta 1	Mus musculus	114-122
21810225-10	2011	The initiation of the AA pathway due to MAF02 particle exposure was demonstrated to depend on the formation of ROS since the presence of the antioxidant N-acetyl-cysteine (NAC) prevented the MAF02-mediated enhancement of free AA, the subsequent conversion to PGE2/TXB2 via the induction of COX-2 and the ERK1/2 and JNK1/2 phosphorylation.	Acetylcysteine	172-175	mitochondrial Cytochrome c oxidase subunit II	Drosophila melanogaster	290-295
23554696-7	2011	Interestingly, EGF could induce a significant production of ROS, and N-acetyl-L-cysteine, a scavenger of ROS which abolished the EGF-induced ROS generation, cell migration, as well as activation of PI3K/Akt and PAK, but not Rac1.	Acetylcysteine	69-88	p21 (RAC1) activated kinase 1	Homo sapiens	211-214
26936454-7	2016	Furthermore, CA generated reactive oxygen species (ROS), and pretreatment with ROS scavenger N-acetyl cysteine (NAC) abrogated CA-induced cleavage of PARP and expression of p53.	Acetylcysteine	93-110	collagen type XI alpha 2 chain	Homo sapiens	150-154
26936454-7	2016	Furthermore, CA generated reactive oxygen species (ROS), and pretreatment with ROS scavenger N-acetyl cysteine (NAC) abrogated CA-induced cleavage of PARP and expression of p53.	Acetylcysteine	112-115	collagen type XI alpha 2 chain	Homo sapiens	150-154
26971531-6	2016	In turn, baicalein increased the generation of reactive oxygen species (ROS); however, an ROS scavenger, N-acetylcysteine, notably attenuated baicalein-mediated loss of MMP and activation of caspases.	Acetylcysteine	105-121	caspase 8	Homo sapiens	191-199
20970410-9	2011	(b) Xenobiochemical aspects of PAP derivatives, specifically: the stereospecific hydrolysis of OPAP and OOPAP by human pancreatic lipase, the in vitro activation of PAP by human and rat liver microsomes as well as by recombinant 450 enzymes, and the formation and stability of GSH and N-acetylcysteine adducts of a highly reactive iminoquinone intermediate generated in the biotransformation of PAP.	Acetylcysteine	285-301	phospholipid phosphatase 1	Mus musculus	31-34
21624350-6	2011	Moreover, when the free radical (ROS) generating capacity of the compounds was studied by 2",7"-dichlorofluorescein-diacetate assay using flow cytometry, we found that a known antioxidant N-acetyl-cysteine almost completely abrogated the H2AX((S139)) phosphorylations and the caspase 3 cleavage and activation.	Acetylcysteine	188-205	H2A.X variant histone	Homo sapiens	238-242
21376115-5	2011	Removal of intracellular ROS by N-acetylcysteine reduced the AMPK activation and IL-8 induction.	Acetylcysteine	32-48	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	61-65
21563917-16	2011	p38 activation at 2 hours after T(3) administration was abolished in NAC-pretreated animals.	Acetylcysteine	69-72	mitogen activated protein kinase 14	Rattus norvegicus	0-3
26643864-8	2016	On the other hand, N-acetylcysteine significantly (P &lt; 0.001) increased SOCS3 gene expression; however, SOCS3 protein was not changed.	Acetylcysteine	19-35	suppressor of cytokine signaling 3	Rattus norvegicus	75-80
26918336-9	2016	NAC inhibited nicotine-mediated increase in ROS production, recovered PKCepsilon gene expression and abrogated increased phosphorylation of GSK3beta.	Acetylcysteine	0-3	glycogen synthase kinase 3 beta	Rattus norvegicus	140-148
21787718-6	2011	The cadmium-induced increase in AKR1C3 protein levels was suppressed by N-acetylcysteine (NAC) and, to a lesser extent, PI3K inhibitor (Ly294002).	Acetylcysteine	72-88	aldo-keto reductase family 1 member C3	Homo sapiens	32-38
21787718-6	2011	The cadmium-induced increase in AKR1C3 protein levels was suppressed by N-acetylcysteine (NAC) and, to a lesser extent, PI3K inhibitor (Ly294002).	Acetylcysteine	90-93	aldo-keto reductase family 1 member C3	Homo sapiens	32-38
26721593-5	2016	Srx depletion also inhibited the growth of A549 cells like Srx inhibition, and the cytotoxic effects of Srx inhibitor were considerably reversed by Srx overexpression or antioxidants such as N-acetyl cysteine and butylated hydroxyanisol.	Acetylcysteine	191-208	sulfiredoxin 1	Homo sapiens	0-3
21721350-1	2011	OBJECTIVE: We sought to investigate the role of hyperbaric oxygen (HBO2), N-acetylcysteine (NAC), and HBO2 plus NAC (HN) on the immunohistochemical expression of caspase-3 and the vascular endothelial growing factor (VEGF) on random skin flaps of rats (modified McFarlane design).	Acetylcysteine	74-90	caspase 3	Rattus norvegicus	162-171
21372137-10	2011	Furthermore, Mct-1 siRNA lowered the level of ROS generated after 15-h exposure to IL-1beta, whereas a ROS scavenger, N-acetylcysteine, suppressed both late phase degradation of IkappaBalpha and Nox-2 expression.	Acetylcysteine	118-134	cytochrome b-245, beta polypeptide	Mus musculus	195-200
26469940-10	2016	We show that by circumventing the xCT-dependent import of L-cystine through addition of N-acetyl-L-cysteine (NAC) as an alternative cysteine source, we were able to restore GSH levels in A-T mutant astroglia providing a possible future avenue for targeted therapeutic intervention.	Acetylcysteine	88-107	solute carrier family 7 (cationic amino acid transporter, y+ system), member 11	Mus musculus	34-37
21131394-10	2011	The changes in oxidant/antioxidant enzymes and IL-6 release were reversed by the antioxidants N-acetyl-cysteine (NAC) and ebselen through inhibition of Smad3 phosphorylation, indicating redox-dependent activation of Smad3 by TGF-beta.	Acetylcysteine	94-111	SMAD family member 3	Homo sapiens	152-157
21131394-10	2011	The changes in oxidant/antioxidant enzymes and IL-6 release were reversed by the antioxidants N-acetyl-cysteine (NAC) and ebselen through inhibition of Smad3 phosphorylation, indicating redox-dependent activation of Smad3 by TGF-beta.	Acetylcysteine	94-111	SMAD family member 3	Homo sapiens	216-221
21131394-10	2011	The changes in oxidant/antioxidant enzymes and IL-6 release were reversed by the antioxidants N-acetyl-cysteine (NAC) and ebselen through inhibition of Smad3 phosphorylation, indicating redox-dependent activation of Smad3 by TGF-beta.	Acetylcysteine	113-116	SMAD family member 3	Homo sapiens	152-157
21131394-10	2011	The changes in oxidant/antioxidant enzymes and IL-6 release were reversed by the antioxidants N-acetyl-cysteine (NAC) and ebselen through inhibition of Smad3 phosphorylation, indicating redox-dependent activation of Smad3 by TGF-beta.	Acetylcysteine	113-116	SMAD family member 3	Homo sapiens	216-221
21081246-8	2011	Incubation of HGF with NAC significantly reduced ROS production and decreased the cell damage and cytotoxicity caused by all materials tested (p&lt;0.001).	Acetylcysteine	23-26	hepatocyte growth factor	Homo sapiens	14-17
22038345-7	2011	Moreover, the CD133(+) cells in SB203580 treatment group had a 21.93+-1.36-fold increase, and 14.50+-1.19-fold increase in NAC treatment group, but only 10.13+-0.57-fold increase in control group.	Acetylcysteine	123-126	prominin 1	Homo sapiens	14-19
26469940-10	2016	We show that by circumventing the xCT-dependent import of L-cystine through addition of N-acetyl-L-cysteine (NAC) as an alternative cysteine source, we were able to restore GSH levels in A-T mutant astroglia providing a possible future avenue for targeted therapeutic intervention.	Acetylcysteine	109-112	solute carrier family 7 (cationic amino acid transporter, y+ system), member 11	Mus musculus	34-37
21728338-6	2011	The reactive oxygen species (ROS) scavenger N-acetylcysteine (NAC) abolished the 15d-PGJ2-induced Nrf2 activation and GCLC expression.	Acetylcysteine	44-60	glutamate-cysteine ligase catalytic subunit	Homo sapiens	118-122
21268080-8	2011	Furthermore, CSE-induced p300 and c-Jun complex formation was inhibited by pretreatment with diphenyleneiodonium chloride, apocynin, N-acetyl-L-cysteine or SP600125.	Acetylcysteine	133-152	E1A binding protein p300	Homo sapiens	25-29
21728338-6	2011	The reactive oxygen species (ROS) scavenger N-acetylcysteine (NAC) abolished the 15d-PGJ2-induced Nrf2 activation and GCLC expression.	Acetylcysteine	62-65	glutamate-cysteine ligase catalytic subunit	Homo sapiens	118-122
26850078-7	2016	Moreover, the MF-induced MPT was attenuated by ROS scavenger (N-acetyl-L-cysteine, NAC) or GSK-3beta inhibitor, and NAC pretreatment prevented GSK-3beta dephosphorylation (Ser(9)) caused by MF exposure.	Acetylcysteine	62-81	glycogen synthase kinase 3 beta	Homo sapiens	143-152
21427628-5	2011	N-acetylcysteine (NAC; 0.25-2 mM), a potent antioxidant, decreased gp91 phox and caspase-3 expression, inhibited apoptosis and restored the glutathione redox ratio.	Acetylcysteine	0-16	caspase 3	Rattus norvegicus	81-90
21029048-12	2011	Dominant-negative Nox4 also mimicked this effect of NAC and DPI.	Acetylcysteine	52-55	NADPH oxidase 4	Mus musculus	18-22
26635914-8	2016	However, the potent antioxidant, N-acetylcysteine (NAC) abrogated the effects of IH by inducing large CD66b(+)/LC3B(+) Gphi and increased both NADPH oxidase expression and phagocytosis.	Acetylcysteine	33-49	microtubule associated protein 1 light chain 3 beta	Homo sapiens	111-115
21427628-5	2011	N-acetylcysteine (NAC; 0.25-2 mM), a potent antioxidant, decreased gp91 phox and caspase-3 expression, inhibited apoptosis and restored the glutathione redox ratio.	Acetylcysteine	18-21	caspase 3	Rattus norvegicus	81-90
26635914-8	2016	However, the potent antioxidant, N-acetylcysteine (NAC) abrogated the effects of IH by inducing large CD66b(+)/LC3B(+) Gphi and increased both NADPH oxidase expression and phagocytosis.	Acetylcysteine	51-54	microtubule associated protein 1 light chain 3 beta	Homo sapiens	111-115
21166495-3	2011	Overexpression of Prdx 6 protein or exposure to N-acetylcysteine (NAC) reversed the apoptotic effect of cisplatin by reducing ROS levels and suppressing the caspase signaling pathway.	Acetylcysteine	66-69	peroxiredoxin 6	Homo sapiens	18-24
28105252-2	2016	Our previous study demonstrated the novel N-acetylcysteine amide (NACA); the amide form of N-acetyl cysteine (NAC) prevented renal tubular cells from contrast-induced apoptosis through inhibiting p38 MAPK pathway in vitro.	Acetylcysteine	91-108	mitogen activated protein kinase 14	Rattus norvegicus	196-199
21873804-11	2011	Moreover, we found that NAC down-regulated the expression of VCAM-1, MMP2 and MMP9, accompanied by inhibition of NF-kappaB activation and reduced expression of RAGE.	Acetylcysteine	24-27	matrix metallopeptidase 9	Mus musculus	78-82
21935824-12	2011	CONCLUSION: NAC treatment had beneficial effects on erythrocyte GSH, serum TNF-?, lung function, and kidney MDA levels in sepsis-induced rats.	Acetylcysteine	12-15	tumor necrosis factor-like	Rattus norvegicus	75-78
21320508-5	2011	N-acetylcysteine, the superoxide dismutase mimetic MnTMPyP, and apocynin significantly attenuated ET-1-mediated inotropic effect, which was accompanied by inhibition of extracellular signal regulated kinase 1/2 (ERK1/2) phosphorylation.	Acetylcysteine	0-16	mitogen activated protein kinase 3	Rattus norvegicus	169-210
28105252-2	2016	Our previous study demonstrated the novel N-acetylcysteine amide (NACA); the amide form of N-acetyl cysteine (NAC) prevented renal tubular cells from contrast-induced apoptosis through inhibiting p38 MAPK pathway in vitro.	Acetylcysteine	66-69	mitogen activated protein kinase 14	Rattus norvegicus	196-199
26734528-1	2015	Linear oligomeric silsesquioxanes with polar side moieties (e.g., carboxylic groups and derivatives of N-acetylcysteine, cysteine hydrochloride or glutathione) can form specific, self-assembled nanostructures when deposited on mica by dip coating.	Acetylcysteine	103-119	MHC class I polypeptide-related sequence A	Homo sapiens	227-231
21490221-8	2011	Correspondingly, xCT deletion in mice elevated the threshold for limbic seizures and abolished the proconvulsive effects of N-acetylcysteine.	Acetylcysteine	124-140	solute carrier family 7 (cationic amino acid transporter, y+ system), member 11	Mus musculus	17-20
22174837-6	2011	RNAi-mediated knockdown of key GSH regulatory enzymes gamma-glutamylcysteine synthetase or glutathione disulfide reductase partially reversed the hypoxia-induced resistance to fenretinide, and increasing GSH levels using N-acetylcysteine augmented the hypoxia-induced resistance in a cell line-specific manner.	Acetylcysteine	221-237	glutamate-cysteine ligase catalytic subunit	Homo sapiens	54-87
21172010-8	2010	The antioxidants, N-acetylcysteine and glutathione, but not vitamin C or tiron, inhibited perifosine-induced elevation of p-c-Jun, DR4 and DR5.	Acetylcysteine	18-34	TNF receptor superfamily member 10a	Homo sapiens	131-134
20816907-8	2010	Normalization of caveolin-1 levels by NAC was accompanied by a reduction in BBB breakdown, indicated by decreased IgG extravasation, normalization of occludin levels and prevention of matrix metalloproteinase-9 up-regulation.	Acetylcysteine	38-41	matrix metallopeptidase 9	Mus musculus	184-210
26734528-6	2015	Specific changes in the morphology of the surface layer were observed when mica was primed with a monolayer of small organic compounds (e.g., N-acetylcysteine, citric acid, thioglycolic or acid).	Acetylcysteine	142-158	MHC class I polypeptide-related sequence A	Homo sapiens	75-79
21242791-11	2011	Further, compared with SBSAL, diaphragm caspase-3 activity was significantly increased in MVSAL (+279%, p &lt; .001), and N-acetylcysteine treatment provided partial protection against caspase-3 activation.	Acetylcysteine	122-138	caspase 3	Rattus norvegicus	185-194
25843654-6	2015	HNE induced the nuclear accumulation of Nrf2 and enhanced UCP3 expression, effects prevented by the antioxidant N-acetylcysteine.	Acetylcysteine	112-128	uncoupling protein 3 (mitochondrial, proton carrier)	Mus musculus	58-62
19840968-9	2010	Moreover, cigarette smoke extract upregulated the expression of TLR9 and the upregulated expression was suppressed by N-acetylcysteine.	Acetylcysteine	118-134	toll like receptor 9	Homo sapiens	64-68
26449648-6	2015	The increase of ATP5b and CTGF protein expression in AGEs-treated renal tubular cells was reversed by antioxidant N-acetylcysteine.	Acetylcysteine	114-130	cellular communication network factor 2	Mus musculus	26-30
20824644-5	2010	Apoptotic markers Fas, FasL, and caspase-8, up-regulated following repeated hCG exposure, were significantly down-regulated following NAC co-incubation.	Acetylcysteine	134-137	Fas ligand	Rattus norvegicus	23-27
21098090-8	2011	17-beta-Estradiol, NAC, and DPI were able to normalize EtOH-induced up-regulation of Nox and RANKL.	Acetylcysteine	19-22	TNF superfamily member 11	Rattus norvegicus	93-98
26446137-10	2015	Further study showed that miR-34a can also aggravate MSC senescence, an effect which was partly abolished by the reactive oxygen species (ROS) scavenger, N-acetylcysteine (NAC).	Acetylcysteine	154-170	microRNA 34a	Homo sapiens	26-33
21115496-8	2011	Finally, when SMS1-null mice were treated with the anti-oxidant N-acetyl cysteine, we observed partial recovery of insulin secretion, indicating that ROS overproduction underlies pancreatic beta-cell dysfunction in SMS1-null mice.	Acetylcysteine	64-81	sphingomyelin synthase 1	Mus musculus	14-18
21115496-8	2011	Finally, when SMS1-null mice were treated with the anti-oxidant N-acetyl cysteine, we observed partial recovery of insulin secretion, indicating that ROS overproduction underlies pancreatic beta-cell dysfunction in SMS1-null mice.	Acetylcysteine	64-81	sphingomyelin synthase 1	Mus musculus	215-219
20824644-7	2010	NAC treatment induced down-regulation of upstream JNK/pJNK and down-stream caspase-3 in the target cells.	Acetylcysteine	0-3	caspase 3	Rattus norvegicus	75-84
20815767-9	2010	Administration of N-acetyl-cysteine prior to APAP-overload prevented GSH depletion and c-Myc degradation.	Acetylcysteine	18-35	MYC proto-oncogene, bHLH transcription factor	Rattus norvegicus	87-92
26446137-10	2015	Further study showed that miR-34a can also aggravate MSC senescence, an effect which was partly abolished by the reactive oxygen species (ROS) scavenger, N-acetylcysteine (NAC).	Acetylcysteine	172-175	microRNA 34a	Homo sapiens	26-33
21253614-9	2011	The suppression of Teff proliferation induced by exogenous TGFbeta treatment could be overcome with NAC.	Acetylcysteine	100-103	transforming growth factor, beta 1	Mus musculus	59-66
26446958-7	2015	Furthermore, both NAC and Trolox increased the activation of the small guanosine triphosphatase (GTPase) RHOA, and blocking downstream RHOA signaling abolished antioxidant-induced migration.	Acetylcysteine	18-21	ras homolog family member A	Mus musculus	105-109
20648652-0	2010	Potential in vivo amelioration by N-acetyl-L-cysteine of oxidative stress in brain in human double mutant APP/PS-1 knock-in mice: toward therapeutic modulation of mild cognitive impairment.	Acetylcysteine	34-53	presenilin 1	Homo sapiens	110-114
20648652-9	2010	Oral administration of NAC also increased the diminished activity of GR and protected against lipid peroxidation in brains of 9-month-old APP/PS-1 mice only.	Acetylcysteine	23-26	glutathione reductase	Mus musculus	69-71
26446958-7	2015	Furthermore, both NAC and Trolox increased the activation of the small guanosine triphosphatase (GTPase) RHOA, and blocking downstream RHOA signaling abolished antioxidant-induced migration.	Acetylcysteine	18-21	ras homolog family member A	Mus musculus	135-139
24677730-3	2015	Pretreatment with reactive oxygen species (ROS) scavenger, N-acetylcysteine (NAC), attenuated NP-induced ROS production, COX-2 expression, and IL-6 and PGE2 release in TM4 cells.	Acetylcysteine	59-75	cytochrome c oxidase II, mitochondrial	Mus musculus	121-126
20653475-6	2010	CONCLUSIONS: NAC prevents the increased expression levels of p53 and CASP8 induced by long-term maintained hypoxia.	Acetylcysteine	13-16	caspase 8	Homo sapiens	69-74
21051528-4	2011	NAC treatment resulted in increased somatic growth relative to controls (4.0 +- 0.1 vs. 3.1 +- 0.1 g/day) and increased hepatic steatosis score (3.5 +- 0.6 vs. 2.7 +- 1.2), associated with suppression of the triglyceride hydrolyzing protein adiponutrin, but produced no elevation in serum alanine aminotransferase (ALT).	Acetylcysteine	0-3	patatin-like phospholipase domain containing 3	Rattus norvegicus	241-252
24677730-3	2015	Pretreatment with reactive oxygen species (ROS) scavenger, N-acetylcysteine (NAC), attenuated NP-induced ROS production, COX-2 expression, and IL-6 and PGE2 release in TM4 cells.	Acetylcysteine	77-80	cytochrome c oxidase II, mitochondrial	Mus musculus	121-126
20557081-10	2010	Additionally, pretreatment of Huh7 cells with antioxidants ascorbic acid and N-acetyl cysteine markedly attenuated the MAA-induced apoptosis by upregulation of Bax, Bak, and PUMA, mitochondrial translocation of cofilin, activation of caspase-3, and cell death.	Acetylcysteine	77-94	cofilin 1	Homo sapiens	211-218
26038117-8	2015	The administration of antioxidant L-N-acetylcysteine did not affect apoptosis, compensatory regeneration, or fibrotic responses but significantly reduced oxidative DNA damage and incidence and multiplicity of live tumors in Mcl-1 knockout mice.	Acetylcysteine	34-52	myeloid cell leukemia sequence 1	Mus musculus	224-229
20151195-8	2010	L-NAME, 5HD, N-acetylcysteine (NAC) and staurosporine inhibited ERK1/2 phosphorylation and also reduced pravastatin-induced cardioprotection, suggesting NO, mitochondrial K(ATP) (mitoK(ATP)) channels, ROS and PKC should be involved in the cardioprotective signaling.	Acetylcysteine	13-29	mitogen activated protein kinase 3	Rattus norvegicus	64-70
21532147-5	2011	Western blotting analysis showed that AGE treatment potentiated to activate extracelluar signal-regulated kinases (ERK1/2) by the induction of intracellular reactive oxygen species (ROS) production, since ROS scavenger N-acetyl-L-cysteine pretreatment significantly inhibited AGE-induced ERK1/2 activation.	Acetylcysteine	219-238	mitogen activated protein kinase 3	Rattus norvegicus	115-121
21532147-5	2011	Western blotting analysis showed that AGE treatment potentiated to activate extracelluar signal-regulated kinases (ERK1/2) by the induction of intracellular reactive oxygen species (ROS) production, since ROS scavenger N-acetyl-L-cysteine pretreatment significantly inhibited AGE-induced ERK1/2 activation.	Acetylcysteine	219-238	mitogen activated protein kinase 3	Rattus norvegicus	288-294
21532147-6	2011	Further, pretreatment with either N-acetyl-L-cysteine or the inhibitor of ERK1/2 activation suppressed AGE-induced proliferation of VSMCs, suggesting a role of ROS/ERK1/2 signaling.	Acetylcysteine	34-53	mitogen activated protein kinase 3	Rattus norvegicus	164-170
20151195-8	2010	L-NAME, 5HD, N-acetylcysteine (NAC) and staurosporine inhibited ERK1/2 phosphorylation and also reduced pravastatin-induced cardioprotection, suggesting NO, mitochondrial K(ATP) (mitoK(ATP)) channels, ROS and PKC should be involved in the cardioprotective signaling.	Acetylcysteine	31-34	mitogen activated protein kinase 3	Rattus norvegicus	64-70
25503516-5	2015	N-acetyl-cysteine (ROS scavenger) or hexamethonium [nicotinic acetylcholine receptor (nAChR) antagonist] attenuated the CSE-induced increase in intracellular ROS, activation of AMPK and NF-kappaB, as well as IL-8 induction, which suggests that nAChRs and ROS are important.	Acetylcysteine	0-17	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	177-181
20080177-7	2010	NAC treatment suppressed the contraction-mediated increase in 2-DG uptake; lactate production; hexokinase, PFK, and G6PDH activities; and gene expression of GLUT4, HKII, and PFK.	Acetylcysteine	0-3	glucose-6-phosphate dehydrogenase	Rattus norvegicus	116-121
21602594-7	2011	Our data suggest that HMGB1 release may be partly an active process triggered by oxidative stress because the antioxidant N-acetylcysteine (NAC) clearly attenuated HMGB1 expression and release.	Acetylcysteine	122-138	high mobility group box 1	Homo sapiens	22-27
21602594-7	2011	Our data suggest that HMGB1 release may be partly an active process triggered by oxidative stress because the antioxidant N-acetylcysteine (NAC) clearly attenuated HMGB1 expression and release.	Acetylcysteine	122-138	high mobility group box 1	Homo sapiens	164-169
21602594-7	2011	Our data suggest that HMGB1 release may be partly an active process triggered by oxidative stress because the antioxidant N-acetylcysteine (NAC) clearly attenuated HMGB1 expression and release.	Acetylcysteine	140-143	high mobility group box 1	Homo sapiens	22-27
21602594-7	2011	Our data suggest that HMGB1 release may be partly an active process triggered by oxidative stress because the antioxidant N-acetylcysteine (NAC) clearly attenuated HMGB1 expression and release.	Acetylcysteine	140-143	high mobility group box 1	Homo sapiens	164-169
25980586-3	2015	AA and GA can be detoxified by glutathione-S-transferase to form AA and isomeric GA glutathione conjugates (AA-, GA2- and GA3-GSH, respectively), which can be further metabolized to mercapturic acids (MAs).	Acetylcysteine	182-199	electron transfer flavoprotein subunit alpha	Homo sapiens	113-116
21208554-9	2011	Pretreatment with antioxidants such as N-acetylcysteine and diphenyleneiodonium significantly inhibited the activation of p38 MAPK compared with LPS control (P&lt;0.05).	Acetylcysteine	39-55	mitogen activated protein kinase 14	Rattus norvegicus	122-125
19885829-7	2010	This increase in PS1 protein expression was prevented by co-treatment with an antioxidant, N-acetylcysteine (NAC).	Acetylcysteine	91-107	presenilin 1	Homo sapiens	17-20
19885829-7	2010	This increase in PS1 protein expression was prevented by co-treatment with an antioxidant, N-acetylcysteine (NAC).	Acetylcysteine	109-112	presenilin 1	Homo sapiens	17-20
19885829-8	2010	EA additionally induced a significant increase in PS1 mRNA expression, which was inhibited by NAC.	Acetylcysteine	94-97	presenilin 1	Homo sapiens	50-53
26240545-10	2015	CONCLUSION: Intravenous administration of NAC NAC in cirrhotic patients undergoing major abdominal surgeries reduces the incidence of cystatin C GFR-based AKI, postoperative renal and liver functions were well-preserved and improved outcome.	Acetylcysteine	42-45	cystatin C	Homo sapiens	134-144
19935772-7	2010	In addition, either DeltaTM-BNIP3 overexpression or N-acetyl-L-cysteine co-treatment decreased lysosomal activation in cells treated with S100A8/A9.	Acetylcysteine	52-71	S100 calcium binding protein A8	Homo sapiens	138-144
20354834-4	2010	NAC administration significantly influenced the resting and post-exercise level of glutathione (+31%) as well as the resting activity of glutathione enzymes (glutathione reductase, -22%; glutathione peroxidase, -18%).	Acetylcysteine	0-3	glutathione-disulfide reductase	Homo sapiens	158-179
21135141-3	2010	We now show that nicotinamide adenine dinucleotide phosphate reduced oxidase (NOX) and NOX-mediated oxidative stress are induced by this pathway and that apoptosis is blocked by both genetic deletion of the NOX subunit NOX2 and by the antioxidant N-acetylcysteine.	Acetylcysteine	247-263	cytochrome b-245, beta polypeptide	Mus musculus	219-223
20936703-10	2010	Antioxidants, catalase (cell-permeable form), and N-acetylcysteine (both L and D-forms) inhibited these events and abolished the GTPP potentiation of NGF-induced neuritogenesis.	Acetylcysteine	50-66	nerve growth factor	Rattus norvegicus	150-153
26240545-10	2015	CONCLUSION: Intravenous administration of NAC NAC in cirrhotic patients undergoing major abdominal surgeries reduces the incidence of cystatin C GFR-based AKI, postoperative renal and liver functions were well-preserved and improved outcome.	Acetylcysteine	46-49	cystatin C	Homo sapiens	134-144
26039957-9	2015	The green fluorescent protein reporter assay revealed that expression of the stress-responsive genes, sod-3 and hsp-16.2, increased significantly following N-acetyl-L-cysteine treatment.	Acetylcysteine	156-175	Superoxide dismutase [Mn] 2, mitochondrial	Caenorhabditis elegans	102-107
21142721-0	2010	Low-level laser therapy associated to N-acetylcysteine lowers macrophage inflammatory protein-2 (MIP-2) mRNA expression and generation of intracellular reactive oxygen species in alveolar macrophages.	Acetylcysteine	38-54	C-X-C motif chemokine ligand 2	Rattus norvegicus	97-102
19696069-5	2010	Sympathetic hyperinnervation was blunted after administering NAC, as assessed by immunofluorescent analysis of tyrosine hydroxylase and western blotting and real-time quantitative RT-PCR of nerve growth factor.	Acetylcysteine	61-64	nerve growth factor	Rattus norvegicus	190-209
19696069-8	2010	Furthermore, the effects of NAC on nerve growth factor were abolished by administering l-buthionine sulfoximinem, an inhibitor of gamma-glutamylcysteine ligase.	Acetylcysteine	28-31	nerve growth factor	Rattus norvegicus	35-54
19696069-9	2010	CONCLUSION: Chronic use of NAC, but not vitamins, after infarction is associated with down-regulation of nerve growth factor proteins, probably through a glutathione-dependent pathway, and thus plays a critical role in the beneficial effect on the arrhythmogenic response to programmed electrical stimulation.	Acetylcysteine	27-30	nerve growth factor	Rattus norvegicus	105-124
21142721-15	2010	CONCLUSION: Results indicate that there is a synergistic action of LLLT with NAC on MIP-2 mRNA expression from LPS- or H(2)O(2)-stimulated AM, and that both ROS intracellular generation and NF-kB signaling seem to be involved.	Acetylcysteine	77-80	C-X-C motif chemokine ligand 2	Rattus norvegicus	84-89
26039957-9	2015	The green fluorescent protein reporter assay revealed that expression of the stress-responsive genes, sod-3 and hsp-16.2, increased significantly following N-acetyl-L-cysteine treatment.	Acetylcysteine	156-175	Heat shock protein hsp-16.2;SHSP domain-containing protein	Caenorhabditis elegans	112-120
24962643-8	2015	Additionally, the NF-kappaB inhibitor N-acetylcysteine (NAC) exerted similar inhibitory effects as ALA on COX-2 and iNOS expression.	Acetylcysteine	38-54	prostaglandin-endoperoxide synthase 2	Rattus norvegicus	106-111
19840221-11	2010	NAC treatment significantly ameliorated decrease in antioxidant defense and prevented cytochrome c release and caspase 3 activation.	Acetylcysteine	0-3	caspase 3	Rattus norvegicus	111-120
24962643-8	2015	Additionally, the NF-kappaB inhibitor N-acetylcysteine (NAC) exerted similar inhibitory effects as ALA on COX-2 and iNOS expression.	Acetylcysteine	56-59	prostaglandin-endoperoxide synthase 2	Rattus norvegicus	106-111
25834400-9	2015	Moreover, PLB induced intracellular reactive oxygen species (ROS) generation and this effect was attenuated by l-glutathione (GSH) and n-acetyl-l-cysteine (NAC).	Acetylcysteine	135-154	phospholamban	Homo sapiens	10-13
20113272-0	2010	Cystatin C and creatinine as markers for radiocontrast-induced nephropathy in patients treated with N-acetylcysteine.	Acetylcysteine	100-116	cystatin C	Homo sapiens	0-10
20826812-8	2010	Moreover, chemical antioxidants, such as N-acetylcysteine and butylated hydroxyanisole, and the NADPH oxidase inhibitor diphenyleneiodonium inhibited Srx induction as well as generation of reactive oxygen species, both of which were also suppressed in Nox2 (NADPH oxidase 2)-deficient bone marrow-derived macrophages.	Acetylcysteine	41-57	cytochrome b-245, beta polypeptide	Mus musculus	252-256
20056085-0	2010	[N-acetylcysteine antagonizes the Interleukin-18-induced expression of TNF-alpha and IL-6 in mouse vascular smooth muscle cells].	Acetylcysteine	1-17	interleukin 18	Mus musculus	34-48
20056085-7	2010	CONCLUSION: N-acetylcysteine antagonizes the production of TNF-alpha and IL-6 induced by IL-18 in VSMC.	Acetylcysteine	12-28	interleukin 18	Mus musculus	89-94
19559059-7	2009	N-Acetylcysteine (NAC) intervention promotes neuroprotection of cutaneous sensory neurons through considerable upregulation of Bcl-2 and downregulation of both Bax and caspase-3 mRNA.	Acetylcysteine	0-16	caspase 3	Rattus norvegicus	168-177
20525644-6	2010	Caspase 3, p38, and p53 inhibitors had no effect on FCCP-induced CASQ2 downregulation; however, it was attenuated by the ROS scavenger N-acetylcysteine (NAC).	Acetylcysteine	135-151	caspase 3	Rattus norvegicus	0-9
19559059-7	2009	N-Acetylcysteine (NAC) intervention promotes neuroprotection of cutaneous sensory neurons through considerable upregulation of Bcl-2 and downregulation of both Bax and caspase-3 mRNA.	Acetylcysteine	18-21	caspase 3	Rattus norvegicus	168-177
25776470-0	2015	N-acetylcysteine relieves oxidative stress and protects hippocampus of rat from radiation-induced apoptosis by inhibiting caspase-3.	Acetylcysteine	0-16	caspase 3	Rattus norvegicus	122-131
19544430-7	2009	Treatment of these cells with the antioxidant N-acetyl-L-cysteine (NAC) or with a p38 MAPK inhibitor restores normal proliferation and reduced expression of p21(cip1) and p27(kip1) in the Atm(-/-) NSCs.	Acetylcysteine	46-65	ataxia telangiectasia mutated	Mus musculus	188-191
20664528-6	2010	When NAC-treated MDSCs were transplanted into infarcted myocardium, we observed significantly improved cardiac function, decreased scar tissue formation, and increased numbers of CD31(+) endothelial cell structures, compared to the injection of untreated and diethyl maleate-treated cells.	Acetylcysteine	5-8	platelet/endothelial cell adhesion molecule 1	Mus musculus	179-183
20636478-5	2010	Pre-treatment with N-acetyl-L-cysteine, which is involved in scavenging reactive oxygen species, prevented PP2A inhibition and subsequent upregulation of survival pathways.	Acetylcysteine	19-38	protein phosphatase 2 (formerly 2A), catalytic subunit, alpha isoform	Mus musculus	107-111
19544430-7	2009	Treatment of these cells with the antioxidant N-acetyl-L-cysteine (NAC) or with a p38 MAPK inhibitor restores normal proliferation and reduced expression of p21(cip1) and p27(kip1) in the Atm(-/-) NSCs.	Acetylcysteine	67-70	ataxia telangiectasia mutated	Mus musculus	188-191
25776470-8	2015	In conclusion, our results demonstrate that NAC inhibits apoptosis induced by irradiation via the inhibition of caspase-3.	Acetylcysteine	44-47	caspase 3	Rattus norvegicus	112-121
20384467-10	2010	NAC protected against oxidative stress through acting on this newly disclosed Nrf2/GR/GSH pathway, by which NAC elevated the biosynthesis of protective GSH to repair and reconstitute the defense system destroyed by phosgene.	Acetylcysteine	0-3	glutathione-disulfide reductase	Homo sapiens	83-85
20384467-10	2010	NAC protected against oxidative stress through acting on this newly disclosed Nrf2/GR/GSH pathway, by which NAC elevated the biosynthesis of protective GSH to repair and reconstitute the defense system destroyed by phosgene.	Acetylcysteine	108-111	glutathione-disulfide reductase	Homo sapiens	83-85
25776470-9	2015	We demonstrated a decrease in caspase-3 mRNA that was present at 24h of NAC treatment.	Acetylcysteine	72-75	caspase 3	Rattus norvegicus	30-39
25717100-6	2015	Targeting mucin disulfide cross-links using current thiol-amino structures such as N-acetylcysteine (NAC) requires high drug concentrations to have mucolytic effects.	Acetylcysteine	83-99	LOC100508689	Homo sapiens	10-15
19693689-3	2010	However, these protective effects were abolished in the presence of either ROS scavenger N-acetylcysteine or ERK 1/2 inhibitor PD98059, and accompanied by prevention of ERK 1/2 phosphorylation and elimination of inhibitory effect on mPTP opening.	Acetylcysteine	89-105	mitogen activated protein kinase 3	Rattus norvegicus	169-176
19486862-5	2009	CSS increased intracellular oxidation, and N-acetylcysteine (NAC), an antioxidant, significantly attenuated the formation of gamma-H2AX, suggesting that reactive oxygen species produced from CSS partially contributed to the phosphorylation.	Acetylcysteine	43-59	H2A.X variant histone	Homo sapiens	125-135
19486862-5	2009	CSS increased intracellular oxidation, and N-acetylcysteine (NAC), an antioxidant, significantly attenuated the formation of gamma-H2AX, suggesting that reactive oxygen species produced from CSS partially contributed to the phosphorylation.	Acetylcysteine	61-64	H2A.X variant histone	Homo sapiens	125-135
25717100-6	2015	Targeting mucin disulfide cross-links using current thiol-amino structures such as N-acetylcysteine (NAC) requires high drug concentrations to have mucolytic effects.	Acetylcysteine	101-104	LOC100508689	Homo sapiens	10-15
23836369-9	2015	N-acetylcysteine, an ROS scavenger, inhibited 2-ABP-induced activation of ERK and JNK, the cell death and caspase-3 activity, which suggested that oxidative stress plays a crucial role in apoptosis through activation of caspase-3 in a ROS/JNK-dependent signaling cascade.	Acetylcysteine	0-16	amine oxidase copper containing 1	Homo sapiens	48-51
25451595-8	2015	Additionally, pretreatment with 2.5 mM N-acetylcysteine (NAC; a glutathione (GSH) precursor) dramatically suppressed the increase in lipid peroxidation, cytotoxicity, apoptotic events, calpain and caspase-12 activity, and ER stress-related molecules in CA-exposed cells.	Acetylcysteine	39-55	caspase 12	Mus musculus	197-207
19131585-4	2009	Flow (10 dynes/cm(2), 6 h)-induced expression of HO-1 protein was abolished when BAECs were preincubated and sheared in the presence of either N(G)-nitro-L-arginine methyl ester or N-acetyl-L-cysteine, suggesting that either NO or ROS up-regulates HO-1.	Acetylcysteine	181-200	heme oxygenase 1	Bos taurus	49-53
20356861-9	2010	A-KG and NAC alone were very effective in restoring the levels of GSH and TAS, but together they significantly resolved the effects of cyanide on antioxidant enzymes, MDA levels, and caspase-3 activity.	Acetylcysteine	9-12	caspase 3	Rattus norvegicus	183-192
26394653-10	2015	NAC also reversed TDT-induced depolarization of Deltapsi, MDC staining, up-regulation of Bax, cleaved-PARP, Beclin-1, LC3-II, and cell viability.	Acetylcysteine	0-3	collagen type XI alpha 2 chain	Homo sapiens	102-106
20217053-5	2010	RESULTS: Sarcosine and N-acetylcysteine, but not LY379268, ameliorated PPI deficits in mGluR5 knockout mice.	Acetylcysteine	23-39	glutamate receptor, ionotropic, kainate 1	Mus musculus	87-93
19428548-10	2009	N-acetylcysteine, an antioxidant precursor of glutathione, inhibited the parthenolide-induced and H(2)O(2)-induced secretion of MIF.	Acetylcysteine	0-16	macrophage migration inhibitory factor	Homo sapiens	128-131
19234179-5	2009	Pretreatment of KB cells with antioxidants vitamin C and N-acetylcysteine or the pharmacological inhibitor PD168393 specific for the epidermal growth factor receptor all inhibited UVB-induced ROS as well as PAF-R agonists, yet had no effect on fMLP-mediated PAF-R agonist production.	Acetylcysteine	57-73	platelet activating factor receptor	Homo sapiens	207-212
25445966-8	2015	Both NAC and GSH, thus attenuated the expression of iNOS and COX-2 by suppressing NF-kappaB activation, indicating that 5-DRL suppresses LPS-induced iNOS and COX-2 expression through downregulation of the ROS-dependent NF-kappaB signaling pathway.	Acetylcysteine	5-8	prostaglandin-endoperoxide synthase 2	Mus musculus	61-66
19234179-5	2009	Pretreatment of KB cells with antioxidants vitamin C and N-acetylcysteine or the pharmacological inhibitor PD168393 specific for the epidermal growth factor receptor all inhibited UVB-induced ROS as well as PAF-R agonists, yet had no effect on fMLP-mediated PAF-R agonist production.	Acetylcysteine	57-73	platelet activating factor receptor	Homo sapiens	258-263
20593142-11	2010	Significant improvements to the erythrocyte ATPase and cardiac markers in patients treated with Mg/NAC correlated with a reduction in postoperative abnormalities.	Acetylcysteine	99-102	dynein axonemal heavy chain 8	Homo sapiens	44-50
25445966-8	2015	Both NAC and GSH, thus attenuated the expression of iNOS and COX-2 by suppressing NF-kappaB activation, indicating that 5-DRL suppresses LPS-induced iNOS and COX-2 expression through downregulation of the ROS-dependent NF-kappaB signaling pathway.	Acetylcysteine	5-8	prostaglandin-endoperoxide synthase 2	Mus musculus	158-163
20114059-7	2010	Attenuation of HNE-mediated activation of caspase 3 in presence of N-acetylcysteine (NAC) indicated the involvement of GSH in the process.	Acetylcysteine	67-83	caspase 3	Rattus norvegicus	42-51
20114059-7	2010	Attenuation of HNE-mediated activation of caspase 3 in presence of N-acetylcysteine (NAC) indicated the involvement of GSH in the process.	Acetylcysteine	85-88	caspase 3	Rattus norvegicus	42-51
19095747-7	2009	JP-8-induced COX-2 expression was also reduced to background in the catalase and SOD transfected cells, or in cultures treated with N-acetylcysteine (NAC).	Acetylcysteine	132-148	cytochrome c oxidase II, mitochondrial	Mus musculus	13-18
19095747-7	2009	JP-8-induced COX-2 expression was also reduced to background in the catalase and SOD transfected cells, or in cultures treated with N-acetylcysteine (NAC).	Acetylcysteine	150-153	cytochrome c oxidase II, mitochondrial	Mus musculus	13-18
25392528-8	2014	Furthermore, reactive oxygen species scavenger (N-acetyl-l-cysteine) and the ERK inhibitor (FR180204) impaired LPS-induced PARP activation and HMGB1 release.	Acetylcysteine	48-67	high mobility group box 1	Mus musculus	143-148
19095747-8	2009	When NAC was injected into JP-8-treated mice, dermal COX-2 expression, and JP-8-induced immune suppression was inhibited.	Acetylcysteine	5-8	cytochrome c oxidase II, mitochondrial	Mus musculus	53-58
19014919-7	2009	N-acetyl-l-cysteine pre-treatment rescued cells from MSt-2-induced ROS formation, mitochondrial membrane potential (Delta psi(m)) loss, Fas expression, caspase-8 and -3 activation and DNA fragmentation.	Acetylcysteine	0-19	caspase 8	Homo sapiens	152-168
20177149-2	2010	In the present study, we found that the co-treatment with hepatocyte growth factor (HGF) and TGF-beta1 resulted in enhanced migration of HaCaT cells compared with either growth factor alone, and that N-acetylcysteine, an antioxidant agent, was the most effective among several inhibitors tested, suggesting the involvement of reactive oxygen species (ROS).	Acetylcysteine	200-216	hepatocyte growth factor	Homo sapiens	58-82
20177149-2	2010	In the present study, we found that the co-treatment with hepatocyte growth factor (HGF) and TGF-beta1 resulted in enhanced migration of HaCaT cells compared with either growth factor alone, and that N-acetylcysteine, an antioxidant agent, was the most effective among several inhibitors tested, suggesting the involvement of reactive oxygen species (ROS).	Acetylcysteine	200-216	hepatocyte growth factor	Homo sapiens	84-87
25016575-0	2014	N-acetyl cysteine regulates the phosphorylation of JAK proteins following CD40-activation of human memory B cells.	Acetylcysteine	0-17	Janus kinase 2	Homo sapiens	51-54
20066544-9	2010	TPMT testing before azathioprine, NAC, and steroids was the most effective and most costly strategy.	Acetylcysteine	34-37	thiopurine S-methyltransferase	Homo sapiens	0-4
19019832-8	2009	RNA gel shift assay showed significant reduction in 3"-UTR-binding protein complex by ROS in both cell types that was reversed by the antioxidant N-acetylcysteine suggesting that ROS affects RNA-protein complex formation to promote Cp mRNA decay.	Acetylcysteine	146-162	ceruloplasmin	Bos taurus	232-234
20066544-14	2010	TPMT testing before initiating therapy with azathioprine, NAC, and steroids is a cost-effective treatment strategy for IPF.	Acetylcysteine	58-61	thiopurine S-methyltransferase	Homo sapiens	0-4
25016575-0	2014	N-acetyl cysteine regulates the phosphorylation of JAK proteins following CD40-activation of human memory B cells.	Acetylcysteine	0-17	CD40 molecule	Homo sapiens	74-78
25016575-9	2014	Furthermore, two kinases involved in STAT3 activation, known as JAK2 and JAK3, appeared down-regulated in presence of NAC.	Acetylcysteine	118-121	Janus kinase 2	Homo sapiens	64-68
18849615-8	2009	Treatment with N-acetylcysteine reversed the augmented Gadd45a mRNA response and caused the suppressed IFN-gamma mRNA response to recover.	Acetylcysteine	15-31	growth arrest and DNA damage inducible alpha	Homo sapiens	55-62
25016575-11	2014	The decrease in the phosphorylation of JAK2 and JAK3, earlier in the process, could explain the downregulation of STAT3 and offer a hypothesis on the mechanism of action of NAC antioxidant properties which were confirmed by a decrease in the level of S-glutathionylation of proteins.	Acetylcysteine	173-176	Janus kinase 2	Homo sapiens	39-43
25123537-11	2014	The suppressive effect was also reversed by co-treatment with N-acetylcysteine or NS-398 (a selective cyclooxygenase-2 inhibitor).	Acetylcysteine	62-78	prostaglandin-endoperoxide synthase 2	Mus musculus	102-118
19644561-6	2009	p,p"-DDE could induce increases in FasL mRNA and protein, which could be blocked by an antioxidant agent, N-acetyl-l-cysteine (NAC).	Acetylcysteine	106-125	Fas ligand	Rattus norvegicus	35-39
19644561-6	2009	p,p"-DDE could induce increases in FasL mRNA and protein, which could be blocked by an antioxidant agent, N-acetyl-l-cysteine (NAC).	Acetylcysteine	127-130	Fas ligand	Rattus norvegicus	35-39
20206069-9	2010	In the NAC group, mean blood beta-2 microglobulin significantly decreased from 2.38 + or - 0.58 to 1.71 + or - 0.38 mg/dl (p&lt;0.01), and in the aminophylline group, mean urinary beta-2 microglobulin concentration significantly decreased from 337 + or - 31.0 to 239 + or - 34 microg/ml (p&lt;0.01).	Acetylcysteine	7-10	potassium calcium-activated channel subfamily M regulatory beta subunit 2	Homo sapiens	29-35
19935767-3	2010	Treatment with an antioxidant (N-acetyl cysteine) or Nox inhibitors strongly inhibited the expression of MMPs by LPS and inhibited cell migration.	Acetylcysteine	31-48	matrix metallopeptidase 13	Mus musculus	105-109
24969774-6	2014	Injection of reactive oxygen species inhibitor N-acetylcysteine attenuated HFD-induced HSPC expansion, leukocytosis, and atherosclerosis in SR-BI(-/-) mice.	Acetylcysteine	47-63	scavenger receptor class B, member 1	Mus musculus	140-145
19725096-7	2010	NAC prevented NO-induced apoptosis, ROS overproduction, p53 up-regulation, and caspase-3 activation.	Acetylcysteine	0-3	caspase 3	Rattus norvegicus	79-88
19725096-8	2010	The protective effects of NAC were significantly blocked by buthionine sulfoximine, a glutathione synthetase inhibitor, indicating that the apoptosis-preventing activity of NAC was mediated by glutathione.	Acetylcysteine	26-29	glutathione synthetase	Rattus norvegicus	86-108
18667743-0	2008	N-acetylcysteine effect on serum creatinine and cystatin C levels in CKD patients.	Acetylcysteine	0-16	cystatin C	Homo sapiens	48-58
19725096-8	2010	The protective effects of NAC were significantly blocked by buthionine sulfoximine, a glutathione synthetase inhibitor, indicating that the apoptosis-preventing activity of NAC was mediated by glutathione.	Acetylcysteine	173-176	glutathione synthetase	Rattus norvegicus	86-108
25257100-3	2014	Previously, we demonstrated in human MIA PaCa-2 pancreatic cancer cells that N-acetyl-l-cysteine (NAC), a glutathione (GSH) precursor, prevents NFkappaB activation via S-glutathionylation of p65-NFkappaB, thereby blunting expression of survival genes.	Acetylcysteine	77-96	RELA proto-oncogene, NF-kB subunit	Homo sapiens	191-194
18675929-4	2008	Competition experiments, using PAPA-NONOate as NO donor, showed that 3-hydroxyanthranilic acid is a more potent NO scavenger than N-acetylcysteine.	Acetylcysteine	130-146	pappalysin 1	Homo sapiens	31-35
25257100-3	2014	Previously, we demonstrated in human MIA PaCa-2 pancreatic cancer cells that N-acetyl-l-cysteine (NAC), a glutathione (GSH) precursor, prevents NFkappaB activation via S-glutathionylation of p65-NFkappaB, thereby blunting expression of survival genes.	Acetylcysteine	98-101	RELA proto-oncogene, NF-kB subunit	Homo sapiens	191-194
18599801-11	2008	Pretreatment with the nonspecific antioxidant N-acetylcysteine and the Rho kinase inhibitors (Fasudil and Y-27632) prevented MLC and MYPT-1 phosphorylation by UFP suggesting a O(2)(.-)-mediated mechanism for PM(2.5) and UFP effects.	Acetylcysteine	46-62	protein phosphatase 1 regulatory subunit 12A	Homo sapiens	133-139
18802057-9	2008	In contrast to Nrf2(+/+) DCs, coincubation of Nrf2(-/-) DCs with PM and the antioxidant N-acetyl cysteine attenuated PM-induced up-regulation of CD80 and CD86.	Acetylcysteine	88-105	CD80 molecule	Homo sapiens	145-149
18802057-9	2008	In contrast to Nrf2(+/+) DCs, coincubation of Nrf2(-/-) DCs with PM and the antioxidant N-acetyl cysteine attenuated PM-induced up-regulation of CD80 and CD86.	Acetylcysteine	88-105	CD86 molecule	Homo sapiens	154-158
20137579-12	2010	(2) The serum cTnI concentration of the CIH and NAC groups was significantly higher than that of the control group (P &lt; 0.01).	Acetylcysteine	48-51	troponin I, cardiac 3	Mus musculus	14-18
19885844-7	2010	AGEs-activated EGFR and ERK1/2 were attenuated by an anti-oxidant (NAC) and an EGFR inhibitor (Iressa).	Acetylcysteine	67-70	mitogen activated protein kinase 3	Rattus norvegicus	24-30
25257100-10	2014	Compared to untreated tumors, gemcitabine treatment alone increased p65-NFkappaB nuclear translocation (3.7-fold) and DNA binding (2.5-fold), and these effects were blunted by NAC.	Acetylcysteine	176-179	RELA proto-oncogene, NF-kB subunit	Homo sapiens	68-71
19815813-10	2010	Blocking tyrosine nitration of PI 3-kinase with epicatechin or NAC restored Akt phosphorylation, and inhibited vaso-obliteration at p12 and neovascularization at p17 comparable with FeTPPS.	Acetylcysteine	63-66	DNA polymerase epsilon 3, accessory subunit	Homo sapiens	162-165
18419763-6	2008	Inhibition of reactive oxygen species (ROS) by N-acetyl-cysteine or diphenylene iodonium significantly suppressed the expression of MMP-3, MMP-9, NO and TNF-alpha in LPS-stimulated microglia, suggesting that ROS is an early signaling inducer in LPS-stimulated microglial cells.	Acetylcysteine	47-64	matrix metallopeptidase 9	Mus musculus	139-144
24976129-6	2014	In addition, the N-acetylcysteine inhibited ROS/RNS generation, elevation of antioxidants level, expression of ERK1/2, Akt, tuberin phosphorylation, resulted in deceased 8-OHdG accumulation and upregulation of OGG1 protein expression suggesting no involvement of Akt and ERK1/2MAPK pathways after CEES and LPS challenge.	Acetylcysteine	17-33	mitogen-activated protein kinase 3	Mus musculus	111-117
18385389-3	2008	METHODS: We investigated the effects of NAC on oxidative stress and oxidation-associated signals, such as p38 mitogen-activated protein kinase (MAPK), NF-kappaB and TNF-alpha, in CDDP-induced acute renal failure (ARF) rats, in comparison to the effects of melatonin (MT), one of the physiological TNF-alpha inhibitors, and pyrrolidine dithiocarbamate (PDTC), a NF-kappaB inhibitor.	Acetylcysteine	40-43	mitogen activated protein kinase 14	Rattus norvegicus	106-109
18385389-4	2008	RESULTS: NAC blocked oxidative stress, p38 MAPK activation, caspase-3 cleavage, tissue apoptosis, renal dysfunction and morphological damage induced by CDDP.	Acetylcysteine	9-12	mitogen activated protein kinase 14	Rattus norvegicus	39-42
20562516-7	2010	An antioxidant drug, N-acetyl-L-cysteine (NAC) inhibited TNF-induced VCAM-1.	Acetylcysteine	21-40	vascular cell adhesion molecule 1	Rattus norvegicus	69-75
20562516-7	2010	An antioxidant drug, N-acetyl-L-cysteine (NAC) inhibited TNF-induced VCAM-1.	Acetylcysteine	42-45	vascular cell adhesion molecule 1	Rattus norvegicus	69-75
18385389-4	2008	RESULTS: NAC blocked oxidative stress, p38 MAPK activation, caspase-3 cleavage, tissue apoptosis, renal dysfunction and morphological damage induced by CDDP.	Acetylcysteine	9-12	caspase 3	Rattus norvegicus	60-69
19796678-7	2009	These results support the hypothesis that exposure of exponentially growing human breast and prostate epithelial cells to PCBs causes increased steady-state levels of intracellular O(2)(*-) and H(2)O(2), induction of MnSOD or CuZnSOD activity, and clonogenic cell killing that could be inhibited by a clinically relevant thiol antioxidant, NAC, as well as by catalase and superoxide dismutase after PCB exposure.	Acetylcysteine	340-343	superoxide dismutase 2	Homo sapiens	217-222
24976129-6	2014	In addition, the N-acetylcysteine inhibited ROS/RNS generation, elevation of antioxidants level, expression of ERK1/2, Akt, tuberin phosphorylation, resulted in deceased 8-OHdG accumulation and upregulation of OGG1 protein expression suggesting no involvement of Akt and ERK1/2MAPK pathways after CEES and LPS challenge.	Acetylcysteine	17-33	mitogen-activated protein kinase 3	Mus musculus	271-277
18385389-8	2008	CONCLUSIONS: These data suggest that oxidative stress and p38 MAPK-mediated apoptotic cell death pathways are involved, at least in part, in the pathogenesis of CDDP-induced ARF, and negative regulation of p38 MAPK activation through inhibition of oxidative stress appears to play a central role in the beneficial effects of NAC.	Acetylcysteine	325-328	mitogen activated protein kinase 14	Rattus norvegicus	58-61
18385389-8	2008	CONCLUSIONS: These data suggest that oxidative stress and p38 MAPK-mediated apoptotic cell death pathways are involved, at least in part, in the pathogenesis of CDDP-induced ARF, and negative regulation of p38 MAPK activation through inhibition of oxidative stress appears to play a central role in the beneficial effects of NAC.	Acetylcysteine	325-328	mitogen activated protein kinase 14	Rattus norvegicus	206-209
24907532-9	2014	The preservation of the intracellular GSH contents with N-acetyl-L-cysteine (NAC), GSH and vitamin C abolished the effect of bornyl caffeate on the activation of p38 MAPK and JNK, preserved the integrity of mitochondrial membrane and ultimately rescued the cells from drug-induced cell death.	Acetylcysteine	56-75	mitogen activated protein kinase 14	Rattus norvegicus	162-165
18496137-9	2008	Caspase-3 activity (0.33% +/- 0.1%*) and apoptotic cells (12% +/- 1%*) were also comparably reduced by NAC.	Acetylcysteine	103-106	caspase 3	Rattus norvegicus	0-9
18504181-0	2008	[Effect of N-acetylcysteine on HMGB1 and RAGE expression in the lungs of asthmatic mice].	Acetylcysteine	11-27	high mobility group box 1	Mus musculus	31-36
18504181-5	2008	After NAC treatment, both of HMGB1 and RAGE mRNA levels (0.98-/+0.05 and 1.58-/+0.21) were significantly higher than those in the other two groups (P&lt;0.05).	Acetylcysteine	6-9	high mobility group box 1	Mus musculus	29-34
20029548-1	2009	This study was undertaken to test whether Ca(2+)-handling abnormalities in cardiomyocytes after ischemia-reperfusion (I/R) are prevented by antioxidants such as N-acetyl L-cysteine (NAC), which is known to reduce oxidative stress by increasing the glutathione redox status, and N-(2-mercaptopropionyl)-glycine (MPG), which scavenges both peroxynitrite and hydroxyl radicals.	Acetylcysteine	161-180	N-methylpurine-DNA glycosylase	Rattus norvegicus	311-314
20029548-6	2009	Furthermore, reduction in the isoproterenol-, ATP-, ouabain-, and caffeine-induced increases in [Ca(2+)](i) in cardiomyocytes from I/R hearts were limited by treatment with NAC or MPG.	Acetylcysteine	173-176	N-methylpurine-DNA glycosylase	Rattus norvegicus	180-183
24907532-9	2014	The preservation of the intracellular GSH contents with N-acetyl-L-cysteine (NAC), GSH and vitamin C abolished the effect of bornyl caffeate on the activation of p38 MAPK and JNK, preserved the integrity of mitochondrial membrane and ultimately rescued the cells from drug-induced cell death.	Acetylcysteine	77-80	mitogen activated protein kinase 14	Rattus norvegicus	162-165
24799199-7	2014	In addition, NAC pretreatment partly ameliorated OTA-induced S-phase arrest by preventing the down-regulation of cyclin A2, cyclin E1 and CDK2 expression in HEK-293 cells.	Acetylcysteine	13-16	cyclin dependent kinase 2	Homo sapiens	138-142
19467228-6	2009	Both basal and induced shedding of EPCR was blocked by the metalloproteinase inhibitors, TAPI-0 and GM6001, and by the reduced non-protein thiols, glutathione, dihydrolipoic acid, dithiothreitol, and N-acetyl-l-cysteine.	Acetylcysteine	200-219	protein C receptor	Homo sapiens	35-39
18187174-8	2008	In addition, the downstream targets of p27, including CDK4, cyclin D1 and phosphorylated-Rb proteins, increased in 1 microM tt-DDE-treated cells and these changes were prevented by NAC co-treatment.	Acetylcysteine	181-184	cyclin dependent kinase 4	Homo sapiens	54-58
18187174-8	2008	In addition, the downstream targets of p27, including CDK4, cyclin D1 and phosphorylated-Rb proteins, increased in 1 microM tt-DDE-treated cells and these changes were prevented by NAC co-treatment.	Acetylcysteine	181-184	cyclin D1	Homo sapiens	60-69
24442604-8	2014	NAC treatment effectively attenuated histopathologic, peroxidative, and apoptotic changes, as well as reducing alterations in SP-D expression in the lung tissue.	Acetylcysteine	0-3	surfactant protein D	Rattus norvegicus	126-130
17918745-3	2008	Furthermore, we observed that N-acetyl-L-cysteine, an inhibitor of tyrosine kinases, suppressed ebselen-induced MAPK activation and buthionine sulfoximine, an activator of protein tyrosine phosphatases, enhanced the effect, indicating that ebselen activated MEK1/2 through one or more tyrosine kinases.	Acetylcysteine	30-49	mitogen activated protein kinase 3	Rattus norvegicus	112-116
19322029-9	2009	In addition, N-acetylcysteine the ROS scavenger, depressed effects of Ang II in a manner similar to STS.	Acetylcysteine	13-29	angiogenin	Homo sapiens	70-73
19409917-11	2009	Pretreatment of Ca9-22 cells with N-acetylcysteine, a thiol antioxidant, abolished all of ovatodiolide-induced effects, including ROS generation, down-regulation of FLIP, caspase activation, apoptosis as well as cell cycle arrest.	Acetylcysteine	34-50	caspase 8	Homo sapiens	171-178
24726884-8	2014	N-acetylcysteine (NAC), an antioxidant, suppressed the phosphorylation of ATM and p53 and, to a less extent, Chk2, but NAC increased the phosphorylation and nuclear foci formation of H2AX.	Acetylcysteine	0-16	ataxia telangiectasia mutated	Mus musculus	74-77
18068289-9	2008	FA and NAC co-treated rats showed a significant decrease in the activities of circulatory lactate dehydrogenase and alkaline phosphatase, the levels of lipid peroxidative markers (in circulation, lung and liver), DNA single stranded breaks (comet parameters), micronuclei frequency (in the whole blood) and expression of cyclooxygenase-2 and Nf-kappaB (in lung and liver tissues), and significant increase in antioxidant status (in circulation, lung and liver).	Acetylcysteine	7-10	prostaglandin-endoperoxide synthase 2	Rattus norvegicus	321-337
24726884-8	2014	N-acetylcysteine (NAC), an antioxidant, suppressed the phosphorylation of ATM and p53 and, to a less extent, Chk2, but NAC increased the phosphorylation and nuclear foci formation of H2AX.	Acetylcysteine	0-16	checkpoint kinase 2	Mus musculus	109-113
19356721-3	2009	Furthermore, pretreatment of cells with l-N-acetylcysteine (an antioxidant) inhibited CoCl(2)-stimulated osteopontin protein expression and p38MAPK phosphorylation, but not Akt/PKB phosphorylation.	Acetylcysteine	40-58	secreted phosphoprotein 1	Rattus norvegicus	105-116
18667818-9	2008	Moreover, the quenching of ROS generation by N-acetyl-L-cysteine administration, a scavenger of ROS, reversed the sanguinarine-induced apoptosis effects via inhibition of ROS production, MMP collapse, tBid expression and the subsequent activation of caspases.	Acetylcysteine	45-64	caspase 8	Homo sapiens	250-258
24726884-8	2014	N-acetylcysteine (NAC), an antioxidant, suppressed the phosphorylation of ATM and p53 and, to a less extent, Chk2, but NAC increased the phosphorylation and nuclear foci formation of H2AX.	Acetylcysteine	18-21	ataxia telangiectasia mutated	Mus musculus	74-77
19356721-3	2009	Furthermore, pretreatment of cells with l-N-acetylcysteine (an antioxidant) inhibited CoCl(2)-stimulated osteopontin protein expression and p38MAPK phosphorylation, but not Akt/PKB phosphorylation.	Acetylcysteine	40-58	mitogen activated protein kinase 14	Rattus norvegicus	140-147
17964282-3	2007	Valsartan, a selective Ang II type 1 (AT1) receptor blocker, and N-acetylcysteine, an antioxidant, inhibited both of these modifications, indicating the contribution of AT1 receptor and reactive oxygen species to oxidation of Prx2 and phosphorylation of GRP58 by Ang II.	Acetylcysteine	65-81	angiotensin II receptor type 1	Homo sapiens	169-172
24726884-8	2014	N-acetylcysteine (NAC), an antioxidant, suppressed the phosphorylation of ATM and p53 and, to a less extent, Chk2, but NAC increased the phosphorylation and nuclear foci formation of H2AX.	Acetylcysteine	18-21	checkpoint kinase 2	Mus musculus	109-113
24794623-11	2014	CONCLUSIONS: Inflammation scores, cellular infiltration, and expression of VEGF, TGF-beta, and iNOS were reduced by ascorbic acid and/or NAC treatments, thereby decreasing MS development.	Acetylcysteine	137-140	Vegfa	Cavia porcellus	75-79
24794623-11	2014	CONCLUSIONS: Inflammation scores, cellular infiltration, and expression of VEGF, TGF-beta, and iNOS were reduced by ascorbic acid and/or NAC treatments, thereby decreasing MS development.	Acetylcysteine	137-140	nitric oxide synthase, inducible	Cavia porcellus	95-99
19038359-8	2009	Furthermore, we found that H(2)O(2)-induced ROS inhibited serine/threonine protein phosphatases 2A (PP2A) and 5 (PP5), which was abrogated by NAC.	Acetylcysteine	142-145	protein phosphatase 2 (formerly 2A), catalytic subunit, alpha isoform	Mus musculus	100-104
17900531-7	2007	MMP-2 activity is directly inhibited by NAC and GSH, while LA is ineffective.	Acetylcysteine	40-43	matrix metallopeptidase 2	Homo sapiens	0-5
24064905-6	2014	Importantly, the effect of above DNA damage response was prevented by N-acetyl-l-cysteine (a reactive oxygen species scavenger), and NU7026 (a DNA-PK inhibitor) could attenuate DNA-PK catalytic subunit and phosphorylation of H2A.X on Ser139 expression in comparison with HMJ-38 alone treated HUVECs.	Acetylcysteine	70-89	H2A.X variant histone	Homo sapiens	225-230
17893047-6	2007	Pretreatment with MAPK inhibitors SB203580 and U0126, or addition of the exogenous thiol N-acetylcysteine, abrogated both p38(MAPK) and ERK2 activation as well as downstream effects on gene expression.	Acetylcysteine	89-105	mitogen-activated protein kinase 14	Mus musculus	122-125
19038359-8	2009	Furthermore, we found that H(2)O(2)-induced ROS inhibited serine/threonine protein phosphatases 2A (PP2A) and 5 (PP5), which was abrogated by NAC.	Acetylcysteine	142-145	protein phosphatase 5, catalytic subunit	Mus musculus	113-116
19454702-9	2009	In addition, pharmacological blockage of ERK and scavenging of reactive oxygen species with N-acetylcysteine reduced HO-1 gene expression in p38(-/-) MEF, respectively.	Acetylcysteine	92-108	mitogen-activated protein kinase 14	Mus musculus	141-144
24297485-6	2014	An antioxidant, N-acetylcysteine or RAGE-antibodies also restored the decrease in ACE 2 mRNA level in AGEs-exposed mesangial cells.	Acetylcysteine	16-32	angiotensin converting enzyme 2	Homo sapiens	82-87
19101991-6	2009	Additionally, treatment of the cells with the ROS scavengers, N-acetylcysteine and catalase, inhibited the radiation induced CatS expression.	Acetylcysteine	62-78	cathepsin S	Felis catus	125-129
17907002-6	2007	Furthermore, pre-treatment with the ROS scavenger N-acetylcysteine (NAC) and the caspase-8 inhibitor z-IETD-fmk was found to effectively prevent UVB-induced apoptosis, suggesting that UVB-induced HaCaT cell apoptosis was partially due to generation of ROS and activation of the caspase-8 pathway.	Acetylcysteine	50-66	caspase 8	Homo sapiens	278-287
17907002-6	2007	Furthermore, pre-treatment with the ROS scavenger N-acetylcysteine (NAC) and the caspase-8 inhibitor z-IETD-fmk was found to effectively prevent UVB-induced apoptosis, suggesting that UVB-induced HaCaT cell apoptosis was partially due to generation of ROS and activation of the caspase-8 pathway.	Acetylcysteine	68-71	caspase 8	Homo sapiens	278-287
17596533-10	2007	It is concluded that both NAC and taurine significantly attenuated HG-induced activation of the Raf-1/MAPK and the JAK2-STAT1/STAT3 signaling pathways and hypertrophic growth in renal tubular epithelial cells.	Acetylcysteine	26-29	Raf-1 proto-oncogene, serine/threonine kinase	Homo sapiens	96-101
17596533-10	2007	It is concluded that both NAC and taurine significantly attenuated HG-induced activation of the Raf-1/MAPK and the JAK2-STAT1/STAT3 signaling pathways and hypertrophic growth in renal tubular epithelial cells.	Acetylcysteine	26-29	Janus kinase 2	Homo sapiens	115-119
24531650-8	2014	RESULTS: In vivo, N-acetylcysteine ameliorated the D-GalN/LPS-induced hepatotoxicity and reduced GSK3beta activity; GSK3beta inhibition increased hepatic superoxide dismutase activity and the glutathione content, decreased malondialdehyde production in the liver tissues; while GSK3beta inhibition suppressed the JNK activation in the liver and decreased cytochrome c release from mitochondria.	Acetylcysteine	18-34	glycogen synthase kinase 3 beta	Homo sapiens	97-105
19371603-7	2009	The increase in MMP production was abolished by pre-treatment with the antioxidants Tiron and N-acetyl cysteine (NAC) or with the xanthine oxidase inhibitors allopurinol or oxypurinol.	Acetylcysteine	94-111	matrix metallopeptidase 9	Mus musculus	16-19
19371603-7	2009	The increase in MMP production was abolished by pre-treatment with the antioxidants Tiron and N-acetyl cysteine (NAC) or with the xanthine oxidase inhibitors allopurinol or oxypurinol.	Acetylcysteine	113-116	matrix metallopeptidase 9	Mus musculus	16-19
24534112-6	2014	In addition, the cystine-glutamate antiporter inhibitor (S)-4-carboxyphenylglycine (CPG) and the mGluR2 antagonist LY341495 reversed the suppressing effects of NAC on DOI-induced head twitch and molecular responses and increased frequency of excitatory field potentials, supporting that NAC attenuates the 5-HT(2A)R-mediated hallucinogenic effects via increased activity of cystine-glutamate antiporter followed by activation of mGluR2 receptors.	Acetylcysteine	160-163	glutamate receptor, ionotropic, AMPA2 (alpha 2)	Mus musculus	97-103
19714806-7	2009	Intraperitoneal NAC administration prior to the final OVA challenge inhibited Yml/Ym2, SP-D, and FIZZ1 expression in BALF and lung tissue.	Acetylcysteine	16-19	chitinase-like 4	Mus musculus	82-85
17607690-8	2007	In contrast, NAC did not reduce the level of ROS but it prevented the increase of pStat1 induced by H2O2, evidencing a differential effect on ROS formation and on Stat1 phosphorylation.	Acetylcysteine	13-16	signal transducer and activator of transcription 1	Rattus norvegicus	83-88
24534112-6	2014	In addition, the cystine-glutamate antiporter inhibitor (S)-4-carboxyphenylglycine (CPG) and the mGluR2 antagonist LY341495 reversed the suppressing effects of NAC on DOI-induced head twitch and molecular responses and increased frequency of excitatory field potentials, supporting that NAC attenuates the 5-HT(2A)R-mediated hallucinogenic effects via increased activity of cystine-glutamate antiporter followed by activation of mGluR2 receptors.	Acetylcysteine	160-163	glutamate receptor, ionotropic, AMPA2 (alpha 2)	Mus musculus	429-435
24534112-6	2014	In addition, the cystine-glutamate antiporter inhibitor (S)-4-carboxyphenylglycine (CPG) and the mGluR2 antagonist LY341495 reversed the suppressing effects of NAC on DOI-induced head twitch and molecular responses and increased frequency of excitatory field potentials, supporting that NAC attenuates the 5-HT(2A)R-mediated hallucinogenic effects via increased activity of cystine-glutamate antiporter followed by activation of mGluR2 receptors.	Acetylcysteine	287-290	glutamate receptor, ionotropic, AMPA2 (alpha 2)	Mus musculus	97-103
17803476-5	2007	AIM: The aim of this study was to determine the effect of NAC on renal function, measured by serum creatinine and Cystatin C, in patients with stage 3 chronic kidney disease.	Acetylcysteine	58-61	cystatin C	Homo sapiens	114-124
19093139-9	2009	NAC and MPA completely suppressed OA-induced fibronectin secretion and decreased the levels of TGF-beta and cellular ROS.	Acetylcysteine	0-3	transforming growth factor, beta 1	Mus musculus	95-103
24681487-7	2014	Treatment of neurons with antioxidants, such as N-acetylcysteine or vitamin E, or decreasing tau levels in axons restored mitochondrial transport in AFG3L2-depleted neurons.	Acetylcysteine	48-64	AFG3-like AAA ATPase 2	Mus musculus	149-155
18717627-7	2009	Treatment with ROS scavenger N-acetyl-L-cysteine attenuated Ref-1 siRNA-mediated activation of NADPH oxidase and cardiac differentiation.	Acetylcysteine	29-48	apurinic/apyrimidinic endonuclease 1	Mus musculus	60-65
24164541-4	2014	HN2-induced EGFR phosphorylation and IL-6 secretion in NHBECs were inhibited by the antioxidant N-acetyl-L-cysteine (NAC) and by the flavoprotein inhibitor diphenyleneiodonium chloride (DPI).	Acetylcysteine	96-115	MT-RNR2 like 2 (pseudogene)	Homo sapiens	0-3
19220841-7	2009	U18666A led to the phosphorylation of p38 mitogen-activated protein kinase 24 and 48 h after the stimulation and the p38 activation was inhibited in presence of cholesterol-free medium or NAC.	Acetylcysteine	188-191	mitogen-activated protein kinase 14	Mus musculus	38-41
19220841-7	2009	U18666A led to the phosphorylation of p38 mitogen-activated protein kinase 24 and 48 h after the stimulation and the p38 activation was inhibited in presence of cholesterol-free medium or NAC.	Acetylcysteine	188-191	mitogen-activated protein kinase 14	Mus musculus	117-120
17576792-7	2007	In addition, 4"-IAPP treatment significantly increases intracellular reactive oxygen species (ROS) and decreases glutathione (GSH) levels in SH-SY5Y cells, and cell death is significantly attenuated by the common antioxidants alpha-tocopherol, N-acetyl-l-cysteine and GSH, but not by the nonspecific caspase inhibitor N-benzyloxycarbonyl-Val-Ala-Asp-fluoromethyl ketone.	Acetylcysteine	244-263	islet amyloid polypeptide	Homo sapiens	16-20
23640957-7	2014	Furthermore, ROS scavenger N-acetyl L-cysteine attenuated beta-sitosterol-mediated sub-G1 accumulation, PARP cleavage, JNK and AMPK activation in U266 cells.	Acetylcysteine	27-46	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	127-131
24586617-7	2014	Importantly, the addition of the antioxidant N-acetyl cysteine (NAC) to the differentiation medium partially prevents the nuclear accumulation of APE1, increasing the neuronal differentiation of hAT-MASC.	Acetylcysteine	45-62	apurinic/apyrimidinic endodeoxyribonuclease 1	Homo sapiens	146-150
17645304-9	2007	MEPE could also trigger time-dependently extracellular signal-regulated kinase (ERK)1/2 phosphorylation in VSMCs, which was attenuated by antioxidants N-acetylcysteine (NAC) and pyrrolidinedithiocarbamate (PDTC).	Acetylcysteine	151-167	mitogen activated protein kinase 3	Rattus norvegicus	41-87
17645304-9	2007	MEPE could also trigger time-dependently extracellular signal-regulated kinase (ERK)1/2 phosphorylation in VSMCs, which was attenuated by antioxidants N-acetylcysteine (NAC) and pyrrolidinedithiocarbamate (PDTC).	Acetylcysteine	169-172	mitogen activated protein kinase 3	Rattus norvegicus	41-87
19136971-4	2009	NAC treatment of rats restored the ability to induce LTP and LTD by indirectly stimulating mGluR2/3 and mGluR5, respectively.	Acetylcysteine	0-3	glutamate receptor, ionotropic, AMPA2 (alpha 2)	Mus musculus	91-97
19136971-4	2009	NAC treatment of rats restored the ability to induce LTP and LTD by indirectly stimulating mGluR2/3 and mGluR5, respectively.	Acetylcysteine	0-3	glutamate receptor, ionotropic, kainate 1	Mus musculus	104-110
24586617-7	2014	Importantly, the addition of the antioxidant N-acetyl cysteine (NAC) to the differentiation medium partially prevents the nuclear accumulation of APE1, increasing the neuronal differentiation of hAT-MASC.	Acetylcysteine	64-67	apurinic/apyrimidinic endodeoxyribonuclease 1	Homo sapiens	146-150
24211316-0	2014	Priming of beta-2 agonist and antimuscarinic induced physiological responses induced by 1200mg/day NAC in moderate to severe COPD patients: A pilot study.	Acetylcysteine	99-102	potassium calcium-activated channel subfamily M regulatory beta subunit 2	Homo sapiens	11-17
18841985-3	2008	A hydrophilic interaction liquid chromatography tandem mass spectrometry method (HILIC-MS/MS) using a zwitterionic stationary phase (Zic-HILIC) was developed and validated to quantitate the mercapturic acids of AA (AAMA) and glycidamide (GAMA), and AAMA-sulfoxide in human urine.	Acetylcysteine	190-207	Zic family member 1	Homo sapiens	133-136
18847228-7	2008	In addition, we found that the conjugate of HNE to cysteine was produced in much lower yield than HNE-GSH, while that of N-acetylcysteine could not be detected.	Acetylcysteine	121-137	elastase, neutrophil expressed	Homo sapiens	44-47
17371946-5	2007	Gel shifting and chromatin immunoprecipitation assays showed that SMC coculture increased the nuclear factor-kappaB (NF-kappaB)-promoter binding activity in ECs; inhibition of NF-kappaB activation by p65-antisense, lactacystin, and N-acetyl-cysteine blocked the coculture-induced E-selectin promoter activity.	Acetylcysteine	232-249	RELA proto-oncogene, NF-kB subunit	Homo sapiens	200-203
17760840-6	2007	In Ang II treated heart, there was a decreased association of p38MAPKbeta &amp; extracellular-signal regulated kinase (ERK) 1/ 2 (anti-death signalling component) with caveolin while there was an increased association of p38MAPKalpha &amp; Jun N-terminal kinase (JNK) (death signalling component) indicating reduced amount of death signal components and increased amount of anti-death signalling components being available to the Ang II treated heart to generate a survival signal, which was reversed with NAC or apocynin.	Acetylcysteine	506-509	angiogenin	Homo sapiens	3-6
17548252-2	2007	This study aimed to investigate the changes in TLR2/4 gene expression in the liver and lung after I/R injury with or without NAC pretreatment.	Acetylcysteine	125-128	toll-like receptor 2	Mus musculus	47-53
17548252-6	2007	RESULTS: Compared with the I/R group, the expression of TLR2/4 mRNA and protein in the liver and lung in the I/R-NAC group was decreased at the same time point (P&lt;0.05).	Acetylcysteine	113-116	toll-like receptor 2	Mus musculus	56-62
17548252-10	2007	NAC inhibited the activation of TLR2/4 and the induction of TNF-alpha resulting from I/R injury via modulating the redox state, thus it may mitigate liver and lung injury following partial hepatic I/R in mice.	Acetylcysteine	0-3	toll-like receptor 2	Mus musculus	32-38
18506790-8	2008	However, both the antioxidant N-acetyl cysteine (NAC) and the mitochondrial membrane-stabilizing agent cyclosporine A (CsA) partially preserve psi, suppress activation of p38 kinase, and partially protect the cells from Cd(2+)-induced death.	Acetylcysteine	30-47	mitogen-activated protein kinase 14	Mus musculus	171-174
18506790-8	2008	However, both the antioxidant N-acetyl cysteine (NAC) and the mitochondrial membrane-stabilizing agent cyclosporine A (CsA) partially preserve psi, suppress activation of p38 kinase, and partially protect the cells from Cd(2+)-induced death.	Acetylcysteine	49-52	mitogen-activated protein kinase 14	Mus musculus	171-174
24399295-6	2014	The reduced cell surface abundance of VEGFR2 in diabetic mice was reversed by treatment with the antioxidant N-acetyl-L-cysteine, suggesting a causative role for oxidative stress.	Acetylcysteine	109-128	kinase insert domain protein receptor	Mus musculus	38-44
18941206-7	2008	N-acetylcysteine (NAC) completely blocked the induction of fasL mRNA and protein.	Acetylcysteine	0-16	Fas ligand (TNF superfamily, member 6)	Mus musculus	59-63
18941206-7	2008	N-acetylcysteine (NAC) completely blocked the induction of fasL mRNA and protein.	Acetylcysteine	18-21	Fas ligand (TNF superfamily, member 6)	Mus musculus	59-63
18829485-8	2008	The induction of many of these genes with SOD2 knockdown, such as VEGFA and FKBP5, is reversible with the antioxidant N-acetylcysteine, suggesting that this mechanism is directly linked to ROS.	Acetylcysteine	118-134	superoxide dismutase 2	Homo sapiens	42-46
18829485-10	2008	SOD2 knockdown-induced AR activation was confirmed by electrophoretic mobility shift assay and luciferase activity, and both were readily reversible with N-acetylcysteine.	Acetylcysteine	154-170	superoxide dismutase 2	Homo sapiens	0-4
17395153-10	2007	NAC co-treatment also suppressed STC1 expression but had no effect on IDAM-induced hsp70 expression.	Acetylcysteine	0-3	stanniocalcin 1	Homo sapiens	33-37
17363366-9	2007	Treatment of BAEC with EGCG generated intracellular H(2)O(2) (assessed with H(2)O(2)-specific fluorescent dye CM-H(2)DCF-DA), whereas treatment with N-acetylcysteine inhibited EGCG-stimulated phosphorylation of Fyn, Akt, and eNOS.	Acetylcysteine	149-165	FYN proto-oncogene, Src family tyrosine kinase	Rattus norvegicus	211-214
24157283-9	2014	Additionally, exposure of Neuro-2a cells to iAs triggered endoplasmic reticulum (ER) stress identified through several key molecules (GRP 78, CHOP, XBP-1, and caspase-12), which was prevented by NAC.	Acetylcysteine	195-198	caspase 12	Mus musculus	159-169
17253623-7	2007	Protection by NAC was associated with the following factors: (1) reduced isoprostane activation and nitrotyrosine formation; (2) increased levels of the antioxidants glutathione, thioredoxin-2, and (3) inhibition of caspase-3, calpain, and caspase-1 activation.	Acetylcysteine	14-17	caspase 3	Rattus norvegicus	216-225
25048265-6	2014	The gene expression profiles in bone marrow cells indicated the upregulation of the Fasl gene, which can be suppressed by NAC administration.	Acetylcysteine	122-125	Fas ligand (TNF superfamily, member 6)	Mus musculus	84-88
17237288-7	2007	The antioxidant N-acetylcysteine attenuated cathepsin D relocation into the cytosol, suggesting that lysosomal destabilization is dependent on elevation of reactive oxygen species and precedes mitochondrial dysfunction.	Acetylcysteine	16-32	cathepsin D	Homo sapiens	44-55
18614529-4	2008	N-Acetyl-l-cysteine reduced oxidative stress, prevented CCTalpha cross-linking, and restored CCT function in 15d-PGJ2-treated cells.	Acetylcysteine	0-19	phosphate cytidylyltransferase 1A, choline	Homo sapiens	56-64
16563723-7	2006	PEITC and NAC-PEITC treatment caused dose-dependent decreases in MMP-2/MMP-9 and MT1-MMP mRNA levels, as determined by reverse transcription polymerase chain reaction.	Acetylcysteine	10-13	matrix metallopeptidase 2	Homo sapiens	65-70
24693334-3	2014	Biochemical analysis demonstrated that the NAC treatment also antagonized hyperphosphorylation of cardiac ryanodine receptors (RyR2) and significantly restored depleted protein levels of both RyR2 and calstabin2.	Acetylcysteine	43-46	ryanodine receptor 2	Rattus norvegicus	127-131
16563723-7	2006	PEITC and NAC-PEITC treatment caused dose-dependent decreases in MMP-2/MMP-9 and MT1-MMP mRNA levels, as determined by reverse transcription polymerase chain reaction.	Acetylcysteine	10-13	matrix metallopeptidase 14	Homo sapiens	81-88
18596559-0	2008	Effect of steroids, acetyl-cysteine and calcium-activated chloride channel inhibitors on allergic mucin expression in sinus mucosa.	Acetylcysteine	20-35	LOC100508689	Homo sapiens	98-103
18657320-0	2008	DNA-binding activity of NF-kappaB and phosphorylation of p65 are induced by N-acetylcysteine through phosphatidylinositol (PI) 3-kinase.	Acetylcysteine	76-92	RELA proto-oncogene, NF-kB subunit	Homo sapiens	57-60
17030433-0	2006	Antioxidant N-acetylcysteine inhibits the activation of JNK3 mediated by the GluR6-PSD95-MLK3 signaling module during cerebral ischemia in rat hippocampus.	Acetylcysteine	12-28	glutamate ionotropic receptor kainate type subunit 2	Rattus norvegicus	77-82
18657320-5	2008	The phosphorylation of p65 at serine 536 was induced by NAC, which is known to contribute to the enhancement of DNA-binding activity of NF-kappaB, however, NAC did not directly phosphorylate p65.	Acetylcysteine	56-59	RELA proto-oncogene, NF-kB subunit	Homo sapiens	23-26
17030433-0	2006	Antioxidant N-acetylcysteine inhibits the activation of JNK3 mediated by the GluR6-PSD95-MLK3 signaling module during cerebral ischemia in rat hippocampus.	Acetylcysteine	12-28	discs large MAGUK scaffold protein 4	Rattus norvegicus	83-88
18657320-5	2008	The phosphorylation of p65 at serine 536 was induced by NAC, which is known to contribute to the enhancement of DNA-binding activity of NF-kappaB, however, NAC did not directly phosphorylate p65.	Acetylcysteine	156-159	RELA proto-oncogene, NF-kB subunit	Homo sapiens	23-26
18657320-6	2008	The NAC-induced DNA-binding activity of NF-kappaB and phosphorylation of p65 were sensitive to a phosphatidylinositol (PI) 3-kinase inhibitor, partially sensitive to an IkappaB kinase (IKK) inhibitor, but not sensitive to a Bruton"s tyrosine kinase (Btk) inhibitor.	Acetylcysteine	4-7	RELA proto-oncogene, NF-kB subunit	Homo sapiens	73-76
17030433-8	2006	Results indicate that NAC distinctly inhibited the association of PSD95 with GluR6 and MLK3, the autophosphorylation of MLK3, the combination of MLK3 with JNK3 and JNK3 activation.	Acetylcysteine	22-25	discs large MAGUK scaffold protein 4	Rattus norvegicus	66-71
17030433-8	2006	Results indicate that NAC distinctly inhibited the association of PSD95 with GluR6 and MLK3, the autophosphorylation of MLK3, the combination of MLK3 with JNK3 and JNK3 activation.	Acetylcysteine	22-25	glutamate ionotropic receptor kainate type subunit 2	Rattus norvegicus	77-82
24693334-3	2014	Biochemical analysis demonstrated that the NAC treatment also antagonized hyperphosphorylation of cardiac ryanodine receptors (RyR2) and significantly restored depleted protein levels of both RyR2 and calstabin2.	Acetylcysteine	43-46	ryanodine receptor 2	Rattus norvegicus	192-196
18353867-7	2008	Among several antioxidants tried, only N-acetylcysteine effectively inhibits TGFbeta-mediated activation of TGase2.	Acetylcysteine	39-55	transforming growth factor, beta 1	Mus musculus	77-84
24515807-19	2014	Mercury has a high affinity for thiol groups ( -SH) and seleno groups ( -SeH) that are present in amino acids as cysteine and N-acetyl cysteine, lipoic acid, proteins, and enzymes.	Acetylcysteine	126-143	epoxide hydrolase 2	Homo sapiens	73-76
18645026-7	2008	Pretreatment with an antioxidant (N-acetylcysteine) or a c-Jun NH(2)-terminal kinase inhibitor (SP600125) effectively prevented Andro-induced p53 activation and DR4 up-regulation and eventually blocked the Andro-induced sensitization on TRAIL-induced apoptosis.	Acetylcysteine	34-50	TNF receptor superfamily member 10a	Homo sapiens	161-164
17936662-11	2008	The anti-oxidant, N-acetyl cysteine, inhibited TNF-alpha-induced PAPP-A expression without altering the induction in VCAM, ICAM, and MCP-1.	Acetylcysteine	18-35	pappalysin 1	Homo sapiens	65-71
18628592-6	2008	Treatment with N-acetyl-L-cysteine also inhibited expression of apoptotic proteins such as Bax and Smac and abrogated caspase-8 activation.	Acetylcysteine	15-34	caspase 8	Homo sapiens	118-127
18353872-7	2008	High glucose increased the generation of ROS, whereas both alpha-lipoic acid and N-acetylcysteine scavenged the ROS and decreased high glucose-induced tyrosine phosphorylation of IkappaBalpha, nuclear translocation of p65, and NF-kappaB DNA binding activity.	Acetylcysteine	81-97	RELA proto-oncogene, NF-kB subunit	Homo sapiens	218-221
23726389-8	2013	It also inhibited Fas, caspase-3, caspase-8 and integrin alphavbeta6 (alphavbeta6) gene expressions in the NAC-treated piglets.	Acetylcysteine	107-110	caspase 8	Homo sapiens	34-43
24016823-8	2013	Treatment with N-acetyl-L-cysteine (NAC), an antioxidant, inhibited WFA-induced loss of type II collagen expression and increase in COX-2 expression, accompanied by inhibition of reactive oxygen species production.	Acetylcysteine	15-34	prostaglandin G/H synthase 2	Oryctolagus cuniculus	132-137
18311190-5	2008	B(1) receptor mRNA was markedly increased in retinas of diabetic rats, and this was prevented by N-acetyl-L-cysteine (1 g kg(-1) day(-1) for 7 days).	Acetylcysteine	97-116	UDP glucuronosyltransferase family 1 member A1	Rattus norvegicus	0-4
24016823-8	2013	Treatment with N-acetyl-L-cysteine (NAC), an antioxidant, inhibited WFA-induced loss of type II collagen expression and increase in COX-2 expression, accompanied by inhibition of reactive oxygen species production.	Acetylcysteine	36-39	prostaglandin G/H synthase 2	Oryctolagus cuniculus	132-137
24008628-4	2013	Here, we observed that cross-linking of CD80 and CD86 in EBV-transformed B cells induced apoptosis through caspase-dependent release of apoptosis-related molecules, cytochrome c and apoptosis-inducing factor (AIF) from mitochondria, because Z-VAD-fmk (N-benzyloxycarbonyl-Val-Ala-Asp-fluoromethylketone) and N-acetylcysteine (NAC) blocked apoptosis and disruption of mitochondria.	Acetylcysteine	308-324	CD80 molecule	Homo sapiens	40-44
18325578-10	2008	CONCLUSION: SFN and NAC upregulate T(H)1 immunity in aging through a restoration of redox equilibrium.	Acetylcysteine	20-23	heart and neural crest derivatives expressed 1	Mus musculus	35-40
24008628-4	2013	Here, we observed that cross-linking of CD80 and CD86 in EBV-transformed B cells induced apoptosis through caspase-dependent release of apoptosis-related molecules, cytochrome c and apoptosis-inducing factor (AIF) from mitochondria, because Z-VAD-fmk (N-benzyloxycarbonyl-Val-Ala-Asp-fluoromethylketone) and N-acetylcysteine (NAC) blocked apoptosis and disruption of mitochondria.	Acetylcysteine	308-324	CD86 molecule	Homo sapiens	49-53
24179013-6	2013	Finally, treatment with the antioxidative compounds N-acetyl cysteine or MP865, but not with placebo, was associated with higher plasma FGF-19 (NAC and MP865 coefficients -0.28 and -0.23, P &lt; 0.05, respectively).	Acetylcysteine	52-69	fibroblast growth factor 19	Homo sapiens	136-142
18437082-0	2008	N-acetylcysteine derivative inhibits CD40-dependent proinflammatory properties of human pancreatic duct cells.	Acetylcysteine	0-16	CD40 molecule	Homo sapiens	37-41
25610275-10	2013	Erdosteine and NAC significantly reduced the local induction of bax and caspase 3 and significantly increased the reduced local production of bcl-2.	Acetylcysteine	15-18	caspase 3	Rattus norvegicus	72-81
18437082-3	2008	In this article, we investigated whether a salt derivative of N-acetyl-L-cysteine, Nacystelyn, could modulate CD40 expression on duct cells and the response of activated duct cells to CD40 engagement.	Acetylcysteine	62-81	CD40 molecule	Homo sapiens	110-114
18437082-3	2008	In this article, we investigated whether a salt derivative of N-acetyl-L-cysteine, Nacystelyn, could modulate CD40 expression on duct cells and the response of activated duct cells to CD40 engagement.	Acetylcysteine	62-81	CD40 molecule	Homo sapiens	184-188
23900601-6	2013	Moreover, the combined treatment induced intracellular reactive oxygen species (ROS) and the radical scavenger N-acetyl-L-cysteine (NAC) blocked the intracellular ROS and apoptosis induced by OBP-801 and LY294002.	Acetylcysteine	111-130	odorant binding protein 2A	Homo sapiens	192-195
18630824-7	2008	NAC is indicated if the serum acetaminophen level drawn 4 hours after ingestion and plotted on the nomograme falls above the "200 mg/L-4 hours" line.	Acetylcysteine	0-3	ribosomal protein L4	Homo sapiens	133-136
18219322-6	2008	TNF-induced SENP1 nuclear translocation is specifically blocked by antioxidants such as N-acetyl-cysteine, suggesting that TNF-induced translocation of SENP1 is ROS dependent.	Acetylcysteine	88-105	SUMO1/sentrin specific peptidase 1	Mus musculus	12-17
18219322-6	2008	TNF-induced SENP1 nuclear translocation is specifically blocked by antioxidants such as N-acetyl-cysteine, suggesting that TNF-induced translocation of SENP1 is ROS dependent.	Acetylcysteine	88-105	SUMO1/sentrin specific peptidase 1	Mus musculus	152-157
23695982-9	2013	Pretreatment with a thiol-containing reactive oxygen species (ROS) scavenger N-acetyl cysteine, but not other ROS inhibitors without thiol groups, suppressed CuB-induced actin aggregation, cofilin hyperactivation and cofilin-actin rod formation, suggesting that thiol oxidation might be involved in these processes.	Acetylcysteine	77-94	cofilin 1	Homo sapiens	189-196
17979115-8	2008	These results suggest that NAC might exert its osteogenic activity via increased glutathione synthesis and inhibition of RhoA activation.	Acetylcysteine	27-30	ras homolog family member A	Mus musculus	121-125
17980396-9	2008	Pretreatment with cell-permeable catalase, N-acetyl-L-cysteine or GSH-monoethyl ester markedly reduced expression of NQO-1 and GCLC under HOCl challenge conditions, suggesting intracellular ROS-scavenging capacity affects HOCl-induced Nrf2 activation.	Acetylcysteine	43-62	glutamate-cysteine ligase catalytic subunit	Homo sapiens	127-131
18032526-8	2008	AGE-induced phosphorylation of FKHRL1 led to a 70% downregulation of MnSOD, an effect partially blocked by a phosphatidylinositol 3-kinase inhibitor (LY-294002) and strongly inhibited by an antioxidant (N-acetylcysteine).	Acetylcysteine	203-219	superoxide dismutase 2	Homo sapiens	69-74
17913704-5	2007	Treatment with either neutralizing anti-TNFR1 antibodies or the glutathione precursor, N-acetylcysteine (NAC), favored the emergence of TNFR2 signaling that mediated a positive effect of TNFalpha on [Ca(2+)] transient and cell fractional shortening.	Acetylcysteine	87-103	TNF receptor superfamily member 1B	Rattus norvegicus	136-141
17913704-5	2007	Treatment with either neutralizing anti-TNFR1 antibodies or the glutathione precursor, N-acetylcysteine (NAC), favored the emergence of TNFR2 signaling that mediated a positive effect of TNFalpha on [Ca(2+)] transient and cell fractional shortening.	Acetylcysteine	105-108	TNF receptor superfamily member 1B	Rattus norvegicus	136-141
17913704-10	2007	In vivo NAC treatment proved to be a unique tool to selectively neutralize TNFR1-mediated effects of TNFalpha while releasing TNFR2 pathways.	Acetylcysteine	8-11	TNF receptor superfamily member 1B	Rattus norvegicus	126-131
23695982-9	2013	Pretreatment with a thiol-containing reactive oxygen species (ROS) scavenger N-acetyl cysteine, but not other ROS inhibitors without thiol groups, suppressed CuB-induced actin aggregation, cofilin hyperactivation and cofilin-actin rod formation, suggesting that thiol oxidation might be involved in these processes.	Acetylcysteine	77-94	cofilin 1	Homo sapiens	217-224
23398207-6	2013	Furthermore, (-)- gossypol treatment increased the translocation of high mobility group box 1 (HMGB1) from nuclei to cytoplasm, which can be suppressed by NAC pretreatment.	Acetylcysteine	155-158	high mobility group box 1	Homo sapiens	68-93
17727829-6	2007	N-Acetyl-l-cysteine (NAC) pretreatment resulted in the increase in glutathione concentration, reduction of intracellular ROS, complete inhibition of DNA fragmentation, mitochondrial membrane potential (MMP) collapse, Fas externalization and caspase-8 activation.	Acetylcysteine	0-19	caspase 8	Homo sapiens	241-250
17936186-6	2007	NAC inhibits HEMA-mediated toxicity through induction of differentiation in DPSCs, because the genes for dentin sialoprotein, osteopontin (OPN), osteocalcin, and alkaline phosphatase, which are induced during differentiation, are also induced by NAC.	Acetylcysteine	0-3	dentin sialophosphoprotein	Homo sapiens	105-124
23398207-6	2013	Furthermore, (-)- gossypol treatment increased the translocation of high mobility group box 1 (HMGB1) from nuclei to cytoplasm, which can be suppressed by NAC pretreatment.	Acetylcysteine	155-158	high mobility group box 1	Homo sapiens	95-100
17635921-5	2007	Nicotine-induced AMPK phosphorylation appeared to be mediated by reactive oxygen species based on the finding that nicotine significantly increased superoxide anions and 3-nitrotyrosine-positive proteins, exogenous peroxynitrite (ONOO(-)) mimicked the effects of nicotine on AMPK, and N-acetylcysteine (NAC) abolished nicotine-enhanced AMPK phosphorylation.	Acetylcysteine	285-301	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	17-21
23943180-3	2013	acetylcysteine is most often used as an antidote for acetaminophen overdose due to its ability to increase levels of glutathione; however, it is also used to treat NAI-ALF and severe alcoholic hepatitis and to prevent CIN.	Acetylcysteine	0-14	afamin	Homo sapiens	168-171
17635921-5	2007	Nicotine-induced AMPK phosphorylation appeared to be mediated by reactive oxygen species based on the finding that nicotine significantly increased superoxide anions and 3-nitrotyrosine-positive proteins, exogenous peroxynitrite (ONOO(-)) mimicked the effects of nicotine on AMPK, and N-acetylcysteine (NAC) abolished nicotine-enhanced AMPK phosphorylation.	Acetylcysteine	303-306	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	17-21
23851285-3	2013	The antioxidant, N-acetylcysteine (NAC), abolished PTTH-induced increase in fluorescence.	Acetylcysteine	17-33	prothoracicotropic hormone	Bombyx mori	51-55
17340120-9	2007	The addition of NAC impeded the oxidative effects of SA exposure, decreasing the production of thiobarbituric acid-reactive substances and significantly diminishing the up regulation of CK18 mRNA and protein.	Acetylcysteine	16-19	keratin 18	Mus musculus	186-190
23851285-3	2013	The antioxidant, N-acetylcysteine (NAC), abolished PTTH-induced increase in fluorescence.	Acetylcysteine	35-38	prothoracicotropic hormone	Bombyx mori	51-55
17458516-7	2007	Remarkably, N-acetyl-L-cysteine caused a 3-fold increase in sICAM-1 by p42/44 MAPK-, p38 MAPK- and PKC-independent mechanisms.	Acetylcysteine	12-31	mitogen activated protein kinase 14	Rattus norvegicus	85-88
23851285-7	2013	In addition, PTTH-stimulated ecdysteroidogenesis was greatly inhibited by treatment with either NAC or mitochondrial inhibitors (rotenone, antimycin A, FCCP, and DPI), but not with apocynin.	Acetylcysteine	96-99	prothoracicotropic hormone	Bombyx mori	13-17
24037197-7	2013	NAC treatment of ECwt-infected mice reduced Hsc70 and PDI expression to levels similar to those observed in villi from uninfected control mice.	Acetylcysteine	0-3	heat shock protein 8	Mus musculus	44-49
17594730-11	2007	Mucolytics that depolymerize mucin, such as N-acetylcysteine, have no proven benefit and carry a risk of epithelial damage when administered via aerosol.	Acetylcysteine	44-60	LOC100508689	Homo sapiens	29-34
17631703-1	2007	OBJECTIVE: To investigate the changes in Toll-like receptor 2/4(TLR2/4) gene expression in liver and lung in ischemia/reperfusion (I/R) injury with or without preconditioning of N-acetyl-L-cysteine (NAC).	Acetylcysteine	199-202	toll-like receptor 2	Mus musculus	41-63
17631703-1	2007	OBJECTIVE: To investigate the changes in Toll-like receptor 2/4(TLR2/4) gene expression in liver and lung in ischemia/reperfusion (I/R) injury with or without preconditioning of N-acetyl-L-cysteine (NAC).	Acetylcysteine	199-202	toll-like receptor 2	Mus musculus	64-70
17631703-4	2007	RESULTS: Compared with I/R group, the expressions of TLR2/4 mRNA and protein in liver and lung in NAC group were decreased at same time points (P&lt;0.05 or P&lt;0.01).	Acetylcysteine	98-101	toll-like receptor 2	Mus musculus	53-59
17631703-7	2007	NAC can inhibit the activation of TLR2/4 and the induction of TNF-alpha resulted from I/R injury via modulating the state of redox process; thus it might mitigate liver and lung injury following partial hepatic I/R in mice.	Acetylcysteine	0-3	toll-like receptor 2	Mus musculus	34-40
17171638-7	2007	Curcumin increased the expression of the phosphorylated forms of PTK, PDK1, and PKC-delta, which was attenuated by either GSH or NAC and potentiated by BSO.	Acetylcysteine	129-132	protein kinase C delta	Homo sapiens	80-89
17593873-5	2007	The anti-oxidant N-acetylcysteine significantly blocked H2O2-induced PEDF overexpression in OUMS-29 cells.	Acetylcysteine	17-33	serpin family F member 1	Homo sapiens	69-73
17308307-5	2007	Blockade of reactive oxygen species production by antioxidant N-acetylcysteine or superoxide scavenger Tiron inhibits GzmK-induced cell death.	Acetylcysteine	62-78	granzyme K	Homo sapiens	118-122
17122189-8	2007	Subsequently, the levels of cardiac free 15-F(2t)-isoprostane, HO-1, Cu-Zn-SOD, total SOD, IL-6, and COX-2 in diabetic rats were decreased by NAC.	Acetylcysteine	142-145	prostaglandin-endoperoxide synthase 2	Rattus norvegicus	101-106
17349922-4	2007	Another antioxidant N-acetylcysteine (NAC) displayed a similar suppressive effect on the entry of phospho-LAT into raft microdomains.	Acetylcysteine	20-36	linker for activation of T cells	Homo sapiens	106-109
17349922-4	2007	Another antioxidant N-acetylcysteine (NAC) displayed a similar suppressive effect on the entry of phospho-LAT into raft microdomains.	Acetylcysteine	38-41	linker for activation of T cells	Homo sapiens	106-109
17164225-8	2007	The antioxidant N-acetyl-L-cysteine and a specific inhibitor of p38 mitogen-activated protein kinase, but not of extracellular signal-regulated kinase 1/2 or c-Jun N-terminal kinase/stress-activated kinases, completely abolished the LOX-induced growth inhibition, indicating a critical role of ROS and p38.	Acetylcysteine	16-35	mitogen-activated protein kinase 14	Mus musculus	64-67
17164225-8	2007	The antioxidant N-acetyl-L-cysteine and a specific inhibitor of p38 mitogen-activated protein kinase, but not of extracellular signal-regulated kinase 1/2 or c-Jun N-terminal kinase/stress-activated kinases, completely abolished the LOX-induced growth inhibition, indicating a critical role of ROS and p38.	Acetylcysteine	16-35	mitogen-activated protein kinase 14	Mus musculus	302-305
17126295-6	2007	On the other hand, the CS-induced phosphorylation of MAPK was enhanced by buthionine sulfoximine (BSO), an activator of protein tyrosine phosphatases (PTPs), but inhibited by N-acetyl-l-cysteine (NAC), an inhibitor of receptor tyrosine kinase.	Acetylcysteine	175-194	mitogen activated protein kinase 3	Rattus norvegicus	53-57
17126295-6	2007	On the other hand, the CS-induced phosphorylation of MAPK was enhanced by buthionine sulfoximine (BSO), an activator of protein tyrosine phosphatases (PTPs), but inhibited by N-acetyl-l-cysteine (NAC), an inhibitor of receptor tyrosine kinase.	Acetylcysteine	196-199	mitogen activated protein kinase 3	Rattus norvegicus	53-57
17034987-4	2007	Moreover, we found increased activation of Caspase 3 in cells from embryos previously exposed to a diabetes-like environment (in vivo, in vitro) compared to cells from control embryos, which was normalized by supplementation of N-acetylcysteine or apoptosis inhibitor.	Acetylcysteine	228-244	caspase 3	Rattus norvegicus	43-52
17023264-9	2006	Supporting this notion, cotreatment with NAC inhibited the TNF-alpha-induced rise in MSK1 and MSK2 kinase activity, while siRNA knock-down experiments showed that MSK2 is the predominant isoform involved in TNF-alpha-induced ET-1 upregulation.	Acetylcysteine	41-44	ribosomal protein S6 kinase A5	Homo sapiens	85-89
17103249-3	2006	In our model of TAA-treated rats the use of the anti-inflammatory drug-indomethacin, and the redox-regulating drug-N-acetylcysteine (NAC), significantly attenuated TAA-induced HSP25 expression and evoked morphological changes of recruited ED1+ macrophages.	Acetylcysteine	115-131	heat shock protein family B (small) member 1	Rattus norvegicus	176-181
16750528-0	2006	A novel antioxidant N-acetylcysteine amide prevents gp120- and Tat-induced oxidative stress in brain endothelial cells.	Acetylcysteine	20-36	tyrosine aminotransferase	Homo sapiens	63-66
16914459-10	2006	Urine NAG/creatinine ratio increased over 30% in 100% of patients in the NAC group vs 92.3% in the placebo group (P=0.081).	Acetylcysteine	73-76	O-GlcNAcase	Homo sapiens	6-9
16914459-12	2006	Serum cystatin C exceeded 1.4 mg litre(-1) in 78.9% in NAC group vs 61.5% in placebo group (P=0.096).	Acetylcysteine	55-58	cystatin C	Homo sapiens	6-16
16896059-9	2006	Pretreatment with 20mM N-acetylcysteine prevented mitochondrial dysfunction, the nuclear translocation of endonuclease G and AIF, and the nuclear DNA fragmentation.	Acetylcysteine	23-39	endonuclease G	Mus musculus	106-120
16697971-7	2006	Loss of DeltaPsi(m), PS externalization and ROS generation were significantly more pronounced in HGF cells than in HSG cells at curcumin concentrations lower than about 15microM, and were inhibited by the addition of the antioxidants N-acetyl-l-cysteine and glutathione.	Acetylcysteine	234-253	hepatocyte growth factor	Homo sapiens	97-100
17034719-1	2006	OBJECTIVE: To explore the effect of N-acetyl L-cysteine (NAC) on expressions of matrix metalloproteinases-2, 9 (MMP-2, MMP-9) in lung fibroblasts of SiO(2) exposed rats.	Acetylcysteine	36-55	matrix metallopeptidase 2	Rattus norvegicus	80-110
17034719-1	2006	OBJECTIVE: To explore the effect of N-acetyl L-cysteine (NAC) on expressions of matrix metalloproteinases-2, 9 (MMP-2, MMP-9) in lung fibroblasts of SiO(2) exposed rats.	Acetylcysteine	36-55	matrix metallopeptidase 2	Rattus norvegicus	112-117
17034719-1	2006	OBJECTIVE: To explore the effect of N-acetyl L-cysteine (NAC) on expressions of matrix metalloproteinases-2, 9 (MMP-2, MMP-9) in lung fibroblasts of SiO(2) exposed rats.	Acetylcysteine	57-60	matrix metallopeptidase 2	Rattus norvegicus	80-110
17034719-1	2006	OBJECTIVE: To explore the effect of N-acetyl L-cysteine (NAC) on expressions of matrix metalloproteinases-2, 9 (MMP-2, MMP-9) in lung fibroblasts of SiO(2) exposed rats.	Acetylcysteine	57-60	matrix metallopeptidase 2	Rattus norvegicus	112-117
17034719-11	2006	CONCLUSION: NAC inhibits the expressions of MMP-2, MMP-9 in lung fibroblasts.	Acetylcysteine	12-15	matrix metallopeptidase 2	Rattus norvegicus	44-49
16760673-0	2006	Activation of ATM and histone H2AX phosphorylation induced by mitoxantrone but not by topotecan is prevented by the antioxidant N-acetyl-L-cysteine.	Acetylcysteine	128-147	H2A.X variant histone	Homo sapiens	22-34
16760673-6	2006	The induction of both ATM activation and H2AX phosphorylation by MXT was prevented to a large extent by N-acetyl-L-cysteine (NAC), a scavenger of reactive oxygen species (ROS).	Acetylcysteine	104-123	H2A.X variant histone	Homo sapiens	41-45
23719546-8	2013	NAC also blunted the increase in phosphorylation of protein kinase B, mammalian target of rapamycin, p70 ribosomal S6 kinase, ribosomal protein S6, and mitogen activated protein kinase p38 at 2 and 8 d after exercise.	Acetylcysteine	0-3	ribosomal protein S6	Homo sapiens	126-146
16872365-3	2006	This constitutive H2AX phosphorylation is markedly reduced by exposure of cells to the reactive oxygen species scavenger N-acetyl-L-cysteine.	Acetylcysteine	121-140	H2A.X variant histone	Homo sapiens	18-22
16872365-9	2006	Also, the degree of attenuation of constitutive H2AX phosphorylation by N-acetyl-L-cysteine was less pronounced in NH32, WTK1, and HL-60, compared to TK6 cells.	Acetylcysteine	72-91	H2A.X variant histone	Homo sapiens	48-52
23395854-4	2013	The antioxidant N-acetylcysteine completely inhibited the increase in HSPA1A and DNAJB1 mRNA levels upon methionine starvation, indicating that this increase is a response to oxidative stress resulting from a lack of methionine.	Acetylcysteine	16-32	DnaJ heat shock protein family (Hsp40) member B1	Homo sapiens	81-87
23325162-6	2013	Those patients with early coma grade who were treated with NAC showed significant improvement in bilirubin and ALT levels when compared to the other three groups (maximum p &lt; 0.02 for NAC 1-2 vs. the 3 other treatments) when predicting death or transplantation.	Acetylcysteine	59-62	nucleus accumbens associated 1	Homo sapiens	187-192
23607780-4	2013	Therefore, we investigated whether NAC may attenuate CPB-induced lung injury by inhibiting TGFbeta1 expression.	Acetylcysteine	35-38	transforming growth factor beta-1 proprotein	Canis lupus familiaris	91-99
16785024-5	2006	BAFF expression was inhibited by treatment with various antioxidants including N-acetyl-L-cysteine (NAC).	Acetylcysteine	79-98	tumor necrosis factor (ligand) superfamily, member 13b	Mus musculus	0-4
16785024-5	2006	BAFF expression was inhibited by treatment with various antioxidants including N-acetyl-L-cysteine (NAC).	Acetylcysteine	100-103	tumor necrosis factor (ligand) superfamily, member 13b	Mus musculus	0-4
23607780-14	2013	Treatment with NAC significantly suppressed the TGFbeta1 expression in the lung tissues at both mRNA and protein levels.	Acetylcysteine	15-18	transforming growth factor beta-1 proprotein	Canis lupus familiaris	48-56
23607780-15	2013	CONCLUSION: Our results suggest that NAC is a potent agent against CPB-induced acute lung injury through inhibiting TGFbeta1 expression.	Acetylcysteine	37-40	transforming growth factor beta-1 proprotein	Canis lupus familiaris	116-124
16753063-4	2006	In previous studies, it has been demonstrated that administration of PA in combination with the free sulfhydryl donor (FSD) agents captopril or N-acetyl cysteine, resulted in angiostatin generation, and anti-angiogenic and anti-tumour activity in murine models.	Acetylcysteine	144-161	plasminogen	Mus musculus	175-186
23449454-6	2013	Statin-induced cytotoxic effects, DNA fragmentation and changes of activation of caspase-3, Akt, Erk and p38 were blocked by antioxidant (N-acetylcysteine) and metabolic products of the HMG-CoA reductase reaction, such as mevalonate, farnesyl pyrophosphate (FPP) and geranylgeranyl pyrophosphate (GGPP).	Acetylcysteine	138-154	mitogen-activated protein kinase 14	Mus musculus	105-108
22729780-6	2013	N-acetyl-L-cysteine prevented mahanine-induced ROS accumulation, aggregation of Hsp90, degradation of client proteins and cell death.	Acetylcysteine	0-19	heat shock protein 86, pseudogene 1	Mus musculus	80-85
16796172-0	2006	[Acetylcysteine in the treatment of severe COPD].	Acetylcysteine	1-15	COPD	Homo sapiens	43-47
16796172-4	2006	In placebo-controlled studies, maintenance therapy with acetylcysteine in patients with chronic bronchitis (usually also COPD) reduced the viscosity of the sputum, the severity of coughing, the number of bacteria in the airways, the number and severity of influenza-like episodes, the number of exacerbations and the number of readmissions.	Acetylcysteine	56-70	COPD	Homo sapiens	121-125
16556443-10	2006	Correspondingly, oral administration with either N-acetylcysteine or ascorbic acid significantly attenuated LPS-induced downregulation of intestinal pregnane X receptor and retinoid X receptor alphalpha.	Acetylcysteine	49-65	retinoid X receptor alpha	Mus musculus	173-202
23111281-7	2013	Systemic administration of the antioxidant N-acetyl cysteine to DRlyp/lyp rats altered abundances of peripheral eosinophils, reduced severity of insulitis, and significantly delayed but did not prevent diabetes onset.	Acetylcysteine	43-60	Insulin dependent diabetes mellitus QTL 2	Rattus norvegicus	66-69
16249273-8	2006	NAC and DPI also inhibited phosphorylation of 4E-BP1 on Thr46 and association of eIF4E with eIF4G, steps that are important in the initiation phase of mRNA translation.	Acetylcysteine	0-3	eukaryotic translation initiation factor 4E	Homo sapiens	81-86
23293188-5	2013	In conclusion, the data suggest marginal benefit of IV acetylcysteine in NAI-ALF with coma grades I-II; however, the routine use of acetylcysteine cannot be recommended.	Acetylcysteine	55-69	afamin	Homo sapiens	77-80
16628006-3	2006	We recently reported that this constitutive H2AX phosphorylation (CHP) is markedly reduced by the antioxidant N-acetyl-L-cysteine (NAC), and postulated that it reflects the oxidative DNA damage ("endogenous DSBs") induced by reactive oxygen species (ROS) generated by metabolic activity during progression through the cell cycle.	Acetylcysteine	110-129	H2A.X variant histone	Homo sapiens	44-48
23222262-7	2013	Removal of intracellular reactive oxygen species by N-acetyl-cysteine reduced the activation of AMP-activated protein kinase, extracellular signal-regulated kinase and Jun N-terminal kinase, and interleukin-8 induction.	Acetylcysteine	52-69	chemokine (C-X-C motif) ligand 15	Mus musculus	195-208
16411658-7	2006	P4501B1 induction was blocked in AKR1A1 transfectants by the AKR1A1 inhibitor (sulfonylnitromethane), the o-quinone scavenger (N-acetyl-l-cysteine), or the cytosolic AhR antagonist (diflubenzuron).	Acetylcysteine	127-146	cytochrome P450 family 1 subfamily B member 1	Homo sapiens	0-7
24475426-2	2013	OBJECTIVES: The aim of this study was to investigate the effect of N-acetyl cysteine (NAC) on the serum levels of Lp(a) and amount of proteinuria in a group of type 2 diabetic patients with diabetic nephropathy.	Acetylcysteine	67-84	lipoprotein(a)	Homo sapiens	114-119
16430375-0	2006	Early, transient increase in complexin I and complexin II in the cerebral cortex following traumatic brain injury is attenuated by N-acetylcysteine.	Acetylcysteine	131-147	complexin 2	Rattus norvegicus	45-57
16154687-5	2005	The antioxidant N-acetylcysteine (NAC) could inhibit the translocation of MLK3 from cytosolic fraction to the membrane fraction and decrease the interactions of MLK3 and PSD-95 in the membrane fraction.	Acetylcysteine	16-32	discs large MAGUK scaffold protein 4	Rattus norvegicus	170-176
16154687-5	2005	The antioxidant N-acetylcysteine (NAC) could inhibit the translocation of MLK3 from cytosolic fraction to the membrane fraction and decrease the interactions of MLK3 and PSD-95 in the membrane fraction.	Acetylcysteine	34-37	discs large MAGUK scaffold protein 4	Rattus norvegicus	170-176
16242670-8	2005	Medium change produced a marked decline in oxidized glutathione and malondialdehyde levels, and the antioxidant N-acetyl-L-cysteine decreased basal ERK1/2 phosphorylation, suggesting a role for oxidative stress in maintaining basal ERK1/2 phosphorylation in cultured hepatocytes.	Acetylcysteine	112-131	mitogen activated protein kinase 3	Rattus norvegicus	148-154
16242670-8	2005	Medium change produced a marked decline in oxidized glutathione and malondialdehyde levels, and the antioxidant N-acetyl-L-cysteine decreased basal ERK1/2 phosphorylation, suggesting a role for oxidative stress in maintaining basal ERK1/2 phosphorylation in cultured hepatocytes.	Acetylcysteine	112-131	mitogen activated protein kinase 3	Rattus norvegicus	232-238
16269967-8	2005	Treatment of VSMC with antioxidants such as N-acetyl-L-cysteine (NAC) or diphenyleneiodonium (DPI) for 24 h decreased the enhanced expression of Gialpha-2 and Gialpha-3 proteins in a concentration-dependent manner in VSMC from SHR.	Acetylcysteine	44-63	G protein subunit alpha i3	Rattus norvegicus	159-168
16269967-8	2005	Treatment of VSMC with antioxidants such as N-acetyl-L-cysteine (NAC) or diphenyleneiodonium (DPI) for 24 h decreased the enhanced expression of Gialpha-2 and Gialpha-3 proteins in a concentration-dependent manner in VSMC from SHR.	Acetylcysteine	65-68	G protein subunit alpha i3	Rattus norvegicus	159-168
16269967-12	2005	In addition, the enhanced activity of extracellular signal-regulated kinase 1/2 in SHR as compared with WKY rats, as demonstrated by enhanced phosphorylation of extracellular signal-regulated kinase 1/2, was also restored to WKY rat levels by NAC or DPI.	Acetylcysteine	243-246	mitogen activated protein kinase 3	Rattus norvegicus	38-79
16280646-4	2005	The suppression of oxidative stress by a potent antioxidant, N-acetyl-l-cysteine or probucol, led to the recovery of insulin biosynthesis and PDX-1 expression in nuclei and improved glucose tolerance in animal models for type 2 diabetes.	Acetylcysteine	61-80	pancreatic and duodenal homeobox 1	Homo sapiens	142-147
16143311-3	2005	During genipin-induced apoptosis, reactive oxygen species (ROS) level was elevated, and N-acetyl-l-cysteine (NAC) and glutathione (GSH) suppressed activation of caspase-3, -7 and -9.	Acetylcysteine	88-107	caspase 3	Rattus norvegicus	161-181
16143311-3	2005	During genipin-induced apoptosis, reactive oxygen species (ROS) level was elevated, and N-acetyl-l-cysteine (NAC) and glutathione (GSH) suppressed activation of caspase-3, -7 and -9.	Acetylcysteine	109-112	caspase 3	Rattus norvegicus	161-181
15829913-9	2005	In addition, administration of N-acetylcysteine (NAC), a precursor of glutathione and a potent antioxidant, attenuated both Tat-induced ERK 1/2 activation and alterations in ZO-1 expression.	Acetylcysteine	31-47	tyrosine aminotransferase	Homo sapiens	124-127
16109311-4	2005	Interestingly, both IL-1beta and TNF-alpha markedly inhibited the expression of MOG, CNPase, and PLP but not MBP, the effect that was blocked by antioxidants such as N-acetylcysteine (NAC) and pyrrolidine dithiocarbamate (PDTC).	Acetylcysteine	166-182	myelin oligodendrocyte glycoprotein	Homo sapiens	80-83
16109311-4	2005	Interestingly, both IL-1beta and TNF-alpha markedly inhibited the expression of MOG, CNPase, and PLP but not MBP, the effect that was blocked by antioxidants such as N-acetylcysteine (NAC) and pyrrolidine dithiocarbamate (PDTC).	Acetylcysteine	184-187	myelin oligodendrocyte glycoprotein	Homo sapiens	80-83
16166335-1	2005	We previously showed that dietary treatment with the N-acetylcysteine conjugate of phenethyl isothiocyanate (PEITC-NAC) inhibited benzo(a)pyrene-induced lung tumorigenesis in A/J mice, and that tumor inhibition was associated with induction of activator protein-1 (AP-1) activity and stimulation of apoptosis in the lungs of mice.	Acetylcysteine	53-69	jun proto-oncogene	Mus musculus	244-263
16166335-1	2005	We previously showed that dietary treatment with the N-acetylcysteine conjugate of phenethyl isothiocyanate (PEITC-NAC) inhibited benzo(a)pyrene-induced lung tumorigenesis in A/J mice, and that tumor inhibition was associated with induction of activator protein-1 (AP-1) activity and stimulation of apoptosis in the lungs of mice.	Acetylcysteine	53-69	jun proto-oncogene	Mus musculus	265-269
16043662-12	2005	Furthermore, the antioxidants MnTMPyP and N-acetylcysteine inhibited the aldosterone-induced increase in ERK1/2 phosphorylation and MMP activities, respectively.	Acetylcysteine	42-58	mitogen activated protein kinase 3	Rattus norvegicus	105-111
15769933-7	2005	N-acetylcysteine (NAC), an antioxidant, and MnTBAP, an inhibitor of superoxide, reduce high NaCl-induced superoxide activity and suppress both high NaCl-induced increase in TonEBP/OREBP transcriptional activity and high NaCl-induced increase in expression of BGT1mRNA, a transcriptional target of TonEBP/OREBP.	Acetylcysteine	0-16	nuclear factor of activated T cells 5	Homo sapiens	173-179
15769933-7	2005	N-acetylcysteine (NAC), an antioxidant, and MnTBAP, an inhibitor of superoxide, reduce high NaCl-induced superoxide activity and suppress both high NaCl-induced increase in TonEBP/OREBP transcriptional activity and high NaCl-induced increase in expression of BGT1mRNA, a transcriptional target of TonEBP/OREBP.	Acetylcysteine	0-16	nuclear factor of activated T cells 5	Homo sapiens	180-185
15769933-7	2005	N-acetylcysteine (NAC), an antioxidant, and MnTBAP, an inhibitor of superoxide, reduce high NaCl-induced superoxide activity and suppress both high NaCl-induced increase in TonEBP/OREBP transcriptional activity and high NaCl-induced increase in expression of BGT1mRNA, a transcriptional target of TonEBP/OREBP.	Acetylcysteine	0-16	solute carrier family 6 member 12	Homo sapiens	259-263
15769933-7	2005	N-acetylcysteine (NAC), an antioxidant, and MnTBAP, an inhibitor of superoxide, reduce high NaCl-induced superoxide activity and suppress both high NaCl-induced increase in TonEBP/OREBP transcriptional activity and high NaCl-induced increase in expression of BGT1mRNA, a transcriptional target of TonEBP/OREBP.	Acetylcysteine	0-16	nuclear factor of activated T cells 5	Homo sapiens	297-303
15769933-7	2005	N-acetylcysteine (NAC), an antioxidant, and MnTBAP, an inhibitor of superoxide, reduce high NaCl-induced superoxide activity and suppress both high NaCl-induced increase in TonEBP/OREBP transcriptional activity and high NaCl-induced increase in expression of BGT1mRNA, a transcriptional target of TonEBP/OREBP.	Acetylcysteine	0-16	nuclear factor of activated T cells 5	Homo sapiens	304-309
15769933-7	2005	N-acetylcysteine (NAC), an antioxidant, and MnTBAP, an inhibitor of superoxide, reduce high NaCl-induced superoxide activity and suppress both high NaCl-induced increase in TonEBP/OREBP transcriptional activity and high NaCl-induced increase in expression of BGT1mRNA, a transcriptional target of TonEBP/OREBP.	Acetylcysteine	18-21	nuclear factor of activated T cells 5	Homo sapiens	173-179
15869837-12	2005	Furthermore, LPS-induced downregulation of PXR, cyp3a11 and mdr1a mRNA in mouse placenta was prevented by N-acetylcysteine (NAC).	Acetylcysteine	106-122	ATP-binding cassette, sub-family B (MDR/TAP), member 1A	Mus musculus	60-65
15869837-12	2005	Furthermore, LPS-induced downregulation of PXR, cyp3a11 and mdr1a mRNA in mouse placenta was prevented by N-acetylcysteine (NAC).	Acetylcysteine	124-127	ATP-binding cassette, sub-family B (MDR/TAP), member 1A	Mus musculus	60-65
15917250-8	2005	Only Yes and JNK activation were sensitive to N-acetylcysteine, inhibitors of NADPH oxidase, PKCzeta, or sphingomyelinase, indicating that the CD95L-induced ROS response is upstream of Yes and JNK but not of Fyn and c-Src activation.	Acetylcysteine	46-62	Fas ligand	Rattus norvegicus	143-148
15761843-7	2005	NAC treatment reduced pancreatic glutathione depletion during the early stages of AP and attenuated the activation of p38-MAPK and NF-kappaB for 48 h following BPDO.	Acetylcysteine	0-3	mitogen activated protein kinase 14	Rattus norvegicus	118-121
15739117-10	2005	On the other hand, the antioxidant N-acetyl-L-cysteine inhibited the stimulation of haeme-oxygenase 1 and c-Myc expression by 30 mmol/l glucose and/or hydrogen peroxide.	Acetylcysteine	35-54	MYC proto-oncogene, bHLH transcription factor	Rattus norvegicus	106-111
15737199-4	2005	Treatment with the antioxidant, N-acetyl-L-cysteine, which suppressed the reduction of the GSH/GSSG ratio, abrogated both the phosphorylation of p38 MAPK and the augmentation of CD86 expression.	Acetylcysteine	32-51	CD86 molecule	Homo sapiens	178-182
15683462-10	2005	Results showed that N-acetylcysteine and glutathion can protect astrocytes against ROS accumulation and caspase-3 activation, whereas 0.1 mM melatonin can inhibit H2O2-induced apoptosis by regulating Bax expression and by inhibiting caspase-3 activation.	Acetylcysteine	20-36	caspase 3	Rattus norvegicus	104-113
15585325-5	2005	In addition, the effect of IL-18 was blocked by the antioxidant, N-acetyl-L-cysteine (NAC), indicating that IL-18 regulates ROI production, which is involved in SCF production.	Acetylcysteine	65-84	interleukin 18	Mus musculus	27-32
15585325-5	2005	In addition, the effect of IL-18 was blocked by the antioxidant, N-acetyl-L-cysteine (NAC), indicating that IL-18 regulates ROI production, which is involved in SCF production.	Acetylcysteine	65-84	interleukin 18	Mus musculus	108-113
15585325-5	2005	In addition, the effect of IL-18 was blocked by the antioxidant, N-acetyl-L-cysteine (NAC), indicating that IL-18 regulates ROI production, which is involved in SCF production.	Acetylcysteine	86-89	interleukin 18	Mus musculus	27-32
15585325-5	2005	In addition, the effect of IL-18 was blocked by the antioxidant, N-acetyl-L-cysteine (NAC), indicating that IL-18 regulates ROI production, which is involved in SCF production.	Acetylcysteine	86-89	interleukin 18	Mus musculus	108-113
15849723-12	2005	N-acetyl-L-cysteine at 50 microM concentration inhibited arsenite-induced NF-kappa B and AP-1.	Acetylcysteine	0-19	jun proto-oncogene	Mus musculus	89-93
15670485-12	2005	At day 0 and day 45 of treatment, the effective PTa increase rate was 72% in the NAC group and 54% in the placebo group.	Acetylcysteine	81-84	pre T cell antigen receptor alpha	Homo sapiens	48-51
15670485-13	2005	The total effective rate (TBil + PTa) was 90% in the NAC group and 69% in the placebo group.	Acetylcysteine	53-56	pre T cell antigen receptor alpha	Homo sapiens	33-36
15670485-16	2005	CONCLUSION: NAC can decrease the level of serum TBil, increase the PTa and reduce the time of hospitalization.	Acetylcysteine	12-15	pre T cell antigen receptor alpha	Homo sapiens	67-70
15489221-10	2004	In contrast, preincubation of cells with the hydroxyl radical scavenger, N-acetylcysteine, significantly attenuated the doxorubicin-mediated phosphorylation and accumulation of p53, p53-DNA binding, and the phosphorylation of H2AX, Nbs1, SMC1, Chk1, and Chk2, suggesting that hydroxyl radicals contribute to the doxorubicin-induced activation of ATM-dependent pathways.	Acetylcysteine	73-89	H2A.X variant histone	Homo sapiens	226-230
16543607-6	2006	H(2)O(2) mimicked the synergistic effects of CSE, while antioxidant N-acetyl-L-cysteine prevented synergistic induction of MUC5AC mucin by CSE.	Acetylcysteine	68-87	LOC100508689	Homo sapiens	130-135
16820894-5	2006	Furthermore, constitutive H2AX phosphorylation in human pulmonary carcinoma A549, lymphoblastoid TK6, and in normal bronchial epithelial cells was reduced following cell exposure to N-acetyl-L-cysteine, a scavenger of reactive oxygen intermediates; the reduction was most pronounced for G(2)M cells.	Acetylcysteine	182-201	H2A.X variant histone	Homo sapiens	26-30
16796172-5	2006	In studies among COPD-patients, acetylcysteine had no effect on the downward trend of the FEV1 but did improve the functional residual capacity; itaffected the number of exacerbations only in those patients who were not on inhaled corticosteroids.	Acetylcysteine	32-46	COPD	Homo sapiens	17-21
15489221-10	2004	In contrast, preincubation of cells with the hydroxyl radical scavenger, N-acetylcysteine, significantly attenuated the doxorubicin-mediated phosphorylation and accumulation of p53, p53-DNA binding, and the phosphorylation of H2AX, Nbs1, SMC1, Chk1, and Chk2, suggesting that hydroxyl radicals contribute to the doxorubicin-induced activation of ATM-dependent pathways.	Acetylcysteine	73-89	checkpoint kinase 2	Homo sapiens	254-258
15813983-10	2004	In the presence of the antioxidants glutathione and N-acetyl-L-cysteine, the PD- and HPD-induced release of ROS, TNF-alpha, and MIP-2 was significantly reduced.	Acetylcysteine	52-71	C-X-C motif chemokine ligand 2	Rattus norvegicus	128-133
24475426-2	2013	OBJECTIVES: The aim of this study was to investigate the effect of N-acetyl cysteine (NAC) on the serum levels of Lp(a) and amount of proteinuria in a group of type 2 diabetic patients with diabetic nephropathy.	Acetylcysteine	86-89	lipoprotein(a)	Homo sapiens	114-119
24112955-4	2013	RESULTS: NAC treatment inhibited fat accumulation and reduced the expression of obesity-related proteins, including monoamine oxidase A, heat shock protein 70 (HSP70), aminoacylase -1 (ACY-1), and transketolase.	Acetylcysteine	9-12	aminoacylase 1	Homo sapiens	168-183
24112955-4	2013	RESULTS: NAC treatment inhibited fat accumulation and reduced the expression of obesity-related proteins, including monoamine oxidase A, heat shock protein 70 (HSP70), aminoacylase -1 (ACY-1), and transketolase.	Acetylcysteine	9-12	aminoacylase 1	Homo sapiens	185-190
15520183-5	2004	Epidermal growth factor receptor activity by asbestos is blocked by N-acetyl-l-cysteine, suggesting that it is an initial redox-activated event leading to downstream AP-1 proto-oncogene up-regulation.	Acetylcysteine	68-87	jun proto-oncogene	Mus musculus	166-170
22982566-4	2012	However, hypoxia further increased the susceptibility of mutant p53 breast cancer SKBR3 cells to lower PRIMA-1 levels, possibly through oxidative stress since this was counteracted by N-acetylcysteine.	Acetylcysteine	184-200	proline rich membrane anchor 1	Homo sapiens	103-110
23206959-2	2012	Investigate the effect of N-acetylcysteine (NAC), which has been studied for its antitumoural properties, on the toxicity of hepatocarcinoma (HCC) cells in vitro when used with the drug interferon alpha-2A (IFN), which is used clinically to treat HCC.	Acetylcysteine	26-42	interferon alpha 2	Homo sapiens	186-205
15569474-17	2004	After treatment with N-acetylcysteine, IFN-gamma increased and the IL-4/IFN-gamma ratio decreased.	Acetylcysteine	21-37	interleukin 4	Rattus norvegicus	67-71
15569474-26	2004	N-acetylcysteine has no effect on IL-4, but increases IFN-gamma levels and brings the IL-4/IFN-gamma ratio back to normal.	Acetylcysteine	0-16	interleukin 4	Rattus norvegicus	86-90
23206959-2	2012	Investigate the effect of N-acetylcysteine (NAC), which has been studied for its antitumoural properties, on the toxicity of hepatocarcinoma (HCC) cells in vitro when used with the drug interferon alpha-2A (IFN), which is used clinically to treat HCC.	Acetylcysteine	26-42	interferon alpha 2	Homo sapiens	207-210
15492272-7	2004	The generation of ROS and activation of NF-kappaB by hPNPase(old-35) are prevented by treatment with a cell-permeable antioxidant, N-acetyl-l-cysteine.	Acetylcysteine	131-150	polyribonucleotide nucleotidyltransferase 1	Homo sapiens	53-67
23206959-2	2012	Investigate the effect of N-acetylcysteine (NAC), which has been studied for its antitumoural properties, on the toxicity of hepatocarcinoma (HCC) cells in vitro when used with the drug interferon alpha-2A (IFN), which is used clinically to treat HCC.	Acetylcysteine	44-47	interferon alpha 2	Homo sapiens	186-205
15492272-8	2004	Infection with Ad.hPNPase(old-35) enhances the production of interleukin (IL)-6 and IL-8, two classical NF-kappaB-responsive cytokines, and this induction is inhibited by N-acetyl-l-cysteine.	Acetylcysteine	171-190	polyribonucleotide nucleotidyltransferase 1	Homo sapiens	18-32
23206959-2	2012	Investigate the effect of N-acetylcysteine (NAC), which has been studied for its antitumoural properties, on the toxicity of hepatocarcinoma (HCC) cells in vitro when used with the drug interferon alpha-2A (IFN), which is used clinically to treat HCC.	Acetylcysteine	44-47	interferon alpha 2	Homo sapiens	207-210
15276019-7	2004	PEDF or an antioxidant, N-acetylcysteine, significantly inhibited the TNF-alpha-induced NF-kappaB activation.	Acetylcysteine	24-40	serpin family F member 1	Homo sapiens	0-4
23206959-4	2012	More importantly, NAC potentiates the cytotoxic effect of IFN, with the best response achieved with 10 mM of NAC and 2.5 x 104 of IFN.	Acetylcysteine	18-21	interferon alpha 2	Homo sapiens	58-61
23206959-4	2012	More importantly, NAC potentiates the cytotoxic effect of IFN, with the best response achieved with 10 mM of NAC and 2.5 x 104 of IFN.	Acetylcysteine	18-21	interferon alpha 2	Homo sapiens	130-133
23206959-4	2012	More importantly, NAC potentiates the cytotoxic effect of IFN, with the best response achieved with 10 mM of NAC and 2.5 x 104 of IFN.	Acetylcysteine	109-112	interferon alpha 2	Homo sapiens	58-61
23206959-7	2012	In a similar way to NAC, RNAi against p65 potentiated the toxic effect of IFN, suggesting that, indeed, NAC may be enhancing the effect of IFN through inhibition of NF-kB.	Acetylcysteine	104-107	RELA proto-oncogene, NF-kB subunit	Homo sapiens	38-41
15355665-13	2004	IL-4 level in the NAC group was 7.99 pg/ml which was similar to that in the smoke exposed group (P &gt; 0.05).	Acetylcysteine	18-21	interleukin 4	Rattus norvegicus	0-4
23206959-7	2012	In a similar way to NAC, RNAi against p65 potentiated the toxic effect of IFN, suggesting that, indeed, NAC may be enhancing the effect of IFN through inhibition of NF-kB.	Acetylcysteine	104-107	interferon alpha 2	Homo sapiens	74-77
23206959-7	2012	In a similar way to NAC, RNAi against p65 potentiated the toxic effect of IFN, suggesting that, indeed, NAC may be enhancing the effect of IFN through inhibition of NF-kB.	Acetylcysteine	104-107	interferon alpha 2	Homo sapiens	139-142
16627882-9	2006	Similarly, increased myelin expression was seen in brain sections from hypothermia plus NAC group, when stained for Luxol Fast Blue (LFB), Myelin Basic Protein (MBP) and Proteolipid protein (PLP).	Acetylcysteine	88-91	proteolipid protein 1	Rattus norvegicus	191-194
22692827-9	2012	The treatment of Batten disease cells with NAC for 48 h attenuated activities of the urea cycle and of DNA repair, as indicated by the substantially decreased expression levels of carbamoyl phosphate synthetase 1, 8-oxoguanine DNA glycosylase 1 and DNA polymerase beta proteins compared with untreated Batten cells.	Acetylcysteine	43-46	DNA polymerase beta	Homo sapiens	249-268
15056806-3	2004	Adult Sprague-Dawley rats were exposed to either CAPs aerosols (CAPs mass concentration 1060 +/- 300 microg/m(3)) or filtered air (Sham controls) for 5 h. NAC-treated rats received 50 mg/kg (ip) NAC 1 h prior to exposure to CAPs.	Acetylcysteine	155-158	nucleus accumbens associated 1	Rattus norvegicus	195-200
22678775-6	2012	The activation of ERK1/2 proteins by dioscoreanone was due to both an arylating reaction, which was suppressed by N-acetyl cysteine, and a redox cycling reaction of NQOR, which was inhibited by dicoumarol.	Acetylcysteine	114-131	mitogen-activated protein kinase 3	Mus musculus	18-24
15038770-5	2004	In contrast, the increase in Mmp2 mRNA levels in irradiated cells was essentially unchanged after incubation with ActD for up to 12 h. Incubating cells with the antioxidants N-acetylcysteine or ebselen or the MEK pathway inhibitors PD98059 and U0126 prior to irradiation abolished the radiation-induced up-regulation of Mmp2.	Acetylcysteine	174-190	matrix metallopeptidase 2	Rattus norvegicus	29-33
15038770-6	2004	Irradiating NRK52E cells led to reactive oxygen species-mediated Erk1/2 activation; preincubation with NAC prevented the radiation-induced increase in phosphorylated Erk1/2.	Acetylcysteine	103-106	mitogen activated protein kinase 3	Rattus norvegicus	65-71
15038770-6	2004	Irradiating NRK52E cells led to reactive oxygen species-mediated Erk1/2 activation; preincubation with NAC prevented the radiation-induced increase in phosphorylated Erk1/2.	Acetylcysteine	103-106	mitogen activated protein kinase 3	Rattus norvegicus	166-172
15040427-6	2004	N-acetylcysteine (NAC) is an antioxidant which raises intracellular reduced glutathione levels, and blocks the formation of ISCs in vitro.	Acetylcysteine	0-16	NFS1 cysteine desulfurase	Homo sapiens	124-128
16631521-7	2006	ALA significantly increased ROS, and this effect was blocked by N-acetyl-cysteine, which also inhibited ALA-induced activation of p44/42 mitogen-activated protein kinase (MAPK) and AP-1, HO-1 expression, and HO activity.	Acetylcysteine	64-81	interferon induced protein 44	Homo sapiens	130-133
16565438-0	2006	Allyl isothiocyanate and its N-acetylcysteine conjugate suppress metastasis via inhibition of invasion, migration, and matrix metalloproteinase-2/-9 activities in SK-Hep 1 human hepatoma cells.	Acetylcysteine	29-45	matrix metallopeptidase 2	Homo sapiens	119-148
16565438-5	2006	We examined the influence of AITC and NAC-AITC on the gene expression of MMPs and tissue inhibitors of metalloproteinase (TIMPs).	Acetylcysteine	38-41	matrix metallopeptidase 2	Homo sapiens	73-77
16565438-6	2006	Gelatin zymography also revealed a significant downregulation of MMP-2/-9 expression in SK-Hep1 cells treated with 0.1-5 microM AITC and NAC-AITC compared with controls.	Acetylcysteine	137-140	matrix metallopeptidase 2	Homo sapiens	65-73
16565438-7	2006	Reverse transcriptase polymerase chain reaction revealed dose-dependent decreases in MMP-2/-9 messenger RNA levels in both AITC-treated and NAC-AITC-treated cells.	Acetylcysteine	140-143	matrix metallopeptidase 2	Homo sapiens	85-93
23088864-8	2012	NAC still caused analgesia in mGlu3(-/-) mice, but was inactive in mGlu2(-/-) mice.	Acetylcysteine	0-3	glutamate receptor, metabotropic 3	Mus musculus	30-35
16081117-9	2006	NAC also abrogated APAP-induced increases in TNFalpha, KC/gro, and IL-10, but augmented expression of the anti-inflammatory cytokines interleukin-4 (IL-4) and transforming growth factor-beta (TGFbeta).	Acetylcysteine	0-3	transforming growth factor, beta 1	Mus musculus	192-199
15982852-4	2006	The antioxidant N-acetyl-L-cysteine (NAC) inhibited IL-3-induced tyrosine phosphorylation of Jak2, IL-3 receptor betac subunit (IL-3Rbetac), and STAT5 as well as activation-specific phosphorylation of Akt, MEK, and ERK, while treatment of cells with H2O2 activated these signaling events.	Acetylcysteine	16-35	midkine	Mus musculus	206-209
15982852-4	2006	The antioxidant N-acetyl-L-cysteine (NAC) inhibited IL-3-induced tyrosine phosphorylation of Jak2, IL-3 receptor betac subunit (IL-3Rbetac), and STAT5 as well as activation-specific phosphorylation of Akt, MEK, and ERK, while treatment of cells with H2O2 activated these signaling events.	Acetylcysteine	16-35	Eph receptor B2	Mus musculus	215-218
15982852-4	2006	The antioxidant N-acetyl-L-cysteine (NAC) inhibited IL-3-induced tyrosine phosphorylation of Jak2, IL-3 receptor betac subunit (IL-3Rbetac), and STAT5 as well as activation-specific phosphorylation of Akt, MEK, and ERK, while treatment of cells with H2O2 activated these signaling events.	Acetylcysteine	37-40	midkine	Mus musculus	206-209
15982852-4	2006	The antioxidant N-acetyl-L-cysteine (NAC) inhibited IL-3-induced tyrosine phosphorylation of Jak2, IL-3 receptor betac subunit (IL-3Rbetac), and STAT5 as well as activation-specific phosphorylation of Akt, MEK, and ERK, while treatment of cells with H2O2 activated these signaling events.	Acetylcysteine	37-40	Eph receptor B2	Mus musculus	215-218
14610226-8	2004	Finally, pretreatment of hepatocytes with the antioxidants N-acetylcysteine and vitamin E attenuated pyrazole-mediated increases in CYP2A5 mRNA levels.	Acetylcysteine	59-75	cytochrome P450, family 2, subfamily a, polypeptide 5	Mus musculus	132-138
22854047-7	2012	NAC and FeTPPS prevented the activation of FAK, its association with LMW-PTP and cell migration.	Acetylcysteine	0-3	protein tyrosine kinase 2	Homo sapiens	43-46
14732289-10	2004	Interestingly, N-acetylcysteine (1 mM) enhanced the HO-1 induction of MCGA3, but N-acetylcysteine itself did not induce HO-1.	Acetylcysteine	15-31	heme oxygenase 1	Bos taurus	52-56
22858589-5	2012	The results showed that Cr(VI) at 32muM led to increase in the ROS level, VDAC1 mRNA expression, and the apoptosis rate and a decrease in the ATP level; pretreatment with NAC led to the down-regulation in the levels of ROS, VDAC1 mRNA and apoptosis and the significant up-regulation in the ATP levels.	Acetylcysteine	171-174	voltage dependent anion channel 1	Homo sapiens	74-79
14646616-5	2003	The effect of vitamin C treatment was blocked by the antioxidant N-acetyl-L-cysteine, suggesting that vitamin C affects IL-18 expression by up-regulating intracellular reactive oxygen intermediate (ROI) levels.	Acetylcysteine	65-84	interleukin 18	Mus musculus	120-125
16449798-6	2006	This mechanism is supported by the ability of N-acetyl cysteine (NAC) to prevent dissociation of Trx-ASK1 and activation of the p38 MAPK pathway.	Acetylcysteine	65-68	mitogen-activated protein kinase 14	Mus musculus	128-131
22858589-5	2012	The results showed that Cr(VI) at 32muM led to increase in the ROS level, VDAC1 mRNA expression, and the apoptosis rate and a decrease in the ATP level; pretreatment with NAC led to the down-regulation in the levels of ROS, VDAC1 mRNA and apoptosis and the significant up-regulation in the ATP levels.	Acetylcysteine	171-174	voltage dependent anion channel 1	Homo sapiens	224-229
22713468-12	2012	NAC significantly inhibited the PDGF-BB-induced phosphorylation of p38 and HSP27.	Acetylcysteine	0-3	mitogen activated protein kinase 14	Rattus norvegicus	67-70
16504566-9	2006	Blocking phosphorylation with the protein kinase C inhibitor bisindolylmaleimide, or inhibiting intracellular oxidation by addition of the antioxidant N-acetyl-l-cysteine could reverse the ubiquitination and downregulation of Raf-1 induced by methylglyoxal and phorbol-12-myristate-13-acetate.	Acetylcysteine	151-170	Raf-1 proto-oncogene, serine/threonine kinase	Homo sapiens	226-231
14551238-8	2003	The antioxidant, N-acetyl-cysteine, inhibited pressure-overload-induced LVH in both gp91phox-/- and wild-type mice.	Acetylcysteine	17-34	cytochrome b-245, beta polypeptide	Mus musculus	84-92
22713468-12	2012	NAC significantly inhibited the PDGF-BB-induced phosphorylation of p38 and HSP27.	Acetylcysteine	0-3	heat shock protein family B (small) member 1	Rattus norvegicus	75-80
22554771-9	2012	An antioxidant drug, N-acetyl-l-cysteine significantly inhibited TNF-alpha-induced phosphorylation of p38 and JNK.	Acetylcysteine	21-40	mitogen activated protein kinase 14	Rattus norvegicus	102-105
16137721-7	2005	Both individually and in combination with oltipraz, NAC inhibited apoptosis in the respiratory tract of rats exposed either to MCS or ECS.	Acetylcysteine	52-55	epistatic circling SWR/J	Mus musculus	134-137
16137721-8	2005	Moreover, NAC attenuated the ECS-related overexpression of proapoptotic genes and normalized the levels of proapoptotic proteins in rat lung.	Acetylcysteine	10-13	epistatic circling SWR/J	Mus musculus	29-32
22496405-10	2012	The oxidative stimulus (H(2)O(2)) induced alpha-SMA expression in ARPCs, while the antioxidant N-acetyl-cysteine inhibited BMP-2-induced alpha-SMA expression.	Acetylcysteine	95-112	bone morphogenetic protein 2	Homo sapiens	123-128
16137721-9	2005	The transplacental administration of NAC to mice considerably attenuated gene overexpression in the liver of fetuses exposed to ECS throughout pregnancy.	Acetylcysteine	37-40	epistatic circling SWR/J	Mus musculus	128-131
14556849-8	2003	The phosphorylation of p38 MAPK by V2O5 was inhibited by NAC and catalase, yet the EGF receptor inhibitor AG1478 had no effect on V2O5-induced p38 MAPK activation.	Acetylcysteine	57-60	mitogen activated protein kinase 14	Rattus norvegicus	23-26
12943989-8	2003	It was further shown that p38 MAPK and ERK activation was inhibited by the antioxidant, N-acetylcysteine (NAC), and that a treatment with haloperidol completely blocked the p38 and ERK activation induced by dopamine.	Acetylcysteine	88-104	mitogen activated protein kinase 14	Rattus norvegicus	26-29
12943989-8	2003	It was further shown that p38 MAPK and ERK activation was inhibited by the antioxidant, N-acetylcysteine (NAC), and that a treatment with haloperidol completely blocked the p38 and ERK activation induced by dopamine.	Acetylcysteine	106-109	mitogen activated protein kinase 14	Rattus norvegicus	26-29
12943989-8	2003	It was further shown that p38 MAPK and ERK activation was inhibited by the antioxidant, N-acetylcysteine (NAC), and that a treatment with haloperidol completely blocked the p38 and ERK activation induced by dopamine.	Acetylcysteine	106-109	mitogen activated protein kinase 14	Rattus norvegicus	173-176
12810527-8	2003	N-acetylcysteine supplementation has been shown to reverse the metabolic abnormalities of the GGT-/- mice and in particular to restore the level of IGF-1 and sex steroids in these mice.	Acetylcysteine	0-16	insulin-like growth factor 1	Mus musculus	148-153
12691831-10	2003	NAC treatment also blocked the ischemia/reperfusion-induced expression of tumor necrosis factor and inducible nitric oxide synthase.	Acetylcysteine	0-3	tumor necrosis factor-like	Rattus norvegicus	74-95
16144837-9	2005	When 2-mercaptoethanol was removed from the culture medium, cysteine and GSH in these cells dramatically decreased, and cells started to die within 24 h. N-Acetyl cysteine also rescued xCT(-/-)-derived cells and permitted growth.	Acetylcysteine	154-171	solute carrier family 7 (cationic amino acid transporter, y+ system), member 11	Mus musculus	185-188
15829913-9	2005	In addition, administration of N-acetylcysteine (NAC), a precursor of glutathione and a potent antioxidant, attenuated both Tat-induced ERK 1/2 activation and alterations in ZO-1 expression.	Acetylcysteine	49-52	tyrosine aminotransferase	Homo sapiens	124-127
12406911-4	2003	However, only partial inhibition of Raf-1 and ERK1 stimulation was observed with the antioxidant N-acetylcysteine (N-Ac).	Acetylcysteine	97-113	Raf-1 proto-oncogene, serine/threonine kinase	Homo sapiens	36-41
12406911-4	2003	However, only partial inhibition of Raf-1 and ERK1 stimulation was observed with the antioxidant N-acetylcysteine (N-Ac).	Acetylcysteine	115-119	Raf-1 proto-oncogene, serine/threonine kinase	Homo sapiens	36-41
22231145-10	2012	IL-1beta-induced cPLA2 expression was mediated through recruitment of activator protein 1 (AP-1) to the cPLA2 promoter region, which was attenuated by NAC and overexpression of HO-1.	Acetylcysteine	151-154	phospholipase A2, group IVA (cytosolic, calcium-dependent)	Mus musculus	17-22
16135167-9	2005	CONCLUSIONS: These data suggest that although long-term aerosolized N-acetylcysteine administration did not influence pulmonary function or quality of life, it may delay disease progression as evidenced by exercise desaturation, high-resolution CT, and serum KL-6.	Acetylcysteine	68-84	mucin 1, cell surface associated	Homo sapiens	259-263
22231145-10	2012	IL-1beta-induced cPLA2 expression was mediated through recruitment of activator protein 1 (AP-1) to the cPLA2 promoter region, which was attenuated by NAC and overexpression of HO-1.	Acetylcysteine	151-154	jun proto-oncogene	Mus musculus	70-89
15769933-9	2005	Furthermore, NAC and MnTBAP, but not catalase, blunt high NaCl-induced increase in TonEBP/OREBP transactivation.	Acetylcysteine	13-16	nuclear factor of activated T cells 5	Homo sapiens	83-89
15769933-9	2005	Furthermore, NAC and MnTBAP, but not catalase, blunt high NaCl-induced increase in TonEBP/OREBP transactivation.	Acetylcysteine	13-16	nuclear factor of activated T cells 5	Homo sapiens	90-95
22231145-10	2012	IL-1beta-induced cPLA2 expression was mediated through recruitment of activator protein 1 (AP-1) to the cPLA2 promoter region, which was attenuated by NAC and overexpression of HO-1.	Acetylcysteine	151-154	jun proto-oncogene	Mus musculus	91-95
15888667-6	2005	Pre-treatment with the antioxidant molecule N-acetyl cysteine sharply decreased the level of phospho-ERK1/2 and had no effect on Raf and MEK1/2 activation, suggesting a Raf-independent mechanism.	Acetylcysteine	44-61	zinc fingers and homeoboxes 2	Homo sapiens	169-172
22231145-10	2012	IL-1beta-induced cPLA2 expression was mediated through recruitment of activator protein 1 (AP-1) to the cPLA2 promoter region, which was attenuated by NAC and overexpression of HO-1.	Acetylcysteine	151-154	phospholipase A2, group IVA (cytosolic, calcium-dependent)	Mus musculus	104-109
12675513-8	2003	Our findings establish a previously unrecognised physiological function of cytosolic leucyl aminopeptidase, participating in glutathione metabolism and in the degradation of glutathione S-conjugates via the mercapturic acid pathway.	Acetylcysteine	207-223	leucine aminopeptidase 3	Rattus norvegicus	85-106
22036036-3	2012	On the basis of these findings, we tested whether NAC would reduce ketamine effects on behavior, MMN, and P300 in healthy humans.	Acetylcysteine	50-53	E1A binding protein p300	Homo sapiens	106-110
16037234-5	2005	N-acetyl-L-cysteine, an antioxidant, successfully suppressed the activity of the p38 MAPK signaling pathway along with the inhibition of apoptosis, indicating the involvement of oxidative stress in the MG-induced apoptosis via the p38 MAPK pathway.	Acetylcysteine	0-19	mitogen activated protein kinase 14	Rattus norvegicus	81-84
16037234-5	2005	N-acetyl-L-cysteine, an antioxidant, successfully suppressed the activity of the p38 MAPK signaling pathway along with the inhibition of apoptosis, indicating the involvement of oxidative stress in the MG-induced apoptosis via the p38 MAPK pathway.	Acetylcysteine	0-19	mitogen activated protein kinase 14	Rattus norvegicus	231-234
16120311-10	2002	The addition of the antioxidant N-acetyl-cysteine only rescues cells non-committed to the neuronal lineage, indicating that frataxin deficiency impairs differentiation mechanisms and survival responses through different mechanisms.	Acetylcysteine	32-49	frataxin	Homo sapiens	124-132
22036036-11	2012	NAC merits further investigation as a cognitive enhancing agent due to its ability to increase the P300 amplitude.	Acetylcysteine	0-3	E1A binding protein p300	Homo sapiens	99-103
22326494-10	2012	PFOS induced caspase-3 activity and nucleosomal DNA fragmentation in a dose-dependent manner, which were blocked by pretreatment of NAC.	Acetylcysteine	132-135	caspase 3	Rattus norvegicus	13-22
12387824-7	2002	N-acetylcysteine, an antioxidant, could abrogate the production of pro-MMP-9, H(2)O(2) generation, and activation of NF-kappaB and MMP-9 promoter.	Acetylcysteine	0-16	matrix metallopeptidase 9	Mus musculus	67-76
12387824-7	2002	N-acetylcysteine, an antioxidant, could abrogate the production of pro-MMP-9, H(2)O(2) generation, and activation of NF-kappaB and MMP-9 promoter.	Acetylcysteine	0-16	matrix metallopeptidase 9	Mus musculus	71-76
12168106-8	2002	Co-treatment with NAC markedly prevented dephosphorylation of Akt, activation of caspase 3, and down-regulation of cIAP1.	Acetylcysteine	18-21	baculoviral IAP repeat containing 2	Homo sapiens	115-120
12023963-6	2002	In addition, a fusion between p47(phox) and the TRAF4 C terminus constitutively activated JNK, and this activation was decreased by the antioxidant N-acetyl cysteine.	Acetylcysteine	148-165	TNF receptor associated factor 4	Homo sapiens	48-53
12165081-0	2002	N-acetylcysteine inhibits the induction of an antigen-specific antibody response down-regulating CD40 and CD27 co-stimulatory molecules.	Acetylcysteine	0-16	CD40 molecule	Homo sapiens	97-101
15846509-5	2005	Ang II significantly induced redox-sensitive transcriptional factor NF-kappaB activation and subsequent monocyte chemoattractant protein-1 expression in human umbilical vein ECs (HUVEC), both of which were completely inhibited by PEDF or the anti-oxidant N-acetylcysteine.	Acetylcysteine	255-271	serpin family F member 1	Homo sapiens	230-234
15720785-6	2005	Similar to bacitracin, N-acetylcysteine blocked alphabeta- and beta2-secretion as well as PDI-beta-chain complex formation.	Acetylcysteine	23-39	potassium calcium-activated channel subfamily M regulatory beta subunit 2	Homo sapiens	63-68
16400524-8	2005	NAC treatment also restored cell cycle progression inhibited by rk-2 and down-regulated p53 and nuclear p21(Waf1/Cip1) expression induced by rk-2.These data suggest that rk-2 induces the BCE cell cycle arrest at G(0)-G(1) phase through inhibition of the cyclin D1/CDK4 complex caused by increase of ROS generation and nuclear cyclin-dependent kinase inhibitors.	Acetylcysteine	0-3	cyclin D1	Homo sapiens	254-263
12165081-4	2002	The NAC-induced inhibitory effect might be a functional consequence of: (i) a down-regulation of the expression on the B cell surface of CD40 and CD27 co-stimulatory molecules and (ii) a down-regulation of interleukin (IL-4) production.	Acetylcysteine	4-7	CD40 molecule	Homo sapiens	137-141
16400524-8	2005	NAC treatment also restored cell cycle progression inhibited by rk-2 and down-regulated p53 and nuclear p21(Waf1/Cip1) expression induced by rk-2.These data suggest that rk-2 induces the BCE cell cycle arrest at G(0)-G(1) phase through inhibition of the cyclin D1/CDK4 complex caused by increase of ROS generation and nuclear cyclin-dependent kinase inhibitors.	Acetylcysteine	0-3	cyclin dependent kinase 4	Homo sapiens	264-268
22361928-8	2012	NAC, therefore, may influence mucin expression by acting on oxidative stress and inflammation, and play a role as a mucolytic agent.	Acetylcysteine	0-3	LOC100508689	Homo sapiens	30-35
15378764-4	2004	The ovalbumin-induced degradation of annexin-1 was blocked by pretreatment of mice with the antioxidant N-acetylcysteine (NAC) or with sodium selenite, both of which have previously been shown to exert anti-inflammatory effects in this asthma model.	Acetylcysteine	104-120	annexin A1	Mus musculus	37-46
15378764-4	2004	The ovalbumin-induced degradation of annexin-1 was blocked by pretreatment of mice with the antioxidant N-acetylcysteine (NAC) or with sodium selenite, both of which have previously been shown to exert anti-inflammatory effects in this asthma model.	Acetylcysteine	122-125	annexin A1	Mus musculus	37-46
15378764-5	2004	Ovalbumin challenge also both increased the expression of cPLA(2) in lung tissue and reduced the extent of the interaction between cPLA(2) and annexin-1, and these effects were inhibited by NAC or selenite.	Acetylcysteine	190-193	phospholipase A2, group IVA (cytosolic, calcium-dependent)	Mus musculus	58-65
15378764-5	2004	Ovalbumin challenge also both increased the expression of cPLA(2) in lung tissue and reduced the extent of the interaction between cPLA(2) and annexin-1, and these effects were inhibited by NAC or selenite.	Acetylcysteine	190-193	phospholipase A2, group IVA (cytosolic, calcium-dependent)	Mus musculus	131-138
15378764-5	2004	Ovalbumin challenge also both increased the expression of cPLA(2) in lung tissue and reduced the extent of the interaction between cPLA(2) and annexin-1, and these effects were inhibited by NAC or selenite.	Acetylcysteine	190-193	annexin A1	Mus musculus	143-152
15451797-7	2004	NAC treatment, which replenished cardiac glutathione, had no effect on hypertension but reduced LV remodeling and dysfunction, normalized serum TNF-alpha level, and limited activation of matrix metalloproteinases -2 and -9 and collagen deposition in LV tissues.	Acetylcysteine	0-3	matrix metallopeptidase 2	Rattus norvegicus	187-222
12140766-7	2002	Moreover, DOX-induced apoptosis at 0.001-0.01 microM was only inhibited in HL-60 cells pre-treated with the antioxidant N-acetyl-cysteine in the absence of anti-PR3, revealing that DOX-induced apoptosis in these cells is PR3- and ROS-dependent.	Acetylcysteine	120-137	proteinase 3	Homo sapiens	221-224
11961137-5	2002	Pretreatment of SMCs with N-acetyl-L-cysteine significantly suppressed the MG-induced AR expression, whereas DL-buthionine-(S,R)-sulfoximine further augmented the MG-induced increase in AR mRNA level.	Acetylcysteine	26-45	aldo-keto reductase family 1 member B1	Rattus norvegicus	86-88
21542122-7	2012	Change in serum cystatin-C, a sensitive marker for renal function, was 0.046 +- 0.204 in the NAC group and 0.002 +- 0.260 in the control group (p = 0.07).	Acetylcysteine	93-96	cystatin C	Homo sapiens	16-26
12027535-11	2002	TGFbeta3 mRNA level was markedly reduced by LPS alone, or with both L-NMMA and NAC.	Acetylcysteine	79-82	transforming growth factor beta 3	Homo sapiens	0-8
15289318-7	2004	Dietary supplementation with NAC significantly reduced 8-OH deoxyguanosine level and the frequency of DNA deletions in Atm-deficient mice.	Acetylcysteine	29-32	ataxia telangiectasia mutated	Mus musculus	119-122
15289318-9	2004	Our findings demonstrate that NAC counteracts genetic instability and suggest that genetic instability may be a consequence of oxidative stress in Atm-deficient mice.	Acetylcysteine	30-33	ataxia telangiectasia mutated	Mus musculus	147-150
15289350-12	2004	The antioxidant N-acetyl-l-cysteine somewhat reduced 4-HPR cytotoxicity but did not affect ceramide species increase.	Acetylcysteine	16-35	haptoglobin-related protein	Homo sapiens	55-58
22268121-11	2012	In CLP + NAC rats, alpha-ENaC expression was upregulated, whereas that of NKCC1 was downregulated, although the difference was not significant.	Acetylcysteine	9-12	sodium channel epithelial 1 subunit alpha	Rattus norvegicus	19-29
15240103-5	2004	Aminoguanidine and N-acetyl-L-cysteine also inhibited the MG-induced p38 MAPK activation and apoptosis along with restoration of the intracellular glutathione content.	Acetylcysteine	19-38	mitogen activated protein kinase 14	Rattus norvegicus	69-72
15249511-6	2004	In addition, Db-HAGE-LDL stimulated NF-kappaB activity significantly in ECV 304 and human umbilical vein endothelial cells (2.3-fold above baseline) in a manner inhibitable by a MEK inhibitor PD98059 (10 micromol/L), the antioxidant N-acetyl-l-cysteine, NAC (30 mmol/L), and the NADPH oxidase inhibitor DPI (20 micromol/L).	Acetylcysteine	233-252	DEAD-box helicase 43	Homo sapiens	16-20
11909699-4	2002	Simultaneous incubation with the thiol antioxidant N-acetylcysteine (NAC) inhibited indomethacin-mediated increases in GCLC mRNA, suggesting that increases in GCLC message were triggered by changes in intracellular oxidation/reduction (redox) reactions.	Acetylcysteine	69-72	glutamate-cysteine ligase catalytic subunit	Homo sapiens	119-123
11909699-4	2002	Simultaneous incubation with the thiol antioxidant N-acetylcysteine (NAC) inhibited indomethacin-mediated increases in GCLC mRNA, suggesting that increases in GCLC message were triggered by changes in intracellular oxidation/reduction (redox) reactions.	Acetylcysteine	69-72	glutamate-cysteine ligase catalytic subunit	Homo sapiens	159-163
15203192-9	2004	N-Acetylcysteine, a ROS scavenger, exhibited a response similar to that of DPI and inhibited ET-1-stimulated ERK1/2, PKB, and Pyk2 phosphorylation.	Acetylcysteine	0-16	protein tyrosine kinase 2	Homo sapiens	126-130
22366396-10	2012	Inhibition of ROS by N-acetylcysteine abrogated LA-induced ERK1/2 activation and cytoprotection.	Acetylcysteine	21-37	mitogen activated protein kinase 3	Rattus norvegicus	59-65
15225644-6	2004	Furthermore, G6PD but not PGK1 induction was blocked by the antioxidants glutathione and N-acetylcysteine.	Acetylcysteine	89-105	glucose-6-phosphate dehydrogenase	Rattus norvegicus	13-17
12061835-7	2002	IL-12 dimer formation appears to be reduced by NAC also in vivo, because pretreatment with NAC (1 g/kg, orally), before LPS injection in mice, inhibited peak IL-12 p75 serum levels without affecting those of p40.	Acetylcysteine	47-50	interleukin 2 receptor subunit beta	Homo sapiens	164-167
12061835-7	2002	IL-12 dimer formation appears to be reduced by NAC also in vivo, because pretreatment with NAC (1 g/kg, orally), before LPS injection in mice, inhibited peak IL-12 p75 serum levels without affecting those of p40.	Acetylcysteine	91-94	interleukin 2 receptor subunit beta	Homo sapiens	164-167
11867563-5	2002	NAC significantly reduced both HgCl2-induced early vasculitis and HgCl(2)-enhanced IgE expression on mast cells with a trend to a decrease in HgCl(2)-enhanced IL-4 expression in these cells.	Acetylcysteine	0-3	interleukin 4	Rattus norvegicus	159-163
11858729-7	2002	Pretreatment with an antioxidant, N-acetylcysteine, repressed CYP1B1 increase, suggesting the involvement of UV-B photoproducts.	Acetylcysteine	34-50	cytochrome P450 family 1 subfamily B member 1	Homo sapiens	62-68
22203419-5	2012	Pretreatment with N-acetyl-L: -cysteine (NAC) (a ROS scavenger) attenuated intracellular ROS accumulation, cytotoxicity, and the inhibition of expression and activity of CSE induced by DOX.	Acetylcysteine	18-39	cystathionine gamma-lyase	Rattus norvegicus	170-173
11668087-6	2001	ERK1/2 phosphorylation was suppressed by an inhibitor of tyrosine phosphorylation (genestein), cholesterol-binding reagents (filipin or cyclodextrin), or inhibitors of ROS (diphenyleneiodonium, N-acetylcysteine, or catalase), suggesting a role for both membrane cholesterol and ROS in ERK1/2 activation.	Acetylcysteine	194-210	mitogen-activated protein kinase 3	Bos taurus	0-6
15026306-5	2004	H(2)O(2)-induced AMPKalpha1 activation was blocked in the presence of the antioxidant N-acetyl-l-cysteine (NAC), and H(2)O(2) significantly increased the ratio of oxidized glutathione to glutathione (GSSG/GSH) concentrations, a sensitive marker of oxidative stress.	Acetylcysteine	86-105	protein kinase AMP-activated catalytic subunit alpha 1	Rattus norvegicus	17-27
15026306-5	2004	H(2)O(2)-induced AMPKalpha1 activation was blocked in the presence of the antioxidant N-acetyl-l-cysteine (NAC), and H(2)O(2) significantly increased the ratio of oxidized glutathione to glutathione (GSSG/GSH) concentrations, a sensitive marker of oxidative stress.	Acetylcysteine	107-110	protein kinase AMP-activated catalytic subunit alpha 1	Rattus norvegicus	17-27
22203419-5	2012	Pretreatment with N-acetyl-L: -cysteine (NAC) (a ROS scavenger) attenuated intracellular ROS accumulation, cytotoxicity, and the inhibition of expression and activity of CSE induced by DOX.	Acetylcysteine	41-44	cystathionine gamma-lyase	Rattus norvegicus	170-173
15075348-8	2004	The antioxidant N-acetyl-L-cysteine inhibited the cytotoxicity/apoptotic effect of S100A8/A9 and DTPA.	Acetylcysteine	16-35	S100 calcium binding protein A8	Homo sapiens	83-89
11585757-7	2001	Moreover, the thiol-antioxidants glutathione and N-acetyl-L-cysteine antagonized the Cpd 5-induced Cdk4 tyrosine phosphorylation, whereas the nonthiol-antioxidants catalase and superoxide dismutase did not.	Acetylcysteine	49-68	cyclin dependent kinase 4	Homo sapiens	99-103
21997484-8	2012	The inhibition of Src by PP2 and ROS production by N-acetyl cysteine inhibited the disassembly of VE-cadherin-p120-catenin complexes, and attenuated high OxPAPC-induced EC barrier disruption.	Acetylcysteine	51-68	catenin delta 1	Homo sapiens	110-122
22131350-5	2012	Furthermore, the anticancer activity of NAC-AITC is associated with the modulation of several important molecular targets, including downregulation of both alpha-tubulin and beta-tubulin, activation of caspase-3 and downregulation of vascular endothelial growth factor.	Acetylcysteine	40-43	caspase 3	Rattus norvegicus	202-211
11710991-7	2001	N-acetylcysteine or catalase prevented FSK-induced suppression of antigen-induced proliferation and the loss of carboxy-terminal epitopes of p56(lck).	Acetylcysteine	0-16	interferon-induced protein with tetratricopeptide repeats 1	Mus musculus	141-144
11710991-7	2001	N-acetylcysteine or catalase prevented FSK-induced suppression of antigen-induced proliferation and the loss of carboxy-terminal epitopes of p56(lck).	Acetylcysteine	0-16	lymphocyte protein tyrosine kinase	Mus musculus	145-148
15228596-5	2004	H(2)O(2) caused a time- and concentration-dependent increase in MAPK phosphorylation, an effect that was totally blocked by N-acetyl-L-cysteine.	Acetylcysteine	124-143	mitogen activated protein kinase 3	Rattus norvegicus	64-68
22739240-7	2012	The H(2)O(2)-induced gene repression or activation of SP-A, SP-B, SP-D and ABCA3 was blocked by pretreatment with the antioxidants N-acetyl-L-cysteine (NAC) and catalase.	Acetylcysteine	131-150	surfactant protein A1	Homo sapiens	54-58
14984365-5	2004	Following H/R, STAT1 was activated and sequential phosphorylation of Tyr701 and Ser727 was observed, which could be inhibited by the antioxidant N-acetyl-L-cysteine.	Acetylcysteine	145-164	signal transducer and activator of transcription 1	Rattus norvegicus	15-20
11507166-8	2001	Application of the antioxidants N-acetylcysteine (20 mM) or dithiothreitol (5 mM) suppressed concentric contraction-induced increase in MAPK(erk1/2) phosphorylation.	Acetylcysteine	32-48	mitogen activated protein kinase 3	Rattus norvegicus	141-147
22739240-7	2012	The H(2)O(2)-induced gene repression or activation of SP-A, SP-B, SP-D and ABCA3 was blocked by pretreatment with the antioxidants N-acetyl-L-cysteine (NAC) and catalase.	Acetylcysteine	131-150	surfactant protein B	Homo sapiens	60-64
21806545-9	2012	Atorvastatin, SP600125, JNK siRNA (small interfering RNA) and NAC (N-acetylcysteine) completely attenuated the leptin and phospho-JNK protein expression induced by Ang II.	Acetylcysteine	62-65	angiogenin	Homo sapiens	164-167
16997736-2	2004	Here we show that SU5416 induces the expression of heme oxygenase-1 in the lung tissue and that administration of antioxidant N-acetyl-l-cysteine protects alveolar septal cells against apoptosis, as demonstrated by caspase-3 lung immunohistochemistry, and against emphysema.	Acetylcysteine	126-145	caspase 3	Rattus norvegicus	215-224
11485390-9	2001	Cotreatment of H4IIEC3 cells with CA and the antioxidant N-acetylcysteine or calphostin C, a specific inhibitor of protein kinase C (PKC), blocked the AP-1 activation and the expression of the AP-1-driven luciferase reporter gene.	Acetylcysteine	57-73	Jun proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	151-155
21806545-9	2012	Atorvastatin, SP600125, JNK siRNA (small interfering RNA) and NAC (N-acetylcysteine) completely attenuated the leptin and phospho-JNK protein expression induced by Ang II.	Acetylcysteine	67-83	angiogenin	Homo sapiens	164-167
11485390-9	2001	Cotreatment of H4IIEC3 cells with CA and the antioxidant N-acetylcysteine or calphostin C, a specific inhibitor of protein kinase C (PKC), blocked the AP-1 activation and the expression of the AP-1-driven luciferase reporter gene.	Acetylcysteine	57-73	Jun proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	193-197
21806545-11	2012	Addition of atorvastatin and NAC significantly attenuated the formation of ROS induced by Ang II.	Acetylcysteine	29-32	angiogenin	Homo sapiens	90-93
11448159-6	2001	Both oxidase inhibitors and the thiol antioxidant N-acetyl cysteine decreased Tat-induced JNK1 activation in parallel with reduction in oxidant levels.	Acetylcysteine	50-67	tyrosine aminotransferase	Homo sapiens	78-81
15050407-6	2004	Mercury-activated p38 was decreased by pretreatment of cells with antioxidants, N-acetylcysteine (NAC) and silymarin, indicating that mercury-induced ROS were involved in p38 activation.	Acetylcysteine	80-96	mitogen-activated protein kinase 14	Mus musculus	18-21
22946344-7	2012	CDDO-Me down-regulated p-Akt, p-mTOR and NF-kappaB (p65) but increased the activation of Erk1/2 and NAC blocked the modulation of these cell signaling proteins by CDDO-Me.	Acetylcysteine	100-103	RELA proto-oncogene, NF-kB subunit	Homo sapiens	52-55
15050407-6	2004	Mercury-activated p38 was decreased by pretreatment of cells with antioxidants, N-acetylcysteine (NAC) and silymarin, indicating that mercury-induced ROS were involved in p38 activation.	Acetylcysteine	80-96	mitogen-activated protein kinase 14	Mus musculus	171-174
15050407-6	2004	Mercury-activated p38 was decreased by pretreatment of cells with antioxidants, N-acetylcysteine (NAC) and silymarin, indicating that mercury-induced ROS were involved in p38 activation.	Acetylcysteine	98-101	mitogen-activated protein kinase 14	Mus musculus	18-21
15050407-6	2004	Mercury-activated p38 was decreased by pretreatment of cells with antioxidants, N-acetylcysteine (NAC) and silymarin, indicating that mercury-induced ROS were involved in p38 activation.	Acetylcysteine	98-101	mitogen-activated protein kinase 14	Mus musculus	171-174
15040427-6	2004	N-acetylcysteine (NAC) is an antioxidant which raises intracellular reduced glutathione levels, and blocks the formation of ISCs in vitro.	Acetylcysteine	18-21	NFS1 cysteine desulfurase	Homo sapiens	124-128
11441839-4	2001	Broilers treated with AFB1 plus NAC were shown to be partially protected against deleterious effects on BW (57.8%), daily weight gain (49.1%), feed conversion index (21.4%), plasma and hepatic total protein concentration (45.2, 66.7%), plasma alanine aminotransferase (67.4%), hepatic glutathione-S-transferase (18.8%), and reduced glutathione liver concentration (75.0%).	Acetylcysteine	32-35	glutathione S-transferase alpha 3	Gallus gallus	285-310
11375274-6	2001	Thrombin-mediated upregulation of IGF-1R mRNA and protein levels was protein kinase C independent but was completely inhibited by the protein tyrosine kinase inhibitor genistein and by the antioxidants N-acetyl-L-cysteine and pyrrolidinedithiocarbamate, suggesting the involvement of reactive oxygen species.	Acetylcysteine	202-221	insulin-like growth factor 1 receptor	Rattus norvegicus	34-40
15040427-7	2004	NAC, in a phase II human trial, caused a downward trend in ISCs, significantly decreased dense cells, and substantially decreased the rate of VOC episodes.	Acetylcysteine	0-3	NFS1 cysteine desulfurase	Homo sapiens	59-63
22044588-8	2012	Furthermore, the activation of Bnip3 and mitophagy due to p53/TIGAR inhibition were reversed with antioxidant N-acetyl-cysteine, indicating that this adaptive response requires ROS signal.	Acetylcysteine	110-127	BCL2/adenovirus E1B interacting protein 3	Mus musculus	31-36
14729376-6	2004	Antioxidant N-acetylcysteine also decreased angiotensin II-increased protein synthesis and beta-myosin heavy chain promoter activity.	Acetylcysteine	12-28	myosin heavy chain 7	Rattus norvegicus	91-114
14729376-7	2004	Furthermore, trilinolein and N-acetylcysteine decreased angiotensin II- or hydrogen peroxide (H2O2)-activated mitogen-activated protein kinases (MAPKs) phosphorylation, and activator protein-1 (AP-1)- [or nuclear factor-kappaB (NF-kappaB)]-reporter activities.	Acetylcysteine	29-45	Jun proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	173-192
14730207-11	2004	Furthermore, E(2) and antioxidants, such as N-acetyl cysteine and diphenylene iodonium, decreased Ang-II-induced cell proliferation, ET-1 promoter activity, ET-1 mRNA, ERK phosphorylation, and activator protein-1-mediated reporter activity.	Acetylcysteine	44-61	Jun proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	193-212
11230331-5	2001	Preincubation of vascular smooth muscle cells with N:-acetylcysteine (NAC), a potent antioxidant, almost completely inhibited the Ang II-induced downregulation of AT(1)-R mRNA.	Acetylcysteine	51-68	angiotensin II receptor, type 1a	Rattus norvegicus	163-170
11230331-5	2001	Preincubation of vascular smooth muscle cells with N:-acetylcysteine (NAC), a potent antioxidant, almost completely inhibited the Ang II-induced downregulation of AT(1)-R mRNA.	Acetylcysteine	70-73	angiotensin II receptor, type 1a	Rattus norvegicus	163-170
11230331-6	2001	The effect of NAC was due to stabilization of the AT(1)-R mRNA that was destabilized by Ang II.	Acetylcysteine	14-17	angiotensin II receptor, type 1a	Rattus norvegicus	50-57
22286146-4	2012	OBJECTIVES: To determine if RyR-mediated Ca(2+) release activated by the specific agonist 4-chloro-m-cresol (4-CMC) induces fragmentation of the mitochondrial network, and to ascertain if NAC prevents the mitochondrial fragmentation induced by AbetaOs and/or 4-CMC.	Acetylcysteine	188-191	ryanodine receptor 2	Rattus norvegicus	28-31
11112425-0	2000	Regulation of HGF/SF gene expression in MRC-5 cells by N-acetylcysteine.	Acetylcysteine	55-71	hepatocyte growth factor	Homo sapiens	14-20
11112425-1	2000	The effect of N-acetylcysteine (NAC) on levels of hepatocyte growth factor/scatter factor (HGF/SF) gene transcripts was investigated in the human lung embryonic fibroblast cell line, MRC-5.	Acetylcysteine	14-30	hepatocyte growth factor	Homo sapiens	91-97
11112425-1	2000	The effect of N-acetylcysteine (NAC) on levels of hepatocyte growth factor/scatter factor (HGF/SF) gene transcripts was investigated in the human lung embryonic fibroblast cell line, MRC-5.	Acetylcysteine	32-35	hepatocyte growth factor	Homo sapiens	91-97
11112425-2	2000	NAC increased expression of HGF/SF mRNA, in a dose- and time-dependent fashion, by a mechanism independent of glutathione synthesis but sensitive to oxidant stress induced by H(2)O(2).	Acetylcysteine	0-3	hepatocyte growth factor	Homo sapiens	28-34
11112425-5	2000	Primer extension analysis demonstrated that NAC enhanced the expression of HGF/SF mRNA transcribed from the main transcription initiation site.	Acetylcysteine	44-47	hepatocyte growth factor	Homo sapiens	75-81
11112425-6	2000	Although the 5" flanking region of the HGF/SF gene contains a sequence at -1019 to -1011 with homology to the NF-kappaB response element, electrophoretic mobility shift assay demonstrated that this site did not bind nuclear factors in MRC-5 cells in the presence or absence of NAC.	Acetylcysteine	277-280	hepatocyte growth factor	Homo sapiens	39-45
14710110-0	2003	Mechanisms of matrix metalloproteinase-9 and matrix metalloproteinase-2 inhibition by N-acetylcysteine in the human term decidua and fetal membranes.	Acetylcysteine	86-102	matrix metallopeptidase 2	Homo sapiens	45-71
14710110-6	2003	RESULTS: N-acetylcysteine had a direct inhibitory effect on matrix metalloproteinase-2 and matrix metalloproteinase-9 activity, regardless of tissue origin, starting at 1.0 mmol/L.	Acetylcysteine	9-25	matrix metallopeptidase 2	Homo sapiens	60-117
14710110-13	2003	CONCLUSION: N-acetylcysteine, at higher concentrations, has an inhibitory effect on matrix metalloproteinase-2 and matrix metalloproteinase-9 activity, regardless of the tissue origin and the differential effect on secretion depending on the tissue and N-acetylcysteine concentration.	Acetylcysteine	12-28	matrix metallopeptidase 2	Homo sapiens	84-141
22286146-9	2012	In addition, we confirmed that preincubation with NAC abolished the stimulation of RyR-mediated Ca(2+) release induced by AbetaOs or 4-CMC.	Acetylcysteine	50-53	ryanodine receptor 2	Rattus norvegicus	83-86
14588144-3	2003	The increases of DNA fragmentation, Bax/Bcl-2 ratio, and caspase activities were abrogated by BAPTA-AM (an intracellular Ca(2+) chelator) and N-acetyl-L-cysteine (an antioxidant), and augmented by wortmannin [a phosphatidylinositol 3-kinase (PI3K) inhibitor].	Acetylcysteine	142-161	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Bos taurus	211-240
11053552-5	2000	On individual immediate cotreatment, some molecules exhibited selective protection against only one mustard, such as DMTU and WR-1065 against HN2 and DOX against SM, whereas NAC and L-TC were effective against both SM and HN2 cytotoxicity.	Acetylcysteine	174-177	MT-RNR2 like 2 (pseudogene)	Homo sapiens	222-225
22286146-10	2012	CONCLUSION: The present results strongly suggest that the general antioxidant NAC prevents AbetaO-induced mitochondrial fragmentation by preventing RyR-mediated Ca(2+)-induced Ca(2+) release.	Acetylcysteine	78-81	ryanodine receptor 2	Rattus norvegicus	148-151
21790669-7	2011	In ethanol-fed rats, NAC reduced inflammation, converted the steatosis from a predominantly microvesicular to a mainly macrovesicular histological pattern, reduced pro-inflammatory cytokine gene expression, ceramide load, and acid sphingomyelinase activity, and increased expression of IGF-1 receptor and IGF-2 in liver.	Acetylcysteine	21-24	insulin-like growth factor 1 receptor	Rattus norvegicus	286-300
11001759-5	2000	The antioxidant N-acetylcysteine partially abrogated the glucose-induced increase in ERK5 activity but had no effect on the increase in JNK1 activity.	Acetylcysteine	16-32	mitogen-activated protein kinase 7	Bos taurus	85-89
10775566-4	2000	Preincubation of VSMCs with either N-acetyl-L-cysteine and/or alpha-lipoic acid significantly decreased bradykinin-induced cytosolic and nuclear phosphorylation of p42(mapk) and p44(mapk).	Acetylcysteine	35-54	interferon induced protein 44	Homo sapiens	168-172
10775566-4	2000	Preincubation of VSMCs with either N-acetyl-L-cysteine and/or alpha-lipoic acid significantly decreased bradykinin-induced cytosolic and nuclear phosphorylation of p42(mapk) and p44(mapk).	Acetylcysteine	35-54	interferon induced protein 44	Homo sapiens	178-181
10775566-4	2000	Preincubation of VSMCs with either N-acetyl-L-cysteine and/or alpha-lipoic acid significantly decreased bradykinin-induced cytosolic and nuclear phosphorylation of p42(mapk) and p44(mapk).	Acetylcysteine	35-54	interferon induced protein 44	Homo sapiens	182-186
14652680-8	2003	The effect of cigarette smoke solution from IR5F cigarettes upon the beta-hexosaminidase release elicited by compound 48/80 (in quercetin-treated cells) and by concanavalin A (in cells cultured on fibronectin-coated wells) could be prevented by N-acetyl-L-cysteine, but not with either hemoglobin, alpha-tocopherol, catalase or palmitoylethanolamide.	Acetylcysteine	245-264	O-GlcNAcase	Rattus norvegicus	69-88
14556849-4	2003	V2O5-induced STAT-1 activation was blocked by catalase and N-acetyl-L-cysteine (NAC), suggesting vanadium-induced generation of H2O2.	Acetylcysteine	59-78	signal transducer and activator of transcription 1	Rattus norvegicus	13-19
14556849-4	2003	V2O5-induced STAT-1 activation was blocked by catalase and N-acetyl-L-cysteine (NAC), suggesting vanadium-induced generation of H2O2.	Acetylcysteine	80-83	signal transducer and activator of transcription 1	Rattus norvegicus	13-19
14511233-6	2003	Both NAC and GSH completely abolished the TNF-alpha-induced enhancement of CD40 expression, but had no considerable effect on the expression of CD80, CD86 and MHC.	Acetylcysteine	5-8	CD40 antigen	Mus musculus	75-79
14511233-7	2003	The marked decrease of CD40 protein with NAC was also detected by Western blotting, but was not associated with the expression level of CD40 mRNA in DC.	Acetylcysteine	41-44	CD40 antigen	Mus musculus	23-27
14511233-8	2003	Thus, NAC appears to reduce CD40 expression on DC by regulating a post-transcriptional pathway.	Acetylcysteine	6-9	CD40 antigen	Mus musculus	28-32
14511233-9	2003	The inhibitory effect of NAC or GSH on TNF-alpha-induced CD40 expression was released by simply removing these agents from the culture.	Acetylcysteine	25-28	CD40 antigen	Mus musculus	57-61
14511233-10	2003	In contrast, culture of TNF-alpha-treated DC with NAC or GSH markedly decreased the expression of CD40 within 12 hr.	Acetylcysteine	50-53	CD40 antigen	Mus musculus	98-102
10730821-2	2000	In human endothelial cells the intracellular glutathione levels were modulated by N-acetyl-L-cysteine (NAC), a precursor of glutathione and 1,3-bis(chloroethyl)-1-nitrosourea (BCNU), an inhibitor of glutathione reductase.	Acetylcysteine	82-101	glutathione-disulfide reductase	Homo sapiens	199-220
10730821-2	2000	In human endothelial cells the intracellular glutathione levels were modulated by N-acetyl-L-cysteine (NAC), a precursor of glutathione and 1,3-bis(chloroethyl)-1-nitrosourea (BCNU), an inhibitor of glutathione reductase.	Acetylcysteine	103-106	glutathione-disulfide reductase	Homo sapiens	199-220
21963990-6	2011	The antioxidant N-acetylcysteine suppressed all P450-dependent changes in protein secretion except for CD14.	Acetylcysteine	16-32	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	48-52
10657671-6	2000	The membrane anchorage of LAT, and consequently the phosphorylation of LAT and the cellular activation of the synovial fluid T lymphocytes upon TCR engagement, is restored in synovial fluid T lymphocytes after supplementation of the intracellular glutathione levels with N-acetyl-l -cysteine.	Acetylcysteine	271-291	linker for activation of T cells	Homo sapiens	26-29
12942544-6	2003	Pretreatment of cells with either GSE or NAC increased the early LPS-stimulated activation of p42/44 but had little effect on the sustained phase.	Acetylcysteine	41-44	erythrocyte membrane protein band 4.2	Bos taurus	94-97
14766088-6	2003	Treatment with N-acetyl-L-cysteine and catalase could inhibit lens opacification, apoptosis and caspase-3 activation induced by H(2)O(2).	Acetylcysteine	15-34	caspase 3	Rattus norvegicus	96-105
14766088-8	2003	CONCLUSION: These data indicate that antioxidants N-acetyl-L-cysteine and catalase, possibly through regulation of the activity of caspase-3, can prevent lens opacification and apoptosis of lens epithelial cells.	Acetylcysteine	50-69	caspase 3	Rattus norvegicus	131-140
10657671-6	2000	The membrane anchorage of LAT, and consequently the phosphorylation of LAT and the cellular activation of the synovial fluid T lymphocytes upon TCR engagement, is restored in synovial fluid T lymphocytes after supplementation of the intracellular glutathione levels with N-acetyl-l -cysteine.	Acetylcysteine	271-291	linker for activation of T cells	Homo sapiens	71-74
22122305-13	2011	NAC also inhibited the transcription of NFkappaB, IL-6, TNF-alpha and COX2 usually induced by LPS.	Acetylcysteine	0-3	cytochrome c oxidase II, mitochondrial	Mus musculus	70-74
21981804-4	2011	NAC strongly depressed phosphorylation of p38 mitogen-activated protein kinase (p38 MAPK), which is necessary for inducing TNFalpha in microglia.	Acetylcysteine	0-3	mitogen activated protein kinase 14	Rattus norvegicus	42-78
21981804-4	2011	NAC strongly depressed phosphorylation of p38 mitogen-activated protein kinase (p38 MAPK), which is necessary for inducing TNFalpha in microglia.	Acetylcysteine	0-3	mitogen activated protein kinase 14	Rattus norvegicus	80-88
21710343-1	2011	BACKGROUND: The aim of this study was to assess the effects of N-acetylcysteine (N-ACC) on contrast-induced nephropathy (CIN) defined by Cystatin C (Cys-C) serum levels and to evaluate the influence of Cys-C on clinical outcome in patients with ST-elevation myocardial infarction (STEMI).	Acetylcysteine	63-79	cystatin C	Homo sapiens	137-147
10508828-7	1999	Finally, although concomitant ingestion of N-acetylcysteine had no effect (p &gt; 0.05) on MMP production, it increased (p &gt; 0.05) lung glutathione levels, blocked (p &lt; 0.05) MMP-9 and MMP-2 activation, and decreased (p &lt; 0.05) levels of the 7S fragment of type IV collagen.	Acetylcysteine	43-59	matrix metallopeptidase 2	Rattus norvegicus	191-196
12745250-6	2003	In agreement with this hypothesis was the finding that the physiologic reductant N-acetylcysteine decreased Grx-1 expression whereas tert-butyl hydroperoxide increased Grx-1 expression.	Acetylcysteine	81-97	glutaredoxin	Homo sapiens	108-113
12649745-5	2003	The L-PAM-induced accumulation of B7-1 mRNA was prevented with the antioxidant N-acetyl- L-cysteine (NAC), indicating that reactive oxygen species are important for the transcriptional regulation.	Acetylcysteine	79-99	peptidylglycine alpha-amidating monooxygenase	Mus musculus	6-9
12649745-5	2003	The L-PAM-induced accumulation of B7-1 mRNA was prevented with the antioxidant N-acetyl- L-cysteine (NAC), indicating that reactive oxygen species are important for the transcriptional regulation.	Acetylcysteine	101-104	peptidylglycine alpha-amidating monooxygenase	Mus musculus	6-9
12504805-6	2003	Moreover, blocking the oxidative activation of the protein kinase C pathway by N-acetylcysteine inhibited glucose effects on NGF synthesis.	Acetylcysteine	79-95	nerve growth factor	Rattus norvegicus	125-128
21843581-10	2011	As expected, NAC suppressed the expression of iNOS, COX-2, and TNF-alpha by blocking proteasome-mediated degradation.	Acetylcysteine	13-16	prostaglandin-endoperoxide synthase 2	Mus musculus	52-57
21961969-7	2011	Furthermore, N-Acetyl-L-cysteine (NAC) or 1,2-bisethane-N,N,N",N"-tetraacetic acid tetrakis ester (BAPTA-AM) could decrease the apoptosis rate, the release of cyto-c and cleaved caspase-3 in SDT group, SERCA(2) degradation was found in SDT group and could also be prevented by the addition of NAC.	Acetylcysteine	13-32	caspase 3	Rattus norvegicus	178-187
12065696-6	2002	The ROS signal further activated caspase-3, an important effector caspase, which could be inhibited by antioxidants (Trolox or N-acetyl cysteine).	Acetylcysteine	127-144	caspase 3	Rattus norvegicus	33-42
12065697-8	2002	Ethanol- and acetaldehyde-induced activation of activator protein-1 and MAP kinases was blocked by the antioxidant N-acetyl-cysteine, suggesting a role of oxidative stress in the signal transduction.	Acetylcysteine	115-132	Jun proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	48-67
21961969-7	2011	Furthermore, N-Acetyl-L-cysteine (NAC) or 1,2-bisethane-N,N,N",N"-tetraacetic acid tetrakis ester (BAPTA-AM) could decrease the apoptosis rate, the release of cyto-c and cleaved caspase-3 in SDT group, SERCA(2) degradation was found in SDT group and could also be prevented by the addition of NAC.	Acetylcysteine	34-37	caspase 3	Rattus norvegicus	178-187
21712056-10	2011	The ability of BRS-3 to regulate EGFR transactivation in NCI-H1299-BRS-3 cells was reduced by AG1478 or gefitinib (EGFR tyrosine kinase inhibitors), GM6001 (matrix metalloprotease inhibitor), PP2 (Src inhibitor), N-acetylcysteine (anti-oxidant), Tiron (superoxide scavenger) and DPI (NADPH oxidase inhibitor).	Acetylcysteine	215-229	bombesin receptor subtype 3	Homo sapiens	15-20
21433060-5	2011	Anti-oxidants such as vitamin C or N-acetyl cysteine (NAC) blocked the strain-mediated increases of Cx 43, Nkx 2.5, and alpha5/beta1 integrins.	Acetylcysteine	35-52	gap junction protein, alpha 3	Mus musculus	100-105
12051701-4	2002	Exposure of pyruvate treated cells to the antioxidant and glutathione precursor N-acetylcysteine restores cell growth and reverses the increase in senescence-associated beta-galactosidase activity.	Acetylcysteine	80-96	galactosidase beta 1	Homo sapiens	169-187
12003792-6	2002	Nrf-1 and -2 activation by bleomycin is inhibited by the ROS quenching agent N-acetylcysteine (NAC), but not by U-0126, a MEK1/2 inhibitor that blocks bleomycin-induced MAPK activation.	Acetylcysteine	77-93	nuclear respiratory factor 1	Homo sapiens	0-12
12003792-6	2002	Nrf-1 and -2 activation by bleomycin is inhibited by the ROS quenching agent N-acetylcysteine (NAC), but not by U-0126, a MEK1/2 inhibitor that blocks bleomycin-induced MAPK activation.	Acetylcysteine	95-98	nuclear respiratory factor 1	Homo sapiens	0-12
21433060-5	2011	Anti-oxidants such as vitamin C or N-acetyl cysteine (NAC) blocked the strain-mediated increases of Cx 43, Nkx 2.5, and alpha5/beta1 integrins.	Acetylcysteine	35-52	NK2 homeobox 5	Mus musculus	107-114
21433060-5	2011	Anti-oxidants such as vitamin C or N-acetyl cysteine (NAC) blocked the strain-mediated increases of Cx 43, Nkx 2.5, and alpha5/beta1 integrins.	Acetylcysteine	54-57	gap junction protein, alpha 3	Mus musculus	100-105
12039859-5	2002	Diamide caused a rapid increase in oxidized glutathione (GSSG) and a loss of mitochondrial cytochrome c in 15-30 min, caspase-3 activation in 2 h, and apoptosis in 24 h. N-Acetyl cysteine attenuated GSSG elevation and diamide-induced apoptosis.	Acetylcysteine	170-187	caspase 3	Rattus norvegicus	118-127
21433060-5	2011	Anti-oxidants such as vitamin C or N-acetyl cysteine (NAC) blocked the strain-mediated increases of Cx 43, Nkx 2.5, and alpha5/beta1 integrins.	Acetylcysteine	54-57	NK2 homeobox 5	Mus musculus	107-114
21860597-6	2011	Pre-treatment of WEHI-231 cells with the antioxidant N-acetyl-L-cysteine (NAC) strongly inhibited CD40-mediated prevention of the recovery of Ca(2+) signaling.	Acetylcysteine	53-72	CD40 antigen	Mus musculus	98-102
12101081-12	2002	the increase in MIP-1 alpha mRNA expression induced by nicotine was attenuated by co-treatment with the antioxidant N-acetylcysteine (NAC), at doses of 10 and 20 mM, suggesting that the induction of MIP-1 alpha mRNA is mediated via the generation of reactive oxygen species (ROS).	Acetylcysteine	116-132	C-C motif chemokine ligand 3	Rattus norvegicus	16-27
12101081-12	2002	the increase in MIP-1 alpha mRNA expression induced by nicotine was attenuated by co-treatment with the antioxidant N-acetylcysteine (NAC), at doses of 10 and 20 mM, suggesting that the induction of MIP-1 alpha mRNA is mediated via the generation of reactive oxygen species (ROS).	Acetylcysteine	116-132	C-C motif chemokine ligand 3	Rattus norvegicus	199-210
12101081-12	2002	the increase in MIP-1 alpha mRNA expression induced by nicotine was attenuated by co-treatment with the antioxidant N-acetylcysteine (NAC), at doses of 10 and 20 mM, suggesting that the induction of MIP-1 alpha mRNA is mediated via the generation of reactive oxygen species (ROS).	Acetylcysteine	134-137	C-C motif chemokine ligand 3	Rattus norvegicus	16-27
12101081-12	2002	the increase in MIP-1 alpha mRNA expression induced by nicotine was attenuated by co-treatment with the antioxidant N-acetylcysteine (NAC), at doses of 10 and 20 mM, suggesting that the induction of MIP-1 alpha mRNA is mediated via the generation of reactive oxygen species (ROS).	Acetylcysteine	134-137	C-C motif chemokine ligand 3	Rattus norvegicus	199-210
21860597-6	2011	Pre-treatment of WEHI-231 cells with the antioxidant N-acetyl-L-cysteine (NAC) strongly inhibited CD40-mediated prevention of the recovery of Ca(2+) signaling.	Acetylcysteine	74-77	CD40 antigen	Mus musculus	98-102
21325641-10	2011	NAC pretreatment blunted IRB-induced cytokine upregulation in the diaphragm and resulted in decreased ERK1/2, P38, and NF-kappaB/p65 phosphorylation.	Acetylcysteine	0-3	mitogen activated protein kinase 3	Rattus norvegicus	102-108
21325641-10	2011	NAC pretreatment blunted IRB-induced cytokine upregulation in the diaphragm and resulted in decreased ERK1/2, P38, and NF-kappaB/p65 phosphorylation.	Acetylcysteine	0-3	mitogen activated protein kinase 14	Rattus norvegicus	110-113
21131132-9	2011	Expression of CD11a (p &lt; 0.05), CD18 (p &lt; 0.05) and CD97 (p &lt; 0.01) on the granulocytes were significantly lower in the NAC treated group, similarly to lymphocyte CD 49d (p &lt; 0.05) and monocyte CD 49d (p &lt; 0.01) and CD 97 (p &lt; 0.05) expression.	Acetylcysteine	129-132	integrin subunit alpha L	Homo sapiens	14-19
20836702-8	2011	Selective inhibition of the NADPH oxidase or N-acetyl L-cysteine also prevented the enhanced translocation of p65 in hippocampal cells, while N-acetyl L-cysteine abolished the increase in RyR2 protein content induced by high frequency stimulation.	Acetylcysteine	45-64	RELA proto-oncogene, NF-kB subunit	Homo sapiens	110-113
11937102-2	2002	In the present study, we explored whether endogenous CGRP is involved in reversal of tolerance to nitroglycerin with N-acetylcysteine or captopril in rats in vivo and vitro.	Acetylcysteine	117-133	calcitonin-related polypeptide alpha	Rattus norvegicus	53-57
11937102-9	2002	The present results suggest that reversal of tolerance to nitroglycerin with N-acetylcysteine or captopril is related to the increased release of CGRP in the rat.	Acetylcysteine	77-93	calcitonin-related polypeptide alpha	Rattus norvegicus	146-150
20969478-8	2011	Antioxidants such as ethyl pyruvate, quercetin, green tea, N-acetylcysteine, and curcumin are protective in the setting of experimental infection/sepsis and injury including ischemia-reperfusion, partly through attenuating HMGB1 release and systemic accumulation.	Acetylcysteine	59-75	high mobility group box 1	Homo sapiens	223-228
11820776-4	2002	The results showed: (i) significant alterations of RBC ultrastructure; (ii) relevant changes of spectrin cytoskeleton; (iii) altered insulin receptor distribution; and (iv) that treatment with the antioxidizing drug N-acetylcysteine was capable of significantly counteracting these changes.	Acetylcysteine	216-232	insulin receptor	Homo sapiens	133-149
11820781-7	2002	Suppression of ROS formation by antioxidant N-acetylcysteine (NAC) downregulated the induction of MRP1 and MRP3 expression.	Acetylcysteine	44-60	ATP binding cassette subfamily C member 3	Homo sapiens	107-111
11820781-7	2002	Suppression of ROS formation by antioxidant N-acetylcysteine (NAC) downregulated the induction of MRP1 and MRP3 expression.	Acetylcysteine	62-65	ATP binding cassette subfamily C member 3	Homo sapiens	107-111
12361192-12	2002	A significant decrease in systolic and diastolic 24-h blood pressure (24 hBP) and daytime BP (dtBP) was achieved with the combination of ACEI and NAC (ACEI + NAC) when compared to the period with only ACEI: 24 hBP = 146.1 +/- 4.2 vs 137 +/- 3.1 (p &lt; 0.05) and 89.2 +/- 2.8 vs 83.5 +/- 3.7mmHg (p = 0.01).	Acetylcysteine	146-149	heme binding protein 1	Homo sapiens	73-76
12361192-12	2002	A significant decrease in systolic and diastolic 24-h blood pressure (24 hBP) and daytime BP (dtBP) was achieved with the combination of ACEI and NAC (ACEI + NAC) when compared to the period with only ACEI: 24 hBP = 146.1 +/- 4.2 vs 137 +/- 3.1 (p &lt; 0.05) and 89.2 +/- 2.8 vs 83.5 +/- 3.7mmHg (p = 0.01).	Acetylcysteine	146-149	heme binding protein 1	Homo sapiens	74-76
12361192-12	2002	A significant decrease in systolic and diastolic 24-h blood pressure (24 hBP) and daytime BP (dtBP) was achieved with the combination of ACEI and NAC (ACEI + NAC) when compared to the period with only ACEI: 24 hBP = 146.1 +/- 4.2 vs 137 +/- 3.1 (p &lt; 0.05) and 89.2 +/- 2.8 vs 83.5 +/- 3.7mmHg (p = 0.01).	Acetylcysteine	146-149	heme binding protein 1	Homo sapiens	210-213
12361192-12	2002	A significant decrease in systolic and diastolic 24-h blood pressure (24 hBP) and daytime BP (dtBP) was achieved with the combination of ACEI and NAC (ACEI + NAC) when compared to the period with only ACEI: 24 hBP = 146.1 +/- 4.2 vs 137 +/- 3.1 (p &lt; 0.05) and 89.2 +/- 2.8 vs 83.5 +/- 3.7mmHg (p = 0.01).	Acetylcysteine	158-161	heme binding protein 1	Homo sapiens	73-76
12361192-12	2002	A significant decrease in systolic and diastolic 24-h blood pressure (24 hBP) and daytime BP (dtBP) was achieved with the combination of ACEI and NAC (ACEI + NAC) when compared to the period with only ACEI: 24 hBP = 146.1 +/- 4.2 vs 137 +/- 3.1 (p &lt; 0.05) and 89.2 +/- 2.8 vs 83.5 +/- 3.7mmHg (p = 0.01).	Acetylcysteine	158-161	heme binding protein 1	Homo sapiens	74-76
12361192-12	2002	A significant decrease in systolic and diastolic 24-h blood pressure (24 hBP) and daytime BP (dtBP) was achieved with the combination of ACEI and NAC (ACEI + NAC) when compared to the period with only ACEI: 24 hBP = 146.1 +/- 4.2 vs 137 +/- 3.1 (p &lt; 0.05) and 89.2 +/- 2.8 vs 83.5 +/- 3.7mmHg (p = 0.01).	Acetylcysteine	158-161	heme binding protein 1	Homo sapiens	210-213
12361192-16	2002	In conclusion, the addition of NAC to an ACEI potentiates its antihypertensive effect during 24hBP and dtBP in smoker hypertensives.	Acetylcysteine	31-34	heme binding protein 1	Homo sapiens	95-98
21345685-6	2011	N-acetylcysteine (NAC) treatment abolished p38 phosphorylation as well as HO-1 induction caused by SC-1, indicating that ROS are upstream signals of p38 in Nrf2/ARE activation by SC-1.	Acetylcysteine	0-16	mitogen activated protein kinase 14	Rattus norvegicus	43-46
21345685-6	2011	N-acetylcysteine (NAC) treatment abolished p38 phosphorylation as well as HO-1 induction caused by SC-1, indicating that ROS are upstream signals of p38 in Nrf2/ARE activation by SC-1.	Acetylcysteine	0-16	mitogen activated protein kinase 14	Rattus norvegicus	149-152
21345685-6	2011	N-acetylcysteine (NAC) treatment abolished p38 phosphorylation as well as HO-1 induction caused by SC-1, indicating that ROS are upstream signals of p38 in Nrf2/ARE activation by SC-1.	Acetylcysteine	18-21	mitogen activated protein kinase 14	Rattus norvegicus	43-46
11782348-11	2002	The AP-1 binding activity was remarkably increased in lung tissue from both the BITC-NAC and PEITC-NAC groups.	Acetylcysteine	85-88	jun proto-oncogene	Mus musculus	4-8
21345685-6	2011	N-acetylcysteine (NAC) treatment abolished p38 phosphorylation as well as HO-1 induction caused by SC-1, indicating that ROS are upstream signals of p38 in Nrf2/ARE activation by SC-1.	Acetylcysteine	18-21	mitogen activated protein kinase 14	Rattus norvegicus	149-152
11782348-14	2002	This study demonstrates the chemopreventive efficacy of the NAC conjugates of PEITC and BITC administered in the diet after a single dose of B(a)P for lung tumorigenesis and provides the first in vivo evidence that activation of MAP kinases, AP-1 transcription factors, p53 phosphorylation, and the induction of apoptosis may be involved in the chemopreventive activity of these compounds.	Acetylcysteine	60-63	jun proto-oncogene	Mus musculus	242-246
21488133-6	2011	The adducts formed between beta-apo-8-carotenal (BA8C) and N-acetylcysteine and BA8C and N-acetyllysine were confirmed by HPLC and ESI-MS. Our results suggest that CDA could alter protein function by post-translational interaction with cysteine and lysine by thioether linkage and by schiff"s based bonds, respectively.	Acetylcysteine	59-75	cytidine deaminase	Homo sapiens	164-167
11709424-5	2001	IL-1 beta treatment stimulated superoxide production in VSM cells that was inhibited by pretreatment of cells with the superoxide scavenger N-acetyl-L-cysteine (NAC) and also by overexpression of the human manganese superoxide dismutase (MnSOD) gene.	Acetylcysteine	140-159	superoxide dismutase 2	Homo sapiens	238-243
11709424-5	2001	IL-1 beta treatment stimulated superoxide production in VSM cells that was inhibited by pretreatment of cells with the superoxide scavenger N-acetyl-L-cysteine (NAC) and also by overexpression of the human manganese superoxide dismutase (MnSOD) gene.	Acetylcysteine	161-164	superoxide dismutase 2	Homo sapiens	206-236
11709424-5	2001	IL-1 beta treatment stimulated superoxide production in VSM cells that was inhibited by pretreatment of cells with the superoxide scavenger N-acetyl-L-cysteine (NAC) and also by overexpression of the human manganese superoxide dismutase (MnSOD) gene.	Acetylcysteine	161-164	superoxide dismutase 2	Homo sapiens	238-243
20959139-6	2011	In addition, NAD(P)H oxidase inhibitor DPI and N-acetylcysteine (NAC), a scavenger of superoxide anion (O2-) also inhibited the enhanced phosphorylation of PDGFR and IGF-1R and c-Src in VSMC from SHR to control levels.	Acetylcysteine	47-63	insulin-like growth factor 1 receptor	Rattus norvegicus	166-172
11532856-6	2001	Third, consistent with these data, N-acetylcysteine reduced the stimulatory effect of HGF on stress kinase activities, while p42/44 mitogen activated kinase (MAPK) was unmodified, suggesting an involvement of c-Jun-N-terminal kinase (JNK) and p38 MAPK in HIF-1 activation.	Acetylcysteine	35-51	hepatocyte growth factor	Homo sapiens	86-89
11322781-9	2001	Antioxidants such as catalase or N-acetyl-cysteine decreased Ang II-activated ERK phosphorylation and inhibited Ang II-induced beta-MyHC promoter activity.	Acetylcysteine	33-50	myosin heavy chain 7	Rattus norvegicus	127-136
11226137-6	2001	We conclude: first, that the biphasic changes recorded in mitochondrial inner membrane potential by the effect of cocaine, were parallel to apoptosis; second, that caspase-3 activity and cleavage to it p20 subunit increased sharply in parallel to the translocation of cytochrome c from mitochondria to cytosol; and third, that the antioxidants, NAC or DFO exerted a noticeable protective role in counteracting the cytotoxicity of cocaine, these effects being more pronounced in the case of DFO than NAC.	Acetylcysteine	499-502	caspase 3	Rattus norvegicus	164-173
20959139-6	2011	In addition, NAD(P)H oxidase inhibitor DPI and N-acetylcysteine (NAC), a scavenger of superoxide anion (O2-) also inhibited the enhanced phosphorylation of PDGFR and IGF-1R and c-Src in VSMC from SHR to control levels.	Acetylcysteine	65-68	insulin-like growth factor 1 receptor	Rattus norvegicus	166-172
21283817-7	2011	Furthermore, chronic CSE treatment was found to increase ROS (reactive oxygen species) production, and application of the ROS scavengers N-acetylcysteine abrogated the expression of PDK2 and HIF1alpha.	Acetylcysteine	137-153	pyruvate dehydrogenase kinase 2	Homo sapiens	182-186
11167995-5	2001	This response is paralleled by increased NF-kappaB p65/p50 binding activity, and it is inhibited by pretreatment with N-acetyl-L-cysteine.	Acetylcysteine	118-137	RELA proto-oncogene, NF-kB subunit	Homo sapiens	51-54
21127198-12	2011	We observed that DBA-induced induction of DR5 and DR4 was mediated through generation of reactive oxygen species (ROS), as N-acetylcysteine blocked the induction of death receptors and suppression of cell survival proteins by DBA.	Acetylcysteine	123-139	TNF receptor superfamily member 10a	Homo sapiens	50-53
11140262-8	2000	However, full protection against photoinactivation of the apo form is observed after incubation with N-acetylcysteine but the latter only partially protects the aconitase function of the holo-IRP-1 from photoinactivation.	Acetylcysteine	101-117	aconitase 1	Homo sapiens	192-197
10837337-9	2000	Cellular levels of reduced thiols correlated with cell death, and pretreatment with N-acetylcysteine (NAC) fully protected from cell death in either PAPA/NO or SIN-1 exposure.	Acetylcysteine	84-100	pappalysin 1	Homo sapiens	149-156
10837337-9	2000	Cellular levels of reduced thiols correlated with cell death, and pretreatment with N-acetylcysteine (NAC) fully protected from cell death in either PAPA/NO or SIN-1 exposure.	Acetylcysteine	102-105	pappalysin 1	Homo sapiens	149-156
10653697-9	2000	We propose that the mod gene product is normally responsible for removing N-acetyl-cysteine from actin.	Acetylcysteine	74-91	modulo	Drosophila melanogaster	20-23
20940016-7	2011	By applying specific inhibitors in rat mesangial cells, ERK1/2 and p38 MAPK signaling pathways were demonstrated to be involved in the lipopolysaccharide-induced inflammatory responses, and were inhibited by SnPP and N-acetylcysteine treatment.	Acetylcysteine	217-233	mitogen activated protein kinase 3	Rattus norvegicus	56-62
10653697-10	2000	The biological significance of this process is demonstrated by observations that retention of the N-acetyl-cysteine in ACT88F affects the flight muscle function of mod(-) flies.	Acetylcysteine	98-115	modulo	Drosophila melanogaster	164-167
10652256-7	2000	The HNE-mediated activation of caspases, cleavage of PARP and DNA fragmentation were blocked by antioxidants cysteine, N-acety-L-cysteine and dithiothreitol, but not by two other HNE-reactive amino acids lysine and histidine, or by cystine, the oxidized form of cysteine.	Acetylcysteine	119-137	caspase 8	Homo sapiens	31-39
20940016-7	2011	By applying specific inhibitors in rat mesangial cells, ERK1/2 and p38 MAPK signaling pathways were demonstrated to be involved in the lipopolysaccharide-induced inflammatory responses, and were inhibited by SnPP and N-acetylcysteine treatment.	Acetylcysteine	217-233	mitogen activated protein kinase 14	Rattus norvegicus	67-70
20940016-7	2011	By applying specific inhibitors in rat mesangial cells, ERK1/2 and p38 MAPK signaling pathways were demonstrated to be involved in the lipopolysaccharide-induced inflammatory responses, and were inhibited by SnPP and N-acetylcysteine treatment.	Acetylcysteine	217-233	mitogen activated protein kinase 3	Rattus norvegicus	71-75
22072928-6	2011	NAC also inhibited both adipogenic transcription factors CCAAT/enhancer binding protein beta (C/EBP beta) and peroxisomal proliferator activated receptor gamma (PPAR gamma) expression; we suggested that intracellular GSH content could be responsible for these effects.	Acetylcysteine	0-3	CCAAT enhancer binding protein beta	Homo sapiens	57-92
10573084-4	1999	N-Acetylcysteine (NAC) is an antioxidant that inhibits the B7-1/CD28 expression in vitro, and it may contrabalance the effects of free radicals and oxidative stress; it has been tested in eight patients with steroid-resistant acute GVHD.	Acetylcysteine	0-16	CD28 molecule	Homo sapiens	64-68
10573084-4	1999	N-Acetylcysteine (NAC) is an antioxidant that inhibits the B7-1/CD28 expression in vitro, and it may contrabalance the effects of free radicals and oxidative stress; it has been tested in eight patients with steroid-resistant acute GVHD.	Acetylcysteine	18-21	CD80 molecule	Homo sapiens	59-63
10573084-4	1999	N-Acetylcysteine (NAC) is an antioxidant that inhibits the B7-1/CD28 expression in vitro, and it may contrabalance the effects of free radicals and oxidative stress; it has been tested in eight patients with steroid-resistant acute GVHD.	Acetylcysteine	18-21	CD28 molecule	Homo sapiens	64-68
22072928-6	2011	NAC also inhibited both adipogenic transcription factors CCAAT/enhancer binding protein beta (C/EBP beta) and peroxisomal proliferator activated receptor gamma (PPAR gamma) expression; we suggested that intracellular GSH content could be responsible for these effects.	Acetylcysteine	0-3	CCAAT enhancer binding protein beta	Homo sapiens	94-104
10573084-9	1999	We noticed significant decrease in CD80, CD25, and CD8+ cells after NAC therapy.	Acetylcysteine	68-71	CD80 molecule	Homo sapiens	35-39
20524210-8	2011	Moreover, the inhibition in TSP-1 mRNA expression by CoCl(2) was blocked by the addition of the potent antioxidant, N-acetylcysteine (NAC).	Acetylcysteine	116-132	thrombospondin 1	Rattus norvegicus	28-33
20524210-8	2011	Moreover, the inhibition in TSP-1 mRNA expression by CoCl(2) was blocked by the addition of the potent antioxidant, N-acetylcysteine (NAC).	Acetylcysteine	134-137	thrombospondin 1	Rattus norvegicus	28-33
10533675-0	1999	Antagonistic effects of pyrrolidine dithiocarbamate and N-acetyl-L-cysteine on surfactant protein A and B mRNAs.	Acetylcysteine	56-75	surfactant protein A1	Homo sapiens	79-105
21991373-3	2011	Furthermore, both antioxidants diphenyliodonium and N-acetylcysteine or overexpression of zebrafish catalase in GF-1 cells also reduced ROS production and protected cells for enhancing host survival rate due to RGNNV infection.	Acetylcysteine	52-68	endothelin receptor Ba	Danio rerio	136-139
10447747-11	1999	LPS treatment for 4 hr also significantly activated NF-kappaB binding, which could also be attenuated by pretreatment with N-acetylcysteine at the doses that reduced MIP-2 mRNA expression.	Acetylcysteine	123-139	C-X-C motif chemokine ligand 2	Rattus norvegicus	166-171
10220113-5	1999	Phenyl-tert-butyl nitrone (PBN), a nitrone-based free radical trap and N-acetyl-cysteine (NAC), a thiol reducing agent, were examined for their effects on the phosphorylation of p38 as well as phosphatase activity.	Acetylcysteine	71-88	mitogen activated protein kinase 14	Rattus norvegicus	178-181
21209852-8	2010	Moreover, in the breast cancer cell, LPA treatment resulted in remarkable production of reactive oxygen species (ROS), while LPA-induced ROS generation, PI3K/PAK1/ERK activation and cell migration could be inhibited by N-acetyl-L-Cysteine, a scavenger of ROS.	Acetylcysteine	219-238	p21 (RAC1) activated kinase 1	Homo sapiens	158-162
10220113-6	1999	Pretreatment of cells with either PBN or NAC at 1.0 mM suppressed IL1beta H2O2, and sorbitol-mediated activation of p38 and significantly increased phosphatase activity.	Acetylcysteine	41-44	mitogen activated protein kinase 14	Rattus norvegicus	116-119
20524045-7	2010	Treatment with the antioxidant N-acetyl-L-cysteine (NAC) blunted the increase in Zn(2+) levels and reduced LC3-II conversion, cathepsin D release and cell death induced by tamoxifen.	Acetylcysteine	31-50	cathepsin D	Homo sapiens	126-137
9927752-5	1999	When the mouse erythroleukaemic cell line MEL was induced with dimethylsulphoxide (DMSO), NaB or NAC, GATA-1 binding activity fell with DMSO, rose significantly with NaB and remained at about the same level in NAC-induced cells.	Acetylcysteine	97-100	GATA binding protein 1	Mus musculus	102-108
9927752-5	1999	When the mouse erythroleukaemic cell line MEL was induced with dimethylsulphoxide (DMSO), NaB or NAC, GATA-1 binding activity fell with DMSO, rose significantly with NaB and remained at about the same level in NAC-induced cells.	Acetylcysteine	210-213	GATA binding protein 1	Mus musculus	102-108
9741582-7	1998	MnSOD gene induction due to ONOO- was inhibited effectively by L-cysteine (10 mM) and partially inhibited by N-acetyl cysteine (50 mM) or pyrrole dithiocarbamate (10 mM).	Acetylcysteine	109-126	superoxide dismutase 2	Homo sapiens	0-5
21121367-6	2010	SWCNT induced nuclear NF-kB/P65 translocation can be inhibited by N-acetylcysteine, indicating elevated ICAM-1 and VCAM-1 expression is mediated by oxidative stress in RAECs, and may play important inflammatory roles in SWCNT-induced vascular endothelium damage.	Acetylcysteine	66-82	vascular cell adhesion molecule 1	Rattus norvegicus	115-121
9726778-8	1998	TNF-alpha production was inhibitable by the antioxidant N-acetylcysteine (NAC).	Acetylcysteine	56-72	eiger	Drosophila melanogaster	0-9
9726778-8	1998	TNF-alpha production was inhibitable by the antioxidant N-acetylcysteine (NAC).	Acetylcysteine	74-77	eiger	Drosophila melanogaster	0-9
10447747-5	1999	This increase by LPS was attenuated by co-treatment with the antioxidants N-acetylcysteine and dimethylsulphoxide, suggesting that the induction of MIP-2 mRNA is mediated via the generation of reactive oxygen species.	Acetylcysteine	74-90	C-X-C motif chemokine ligand 2	Rattus norvegicus	148-153
20826812-8	2010	Moreover, chemical antioxidants, such as N-acetylcysteine and butylated hydroxyanisole, and the NADPH oxidase inhibitor diphenyleneiodonium inhibited Srx induction as well as generation of reactive oxygen species, both of which were also suppressed in Nox2 (NADPH oxidase 2)-deficient bone marrow-derived macrophages.	Acetylcysteine	41-57	cytochrome b-245, beta polypeptide	Mus musculus	258-273
10204800-8	1999	N-acetylcysteine (4 mM) completely blocked the anti-proliferative and apoptotic-inducing effects of 4-HPR, suggesting that an oxidative mechanism may be involved.	Acetylcysteine	0-16	haptoglobin-related protein	Homo sapiens	102-105
20932820-8	2010	In addition, co-treatment of rats with TD and N-acetylcysteine prevented the increase in CD11b/c and CD68, but did not alter the onset of neurological impairment.	Acetylcysteine	46-62	Cd68 molecule	Rattus norvegicus	101-105
9862355-5	1998	Blocking ROI production by preincubation with the antioxidant N-acetyl-L-cysteine inhibits JNK activation, NF-kappaB-driven luciferase activity, and IL-6 secretion following CD40 ligation, suggesting a role for ROI in CD40-mediated signaling events.	Acetylcysteine	62-81	CD40 antigen	Mus musculus	174-178
9862355-5	1998	Blocking ROI production by preincubation with the antioxidant N-acetyl-L-cysteine inhibits JNK activation, NF-kappaB-driven luciferase activity, and IL-6 secretion following CD40 ligation, suggesting a role for ROI in CD40-mediated signaling events.	Acetylcysteine	62-81	CD40 antigen	Mus musculus	218-222
9668065-10	1998	The antioxidants N-acetyl cysteine, 1,1,3,3-tetramethyl-2-thiourea, and vitamin E inhibited both UVB-induced PAF biosynthesis as well as the augmentation of UVB-induced apoptosis in PAF-R-expressing KB clones, suggesting the possibility that UVB stimulates the production of oxidized lipid species with PAF-R agonistic activity in this model system.	Acetylcysteine	17-34	platelet activating factor receptor	Homo sapiens	182-187
9668065-10	1998	The antioxidants N-acetyl cysteine, 1,1,3,3-tetramethyl-2-thiourea, and vitamin E inhibited both UVB-induced PAF biosynthesis as well as the augmentation of UVB-induced apoptosis in PAF-R-expressing KB clones, suggesting the possibility that UVB stimulates the production of oxidized lipid species with PAF-R agonistic activity in this model system.	Acetylcysteine	17-34	platelet activating factor receptor	Homo sapiens	303-308
9862377-7	1998	The FasL-induced cell death pathway in microglia involves reactive oxygen intermediates because the antioxidants N-acetylcysteine and glutathione interfere with induction of apoptosis.	Acetylcysteine	113-129	Fas ligand (TNF superfamily, member 6)	Mus musculus	4-8
20674558-6	2010	DP increased the levels of reactive oxygen species (ROS) in HepG2 cells, and antioxidant N-acetylcysteine (NAC) completely blocked DP-induced ROS accumulation and the disruption of the balance between Bax and Bcl-2 proteins, and effectively blocked the decreased MMP and apoptosis, but had no effect on the activation of caspase-8 and the up-regulations of DR4 and DR5 induced by DP.	Acetylcysteine	89-105	caspase 8	Homo sapiens	321-330
20674558-6	2010	DP increased the levels of reactive oxygen species (ROS) in HepG2 cells, and antioxidant N-acetylcysteine (NAC) completely blocked DP-induced ROS accumulation and the disruption of the balance between Bax and Bcl-2 proteins, and effectively blocked the decreased MMP and apoptosis, but had no effect on the activation of caspase-8 and the up-regulations of DR4 and DR5 induced by DP.	Acetylcysteine	89-105	TNF receptor superfamily member 10a	Homo sapiens	357-360
20674558-6	2010	DP increased the levels of reactive oxygen species (ROS) in HepG2 cells, and antioxidant N-acetylcysteine (NAC) completely blocked DP-induced ROS accumulation and the disruption of the balance between Bax and Bcl-2 proteins, and effectively blocked the decreased MMP and apoptosis, but had no effect on the activation of caspase-8 and the up-regulations of DR4 and DR5 induced by DP.	Acetylcysteine	107-110	caspase 8	Homo sapiens	321-330
9641697-10	1998	Similarly, NAC treatment of explanted lesions abolished in situ gelatinolytic activity and MMP-9 expression.	Acetylcysteine	11-14	matrix metalloproteinase-9	Oryctolagus cuniculus	91-96
20674558-6	2010	DP increased the levels of reactive oxygen species (ROS) in HepG2 cells, and antioxidant N-acetylcysteine (NAC) completely blocked DP-induced ROS accumulation and the disruption of the balance between Bax and Bcl-2 proteins, and effectively blocked the decreased MMP and apoptosis, but had no effect on the activation of caspase-8 and the up-regulations of DR4 and DR5 induced by DP.	Acetylcysteine	107-110	TNF receptor superfamily member 10a	Homo sapiens	357-360
9794418-2	1998	We identified a rapid and delayed phase of MAPK activation with distinctive activity increases at 5 to 15 min and 15 to 24 h. Rapid and late MAPK activation were attenuated by the redox-modulating agent N-acetylcysteine.	Acetylcysteine	203-219	mitogen activated protein kinase 3	Rattus norvegicus	43-47
9794418-2	1998	We identified a rapid and delayed phase of MAPK activation with distinctive activity increases at 5 to 15 min and 15 to 24 h. Rapid and late MAPK activation were attenuated by the redox-modulating agent N-acetylcysteine.	Acetylcysteine	203-219	mitogen activated protein kinase 3	Rattus norvegicus	141-145
20550428-10	2010	NAC application eliminated the decreasing effects of fenthion on GST activity in this tissue.	Acetylcysteine	0-3	glutathione S-transferase	Oreochromis niloticus	65-68
9747602-5	1998	Addition of the antioxidant N-acetylcysteine (NAC, 1.0 mM) decreased ROFA and alpha-quartz-mediated IL-8 production by approximately 50% in normal and TNF-alpha-primed A549 cells.	Acetylcysteine	28-44	eiger	Drosophila melanogaster	151-160
9545524-8	1998	Augmentation of glutathione levels by pretreatment of cells with N-acetyl-L-cysteine attenuated the effect of PGA2 on IGF-I and Waf1 gene expression.	Acetylcysteine	65-84	cyclin-dependent kinase inhibitor 1A	Rattus norvegicus	128-132
9571990-9	1998	NAC prevented activation of mitogen-activated protein (MAP) kinases p42MAPK and p44MAPK and inhibited expression of cyclin D1, but had no effect on the levels of proliferating cell nuclear antigen.	Acetylcysteine	0-3	mitogen-activated protein kinase 3	Mus musculus	80-87
9747602-5	1998	Addition of the antioxidant N-acetylcysteine (NAC, 1.0 mM) decreased ROFA and alpha-quartz-mediated IL-8 production by approximately 50% in normal and TNF-alpha-primed A549 cells.	Acetylcysteine	46-49	eiger	Drosophila melanogaster	151-160
20970637-7	2010	An early decrease in pH values was detected in the NAC-treated group at 5 minutes before reperfusion (I-3; P=.051).	Acetylcysteine	51-54	brain protein I3	Homo sapiens	102-105
20970637-8	2010	We concluded that intraoperative NAC administration during the anhepatic phase of liver transplantation significantly decreased recipient pH values at 5 and 20 minutes after reperfusion, a decrease that was detected at 5 minutes before reperfusion (I-3).	Acetylcysteine	33-36	brain protein I3	Homo sapiens	249-252
20713718-7	2010	Moreover, treatment with antioxidants alpha-tocopherol and N-acetylcysteine (NAC) attenuated paraquat-induced implantation failure in P(4)-treated Fkbp52(-/-) mice.	Acetylcysteine	59-75	FK506 binding protein 4	Mus musculus	147-153
9722530-4	1998	H2O2 (10 mM) specifically activated the HDC promoter 10-12-fold, and this activation was blocked by both mannitol and N-acetylcysteine.	Acetylcysteine	118-134	histidine decarboxylase	Homo sapiens	40-43
9680182-2	1998	We describe a procedure based on the use of the enzyme acylase, which hydrolyzes N-acetylcysteine to cysteine.	Acetylcysteine	81-97	aminoacylase 1	Homo sapiens	55-62
9670954-6	1998	The activation of JNK by HIV-tat appears to be mediated through generation of free radical species, since pretreatment of cells with N-acetylcysteine (NAC) abolished the effect.	Acetylcysteine	133-149	tyrosine aminotransferase	Homo sapiens	29-32
9531254-7	1998	The role of redox-sensitive mechanisms in this process was further supported by the observation that HNE-induced DNA synthesis and AP-1 activation were inhibited by the antioxidants N-acetylcysteine and pyrrolidine dithiocarbamate.	Acetylcysteine	182-198	Jun proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	131-135
9457054-5	1998	N-Acetylcysteine (1 mM) interfered with NO-mediated apoptotic signaling, blocking DNA fragmentation as well as PARP and U1 snRNP cleavage.	Acetylcysteine	0-16	RNA, U1 small nuclear 1	Homo sapiens	120-128
9396727-7	1997	When cells were incubated in the presence of ALA or succinylacetone methyl ester, N-acetylcysteine inhibited IRP1 activation, suggesting that the observed effect is mediated by an oxidative process.	Acetylcysteine	82-98	aconitase 1	Homo sapiens	109-113
9440542-8	1997	NAC inhibited the generation of Smu/Sepsilon switch fragments in normal human B cells costimulated with IL-4 and anti-CD40 monoclonal antibody.	Acetylcysteine	0-3	CD40 molecule	Homo sapiens	118-122
9670954-6	1998	The activation of JNK by HIV-tat appears to be mediated through generation of free radical species, since pretreatment of cells with N-acetylcysteine (NAC) abolished the effect.	Acetylcysteine	151-154	tyrosine aminotransferase	Homo sapiens	29-32
20713718-7	2010	Moreover, treatment with antioxidants alpha-tocopherol and N-acetylcysteine (NAC) attenuated paraquat-induced implantation failure in P(4)-treated Fkbp52(-/-) mice.	Acetylcysteine	77-80	FK506 binding protein 4	Mus musculus	147-153
20713718-8	2010	Functional analyses using mouse embryonic fibroblasts show that Fkbp52 deficiency associated with reduced PRDX6 levels promotes H(2)O(2)-induced cell death, which is reversed by the addition of NAC or by forced expression of PRDX6, suggesting that Fkbp52 deficiency diminishes the threshold against OS by reducing PRDX6 levels.	Acetylcysteine	194-197	FK506 binding protein 4	Mus musculus	64-70
9287988-8	1997	Pretreatment with either the antioxidant N-acetyl cysteine or IL-1RA was sufficient to prevent almost completely down-regulation of IRP activity.	Acetylcysteine	41-58	caspase 3	Rattus norvegicus	132-135
20657580-2	2010	Metronidazole, a bactericide, or N-acetylcysteine, a precursor of sulfide-buffering glutathione, substantially prolonged the lifespan of Ethe1-deficient mice, with the combined treatment being additive.	Acetylcysteine	33-49	ethylmalonic encephalopathy 1	Mus musculus	137-142
20804648-14	2010	NAC may exert a protective effect on HLI through attenuation of hyperoxia-induced p38 MAPK activation.	Acetylcysteine	0-3	mitogen activated protein kinase 14	Rattus norvegicus	82-85
20388507-7	2010	The transactivation of the EGF receptor and the increase in reactive oxygen species caused by NMB-like peptides was inhibited by N-acetylcysteine (NAC) or Tiron.	Acetylcysteine	129-145	neuromedin B	Homo sapiens	94-97
20388507-7	2010	The transactivation of the EGF receptor and the increase in reactive oxygen species caused by NMB-like peptides was inhibited by N-acetylcysteine (NAC) or Tiron.	Acetylcysteine	147-150	neuromedin B	Homo sapiens	94-97
20417223-8	2010	The role of thiol oxidation in the initiation of mono-DC activation was confirmed by a pre-treatment with N-acetyl-l-cysteine which strongly decreased chemical-induced CD86 overexpression.	Acetylcysteine	106-125	CD86 molecule	Homo sapiens	168-172
20453393-8	2010	The antioxidant, N-acetyl-L-cysteine, suppressed glucose-induced osteopontin expression by decreasing ROS concentration.	Acetylcysteine	17-36	secreted phosphoprotein 1	Rattus norvegicus	65-76
20037173-10	2010	However, NAC pretreatment significantly improved renal function and decreased the activation of ERK, JNK, Bax and Bad, whereas it increased Bcl-2 and Bcl-xL.	Acetylcysteine	9-12	Bcl2-like 1	Rattus norvegicus	150-156
20233320-8	2010	Pharmacological agents NAC, U0126, and PD98059 were found to decrease the CsA-induced PAI-1 mRNA and protein expression (P &lt; 0.05).	Acetylcysteine	23-26	ERCC excision repair 8, CSA ubiquitin ligase complex subunit	Homo sapiens	74-77
20654106-10	2010	The band density ratio of pp38 and p38 was significantly upregulated in H/R group (13.4 vs. 3.89), the mRNA and protein expressions of bcl2 were significantly lower and bax expressions were significantly higher in H/R group than those in control group and these changes could also be attenuated by NAC.	Acetylcysteine	298-301	mitogen activated protein kinase 14	Rattus norvegicus	27-30
20654106-11	2010	CONCLUSION: NAC significantly reduced apoptosis through inhibiting the phosphorylation of p38 signal pathway.	Acetylcysteine	12-15	mitogen activated protein kinase 14	Rattus norvegicus	90-93
20093493-8	2010	In addition, NAC reduced PCNA and cyclin D1 immunostainings, as well as thyroid weight, whereas 15dPGJ2 influenced neither thyroid weight nor cell proliferation.	Acetylcysteine	13-16	cyclin D1	Homo sapiens	34-43
20179891-7	2010	NAC also decreased the expression of TNF-alpha mRNA and Caspase-3 mRNA in gastric mucosa.	Acetylcysteine	0-3	caspase 3	Rattus norvegicus	56-65
20179891-11	2010	In addition, vanilloid receptor subtype 1 may be involved in the protective mechanism of NAC against GI/R injury.	Acetylcysteine	89-92	transient receptor potential cation channel, subfamily V, member 1	Rattus norvegicus	13-41
19965809-0	2010	N-acetylcysteine inhibits RhoA and promotes apoptotic cell clearance during intense lung inflammation.	Acetylcysteine	0-16	ras homolog family member A	Mus musculus	26-30
19965809-7	2010	NAC enhanced the clearance of apoptotic cells and inhibited RhoA activity in alveolar macrophages at 3 days post LPS treatment.	Acetylcysteine	0-3	ras homolog family member A	Mus musculus	60-64
19965809-8	2010	NAC suppressed LPS-induced proinflammatory mediators, enhanced the production of transforming growth factor-beta1, reduced the accumulation of inflammatory cells, and reduced levels of protein and lactate dehydrogenase in bronchoalveolar lavage fluid.	Acetylcysteine	0-3	transforming growth factor, beta 1	Mus musculus	81-113
19965809-9	2010	In the presence of ex vivo apoptotic cells, alveolar macrophages exposed to LPS or LPS + NAC had reduced tumor necrosis factor-alpha levels and increased transforming growth factor-beta1 levels.	Acetylcysteine	89-92	transforming growth factor, beta 1	Mus musculus	154-186
19965809-11	2010	CONCLUSIONS: These results indicate that NAC can expedite the resolution of LPS-induced pulmonary inflammation through the inhibition of RhoA activity and the enhancement of apoptotic cell clearance.	Acetylcysteine	41-44	ras homolog family member A	Mus musculus	137-141
18793808-2	2010	To date, the effect of acetylcysteine on cystatin C-based CIN has not been described.	Acetylcysteine	23-37	cystatin C	Homo sapiens	41-51
18793808-6	2010	RESULTS: The overall incidence of cystatin C-based CIN among all study subjects was 10.2% (5.0% in N-acetylcysteine group and 15.1% in control group, p&lt;0.05) and that of serum creatinine-based CIN was 6% (3.8% in N-acetylcysteine group and 8.1% in control group, p=NS).	Acetylcysteine	99-115	cystatin C	Homo sapiens	34-44
18793808-6	2010	RESULTS: The overall incidence of cystatin C-based CIN among all study subjects was 10.2% (5.0% in N-acetylcysteine group and 15.1% in control group, p&lt;0.05) and that of serum creatinine-based CIN was 6% (3.8% in N-acetylcysteine group and 8.1% in control group, p=NS).	Acetylcysteine	216-232	cystatin C	Homo sapiens	34-44
18793808-8	2010	Multivariate logistic regression analysis showed that N-acetylcysteine administration was independently protective against the development of cystatin C-based CIN (Odd ratio[95% confidence interval] 0.255[0.066 to 0.994]) but there was a trend toward protection against that of serum creatinine-based CIN.	Acetylcysteine	54-70	cystatin C	Homo sapiens	142-152
18793808-9	2010	CONCLUSIONS: This study suggests that in patients with apparently normal renal function, prophylactic oral N-acetylcysteine administration is effective at preventing cystatin C-based CIN development after elective coronary angiography and/or intervention, and that serum cystatin C might be a more sensitive marker of the early CIN than serum creatinine.	Acetylcysteine	107-123	cystatin C	Homo sapiens	166-176
18793808-9	2010	CONCLUSIONS: This study suggests that in patients with apparently normal renal function, prophylactic oral N-acetylcysteine administration is effective at preventing cystatin C-based CIN development after elective coronary angiography and/or intervention, and that serum cystatin C might be a more sensitive marker of the early CIN than serum creatinine.	Acetylcysteine	107-123	cystatin C	Homo sapiens	271-281
19962414-5	2010	Reactive oxygen species (ROS) appeared to be involved in MMP-9 expression because treatment with the free radical scavenger, N-acetylcysteine (NAC), suppressed both 6-OHDA- and MPP(+)-induced MMP-9 promoter activities.	Acetylcysteine	125-141	matrix metallopeptidase 9	Mus musculus	57-62
19962414-5	2010	Reactive oxygen species (ROS) appeared to be involved in MMP-9 expression because treatment with the free radical scavenger, N-acetylcysteine (NAC), suppressed both 6-OHDA- and MPP(+)-induced MMP-9 promoter activities.	Acetylcysteine	125-141	M-phase phosphoprotein 6	Homo sapiens	177-180
19962414-5	2010	Reactive oxygen species (ROS) appeared to be involved in MMP-9 expression because treatment with the free radical scavenger, N-acetylcysteine (NAC), suppressed both 6-OHDA- and MPP(+)-induced MMP-9 promoter activities.	Acetylcysteine	125-141	matrix metallopeptidase 9	Mus musculus	192-197
19962414-5	2010	Reactive oxygen species (ROS) appeared to be involved in MMP-9 expression because treatment with the free radical scavenger, N-acetylcysteine (NAC), suppressed both 6-OHDA- and MPP(+)-induced MMP-9 promoter activities.	Acetylcysteine	143-146	matrix metallopeptidase 9	Mus musculus	57-62
19962414-5	2010	Reactive oxygen species (ROS) appeared to be involved in MMP-9 expression because treatment with the free radical scavenger, N-acetylcysteine (NAC), suppressed both 6-OHDA- and MPP(+)-induced MMP-9 promoter activities.	Acetylcysteine	143-146	M-phase phosphoprotein 6	Homo sapiens	177-180
19962414-5	2010	Reactive oxygen species (ROS) appeared to be involved in MMP-9 expression because treatment with the free radical scavenger, N-acetylcysteine (NAC), suppressed both 6-OHDA- and MPP(+)-induced MMP-9 promoter activities.	Acetylcysteine	143-146	matrix metallopeptidase 9	Mus musculus	192-197
19968960-3	2010	TGF-beta1-induced reduction of Grx1 expression caused an increase of intracellular reactive oxygen species (ROS) in EpRas cells, and pre-treatment of the ROS scavenger N-acetylcysteine (NAC) inhibited TGF-beta1-induced EMT.	Acetylcysteine	168-184	transforming growth factor, beta 1	Mus musculus	0-9
19968960-3	2010	TGF-beta1-induced reduction of Grx1 expression caused an increase of intracellular reactive oxygen species (ROS) in EpRas cells, and pre-treatment of the ROS scavenger N-acetylcysteine (NAC) inhibited TGF-beta1-induced EMT.	Acetylcysteine	168-184	transforming growth factor, beta 1	Mus musculus	201-210
19968960-3	2010	TGF-beta1-induced reduction of Grx1 expression caused an increase of intracellular reactive oxygen species (ROS) in EpRas cells, and pre-treatment of the ROS scavenger N-acetylcysteine (NAC) inhibited TGF-beta1-induced EMT.	Acetylcysteine	186-189	transforming growth factor, beta 1	Mus musculus	0-9
20368026-2	2010	The aim of this study was to illustrate the roles of adenovirus E1A protein on the transactivation of NF-kappaB, AP-1 in response to inflammatory stimuli and the effect of N-Acetylcysteine (NAC) upon the transactivation of NF-kappaB and AP-1 in cells stably expressing E1A protein.	Acetylcysteine	190-193	Jun proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	237-241
19635476-7	2009	EGF-stimulated cell adhesion or migration in cell culture was greatly suppressed in the presence of NAC while EGF-facilitated epithelial cell wound healing in corneal organ culture was also blocked by NAC.	Acetylcysteine	100-103	pro-epidermal growth factor	Oryctolagus cuniculus	0-3
19635476-7	2009	EGF-stimulated cell adhesion or migration in cell culture was greatly suppressed in the presence of NAC while EGF-facilitated epithelial cell wound healing in corneal organ culture was also blocked by NAC.	Acetylcysteine	201-204	pro-epidermal growth factor	Oryctolagus cuniculus	0-3
19635476-7	2009	EGF-stimulated cell adhesion or migration in cell culture was greatly suppressed in the presence of NAC while EGF-facilitated epithelial cell wound healing in corneal organ culture was also blocked by NAC.	Acetylcysteine	201-204	pro-epidermal growth factor	Oryctolagus cuniculus	110-113
20104683-9	2009	CONCLUSION: N-acetylcysteine can inhibit the activation of TLR2/4 and reduce TNF-alpha secretion resulted from I/R injury it might abate liver and lung injury following partial hepatic ischemia-reperfusion in mice.	Acetylcysteine	12-28	toll-like receptor 2	Mus musculus	59-65
19553350-8	2009	Interestingly, hydrogen peroxide increased HDAC-2 activity, and the treatment with an antioxidant, N-acetylcysteine, almost completely reduced TGF-beta1-induced activation of HDAC-2.	Acetylcysteine	99-115	histone deacetylase 2	Rattus norvegicus	43-49
19553350-8	2009	Interestingly, hydrogen peroxide increased HDAC-2 activity, and the treatment with an antioxidant, N-acetylcysteine, almost completely reduced TGF-beta1-induced activation of HDAC-2.	Acetylcysteine	99-115	histone deacetylase 2	Rattus norvegicus	175-181
19482076-6	2009	Our data also reveal that 4-HPR-mediated ROS evoke Akt conformational change by forming an intramolecular disulfide bond; N-acetylcysteine and glutathione, as thiol antioxidants, significantly abate the ROS generation in 4-HPR-exposed cells.	Acetylcysteine	122-138	haptoglobin-related protein	Homo sapiens	28-31
19482076-6	2009	Our data also reveal that 4-HPR-mediated ROS evoke Akt conformational change by forming an intramolecular disulfide bond; N-acetylcysteine and glutathione, as thiol antioxidants, significantly abate the ROS generation in 4-HPR-exposed cells.	Acetylcysteine	122-138	haptoglobin-related protein	Homo sapiens	223-226
19639223-8	2009	Moreover, the antibody recognizing the glutathionylated proteins co-precipitated and -localized with the cytoplasmic inactive form of p65NF-kappaB in H2O2- and NAC-treated cells, even when, in 1 mM NAC-treated cells, a part of p65 was glutathione-free and localized into the nucleus.	Acetylcysteine	160-163	RELA proto-oncogene, NF-kB subunit	Homo sapiens	134-137
9278255-9	1997	In the same system, the antioxidants, N-acetyl-cysteine (NAC) and pyrrolidine dithiocarbamate (PDTC) at concentrations shown to up-regulate the mRNAs of both c-jun and c-fos, also enhance the transactivity of AP-1.	Acetylcysteine	38-55	transcription factor Jun	Oryctolagus cuniculus	158-163
9278255-9	1997	In the same system, the antioxidants, N-acetyl-cysteine (NAC) and pyrrolidine dithiocarbamate (PDTC) at concentrations shown to up-regulate the mRNAs of both c-jun and c-fos, also enhance the transactivity of AP-1.	Acetylcysteine	57-60	transcription factor Jun	Oryctolagus cuniculus	158-163
9003061-8	1997	N-Acetylcysteine reduced (50%) the accumulation of HO-1 mRNA in astroglial cells after PrP 106-126 (25 microM) given for 5 days.	Acetylcysteine	0-16	prion protein	Rattus norvegicus	87-90
9110073-5	1997	NAC-treated and -untreated cells were subjected to FACS analysis of multiple-cell-surface adhesion and activation molecules and the results were compared.	Acetylcysteine	0-3	acyl-CoA synthetase long-chain family member 1	Mus musculus	51-55
9110073-8	1997	RESULTS: Unstimulated, non-dividing PBMC supported high levels of HIV replication when in direct contact with U1 cells in the presence of NAC or OTC; CD2 and CD54 (I-CAM1) were down-regulated on NAC-treated PBMC; and OTC-treated mice produced significantly higher yields of HIV-1 from peritoneal cells than did untreated mice.	Acetylcysteine	195-198	CD2 antigen	Mus musculus	150-153
9110073-8	1997	RESULTS: Unstimulated, non-dividing PBMC supported high levels of HIV replication when in direct contact with U1 cells in the presence of NAC or OTC; CD2 and CD54 (I-CAM1) were down-regulated on NAC-treated PBMC; and OTC-treated mice produced significantly higher yields of HIV-1 from peritoneal cells than did untreated mice.	Acetylcysteine	195-198	intercellular adhesion molecule 1	Mus musculus	158-162
9110073-8	1997	RESULTS: Unstimulated, non-dividing PBMC supported high levels of HIV replication when in direct contact with U1 cells in the presence of NAC or OTC; CD2 and CD54 (I-CAM1) were down-regulated on NAC-treated PBMC; and OTC-treated mice produced significantly higher yields of HIV-1 from peritoneal cells than did untreated mice.	Acetylcysteine	195-198	intercellular adhesion molecule 1	Mus musculus	164-171
8826530-4	1996	NAC also acted in synergy with ciliary neurotrophic factor (CNTF) to prevent killing of oligodendrocytes by TNF-alpha.	Acetylcysteine	0-3	ciliary neurotrophic factor	Mus musculus	31-58
8826530-4	1996	NAC also acted in synergy with ciliary neurotrophic factor (CNTF) to prevent killing of oligodendrocytes by TNF-alpha.	Acetylcysteine	0-3	ciliary neurotrophic factor	Mus musculus	60-64
8826530-5	1996	In analysis of "death by neglect," NAC markedly enhanced the extent of spinal ganglion neuron survival obtained with suboptimal concentrations of nerve growth factor and of oligodendrocyte survival obtained with suboptimal concentrations of CNTF or insulin-like growth factor-1.	Acetylcysteine	35-38	ciliary neurotrophic factor	Mus musculus	241-245
8826530-5	1996	In analysis of "death by neglect," NAC markedly enhanced the extent of spinal ganglion neuron survival obtained with suboptimal concentrations of nerve growth factor and of oligodendrocyte survival obtained with suboptimal concentrations of CNTF or insulin-like growth factor-1.	Acetylcysteine	35-38	insulin-like growth factor 1	Mus musculus	249-277
7755283-7	1995	Treatment of C2C12 cells with H2O2 induces a dose-dependent increase in c-jun/c-fos heterodimer binding, specifically reverted by the cysteine derivative and glutathione precursor N-acetyl-L-cysteine (NAC).	Acetylcysteine	180-199	jun proto-oncogene	Mus musculus	72-77
7755283-7	1995	Treatment of C2C12 cells with H2O2 induces a dose-dependent increase in c-jun/c-fos heterodimer binding, specifically reverted by the cysteine derivative and glutathione precursor N-acetyl-L-cysteine (NAC).	Acetylcysteine	201-204	jun proto-oncogene	Mus musculus	72-77
7755283-8	1995	The observation that the induction by angiotensin II of both the AP1 DNA binding activity and DNA synthesis in quiescent C2C12 myoblasts is abolished by NAC strongly suggests a role for reactive oxygen intermediates (ROIs) in the intracellular transduction of angiotensin II signals for immediate early gene induction and for cell proliferation.	Acetylcysteine	153-156	jun proto-oncogene	Mus musculus	65-68
7757200-7	1995	Dihydrolipoamide, dihydrolipoic acid, Captopril, acetylcysteine, EDTA, DETAPAC, histidine, bathocuproine, GSSG and trypanothione prevented LADH inactivation.	Acetylcysteine	49-63	dihydrolipoamide dehydrogenase	Sus scrofa	139-143
7558175-2	1995	In the present study, NAC treatment of the murine T-cell hybridoma DO-11.10 was found to inhibit apoptosis triggered by anti-CD3 antibody but enhance the process when induced by 6-alpha- methylprednisolone.	Acetylcysteine	22-25	CD3 antigen, epsilon polypeptide	Mus musculus	125-128
7841193-6	1995	N-Acetylcysteine inhibited IL1-induced interleukin-2 in EL4, however, demonstrating that N-acetylcysteine was biologically active.	Acetylcysteine	89-105	interleukin 1 complex	Mus musculus	27-30
7840217-4	1995	IL-1-induced tolerance to IL-1-mediated lung leak and the associated increases in lung catalase, lung G6PDH, and serum catalase activities were all prevented by treating rats with the IL-1-receptor antagonist or with N-acetyl-L-cysteine, an agent that increases intracellular glutathione levels.	Acetylcysteine	217-236	glucose-6-phosphate dehydrogenase	Rattus norvegicus	102-107
9593830-6	1998	N-acetylcysteine (NAC) treatment of Lp(a) decreased (48%) LBS activity while homocysteine treatment had no (89%) effect.	Acetylcysteine	0-16	lipoprotein(a)	Homo sapiens	36-41
9593830-6	1998	N-acetylcysteine (NAC) treatment of Lp(a) decreased (48%) LBS activity while homocysteine treatment had no (89%) effect.	Acetylcysteine	18-21	lipoprotein(a)	Homo sapiens	36-41
9535218-4	1998	Exposure to N-acetylcysteine before treatment with oxLDL, C2-ceramide, TNF-alpha, or H2O2 reversed a decrease in cellular glutathione concentrations as well as the enhanced production of p53 and MnSOD mRNA and protein.	Acetylcysteine	12-28	superoxide dismutase 2	Homo sapiens	195-200
9699154-7	1998	N-acetyl cysteine (NAC) downregulated this gp41 peptide-induced MMP-2 activity in T98G.	Acetylcysteine	0-17	matrix metallopeptidase 2	Homo sapiens	64-69
9699154-7	1998	N-acetyl cysteine (NAC) downregulated this gp41 peptide-induced MMP-2 activity in T98G.	Acetylcysteine	19-22	matrix metallopeptidase 2	Homo sapiens	64-69
9566590-7	1998	The stimulated AP-1 binding was also blocked by the antioxidant N-acetyl-L-cysteine, indicating that reactive oxygen species generated following ATP stimulation were involved in the induction of AP-1 activity.	Acetylcysteine	64-83	Jun proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	15-19
9566590-7	1998	The stimulated AP-1 binding was also blocked by the antioxidant N-acetyl-L-cysteine, indicating that reactive oxygen species generated following ATP stimulation were involved in the induction of AP-1 activity.	Acetylcysteine	64-83	Jun proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	195-199
9521863-4	1998	Removal of NAC from the culture medium stimulates SMCs to synchronously reenter the cell cycle as judged by induction of cyclin D1 and B-myb gene expression during mid and late G1 phase, respectively, and induction of histone gene expression and [3H]thymidine incorporation during S phase.	Acetylcysteine	11-14	cyclin D1	Homo sapiens	121-130
9454905-5	1998	When ER-1 cells were treated with EGF in the presence of N-acetylcysteine, a chemical antioxidant, the reversible or irreversible EGF-induced progression was inhibited.	Acetylcysteine	57-73	epidermal growth factor like 1	Rattus norvegicus	34-37
9454905-5	1998	When ER-1 cells were treated with EGF in the presence of N-acetylcysteine, a chemical antioxidant, the reversible or irreversible EGF-induced progression was inhibited.	Acetylcysteine	57-73	epidermal growth factor like 1	Rattus norvegicus	130-133
9440542-3	1997	In both cell lines, n-acetyl-L-cysteine (NAC), a potent thiol antioxidant, inhibited the triggering of the nuclear expression of NF-kappaB by IL-4 and by anti-CD40 monoclonal antibody.	Acetylcysteine	20-39	CD40 molecule	Homo sapiens	159-163
9440542-3	1997	In both cell lines, n-acetyl-L-cysteine (NAC), a potent thiol antioxidant, inhibited the triggering of the nuclear expression of NF-kappaB by IL-4 and by anti-CD40 monoclonal antibody.	Acetylcysteine	41-44	CD40 molecule	Homo sapiens	159-163
9440542-6	1997	Of note, CD40-mediated enhancement of IL-4-driven germline Cepsilon transcription was markedly decreased by NAC or by a decoy oligodeoxynucleotide for NF-kappaB.	Acetylcysteine	108-111	CD40 molecule	Homo sapiens	9-13
9331086-4	1997	The amount of AFAR protein in selenium-sufficient and -deficient Fischer rats was modulated by treatment with N-acetylcysteine; this antioxidant reduced basal expression of AFAR but did not modulate the relative overexpression of AFAR during selenium deficiency.	Acetylcysteine	110-126	aldo-keto reductase family 7 member A3	Rattus norvegicus	14-18
9331086-4	1997	The amount of AFAR protein in selenium-sufficient and -deficient Fischer rats was modulated by treatment with N-acetylcysteine; this antioxidant reduced basal expression of AFAR but did not modulate the relative overexpression of AFAR during selenium deficiency.	Acetylcysteine	110-126	aldo-keto reductase family 7 member A3	Rattus norvegicus	173-177
9331086-4	1997	The amount of AFAR protein in selenium-sufficient and -deficient Fischer rats was modulated by treatment with N-acetylcysteine; this antioxidant reduced basal expression of AFAR but did not modulate the relative overexpression of AFAR during selenium deficiency.	Acetylcysteine	110-126	aldo-keto reductase family 7 member A3	Rattus norvegicus	173-177
9298175-0	1997	N-acetylcysteine attenuates TNF-alpha-dependent reduction of IL-4-induced Fc epsilon RII expression in human monocytes.	Acetylcysteine	0-16	Fc epsilon receptor II	Homo sapiens	74-88
9298175-4	1997	In the present study, to test our hypothesis, we examined the effect of NAC on TNF-alpha-dependent reduction of IL-4-induced Fc epsilon RII expression in human monocytes.	Acetylcysteine	72-75	Fc epsilon receptor II	Homo sapiens	125-139
9298175-5	1997	NAC attenuated TNF-alpha-dependent reduction of IL-4-induced Fc epsilon RII expression by attenuating TNF-alpha-dependent reduction of Fc epsilon RII mRNA expression.	Acetylcysteine	0-3	Fc epsilon receptor II	Homo sapiens	61-75
9298175-5	1997	NAC attenuated TNF-alpha-dependent reduction of IL-4-induced Fc epsilon RII expression by attenuating TNF-alpha-dependent reduction of Fc epsilon RII mRNA expression.	Acetylcysteine	0-3	Fc epsilon receptor II	Homo sapiens	135-149
8955147-4	1996	N-acetyl-L-cysteine (NAC), which acts as a reductant in cells both by its direct reducing activity and by increasing the synthesis of the cellular antioxidant glutathione, inhibited neuronal differentiation induced by NGF or by the expression of oncogenic ras in PC12 cells.	Acetylcysteine	0-19	nerve growth factor	Rattus norvegicus	218-221
8955147-4	1996	N-acetyl-L-cysteine (NAC), which acts as a reductant in cells both by its direct reducing activity and by increasing the synthesis of the cellular antioxidant glutathione, inhibited neuronal differentiation induced by NGF or by the expression of oncogenic ras in PC12 cells.	Acetylcysteine	21-24	nerve growth factor	Rattus norvegicus	218-221
8955147-5	1996	NAC suppressed NGF-induced c-fos gene expression and AP-1 activation.	Acetylcysteine	0-3	nerve growth factor	Rattus norvegicus	15-18
8955147-7	1996	NAC also suppressed the NGF-induced activation of mitogen-activated protein kinases (MAPKs) and decreased the amount of tyrosine phosphorylation of MAPKs.	Acetylcysteine	0-3	nerve growth factor	Rattus norvegicus	24-27
8955147-12	1996	Thus, NAC suppresses NGF-induced neuronal differentiation by uncoupling the signal transduction from Ras to the MAP kinase cascade in PC12 cells.	Acetylcysteine	6-9	nerve growth factor	Rattus norvegicus	21-24
8900202-9	1996	Both L-histidine and N-acetyl-L-cysteine showed a significant inhibitory effect on PDT-induced SAPK and p38 HOG1 activation.	Acetylcysteine	21-40	mitogen-activated protein kinase 14	Mus musculus	104-107
8905424-0	1996	N-acetylcysteine pretreatment of cardiac surgery patients influences plasma neutrophil elastase and neutrophil influx in bronchoalveolar lavage fluid.	Acetylcysteine	0-16	elastase, neutrophil expressed	Homo sapiens	76-95
8905424-8	1996	NAC pretreatment prevented an increase in plasma neutrophil elastase activity (18.9 +/- 6.9 vs 49.9 +/- 5.6 ng/ml in group 1 at the end of ECC; p = 0.027).	Acetylcysteine	0-3	elastase, neutrophil expressed	Homo sapiens	49-68
8760145-3	1996	Pretreatment of human pulmonary adenocarcinoma cells H441 with the antioxidants N-acetyl-L-cysteine (NAC) and nordihydroguaiaretic acid (NDGA) blocked MnSOD induction by TNF-alpha, implicating ROS as a signaling agent in this pathway.	Acetylcysteine	80-99	superoxide dismutase 2	Homo sapiens	151-156
8574146-5	1995	Interestingly, 5 mM N-acetylcysteine (NAC) acts as an immunoenhancer; mitogenesis was enhanced 2 fold or more in general for control and HIV+ CD4+ T-cells and IL-2 production was enhanced 2-3 fold for anti-CD3 (with PMA or anti-CD28) for both controls and HIV+ CD4+ cells.	Acetylcysteine	20-36	CD28 molecule	Homo sapiens	228-232
8574146-5	1995	Interestingly, 5 mM N-acetylcysteine (NAC) acts as an immunoenhancer; mitogenesis was enhanced 2 fold or more in general for control and HIV+ CD4+ T-cells and IL-2 production was enhanced 2-3 fold for anti-CD3 (with PMA or anti-CD28) for both controls and HIV+ CD4+ cells.	Acetylcysteine	38-41	CD28 molecule	Homo sapiens	228-232
8574146-6	1995	However, NAC suppressed IL-4 production induced by anti-CD3 and anti-CD28 in both control and HIV+ CD4+ T cells.	Acetylcysteine	9-12	CD28 molecule	Homo sapiens	69-73
7507967-2	1994	We report here that NAC completely blocks activation induced death and associated DNA fragmentation of myelin basic protein (MBP) specific T cell hybridomas.	Acetylcysteine	20-23	myelin basic protein	Homo sapiens	103-123
8339559-4	1993	To investigate this hypothesis in keratoconus corneal epithelial extracts and a separate group comprising other corneal disorders, mainly herpes keratitis, we indirectly measured the GSH turnover by assaying the activity of glutathione reductase (GR) which is responsible in producing GSH and glutathione s-transferase (GST), which converts GSH into mercapturic acid.	Acetylcysteine	350-366	glutathione-disulfide reductase	Homo sapiens	224-245
19639223-8	2009	Moreover, the antibody recognizing the glutathionylated proteins co-precipitated and -localized with the cytoplasmic inactive form of p65NF-kappaB in H2O2- and NAC-treated cells, even when, in 1 mM NAC-treated cells, a part of p65 was glutathione-free and localized into the nucleus.	Acetylcysteine	198-201	RELA proto-oncogene, NF-kB subunit	Homo sapiens	134-137
19763043-7	2009	Furthermore, in an in vivo angiogenesis system using a chick chorioallantoic membrane model, TROG dose-dependently inhibited VEGF-induced angiogenesis, which was similar to the inhibitory effect of N-acetylcysteine on VEGF-induced angiogenesis.	Acetylcysteine	198-214	vascular endothelial growth factor A	Gallus gallus	218-222
19664398-7	2009	RESULTS: Treatment with NAC decreased the activity of Caspase-3, the content of GSSG, the values of AI but increased the content of GSH in both non-diabetic and diabetic rats (P&lt;0.05), but there were still significant difference about the values of above parameters between diabetic rats and non-diabetic rats (P&lt;0.05).	Acetylcysteine	24-27	caspase 3	Rattus norvegicus	54-63
1438209-8	1992	Cysteine, glutathione, and N-acetylcysteine also increase the affinity between Lp(a) and fibrin.	Acetylcysteine	27-43	lipoprotein(a)	Homo sapiens	79-84
1904276-8	1991	TFEC metabolites were very reactive with the thiol nucleophiles glutathione and N-acetylcysteine.	Acetylcysteine	80-96	transcription factor EC	Homo sapiens	0-4
19664398-8	2009	CONCLUSION: NAC can attenuated cardiomyocyte apoptosis by decreasing the activity of Caspase-3 and increasing the content of GSH, which has protective effect on ischemic/reperfused myocardium injury in both non-diabetic and diabetic rats, but the cardioprotective effect is less effective in diabetic rats than that in non-diabetic rats.	Acetylcysteine	12-15	caspase 3	Rattus norvegicus	85-94
19953933-13	2009	CONCLUSION: NAC inhibits the atherosclerotic formation, suppresses the levels of ox-LDL, MMP-9 and MMP-2 and downgrades the expression of matrix metalloproteinase mRNA.	Acetylcysteine	12-15	matrix metalloproteinase-9	Oryctolagus cuniculus	89-94
33824697-10	2021	These effects of TGF-beta 1 could be inhibited by the ROS scavenger N-acetylcysteine (NAC), siRNA-mediated knockdown of Smad3 and NOX4, and pharmacological inhibitors SB203580 (p38MAPK inhibitor) and LY294002 (Akt inhibitor).	Acetylcysteine	68-84	transforming growth factor, beta 1	Mus musculus	17-27
33824697-10	2021	These effects of TGF-beta 1 could be inhibited by the ROS scavenger N-acetylcysteine (NAC), siRNA-mediated knockdown of Smad3 and NOX4, and pharmacological inhibitors SB203580 (p38MAPK inhibitor) and LY294002 (Akt inhibitor).	Acetylcysteine	86-89	transforming growth factor, beta 1	Mus musculus	17-27
24915841-2	2014	Bmi-1 was knocked down in human renal proximal tubular epithelial (HK2) cells which were treated with 1 mm NAC for 72 or 96 h, and their phenotypes were compared with control cells.	Acetylcysteine	107-110	BMI1 proto-oncogene, polycomb ring finger	Homo sapiens	0-5
19526394-4	2009	Urine NAG/creatinine increased at deflation and at 3 h thereafter in the NAC group and the ratio was higher than in the placebo group.	Acetylcysteine	73-76	O-GlcNAcase	Homo sapiens	6-9
34780752-7	2021	Just like atractylodin, antioxidant N-acetyl-L-cysteine (NAC) could inhibit TRPC6/p-CaMK4 signaling activation to reduce fructose-induced podocytes hypermotility.	Acetylcysteine	36-55	calcium/calmodulin dependent protein kinase IV	Homo sapiens	84-89
34780752-7	2021	Just like atractylodin, antioxidant N-acetyl-L-cysteine (NAC) could inhibit TRPC6/p-CaMK4 signaling activation to reduce fructose-induced podocytes hypermotility.	Acetylcysteine	57-60	transient receptor potential cation channel subfamily C member 6	Homo sapiens	76-81
34780752-7	2021	Just like atractylodin, antioxidant N-acetyl-L-cysteine (NAC) could inhibit TRPC6/p-CaMK4 signaling activation to reduce fructose-induced podocytes hypermotility.	Acetylcysteine	57-60	calcium/calmodulin dependent protein kinase IV	Homo sapiens	84-89
19350554-7	2009	In contrast, N-acetylcysteine, a potent cysteine reductive compound, significantly prevents up-regulation of HMOX1, GCLM, and CXCL2 genes, and repression of MMP9 and CCL22 genes induced by As(2)O(3).	Acetylcysteine	13-29	C-C motif chemokine ligand 22	Homo sapiens	166-171
34619980-0	2021	N-acetylcysteine inhibits aortic stenosis progression in a murine model by blocking shear-induced activation of platelet latent TGF-beta1.	Acetylcysteine	0-16	transforming growth factor, beta 1	Mus musculus	128-137
19321450-8	2009	Furthermore, both mitogen-activated protein kinase (MAPK)/ERK inhibitor PD98059 and antioxidant N-acetyl-l-cysteine restored normal proliferation of Atm(-/-) astrocytes.	Acetylcysteine	96-115	ataxia telangiectasia mutated	Mus musculus	149-152
34619980-5	2021	N-acetylcysteine (NAC) inhibits WSS-induced TGF-beta1 activation in vitro.	Acetylcysteine	0-16	transforming growth factor, beta 1	Mus musculus	44-53
34619980-5	2021	N-acetylcysteine (NAC) inhibits WSS-induced TGF-beta1 activation in vitro.	Acetylcysteine	18-21	transforming growth factor, beta 1	Mus musculus	44-53
34619980-6	2021	We hypothesize that NAC will inhibit AS progression by inhibiting WSS-induced TGF-beta1 activation.	Acetylcysteine	20-23	transforming growth factor, beta 1	Mus musculus	78-87
34899969-9	2021	Result: NAC could effectively improve the immune status of COPD patients as well as the COPD mouse model by downregulating proinflammation and inflammation cytokines including IL-1beta, interferon- (IFN-) gamma, tumor necrosis factor- (TNF-) alpha, and IL-18.	Acetylcysteine	8-11	interleukin 18	Mus musculus	253-258
34899969-11	2021	Conclusion: NAC could effectively inhibit the production of IL-18 by suppressing NLRP3 expression in macrophages to reduce the production of IFN-gamma in NK cells.	Acetylcysteine	12-15	interleukin 18	Mus musculus	60-65
18783311-9	2009	Downregulation of Nox4, or pretreatment with N-acetylcysteine, attenuated hyperoxia-induced cell migration and capillary tube formation, suggesting that ROS generated by Nox4 regulate endothelial cell motility.	Acetylcysteine	45-61	NADPH oxidase 4	Homo sapiens	170-174
34687865-9	2021	Furthermore, HIV-1 Tat protein-induced epithelial monolayer disruption in HT-29 cells was rescued by antioxidant N-acetylcysteine (NAC).	Acetylcysteine	113-129	tyrosine aminotransferase	Homo sapiens	19-22
34687865-9	2021	Furthermore, HIV-1 Tat protein-induced epithelial monolayer disruption in HT-29 cells was rescued by antioxidant N-acetylcysteine (NAC).	Acetylcysteine	131-134	tyrosine aminotransferase	Homo sapiens	19-22
34601074-9	2021	While expression of TNF-alpha and IL-1beta, latency, as well as density of apoptosis cells in caspase-3 evaluation significantly more decreased in HBO+NAC group compared to other groups.	Acetylcysteine	151-154	caspase 3	Rattus norvegicus	94-103
18716872-3	2009	NAC alone and in combination with 5-ASA suppressed COX2 gene expression and prostaglandin E(2) (PGE(2)) levels to control values.	Acetylcysteine	0-3	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	51-55
19177506-0	2009	A liquid chromatography/tandem mass spectrometry method for detecting UGT-mediated bioactivation of drugs as their N-acetylcysteine adducts in human liver microsomes.	Acetylcysteine	115-131	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	70-73
34390730-9	2021	Indeed, the administration of GSH or N-acetylcysteine improved the expression of GPX4 and viability in MITOL-knockdown NRVMs.	Acetylcysteine	37-53	glutathione peroxidase 4	Rattus norvegicus	81-85
8621460-8	1996	Both H2O2 and MQ-induced up-regulation of MIP-1 alpha mRNA was suppressed by co-treatment with N-acetylcysteine, a synthetic antioxidant.	Acetylcysteine	95-111	C-C motif chemokine ligand 3	Rattus norvegicus	42-53
8626753-8	1996	Further, ERK2 activation by H2O2 was blocked by pretreatment with either N-acetyl-cysteine, o-phenanthroline, or mannitol, indicating that metal-catalyzed free radical formation mediates the initiation of signal transduction by H2O2.	Acetylcysteine	73-90	mitogen activated protein kinase 1	Rattus norvegicus	9-13
19177506-3	2009	In order to detect the UDP-glucuronosyltransferase (UGT)-mediated bioactivation of drugs, an in vitro trapping method using N-acetylcysteine (NAC) as a trapping agent followed by liquid chromatography/tandem mass spectrometry (LC/MS/MS) was developed in this study.	Acetylcysteine	124-140	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	23-50
19177506-3	2009	In order to detect the UDP-glucuronosyltransferase (UGT)-mediated bioactivation of drugs, an in vitro trapping method using N-acetylcysteine (NAC) as a trapping agent followed by liquid chromatography/tandem mass spectrometry (LC/MS/MS) was developed in this study.	Acetylcysteine	124-140	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	52-55
19177506-3	2009	In order to detect the UDP-glucuronosyltransferase (UGT)-mediated bioactivation of drugs, an in vitro trapping method using N-acetylcysteine (NAC) as a trapping agent followed by liquid chromatography/tandem mass spectrometry (LC/MS/MS) was developed in this study.	Acetylcysteine	142-145	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	23-50
19177506-3	2009	In order to detect the UDP-glucuronosyltransferase (UGT)-mediated bioactivation of drugs, an in vitro trapping method using N-acetylcysteine (NAC) as a trapping agent followed by liquid chromatography/tandem mass spectrometry (LC/MS/MS) was developed in this study.	Acetylcysteine	142-145	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	52-55
19063961-9	2009	Activation of JNK and p38MAPK was weaker in TNFalpha plus PY-treated NOS2(-/-) mice and 1400W and NAC blocked the activation of JNK and p38MAPK in wild-type mice.	Acetylcysteine	98-101	mitogen-activated protein kinase 14	Mus musculus	22-29
7827123-2	1995	N-Acetylcysteine was used to lower Lp(a) in the control subjects and their lipoproteins were re-examined after 7 days of treatment.	Acetylcysteine	0-16	lipoprotein(a)	Homo sapiens	35-40
7827123-11	1995	Following treatment with N-acetylcysteine, LDL cholesterol did not change, while Lp(a) decreased significantly by 24% (P &lt; 0.05).	Acetylcysteine	25-41	lipoprotein(a)	Homo sapiens	81-86
19063961-9	2009	Activation of JNK and p38MAPK was weaker in TNFalpha plus PY-treated NOS2(-/-) mice and 1400W and NAC blocked the activation of JNK and p38MAPK in wild-type mice.	Acetylcysteine	98-101	mitogen-activated protein kinase 14	Mus musculus	136-143
7841193-6	1995	N-Acetylcysteine inhibited IL1-induced interleukin-2 in EL4, however, demonstrating that N-acetylcysteine was biologically active.	Acetylcysteine	0-16	interleukin 1 complex	Mus musculus	27-30
8200134-0	1994	Inhibition with N-acetylcysteine of enhanced production of tumor necrosis factor in streptozotocin-induced diabetic rats.	Acetylcysteine	16-32	tumor necrosis factor-like	Rattus norvegicus	59-80
19033392-9	2009	A significant inhibition of the expression of hmox1 and nqo1 mRNAs and CD86 expression was found in 1-chloro 2,4-dinitrobenzene-treated THP-1 cells preincubated with N-acetyl cysteine, a glutathione precursor.	Acetylcysteine	166-183	CD86 molecule	Homo sapiens	71-75
19033395-9	2009	Furthermore, we found that arsenic-induced AhR activation and -enhanced CYP1A1 expression can be further increased by a prooxidant, buthionine-(S,R)-sulfoximine, and suppressed by antioxidants, such as N-acetylcysteine and catalase.	Acetylcysteine	202-218	aryl hydrocarbon receptor	Homo sapiens	43-46
7839688-6	1994	In several studies it has been shown, that Lp(a) concentrations can be reduced mainly by long term treatment with lipid-lowering sustained-release bezafibrate, ACE-inhibitor fosinopril, alpha-tocopheryl-nicotinate and N-acetylcysteine.	Acetylcysteine	218-234	lipoprotein(a)	Homo sapiens	43-48
18791325-10	2009	Intracellular ROS generation, production of ATP and MDA, and caspase-3, -8 and -9 activities were significantly increased in HG-treated RMCs, and were effectively attenuated by addition of NAC.	Acetylcysteine	189-192	caspase 3	Rattus norvegicus	61-81
1836221-2	1991	We determined whether the serum Lp(a) concentration could be decreased in vitro and in vivo by the reducing agent N-acetylcysteine (NAC), a drug used as a mucolytic agent, which acts by cleaving disulphide bonds.	Acetylcysteine	114-130	lipoprotein(a)	Homo sapiens	32-37
18713279-0	2008	The effects of N-acetylcysteine on the expression of matrix metalloproteinase-2 and tissue inhibitor of matrix metalloproteinase-2 in hepatic fibrosis in bile duct ligated rats.	Acetylcysteine	15-31	matrix metallopeptidase 2	Rattus norvegicus	53-130
1836221-2	1991	We determined whether the serum Lp(a) concentration could be decreased in vitro and in vivo by the reducing agent N-acetylcysteine (NAC), a drug used as a mucolytic agent, which acts by cleaving disulphide bonds.	Acetylcysteine	132-135	lipoprotein(a)	Homo sapiens	32-37
1836221-3	1991	High concentrations of NAC (greater than or equal to 8 mg ml-1) resulted in dissociation of the Lp(a) antigen in vitro.	Acetylcysteine	23-26	lipoprotein(a)	Homo sapiens	96-101
1836221-5	1991	In 12 subjects with a high plasma level of Lp(a), median 87.0 mg dl-1 (range 42.0-201.6 mg dl-1), a small but significant decrease in Lp(a) concentration of 7% (P = 0.02) was observed after administration of NAC in a dose of 1.2 g d-1 for 6 weeks.	Acetylcysteine	208-211	lipoprotein(a)	Homo sapiens	43-48
18713279-3	2008	We investigated the effects of N-acetylcysteine on the expression of matrix metalloproteinase-2 and tissue inhibitor of matrix metalloproteinase-2.	Acetylcysteine	31-47	matrix metallopeptidase 2	Rattus norvegicus	69-146
1836221-5	1991	In 12 subjects with a high plasma level of Lp(a), median 87.0 mg dl-1 (range 42.0-201.6 mg dl-1), a small but significant decrease in Lp(a) concentration of 7% (P = 0.02) was observed after administration of NAC in a dose of 1.2 g d-1 for 6 weeks.	Acetylcysteine	208-211	lipoprotein(a)	Homo sapiens	134-139
1836221-6	1991	These results indicate that NAC has only a limited capacity to reduce the concentration of Lp(a), which is not clinically significant.	Acetylcysteine	28-31	lipoprotein(a)	Homo sapiens	91-96
18713279-10	2008	N-acetylcysteine treatment also significantly decreased matrix metalloproteinase-2 activity and normalized tissue inhibitor of matrix metalloproteinase-2 expression.	Acetylcysteine	0-16	matrix metallopeptidase 2	Rattus norvegicus	56-82
18713279-10	2008	N-acetylcysteine treatment also significantly decreased matrix metalloproteinase-2 activity and normalized tissue inhibitor of matrix metalloproteinase-2 expression.	Acetylcysteine	0-16	matrix metallopeptidase 2	Rattus norvegicus	127-153
18713279-11	2008	CONCLUSION: Collectively, N-acetylcysteine showed inhibition of matrix metalloproteinase-2 expression and activity.	Acetylcysteine	26-42	matrix metallopeptidase 2	Rattus norvegicus	64-90
18713279-12	2008	In addition, administration of N-acetylcysteine was associated with downregulation of the expression of tissue inhibitor of matrix metalloproteinase-2 and amelioration of oxidative stress in the liver of bile duct ligated rats.	Acetylcysteine	31-47	matrix metallopeptidase 2	Rattus norvegicus	124-150
1751396-6	1991	When the 19-oxygenated steroids were separately subjected to reaction with N-acetyl-L-cysteine, these rapidly disappeared from the reaction mixture with t1/2 of 25 min (19-OHAT) and 20 s (19-oxo AT).	Acetylcysteine	75-94	interleukin 1 receptor like 1	Homo sapiens	153-163
18926564-7	2008	RESULTS: Repeated exposure of CSE induced TSLP mRNA and protein expression, which was inhibited by treatment with antioxidative N-acetylcysteine and by TNF-alpha receptor I deficiency.	Acetylcysteine	128-144	thymic stromal lymphopoietin	Mus musculus	42-46
33800932-6	2021	Spike and envelope protein disulfide bonds were reduced by Acetylcysteine.	Acetylcysteine	59-73	surface glycoprotein	Severe acute respiratory syndrome coronavirus 2	0-5
28812380-1	2018	OBJECTIVES: In Australia, the treatment guideline for patients with repeated supratherapeutic ingestion (RSTI) of paracetamol recommends an abbreviated acetylcysteine regimen if the paracetamol concentration is low (&lt;10 mg/L) and alanine aminotransferase (ALT) is normal or static after 8 hours of infusion.	Acetylcysteine	152-166	glutamic--pyruvic transaminase	Homo sapiens	233-257
18538675-4	2008	Supplementation of PUVA-treated fibroblasts with alpha-tocopherol (alpha-Toc), N-acetylcysteine (NAC), or alpha-lipoic acid (alpha-LA) abrogated the increased ROS generation and rescued fibroblasts from the ROS-dependent changes into the cellular senescence phenotype, such as cytoplasmic enlargement, enhanced expression of senescence-associated-beta-galactosidase and matrix-metalloproteinase-1, hallmarks of photoaging and intrinsic aging.	Acetylcysteine	79-95	galactosidase beta 1	Homo sapiens	347-365
18538675-4	2008	Supplementation of PUVA-treated fibroblasts with alpha-tocopherol (alpha-Toc), N-acetylcysteine (NAC), or alpha-lipoic acid (alpha-LA) abrogated the increased ROS generation and rescued fibroblasts from the ROS-dependent changes into the cellular senescence phenotype, such as cytoplasmic enlargement, enhanced expression of senescence-associated-beta-galactosidase and matrix-metalloproteinase-1, hallmarks of photoaging and intrinsic aging.	Acetylcysteine	97-100	galactosidase beta 1	Homo sapiens	347-365
34590731-3	2022	The purpose of this study was to examine whether advanced DWI techniques are able to sensitively detect the potential therapeutic effects of the antioxidant N-acetylcysteine (NAC) in a Disc1 svDelta2 preclinical rat model of psychiatric illness.	Acetylcysteine	157-173	DISC1 scaffold protein	Rattus norvegicus	185-199
18657320-8	2008	These results suggest that NAC activates mainly PI3K to phosphorylate p65 and subsequently induces DNA-binding activity of NF-kappaB, independent of its antioxidative function.	Acetylcysteine	27-30	RELA proto-oncogene, NF-kB subunit	Homo sapiens	70-73
34590731-3	2022	The purpose of this study was to examine whether advanced DWI techniques are able to sensitively detect the potential therapeutic effects of the antioxidant N-acetylcysteine (NAC) in a Disc1 svDelta2 preclinical rat model of psychiatric illness.	Acetylcysteine	175-178	DISC1 scaffold protein	Rattus norvegicus	185-199
18486599-3	2008	Unexpectedly LPS in the presence of ROS inhibitor N-acetyl-L-cysteine rapidly induced phosphorylation of eIF2alpha and induction of GADD34 expression.	Acetylcysteine	50-69	eukaryotic translation initiation factor 2A	Mus musculus	105-114
18299995-6	2008	Treatments with the antioxidant N-acetyl-cysteine (NAC) were needed to promote survival in cell recovering from mild proteasome inhibition while overexpression of the antiapoptotic protein Bcl-xL together with NAC attenuated cell death during recovery from potent inhibition.	Acetylcysteine	32-49	BCL2-like 1	Mus musculus	189-195
34958912-0	2022	N-acetylcysteine decreases dopamine transporter availability in the non-lesioned striatum of the 6-OHDA hemiparkinsonian rat.	Acetylcysteine	0-16	solute carrier family 6 member 3	Rattus norvegicus	27-47
34958912-2	2022	The short- and long-term regulatory mechanisms of NAC on the 6-OHDA hemiparkinsonian rat model were longitudinally investigated by performing positron emission tomography (PET) imaging using the specific dopamine transporter (DAT) radioligand (18F)FE-PE2I.	Acetylcysteine	50-53	solute carrier family 6 member 3	Rattus norvegicus	204-224
34958912-2	2022	The short- and long-term regulatory mechanisms of NAC on the 6-OHDA hemiparkinsonian rat model were longitudinally investigated by performing positron emission tomography (PET) imaging using the specific dopamine transporter (DAT) radioligand (18F)FE-PE2I.	Acetylcysteine	50-53	solute carrier family 6 member 3	Rattus norvegicus	226-229
34958912-3	2022	The results demonstrate that after a unilateral dopamine insult NAC has a strong influence on the non-lesioned hemisphere by decreasing the levels of DAT in the striatum early after the lesion.	Acetylcysteine	64-67	solute carrier family 6 member 3	Rattus norvegicus	150-153
34958912-4	2022	We interpret this early and short-term decrease of DAT in the healthy striatum of NAC-treated animals as a beneficial compensatory effect induced by NAC.	Acetylcysteine	82-85	solute carrier family 6 member 3	Rattus norvegicus	51-54
34958912-4	2022	We interpret this early and short-term decrease of DAT in the healthy striatum of NAC-treated animals as a beneficial compensatory effect induced by NAC.	Acetylcysteine	149-152	solute carrier family 6 member 3	Rattus norvegicus	51-54
34801870-10	2022	We also found that either TSH or NAC enhanced PKA, Akt, mTORC, AMPK, Sirtuins, PGC1alpha, NRF-2, mitofusin-2, TFAM and catalase in the N-TSHR-mAb stressed cells.	Acetylcysteine	33-36	transcription factor A, mitochondrial	Rattus norvegicus	110-114
34954677-8	2021	The ROS scavenger N-acetylcysteine (NAC) attenuated BPA-induced the mTOR/ULK1 pathway activation, apoptosis and autophagy.	Acetylcysteine	18-34	unc-51 like autophagy activating kinase 1	Homo sapiens	73-77
34954677-8	2021	The ROS scavenger N-acetylcysteine (NAC) attenuated BPA-induced the mTOR/ULK1 pathway activation, apoptosis and autophagy.	Acetylcysteine	36-39	unc-51 like autophagy activating kinase 1	Homo sapiens	73-77
18174269-0	2008	Improved estimation of glomerular filtration rate by serum cystatin C in preventing contrast induced nephropathy by N-acetylcysteine or zinc--preliminary results.	Acetylcysteine	116-132	cystatin C	Homo sapiens	59-69
34780752-7	2021	Just like atractylodin, antioxidant N-acetyl-L-cysteine (NAC) could inhibit TRPC6/p-CaMK4 signaling activation to reduce fructose-induced podocytes hypermotility.	Acetylcysteine	36-55	transient receptor potential cation channel subfamily C member 6	Homo sapiens	76-81
18642776-0	2008	[Effects of N-acetylcysteine on mRNA expression of monocyte chemotactic protein and macrophage inflammatory protein 2 in acute necrotizing pancreatitis: experiment with rats].	Acetylcysteine	12-28	C-X-C motif chemokine ligand 2	Rattus norvegicus	84-117
34895315-5	2021	Pretreatment with N-acetyl cysteine (ROS scavenger) or 4-phenylbutyric acid (4-PBA; ER stress inhibitor) significantly alleviated apoptosis, mitochondrial ROS production, mitochondrial dysfunction and ER stress response in a dose-dependent manner.	Acetylcysteine	18-35	epiregulin	Homo sapiens	84-86
34895315-5	2021	Pretreatment with N-acetyl cysteine (ROS scavenger) or 4-phenylbutyric acid (4-PBA; ER stress inhibitor) significantly alleviated apoptosis, mitochondrial ROS production, mitochondrial dysfunction and ER stress response in a dose-dependent manner.	Acetylcysteine	18-35	epiregulin	Homo sapiens	201-203
18642776-15	2008	The MCP-1 mRNA expression levels at different time points the NAC group were 0.2497 +/- 0.0168, 0.4457 +/- 0.0097, and 0.6306 +/- 0.0423 respectively, and the MIP-2 mRNA expression levels at the time points 3 h, 6 h, and 12 h of the NAC group were 0.2436 +/- 0.0099, 0.4312 +/- 0.0221, and 0.6302 +/- 0.0288 respectively, all significantly lower than those of the ANP group (all P &lt; 0.05).	Acetylcysteine	62-65	C-X-C motif chemokine ligand 2	Rattus norvegicus	159-164
18642776-20	2008	NAC may have beneficial effects on AP through downregulation of the expression of MCP-1 and MIP-2.	Acetylcysteine	0-3	C-X-C motif chemokine ligand 2	Rattus norvegicus	92-97
17979115-7	2008	We observed that NAC suppressed small GTPase RhoA activity and activation of RhoA by Pasteurella multocida toxin suppressed the osteogenic activity of NAC.	Acetylcysteine	17-20	ras homolog family member A	Mus musculus	45-49
34637923-9	2021	Conversely, suppression of ROS generation by N-acetyl cysteine (NAC) inhibited the M2-like polarization of Prx5-deficient macrophages, increased expression levels of inflammatory factors, inhibited the proliferation and migration of co-cultured lung cancer cells, and suppressed tumor growth in mice.	Acetylcysteine	45-62	peroxiredoxin 5	Mus musculus	107-111
34637923-9	2021	Conversely, suppression of ROS generation by N-acetyl cysteine (NAC) inhibited the M2-like polarization of Prx5-deficient macrophages, increased expression levels of inflammatory factors, inhibited the proliferation and migration of co-cultured lung cancer cells, and suppressed tumor growth in mice.	Acetylcysteine	64-67	peroxiredoxin 5	Mus musculus	107-111
34755672-5	2021	The effects of chrysin, LPS, and their combination on the mRNA expressions of iNOS and COX-2 were detected using RT-PCR; Western blotting was performed to examine the changes in cellular expressions of p-AKT, p-PRAS40, p-mTOR, mTOR, p-P70S6k, p-S6RP and S6RP following the treatments with LPS, N-Acetyl-L-cysteine, and chrysin, alone or in combinations.	Acetylcysteine	294-313	cytochrome c oxidase II, mitochondrial	Mus musculus	87-92
34755672-9	2021	Chrysin treatment significantly reduced the generation of endogenous ROS, and treatment with N-Acetyl-L-cysteine to eliminate intracellular ROS obviously reduced the expressions of iNOS and COX-2 (P < 0.05) and blocked the AKT/mTOR pathway (P < 0.05).	Acetylcysteine	93-112	cytochrome c oxidase II, mitochondrial	Mus musculus	190-195
17979115-7	2008	We observed that NAC suppressed small GTPase RhoA activity and activation of RhoA by Pasteurella multocida toxin suppressed the osteogenic activity of NAC.	Acetylcysteine	151-154	ras homolog family member A	Mus musculus	77-81
18025227-6	2007	Prior administration of the free radical scavengers, tempol and N-acetyl-L-cysteine, abolished the stress induction of p38 activation and the resulting mucosal inflammation and gastric injury.	Acetylcysteine	64-83	mitogen activated protein kinase 14	Rattus norvegicus	119-122
34650666-7	2021	Furthermore, MICAL2 knockdown attenuated intracellular ROS generation, while MICAL2 overexpression led to a decrease in the p-YAP/YAP ratio and promoted YAP nuclear localization and cell proliferation, effects that were reversed by pretreatment with the ROS scavenger N-acetyl-L-cysteine (NAC) and SOD-mimetic drug tempol.	Acetylcysteine	268-287	microtubule associated monooxygenase, calponin and LIM domain containing 2	Homo sapiens	13-19
34650666-7	2021	Furthermore, MICAL2 knockdown attenuated intracellular ROS generation, while MICAL2 overexpression led to a decrease in the p-YAP/YAP ratio and promoted YAP nuclear localization and cell proliferation, effects that were reversed by pretreatment with the ROS scavenger N-acetyl-L-cysteine (NAC) and SOD-mimetic drug tempol.	Acetylcysteine	268-287	microtubule associated monooxygenase, calponin and LIM domain containing 2	Homo sapiens	77-83
34650666-7	2021	Furthermore, MICAL2 knockdown attenuated intracellular ROS generation, while MICAL2 overexpression led to a decrease in the p-YAP/YAP ratio and promoted YAP nuclear localization and cell proliferation, effects that were reversed by pretreatment with the ROS scavenger N-acetyl-L-cysteine (NAC) and SOD-mimetic drug tempol.	Acetylcysteine	268-287	Yes1 associated transcriptional regulator	Homo sapiens	126-129
34650666-7	2021	Furthermore, MICAL2 knockdown attenuated intracellular ROS generation, while MICAL2 overexpression led to a decrease in the p-YAP/YAP ratio and promoted YAP nuclear localization and cell proliferation, effects that were reversed by pretreatment with the ROS scavenger N-acetyl-L-cysteine (NAC) and SOD-mimetic drug tempol.	Acetylcysteine	268-287	Yes1 associated transcriptional regulator	Homo sapiens	130-133
34650666-7	2021	Furthermore, MICAL2 knockdown attenuated intracellular ROS generation, while MICAL2 overexpression led to a decrease in the p-YAP/YAP ratio and promoted YAP nuclear localization and cell proliferation, effects that were reversed by pretreatment with the ROS scavenger N-acetyl-L-cysteine (NAC) and SOD-mimetic drug tempol.	Acetylcysteine	268-287	Yes1 associated transcriptional regulator	Homo sapiens	153-156
34650666-7	2021	Furthermore, MICAL2 knockdown attenuated intracellular ROS generation, while MICAL2 overexpression led to a decrease in the p-YAP/YAP ratio and promoted YAP nuclear localization and cell proliferation, effects that were reversed by pretreatment with the ROS scavenger N-acetyl-L-cysteine (NAC) and SOD-mimetic drug tempol.	Acetylcysteine	289-292	microtubule associated monooxygenase, calponin and LIM domain containing 2	Homo sapiens	13-19
34650666-7	2021	Furthermore, MICAL2 knockdown attenuated intracellular ROS generation, while MICAL2 overexpression led to a decrease in the p-YAP/YAP ratio and promoted YAP nuclear localization and cell proliferation, effects that were reversed by pretreatment with the ROS scavenger N-acetyl-L-cysteine (NAC) and SOD-mimetic drug tempol.	Acetylcysteine	289-292	microtubule associated monooxygenase, calponin and LIM domain containing 2	Homo sapiens	77-83
34650666-7	2021	Furthermore, MICAL2 knockdown attenuated intracellular ROS generation, while MICAL2 overexpression led to a decrease in the p-YAP/YAP ratio and promoted YAP nuclear localization and cell proliferation, effects that were reversed by pretreatment with the ROS scavenger N-acetyl-L-cysteine (NAC) and SOD-mimetic drug tempol.	Acetylcysteine	289-292	Yes1 associated transcriptional regulator	Homo sapiens	126-129
34650666-7	2021	Furthermore, MICAL2 knockdown attenuated intracellular ROS generation, while MICAL2 overexpression led to a decrease in the p-YAP/YAP ratio and promoted YAP nuclear localization and cell proliferation, effects that were reversed by pretreatment with the ROS scavenger N-acetyl-L-cysteine (NAC) and SOD-mimetic drug tempol.	Acetylcysteine	289-292	Yes1 associated transcriptional regulator	Homo sapiens	130-133
34650666-7	2021	Furthermore, MICAL2 knockdown attenuated intracellular ROS generation, while MICAL2 overexpression led to a decrease in the p-YAP/YAP ratio and promoted YAP nuclear localization and cell proliferation, effects that were reversed by pretreatment with the ROS scavenger N-acetyl-L-cysteine (NAC) and SOD-mimetic drug tempol.	Acetylcysteine	289-292	Yes1 associated transcriptional regulator	Homo sapiens	153-156
34684414-8	2021	Moreover, NAC and ALA augmented the expression of GLUT4 and the phosphorylation state of Akt (Ser473) and GSK3beta (Ser9), which improved the intracellular insulin transduction pathway.	Acetylcysteine	10-13	glycogen synthase kinase 3 alpha	Rattus norvegicus	106-114
34791723-8	2021	Furthermore, the addition of a PPAR-gamma antagonist abrogated the suppressive action of ABA on inflammation as well as on ER stress and oxidative stress, while NAC restored the protective effect of ABA in ARDS mice treated with a PPAR-gamma antagonist.	Acetylcysteine	161-164	peroxisome proliferator activated receptor gamma	Mus musculus	231-241
34779196-7	2021	Additionally, the ROS inhibitor N-acetyl-l-cysteine (NAC) inhibited p38 and activated Parkin-mediated mitophagy.	Acetylcysteine	32-51	mitogen-activated protein kinase 14	Mus musculus	68-71
34779196-7	2021	Additionally, the ROS inhibitor N-acetyl-l-cysteine (NAC) inhibited p38 and activated Parkin-mediated mitophagy.	Acetylcysteine	53-56	mitogen-activated protein kinase 14	Mus musculus	68-71
34867200-0	2021	N-Acetyl Cysteine Restores Sirtuin-6 and Decreases HMGB1 Release Following Lipopolysaccharide-Sensitized Hypoxic-Ischemic Brain Injury in Neonatal Mice.	Acetylcysteine	0-17	high mobility group box 1	Mus musculus	51-56
34867200-9	2021	NAC treatment restored sirtuin-6 protein levels, which was associated with reduced extracellular HMGB1 release and reduced thiol oxidation in the blood.	Acetylcysteine	0-3	high mobility group box 1	Mus musculus	97-102
17904098-7	2007	N-acetylcysteine (NAC), a well-known ROS scavenger, suppressed caspase-8 activation and the subsequent cleavage of caspase-9 and caspase-3, indicating the role of ROS in caspase-8-mediated apoptosis.	Acetylcysteine	0-16	caspase 8	Homo sapiens	63-72
34494136-12	2021	In VIC cultures treated with glucose in combination with reactive oxygen species (ROS) inhibitor (N-acetyl-L-cysteine), the expression of NF-kappaB and BMP-2 was significantly suppressed.	Acetylcysteine	98-117	bone morphogenetic protein 2	Homo sapiens	152-157
17904098-7	2007	N-acetylcysteine (NAC), a well-known ROS scavenger, suppressed caspase-8 activation and the subsequent cleavage of caspase-9 and caspase-3, indicating the role of ROS in caspase-8-mediated apoptosis.	Acetylcysteine	0-16	caspase 8	Homo sapiens	170-179
34703944-8	2021	However, we found markedly reduced (p < 0.001) MMP-2 secretion in cells incubated with NAC.	Acetylcysteine	87-90	matrix metallopeptidase 2	Homo sapiens	47-52
17904098-7	2007	N-acetylcysteine (NAC), a well-known ROS scavenger, suppressed caspase-8 activation and the subsequent cleavage of caspase-9 and caspase-3, indicating the role of ROS in caspase-8-mediated apoptosis.	Acetylcysteine	18-21	caspase 8	Homo sapiens	63-72
17904098-7	2007	N-acetylcysteine (NAC), a well-known ROS scavenger, suppressed caspase-8 activation and the subsequent cleavage of caspase-9 and caspase-3, indicating the role of ROS in caspase-8-mediated apoptosis.	Acetylcysteine	18-21	caspase 8	Homo sapiens	170-179
17714694-7	2007	Data on membrane localization, Mg2+ dependence, sensitivity to thiol oxidizing agents and protection by N-acetylcysteine (NAC) and DTT strongly suggest the involvement of PTP1B, the major PTP of human RBC associated to and acting on Band 3.	Acetylcysteine	122-125	protein tyrosine phosphatase receptor type U	Homo sapiens	171-174
34614473-6	2021	Additionally, the expression of NF-kappaB, caspase-1, and NLRP3 were decreased after pretreatment with ROS scavenging agent N-acetylcysteine (NAC, 5 mM pretreated for 2 h) and the NF-kappaB nuclear translocation inhibitor Dehydroxymethylepoxyquinomicin (DHMEQ, 10 mug/mL pretreatment for 4 h) respectively.	Acetylcysteine	124-140	caspase 1	Bos taurus	43-52
34614473-6	2021	Additionally, the expression of NF-kappaB, caspase-1, and NLRP3 were decreased after pretreatment with ROS scavenging agent N-acetylcysteine (NAC, 5 mM pretreated for 2 h) and the NF-kappaB nuclear translocation inhibitor Dehydroxymethylepoxyquinomicin (DHMEQ, 10 mug/mL pretreatment for 4 h) respectively.	Acetylcysteine	124-140	NLR family pyrin domain containing 3	Bos taurus	58-63
34614473-6	2021	Additionally, the expression of NF-kappaB, caspase-1, and NLRP3 were decreased after pretreatment with ROS scavenging agent N-acetylcysteine (NAC, 5 mM pretreated for 2 h) and the NF-kappaB nuclear translocation inhibitor Dehydroxymethylepoxyquinomicin (DHMEQ, 10 mug/mL pretreatment for 4 h) respectively.	Acetylcysteine	142-145	caspase 1	Bos taurus	43-52
17596533-6	2007	Moreover, NAC and taurine increased cyclin D1/cdk4 activation and suppressed p21(Waf1/Cip1) and p27(Kip1) expression in HG-treated cells.	Acetylcysteine	10-13	cyclin D1	Homo sapiens	36-45
34614473-6	2021	Additionally, the expression of NF-kappaB, caspase-1, and NLRP3 were decreased after pretreatment with ROS scavenging agent N-acetylcysteine (NAC, 5 mM pretreated for 2 h) and the NF-kappaB nuclear translocation inhibitor Dehydroxymethylepoxyquinomicin (DHMEQ, 10 mug/mL pretreatment for 4 h) respectively.	Acetylcysteine	142-145	NLR family pyrin domain containing 3	Bos taurus	58-63
34531444-8	2021	The effect was rescued by antioxidant, N-acetyl cysteine, thereby implying a ROS-specific effect and in the trophoblast cells, OS triggers UPR pathway through IRE1alpha-XBP1 axis.	Acetylcysteine	39-56	endoplasmic reticulum to nucleus signaling 1	Homo sapiens	159-168
34528650-1	2021	Well-dispersed chiral Ag2S quantum dots (Ag2S QDs) were facilely synthesized by using N-acetyl-L-cysteine (NALC) as the chiral ligand and loaded onto nanosheets of two-dimensional (2D) few-layer carbon nitride (C3N4).	Acetylcysteine	86-105	angiotensin II receptor type 1	Homo sapiens	22-26
17596533-6	2007	Moreover, NAC and taurine increased cyclin D1/cdk4 activation and suppressed p21(Waf1/Cip1) and p27(Kip1) expression in HG-treated cells.	Acetylcysteine	10-13	cyclin dependent kinase 4	Homo sapiens	46-50
34528650-1	2021	Well-dispersed chiral Ag2S quantum dots (Ag2S QDs) were facilely synthesized by using N-acetyl-L-cysteine (NALC) as the chiral ligand and loaded onto nanosheets of two-dimensional (2D) few-layer carbon nitride (C3N4).	Acetylcysteine	107-111	angiotensin II receptor type 1	Homo sapiens	22-26
34594329-7	2021	Moreover, inhibition of ROS release by scavenger N-acetyl-L-cysteine (NAC) abrogated the importance of ROS in NLRP3 assembly and apoptosis in MAC-T cells.	Acetylcysteine	49-68	NLR family pyrin domain containing 3	Bos taurus	110-115
34594329-7	2021	Moreover, inhibition of ROS release by scavenger N-acetyl-L-cysteine (NAC) abrogated the importance of ROS in NLRP3 assembly and apoptosis in MAC-T cells.	Acetylcysteine	70-73	NLR family pyrin domain containing 3	Bos taurus	110-115
18038907-0	2007	N-acetylcysteine prevents LPS-induced pro-inflammatory cytokines and MMP2 production in gingival fibroblasts.	Acetylcysteine	0-16	matrix metallopeptidase 2	Homo sapiens	69-73
17715118-3	2007	administration of N-acetylcysteine (NAC) on serum levels of creatinine and cystatin C, two markers of renal function, in patients with renal insufficiency who undergo emergency contrast-enhanced CT.	Acetylcysteine	18-34	cystatin C	Homo sapiens	75-85
34588976-10	2021	NAC also activated Sirt1 and preserved its protein level and subsequently promoted mitochondria biogenesis via deacetylating PGC1a.	Acetylcysteine	0-3	peroxisome proliferative activated receptor, gamma, coactivator 1 alpha	Mus musculus	125-130
34753839-9	2021	NAC incorporated at a concentration of 2.5 mM showed higher mineralization and considerably increased gene expression levels of runt-related transcription factor 2 (RUNX2), COL1A1, DSPP, and DMP-1.	Acetylcysteine	0-3	dentin sialophosphoprotein	Homo sapiens	181-185
34146985-6	2021	Cell cycle was arrested in G1 phase by BDE-47; (2) Elevated intracellular ROS, LDH levels and necrosis were found, which was alleviated by pretreatment with ROS scavenger N-acetylcysteine (NAC); (3) AhR plays an essential role in ligand-regulated transcription factor activation by exogenous environmental compounds.	Acetylcysteine	171-187	aryl hydrocarbon receptor	Homo sapiens	199-202
34146985-6	2021	Cell cycle was arrested in G1 phase by BDE-47; (2) Elevated intracellular ROS, LDH levels and necrosis were found, which was alleviated by pretreatment with ROS scavenger N-acetylcysteine (NAC); (3) AhR plays an essential role in ligand-regulated transcription factor activation by exogenous environmental compounds.	Acetylcysteine	189-192	aryl hydrocarbon receptor	Homo sapiens	199-202
17715118-3	2007	administration of N-acetylcysteine (NAC) on serum levels of creatinine and cystatin C, two markers of renal function, in patients with renal insufficiency who undergo emergency contrast-enhanced CT.	Acetylcysteine	36-39	cystatin C	Homo sapiens	75-85
34171382-8	2021	The ROS level in H322M cells was increased after PDTC treatment, and pretreatment with N-acetyl-cysteine (NAC) reversed PDTC-induced ACE2 suppression.	Acetylcysteine	87-104	angiotensin converting enzyme 2	Homo sapiens	133-137
17715118-9	2007	A 25% or greater increase in serum cystatin C concentration was found in nine (22%) of 40 patients in the control group and in seven (17%) of 41 patients in the NAC group (p = 0.59).	Acetylcysteine	161-164	cystatin C	Homo sapiens	35-45
34171382-8	2021	The ROS level in H322M cells was increased after PDTC treatment, and pretreatment with N-acetyl-cysteine (NAC) reversed PDTC-induced ACE2 suppression.	Acetylcysteine	106-109	angiotensin converting enzyme 2	Homo sapiens	133-137
17415663-5	2007	However, depletions in glutathione and Bcl-xL with potent proteasome inhibition exacerbated this response whereupon survival required the cooperative protection of NAC with Bcl-xL overexpression.	Acetylcysteine	164-167	BCL2-like 1	Mus musculus	39-45
34366878-4	2021	Purpose: We hypothesized that survival and lung ciliation, (a) would decrease progressively in Man1a2 +/- heterozygous and Man1a2 -/- null newborn pups compared with WT, and (b) could be enhanced by gestational treatment with N-Acetyl-cysteine (NAC), an antioxidant.	Acetylcysteine	226-243	mannosidase, alpha, class 1A, member 2	Mus musculus	123-129
34366878-4	2021	Purpose: We hypothesized that survival and lung ciliation, (a) would decrease progressively in Man1a2 +/- heterozygous and Man1a2 -/- null newborn pups compared with WT, and (b) could be enhanced by gestational treatment with N-Acetyl-cysteine (NAC), an antioxidant.	Acetylcysteine	245-248	mannosidase, alpha, class 1A, member 2	Mus musculus	123-129
34366878-14	2021	Conclusion: Survival and lung ciliation in the Man1a2 mutant mouse, and its improvement with N-Acetyl cysteine is genotype-dependent.	Acetylcysteine	93-110	mannosidase, alpha, class 1A, member 2	Mus musculus	47-53
34733484-10	2021	The cotreatment with HP and NAC revealed their ability to protect against hematological changes, oxidative damage, histopathological, and immunohistochemical changes, and genotoxicity induced by FA.	Acetylcysteine	28-31	glycogen synthase kinase 3 beta	Rattus norvegicus	195-197
17445339-9	2007	Pre-treatment with NAC prevented this impairment of recovery in MLP male offspring and improved recovery in all females.	Acetylcysteine	19-22	mucin 2, oligomeric mucus/gel-forming	Rattus norvegicus	64-67
34445365-0	2021	Single Dose of N-Acetylcysteine in Local Anesthesia Increases Expression of HIF1alpha, MAPK1, TGFbeta1 and Growth Factors in Rat Wound Healing.	Acetylcysteine	15-31	mitogen activated protein kinase 1	Rattus norvegicus	87-92
34445365-7	2021	On the 14th day, the number of cells stained with anti-CD68 and anti-CD31 antibodies was significantly larger in the tissues treated with 0.03% NAC compared with the control.	Acetylcysteine	144-147	Cd68 molecule	Rattus norvegicus	55-59
34439496-10	2021	Dnmt3b inhibitor 5"-azacytosine, antioxidant N-acetylcysteine, or Oxr1 recombinant protein attenuated loss in miR-29a and FoxO3 to mitigate oxidative stress, senescence, and mineralization matrix underproduction.	Acetylcysteine	45-61	microRNA 29a	Mus musculus	110-117
34193975-10	2021	Furthermore, juvenile (postnatal day 11-25) antioxidant treatment (N-acetyl-cysteine, 900 mg/L drinking water) prevented all these impairments in MAM rats.	Acetylcysteine	67-84	alpha-2-macroglobulin	Rattus norvegicus	146-149
17467183-9	2007	GSH and NAC conjugates of N-Me-alpha-MeDA and alpha-MeDA induced a concentration dependent delayed neuronal death, accompanied by activation of caspase 3, which occurred earlier in hyperthermic conditions.	Acetylcysteine	8-11	caspase 3	Rattus norvegicus	144-153
34250770-11	2021	NAC treatments decreased the expression of MMP2 and MMP9 in rats exposed to single or continuous Cd.	Acetylcysteine	0-3	matrix metallopeptidase 2	Rattus norvegicus	43-47
34102208-0	2021	N-acetylcysteine alleviates ocular surface damage in STZ-induced diabetic mice by inhibiting the ROS/NLRP3/Caspase-1/IL-1beta signaling pathway.	Acetylcysteine	0-16	caspase 1	Mus musculus	107-116
34102208-10	2021	Moreover, NAC markedly attenuated ROS accumulation and decreased NLRP3, IL-1beta and caspase-1 levels in diabetic cornea and conjunctiva.	Acetylcysteine	10-13	caspase 1	Mus musculus	85-94
34102208-11	2021	These results suggest that NAC improves ocular surface damage in STZ-induced diabetic mice, which may be related to the inhibition of the ROS/NLRP3/Caspase-1/IL-1beta signaling pathway.	Acetylcysteine	27-30	caspase 1	Mus musculus	148-157
35507947-8	2022	In addition, the expression of Gdf9, Lif, Bax, and Bcl2 genes were increased and Amh was decreased in groups cultured in the presence of NAC compared to groups cultured without NAC.	Acetylcysteine	137-140	anti-Mullerian hormone	Mus musculus	81-84
34065411-7	2021	Moreover, HepG2 cells under spinning conditions exhibited intensive TGFbeta-induced epithelial-to-mesenchymal transition (EMT) and increased susceptibility to acetaminophen (APAP)-induced hepatotoxicity as well as hepatotoxicity prevention by administration of N-acetylcysteine (NAC).	Acetylcysteine	261-277	transforming growth factor alpha	Homo sapiens	68-75
34065411-7	2021	Moreover, HepG2 cells under spinning conditions exhibited intensive TGFbeta-induced epithelial-to-mesenchymal transition (EMT) and increased susceptibility to acetaminophen (APAP)-induced hepatotoxicity as well as hepatotoxicity prevention by administration of N-acetylcysteine (NAC).	Acetylcysteine	279-282	transforming growth factor alpha	Homo sapiens	68-75
35489181-11	2022	Treatment with NAC+ASA increased the levels of glutamate transporters xCT and GLT-1 in nucleus accumbens, while Lactobacillus-GG administration increased those of the dopamine transporter (DAT).	Acetylcysteine	15-18	solute carrier family 6 member 3	Rattus norvegicus	189-192
35507947-8	2022	In addition, the expression of Gdf9, Lif, Bax, and Bcl2 genes were increased and Amh was decreased in groups cultured in the presence of NAC compared to groups cultured without NAC.	Acetylcysteine	177-180	anti-Mullerian hormone	Mus musculus	81-84
17462539-7	2007	NAC also lowers Akt activity, extracellular signal-regulated kinase 1/2, and the redox-sensitive transcription factor NF-kappaB, all of which are ROS related and seem to be in close connection with cell proliferation.	Acetylcysteine	0-3	mitogen activated protein kinase 3	Rattus norvegicus	30-71
35582415-7	2022	In addition, increased expression of caspase-3, KIM-1 and NGAL suffering from VCM was also reversed by NAC in vivo and in vitro.	Acetylcysteine	103-106	caspase 3	Rattus norvegicus	37-46
35582415-7	2022	In addition, increased expression of caspase-3, KIM-1 and NGAL suffering from VCM was also reversed by NAC in vivo and in vitro.	Acetylcysteine	103-106	lipocalin 2	Rattus norvegicus	58-62
17448897-8	2007	We observed that BzATP stimulates MAP kinase (ERK1/ERK2, p38, and JNK1/JNK2) phosphorylation and that the antioxidants N-acetylcysteine and ascorbic acid strongly attenuate BzATP-mediated JNK1/JNK2 and p38 phosphorylation but only slightly reduce BzATP-induced ERK1/ERK2 phosphorylation.	Acetylcysteine	119-135	mitogen-activated protein kinase 14	Mus musculus	202-205
35582415-8	2022	NAC inhibited ROS production, decreased cell apoptosis by decreasing the Bax/Bcl-2 ratio and caspase-3 expression in HK-2 cells and regulated oxidative stress indicators in the kidney by decreasing GSH, SOD and CAT activity and increasing MDA levels.	Acetylcysteine	0-3	caspase 3	Rattus norvegicus	93-102
35611548-7	2022	In SNUC5/ OXTR cells, the production of intracellular reactive oxygen species (ROS) was significantly higher than that in SNU-C5 cells, and treatment with the ROS scavenger N-acetylcysteine restored the reduced autophagy levels.	Acetylcysteine	173-189	oxytocin receptor	Homo sapiens	10-14
17448897-8	2007	We observed that BzATP stimulates MAP kinase (ERK1/ERK2, p38, and JNK1/JNK2) phosphorylation and that the antioxidants N-acetylcysteine and ascorbic acid strongly attenuate BzATP-mediated JNK1/JNK2 and p38 phosphorylation but only slightly reduce BzATP-induced ERK1/ERK2 phosphorylation.	Acetylcysteine	119-135	mitogen-activated protein kinase 3	Mus musculus	261-265
17158644-5	2007	The enhanced expression of G(i)alpha-2 and G(i)alpha-3 proteins was restored to control levels by antioxidants such as N-acetyl-L-cysteine, alpha-tocopherol, DPI, and apocynin.	Acetylcysteine	119-138	G protein subunit alpha i3	Homo sapiens	43-54
35588920-6	2022	METHODS: Flow cytometric analysis was performed to assess the effects of NAC on SCAP viability.	Acetylcysteine	73-76	SREBF chaperone	Homo sapiens	80-84
35588920-11	2022	SCAP pre-treated with NAC had a significantly lower immune cell-mediated cytotoxicity to non-activated and activated PBMCs.	Acetylcysteine	22-25	SREBF chaperone	Homo sapiens	0-4
35588920-12	2022	The ELISA results showed that SCAP pre-treated with NAC induced lower levels of proinflammatory cytokines.	Acetylcysteine	52-55	SREBF chaperone	Homo sapiens	30-34
35123993-8	2022	Interestingly, NAC can block HQ-induced AhR activation and DNA damage and apoptosis.	Acetylcysteine	15-18	aryl hydrocarbon receptor	Homo sapiens	40-43
35123263-0	2022	The function of SARS-CoV-2 spike protein is impaired by disulfide-bond disruption with mutation at cysteine-488 and by thiol-reactive N-acetyl-cysteine and glutathione.	Acetylcysteine	134-151	surface glycoprotein	Severe acute respiratory syndrome coronavirus 2	27-32
35588920-13	2022	CONCLUSIONS: SCAP pre-treated with NAC have a higher chance of surviving the activated immune system.	Acetylcysteine	35-38	SREBF chaperone	Homo sapiens	13-17
17174578-4	2007	Moreover, NAC treatment inhibited an increase in the number of cells expressing high levels of erythroid-specific antigen TER119.	Acetylcysteine	10-13	lymphocyte antigen 76	Mus musculus	122-128
35143901-8	2022	Further treatment of UT-B-overexpressing B16 cells with reactive oxygen species scavenging agent N-acetyl-l-cysteine and coenzyme Q10 restored cell viability and mitochondrial function and increased polyamine production.	Acetylcysteine	97-116	solute carrier family 14 (urea transporter), member 1	Mus musculus	21-25
17334226-8	2007	Inhibition of Tat-induced ROS generation by N-acetyl cysteine, vitamin C and diphenyl iodonium suppressed Tat-induced NF-kappaB activation, ICAM-1 and VCAM-1 expression, and monocyte adhesion in CRT-MG.	Acetylcysteine	44-61	tyrosine aminotransferase	Homo sapiens	14-17
17334226-8	2007	Inhibition of Tat-induced ROS generation by N-acetyl cysteine, vitamin C and diphenyl iodonium suppressed Tat-induced NF-kappaB activation, ICAM-1 and VCAM-1 expression, and monocyte adhesion in CRT-MG.	Acetylcysteine	44-61	tyrosine aminotransferase	Homo sapiens	106-109
17869641-7	2007	Serum deprivation (0.5% FBS) producing ROS and exogenous H(2)O(2) treatment also enhanced mBAFF promoter activity, which was reduced by N-acetyl-l-cysteine (NAC), a well-known ROS scavenger.	Acetylcysteine	136-155	tumor necrosis factor (ligand) superfamily, member 13b	Mus musculus	90-95
35420738-0	2022	Diverse Impact of N-Acetylcysteine or Alpha-Lipoic Acid Supplementation during High-Fat Diet Regime on Matrix Metalloproteinase-2 and Matrix Metalloproteinase-9 in Visceral and Subcutaneous Adipose Tissue.	Acetylcysteine	18-34	matrix metallopeptidase 2	Rattus norvegicus	103-129
35420738-6	2022	Real-time PCR and western blot approaches were used to check whether NAC or ALA impacts MMP2/9 expression.	Acetylcysteine	69-72	matrix metallopeptidase 2	Rattus norvegicus	88-94
35420738-8	2022	Moreover, NAC and ALA have a divergent impact on MMP2 and MMP9 expression in different adipose tissue localization.	Acetylcysteine	10-13	matrix metallopeptidase 2	Rattus norvegicus	49-53
35420738-9	2022	CONCLUSION: Based on our results, we speculate that NAC and ALA have a prominent effect on the MMP2/9 functions under obesity conditions.	Acetylcysteine	52-55	matrix metallopeptidase 2	Rattus norvegicus	95-101
35394351-6	2022	However, ROS scavenger N-acetylcysteine (NAC) attenuated the above effects and restored the effects of GO on protein expressions related to apoptosis, autophagy and AMPK/mTOR/ULK1 signal pathways.	Acetylcysteine	23-39	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	165-169
17869641-7	2007	Serum deprivation (0.5% FBS) producing ROS and exogenous H(2)O(2) treatment also enhanced mBAFF promoter activity, which was reduced by N-acetyl-l-cysteine (NAC), a well-known ROS scavenger.	Acetylcysteine	157-160	tumor necrosis factor (ligand) superfamily, member 13b	Mus musculus	90-95
35394351-6	2022	However, ROS scavenger N-acetylcysteine (NAC) attenuated the above effects and restored the effects of GO on protein expressions related to apoptosis, autophagy and AMPK/mTOR/ULK1 signal pathways.	Acetylcysteine	23-39	unc-51 like autophagy activating kinase 1	Homo sapiens	175-179
35394351-6	2022	However, ROS scavenger N-acetylcysteine (NAC) attenuated the above effects and restored the effects of GO on protein expressions related to apoptosis, autophagy and AMPK/mTOR/ULK1 signal pathways.	Acetylcysteine	41-44	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	165-169
35394351-6	2022	However, ROS scavenger N-acetylcysteine (NAC) attenuated the above effects and restored the effects of GO on protein expressions related to apoptosis, autophagy and AMPK/mTOR/ULK1 signal pathways.	Acetylcysteine	41-44	unc-51 like autophagy activating kinase 1	Homo sapiens	175-179
35065218-6	2022	Pre-treatment with NAC was efficient to prevent cell damage at lower Cl2 concentrations in part by averting the formation of apoptotic-like bodies and increasing the expression of the anti-apoptotic proteins clusterin and phosphorylated tumour protein p53(S46).	Acetylcysteine	19-22	clusterin	Homo sapiens	208-217
17210758-0	2007	N-Acetylcysteine and alpha-cyano-4-hydroxycinnamic acid alter protein kinase C (PKC)-delta and PKC-zeta and diminish dysmorphogenesis in rat embryos cultured with high glucose in vitro.	Acetylcysteine	0-16	protein kinase C, delta	Rattus norvegicus	62-90
35433874-9	2022	CagA+ H. pylori, not CagA- H. pylori, infection significantly increased aortic ROS production, decreased ACh-induced aortic relaxation, and enhanced early atherosclerosis formation, which were prevented with N-acetylcysteine treatment.	Acetylcysteine	208-224	S100 calcium binding protein A8	Homo sapiens	0-4
17210758-8	2007	The activities of embryonic protein kinase C-delta and protein kinase C-zeta were increased in the high glucose environment after 24-h culture, but were normalized by the addition of CHC and NAC as well as respective inhibitor to the culture medium.	Acetylcysteine	191-194	protein kinase C, delta	Rattus norvegicus	28-50
35368869-5	2022	Antioxidant N-acetyl cysteine reduced both MD- and AA+MD-induced autophagy, as well as changes in AMPK/mTORC1/ULK1 activity and cell death triggered by the drug combination.	Acetylcysteine	12-29	CREB regulated transcription coactivator 1	Mus musculus	103-109
17182545-4	2007	Reduction of ROS by the antioxidant N-acetyl-l-cysteine (NAC) prevented the emergence of senescent phenotypes in Atm(-/-) mouse embryonic fibroblasts, hypersensitivity to total body irradiation, and thymic lymphomagenesis in Atm(-/-) mice.	Acetylcysteine	36-55	ataxia telangiectasia mutated	Mus musculus	113-116
35368869-5	2022	Antioxidant N-acetyl cysteine reduced both MD- and AA+MD-induced autophagy, as well as changes in AMPK/mTORC1/ULK1 activity and cell death triggered by the drug combination.	Acetylcysteine	12-29	unc-51 like autophagy activating kinase 1	Homo sapiens	110-114
35280167-7	2022	Furthermore, NAC normalized the altered GSH levels displayed by these animals in the hippocampus and nucleus accumbens, and it partially rescued the altered expression of post-synaptic terminal network genes found in VPA-exposed rats, such as NR2a, MGLUR5, GLUR1, and GLUR2 in nucleus accumbens, and CAMK2, NR1, and GLUR2 in cerebellum.	Acetylcysteine	13-16	calcium/calmodulin-dependent protein kinase II delta	Rattus norvegicus	300-305
35280167-7	2022	Furthermore, NAC normalized the altered GSH levels displayed by these animals in the hippocampus and nucleus accumbens, and it partially rescued the altered expression of post-synaptic terminal network genes found in VPA-exposed rats, such as NR2a, MGLUR5, GLUR1, and GLUR2 in nucleus accumbens, and CAMK2, NR1, and GLUR2 in cerebellum.	Acetylcysteine	13-16	glutamate ionotropic receptor NMDA type subunit 1	Rattus norvegicus	307-310
35123263-5	2022	Consistently, in vitro binding of RBD and ACE2, spike-mediated cell-cell fusion, and pseudotyped viral infection of VeroE6/TMPRSS2 cells were inhibited by the thiol-reactive compounds N-acetylcysteine (NAC) and a reduced form of glutathione (GSH).	Acetylcysteine	184-200	angiotensin-converting enzyme 2	Chlorocebus sabaeus	42-46
35123263-5	2022	Consistently, in vitro binding of RBD and ACE2, spike-mediated cell-cell fusion, and pseudotyped viral infection of VeroE6/TMPRSS2 cells were inhibited by the thiol-reactive compounds N-acetylcysteine (NAC) and a reduced form of glutathione (GSH).	Acetylcysteine	184-200	surface glycoprotein	Severe acute respiratory syndrome coronavirus 2	48-53
17182545-4	2007	Reduction of ROS by the antioxidant N-acetyl-l-cysteine (NAC) prevented the emergence of senescent phenotypes in Atm(-/-) mouse embryonic fibroblasts, hypersensitivity to total body irradiation, and thymic lymphomagenesis in Atm(-/-) mice.	Acetylcysteine	36-55	ataxia telangiectasia mutated	Mus musculus	225-228
17182545-4	2007	Reduction of ROS by the antioxidant N-acetyl-l-cysteine (NAC) prevented the emergence of senescent phenotypes in Atm(-/-) mouse embryonic fibroblasts, hypersensitivity to total body irradiation, and thymic lymphomagenesis in Atm(-/-) mice.	Acetylcysteine	57-60	ataxia telangiectasia mutated	Mus musculus	113-116
17182545-4	2007	Reduction of ROS by the antioxidant N-acetyl-l-cysteine (NAC) prevented the emergence of senescent phenotypes in Atm(-/-) mouse embryonic fibroblasts, hypersensitivity to total body irradiation, and thymic lymphomagenesis in Atm(-/-) mice.	Acetylcysteine	57-60	ataxia telangiectasia mutated	Mus musculus	225-228
17182545-6	2007	Impairment of Ig class switch recombination seen in Atm(-/-) mice was mitigated by NAC, indicating that ROS elevation leads to abnormal response to programmed double-strand breaks in vivo.	Acetylcysteine	83-86	ataxia telangiectasia mutated	Mus musculus	52-55
17182545-7	2007	Significantly, in vivo administration of NAC to Atm(-/-) mice restored normal T cell development and inhibited aberrant V(D)J recombination.	Acetylcysteine	41-44	ataxia telangiectasia mutated	Mus musculus	48-51
16881050-7	2006	The LPS down-regulatory effect on TfR protein expression is abolished by the NADPH oxidase inhibitor diphenyliodonium (DPI) but is not affected by the free radical scavenger N-acetyl-L-cysteine (NAC) or the iNOS inhibitor aminoguanidine (AG).	Acetylcysteine	195-198	transferrin receptor	Mus musculus	34-37
16616762-13	2006	CONCLUSION: These data suggest that the oxidants generated from activated PMNs after ischemia/reperfusion trigger myocardial apoptosis, which is further supported by an anti-oxidant therapy with NAC, potentially mediated by enhanced NFkappaB-TNFalpha signaling pathway, activated caspase-3 and down-regulated Bcl-2.	Acetylcysteine	195-198	caspase 3	Rattus norvegicus	280-289
16863997-6	2006	Importantly, reduction of hydrogen peroxide by administration of the antioxidant N-acetylcysteine to Atm(-/-) mice attenuates the elevation of Nrf-2, c-Myc, and DNA synthesis in their thymocytes, suggesting that ATM may control c-Myc and DNA synthesis during postnatal thymocyte development by preventing accumulation of reactive oxygen species.	Acetylcysteine	81-97	ataxia telangiectasia mutated	Mus musculus	101-104
16863997-6	2006	Importantly, reduction of hydrogen peroxide by administration of the antioxidant N-acetylcysteine to Atm(-/-) mice attenuates the elevation of Nrf-2, c-Myc, and DNA synthesis in their thymocytes, suggesting that ATM may control c-Myc and DNA synthesis during postnatal thymocyte development by preventing accumulation of reactive oxygen species.	Acetylcysteine	81-97	ataxia telangiectasia mutated	Mus musculus	212-215
16356505-5	2006	Pretreatment with the antioxidant, N-acetylcysteine, inhibited chylomicron remnant-induced CD40 protein expression by 60%.	Acetylcysteine	35-51	CD40 molecule	Homo sapiens	91-95
16861926-8	2006	The induction of phosphorylation of H2AX on Ser 139 by NO-ASA was markedly attenuated in the presence of N-acetyl-L-cysteine, a scavenger of reactive oxygen species (ROS).	Acetylcysteine	105-124	H2A.X variant histone	Homo sapiens	36-40
16473382-8	2006	NAC, but not DTT, also decreased the phosphorylation of p38 and JNK supporting a role for oxidative processes in activating these kinases.	Acetylcysteine	0-3	mitogen-activated protein kinase 14	Mus musculus	56-59
16781197-0	2006	Antioxidant N-acetyl cysteine reduces incidence and multiplicity of lymphoma in Atm deficient mice.	Acetylcysteine	12-29	ataxia telangiectasia mutated	Mus musculus	80-83
16574159-0	2006	The effect of N-acetylcysteine in combination with vitamin C on the activity of ornithine decarboxylase of lung carcinoma cells--In vitro.	Acetylcysteine	14-30	ornithine decarboxylase 1	Homo sapiens	80-103
16574159-2	2006	This study assesses the dose-dependent effect of N-acetylcysteine (NAC), a chemopreventive agent, in combination with vitamin C (VC) on the activity of ODC in lung carcinoma cell line, NCI-H82.	Acetylcysteine	49-65	ornithine decarboxylase 1	Homo sapiens	152-155
16574159-2	2006	This study assesses the dose-dependent effect of N-acetylcysteine (NAC), a chemopreventive agent, in combination with vitamin C (VC) on the activity of ODC in lung carcinoma cell line, NCI-H82.	Acetylcysteine	67-70	ornithine decarboxylase 1	Homo sapiens	152-155
16648577-8	2006	Whereas the antioxidant N-acetyl-l-cysteine blocked the generation of reactive oxygen species and activation of JNK and AMPK, it did not block immunotoxin-induced apoptosis.	Acetylcysteine	24-43	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	120-124
16449798-6	2006	This mechanism is supported by the ability of N-acetyl cysteine (NAC) to prevent dissociation of Trx-ASK1 and activation of the p38 MAPK pathway.	Acetylcysteine	46-63	mitogen-activated protein kinase 14	Mus musculus	128-131
15907373-2	2006	The treatment with N-acetyl-cysteine (NAC) completely abolishes the H2O2-induced decrease in eIF4E phosphorylated levels, whereas the decrease in 4E-BP1 phosphorylated levels and eIF4F activity inhibition are significantly but not fully reversed.	Acetylcysteine	19-36	eukaryotic translation initiation factor 4E	Homo sapiens	93-98
15907373-2	2006	The treatment with N-acetyl-cysteine (NAC) completely abolishes the H2O2-induced decrease in eIF4E phosphorylated levels, whereas the decrease in 4E-BP1 phosphorylated levels and eIF4F activity inhibition are significantly but not fully reversed.	Acetylcysteine	38-41	eukaryotic translation initiation factor 4E	Homo sapiens	93-98
16275897-4	2006	N-acetylcysteine, a scavenger of reactive oxygen species (ROS), effectively inhibited the activation of p38 and cellular death, indicating that the activation induced by ROS is an initial step in the process of apoptosis triggered by SA-liposomes.	Acetylcysteine	0-16	mitogen-activated protein kinase 14	Mus musculus	104-107
16024921-5	2005	The general antioxidant N-acetyl-l-cysteine (6 mM), and the superoxide dismutase mimetic TEMPO (2.0 mm) reduced COX-2 levels by 75.6 and 79.8%, respectively.	Acetylcysteine	24-43	cytochrome c oxidase II, mitochondrial	Mus musculus	112-117
16024921-8	2005	The increases in phosphorylation of ERK1/2 and p38 were detected 20 min following the hypertonic treatment and were both prevented by N-acetyl-l-cysteine.	Acetylcysteine	134-153	mitogen-activated protein kinase 3	Mus musculus	36-42
16024921-8	2005	The increases in phosphorylation of ERK1/2 and p38 were detected 20 min following the hypertonic treatment and were both prevented by N-acetyl-l-cysteine.	Acetylcysteine	134-153	mitogen-activated protein kinase 14	Mus musculus	47-50
16098950-3	2005	Dissection of the molecular steps involved in TGF-beta signaling revealed that N-acetyl-L-cysteine dose-dependently abrogated the induction of the TGF-beta1 signaling reporter gene activation, the phosphorylation of Smad2 and Smad3, and the up-regulation of Smad7 mRNA.	Acetylcysteine	79-98	SMAD family member 2	Homo sapiens	216-221
16098950-3	2005	Dissection of the molecular steps involved in TGF-beta signaling revealed that N-acetyl-L-cysteine dose-dependently abrogated the induction of the TGF-beta1 signaling reporter gene activation, the phosphorylation of Smad2 and Smad3, and the up-regulation of Smad7 mRNA.	Acetylcysteine	79-98	SMAD family member 3	Homo sapiens	226-231
16086031-7	2005	Reactive oxygen species (ROS) were also detected within 1 h after AF treatment, and the antioxidant N-acetyl-L-cysteine (NAC) effectively protected the cells from apoptosis by inhibiting the phosphorylation of p38 MAPK and the activation of caspases.	Acetylcysteine	100-119	caspase 8	Homo sapiens	241-249
16382175-5	2005	In H9C2 cells, NAC pretreatment blocked cocaine-mediated increases in CRP, FAS, FAS ligand, and cytokine receptor-like factor1 (CRLF1) expression.	Acetylcysteine	15-18	Fas ligand	Rattus norvegicus	80-90
16088932-5	2005	Pretreatment with the cell-permeable antioxidant, N-acetyl cysteine, prevented cells from H2O2-induced Daxx upregulation and subsequent apoptosis, indicating that the endogenous oxidant regulated Daxx expression.	Acetylcysteine	50-67	death domain associated protein	Homo sapiens	103-107
16088932-5	2005	Pretreatment with the cell-permeable antioxidant, N-acetyl cysteine, prevented cells from H2O2-induced Daxx upregulation and subsequent apoptosis, indicating that the endogenous oxidant regulated Daxx expression.	Acetylcysteine	50-67	death domain associated protein	Homo sapiens	196-200
16168067-7	2005	N-acetyl-cysteine, partially reversed the inhibition of beta-hexosaminidase release suggesting CSS may act via oxidative free radicals.	Acetylcysteine	0-17	O-GlcNAcase	Homo sapiens	56-75
15962302-6	2005	Pretreatment of the cells with N-acetyl-L-cysteine (NAC) significantly prevented suppression of MMPs and uPA secretion, DNA binding activity of NF-kappaB, and in vitro invasion of HT1080 cells by As2O3, suggesting a role of reactive oxygen species (ROS) in this process.	Acetylcysteine	31-50	matrix metallopeptidase 2	Homo sapiens	96-100
15962302-6	2005	Pretreatment of the cells with N-acetyl-L-cysteine (NAC) significantly prevented suppression of MMPs and uPA secretion, DNA binding activity of NF-kappaB, and in vitro invasion of HT1080 cells by As2O3, suggesting a role of reactive oxygen species (ROS) in this process.	Acetylcysteine	52-55	matrix metallopeptidase 2	Homo sapiens	96-100
16253189-12	2005	The phopho-ERK1/2 protein level of the NAC + Aldo group was not significantly different from that of the Aldo group (P &gt; 0.05).	Acetylcysteine	39-42	mitogen activated protein kinase 3	Rattus norvegicus	11-17
16187210-5	2005	In the present study we investigated, in different rat brain areas during aging (6, 12, and 28 months), the effect of 1-year treatment with CR and dietary supplementation with NAC on the expression of subunit 39 kDa and ND-1 (mitochondrial respiratory complex I), subunit IV (complex IV), subunit alpha of F0F1-ATP synthase (complex V) and of adenine nucleotide translocator, isoform 1 (ANT-1).	Acetylcysteine	176-179	solute carrier family 25 member 4	Rattus norvegicus	343-385
16187210-5	2005	In the present study we investigated, in different rat brain areas during aging (6, 12, and 28 months), the effect of 1-year treatment with CR and dietary supplementation with NAC on the expression of subunit 39 kDa and ND-1 (mitochondrial respiratory complex I), subunit IV (complex IV), subunit alpha of F0F1-ATP synthase (complex V) and of adenine nucleotide translocator, isoform 1 (ANT-1).	Acetylcysteine	176-179	solute carrier family 25 member 4	Rattus norvegicus	387-392
15664999-7	2005	In the current study, chronic culturing of HIT-T15 cells with the antioxidant N-acetylcysteine (NAC) prevented loss of MafA protein (late passage = 18.9 +/- 10.4% of early passage, p &lt; 0.001; late passage with NAC = 68.7 +/- 19.7% of early passage, p = not significant) and loss of DNA binding (late passage = 63.7 +/- 9% of early passage, p &lt; 0.02; late passage with NAC = 116 +/- 10% of early passage, p = not significant).	Acetylcysteine	78-94	transcription factor MafA	Mesocricetus auratus	119-123
15664999-7	2005	In the current study, chronic culturing of HIT-T15 cells with the antioxidant N-acetylcysteine (NAC) prevented loss of MafA protein (late passage = 18.9 +/- 10.4% of early passage, p &lt; 0.001; late passage with NAC = 68.7 +/- 19.7% of early passage, p = not significant) and loss of DNA binding (late passage = 63.7 +/- 9% of early passage, p &lt; 0.02; late passage with NAC = 116 +/- 10% of early passage, p = not significant).	Acetylcysteine	96-99	transcription factor MafA	Mesocricetus auratus	119-123
15683462-10	2005	Results showed that N-acetylcysteine and glutathion can protect astrocytes against ROS accumulation and caspase-3 activation, whereas 0.1 mM melatonin can inhibit H2O2-induced apoptosis by regulating Bax expression and by inhibiting caspase-3 activation.	Acetylcysteine	20-36	caspase 3	Rattus norvegicus	233-242
15659314-7	2005	Co-incubation of cells with glutathione, N-acetyl-L-cysteine or glutathione reductase inhibited cytotoxicity and the phosphorylation of p38 MAPK induced by satratoxin H.	Acetylcysteine	41-60	mitogen activated protein kinase 14	Rattus norvegicus	136-139
15573404-0	2005	Downregulation of complexin I and complexin II in the medial thalamus is blocked by N-acetylcysteine in experimental Wernicke"s encephalopathy.	Acetylcysteine	84-100	complexin 2	Rattus norvegicus	34-46
15808665-6	2005	NAC 1: the rats received N-acetylcysteine (150 mg/kg) 15 minutes before 40 minutes of ischemia and 5 minutes before 30 minutes of reperfusion.	Acetylcysteine	25-41	nucleus accumbens associated 1	Rattus norvegicus	0-5
15557194-4	2004	Interestingly, LPS-induced MMP-9 expression and p38 kinase phosphorylation were shown to be suppressed by the antioxidant N-acetylcysteine and the flavoenzyme inhibitor diphenyleneiodonium chloride, but not by pyrrolidine dithiocarbamate, an NF-kappaB inhibitor.	Acetylcysteine	122-138	matrix metallopeptidase 9	Mus musculus	27-32
15557194-4	2004	Interestingly, LPS-induced MMP-9 expression and p38 kinase phosphorylation were shown to be suppressed by the antioxidant N-acetylcysteine and the flavoenzyme inhibitor diphenyleneiodonium chloride, but not by pyrrolidine dithiocarbamate, an NF-kappaB inhibitor.	Acetylcysteine	122-138	mitogen-activated protein kinase 14	Mus musculus	48-51
15385622-5	2004	N-Acetyl-cysteine, a powerful antioxidant in yeast, completely reversed this effect, suggesting that FUS1 and RLM1 activation in response to catecholamines is a result of oxidative stress.	Acetylcysteine	0-17	Fus1p	Saccharomyces cerevisiae S288C	101-105
15385622-5	2004	N-Acetyl-cysteine, a powerful antioxidant in yeast, completely reversed this effect, suggesting that FUS1 and RLM1 activation in response to catecholamines is a result of oxidative stress.	Acetylcysteine	0-17	Rlm1p	Saccharomyces cerevisiae S288C	110-114
15541757-9	2004	Furthermore, these effects of DEP on either HO-1 or TGM-2 were reduced by N-acetyl-l-cysteine (NAC), thus suggesting that oxidative stress caused by this organic fraction of DEP may have induced these cellular responses.	Acetylcysteine	95-98	transglutaminase 2	Rattus norvegicus	52-57
15450951-3	2004	The MMC-induced cell death and decrease in the GSH contents in SCLC cells were inhibited by caspase inhibitors (z-DQMD.fmk, z-IETD.fmk and z-LEHD.fmk) and antioxidants (N-acetylcysteine, dithiothreitol and N-(2-mercaptopropionyl)glycine, melatonin, rutin and carboxy-PTIO).	Acetylcysteine	169-185	caspase 8	Homo sapiens	92-99
15451068-4	2004	N-Acetyl-L-cysteine, an antioxidant, suppresses ROS generation, Akt inactivation, caspase-8 activation, and DNA fragmentation.	Acetylcysteine	0-19	caspase 8	Homo sapiens	82-91
15450387-7	2004	Treatment of amnion and choriodecidual tissues with SASP concentrations greater than 5 mM, 15 mM NAC, 30 microM 15d-PGJ(2) and 30 microM troglitazone significantly reduced the release of PTHrP (p &lt; 0.05).	Acetylcysteine	97-100	parathyroid hormone like hormone	Homo sapiens	187-192
15051799-12	2004	NAC and Trolox also ameliorated AA-mediated Erk1/2 and p38 MAPK activation, suggesting that this activation is associated with ROS and oxidative stress.	Acetylcysteine	0-3	mitogen activated protein kinase 3	Rattus norvegicus	44-50
15203191-4	2004	In primary human and bovine chondrocytes, ROS scavenger and antioxidant N-acetylcysteine (NAC) inhibited TGF-beta1-induced TIMP-3 mRNA and protein increases.	Acetylcysteine	72-88	transforming growth factor beta 1	Bos taurus	105-114
15203191-4	2004	In primary human and bovine chondrocytes, ROS scavenger and antioxidant N-acetylcysteine (NAC) inhibited TGF-beta1-induced TIMP-3 mRNA and protein increases.	Acetylcysteine	90-93	transforming growth factor beta 1	Bos taurus	105-114
15203191-9	2004	TGF-beta1-stimulated Smad2 phosphorylation was inhibited by NAC.	Acetylcysteine	60-63	SMAD family member 2	Homo sapiens	21-26
15173094-8	2004	In addition, l-N-acetylcysteine inhibited the combined therapy-mediated elevation of a proapoptotic BH3-only protein Bim expression, phosphorylation of H2AX, and accumulation of 8-hydroxydeoxyguanosine.	Acetylcysteine	13-31	H2A.X variant histone	Homo sapiens	152-156
15158123-6	2004	Pretreatment of the cells with an antioxidant, N-acetylcysteine (NAC), resulted in the inhibition of p38 MAPK phosphorylation and PKC- translocation during TGD.	Acetylcysteine	47-63	protein kinase C delta	Homo sapiens	130-133
15158123-6	2004	Pretreatment of the cells with an antioxidant, N-acetylcysteine (NAC), resulted in the inhibition of p38 MAPK phosphorylation and PKC- translocation during TGD.	Acetylcysteine	65-68	protein kinase C delta	Homo sapiens	130-133
15039334-7	2004	LPS-stimulated IL-8 expression could be blocked by the antioxidants N-acetyl-L-cysteine and dimethyl sulfoxide at both the protein and mRNA levels.	Acetylcysteine	68-87	chemokine (C-X-C motif) ligand 15	Mus musculus	15-19
14647418-7	2004	Lastly, antioxidants (e.g., L-N-acetylcysteine; L-NAC) opposed adaphostin-mediated mitochondrial dysfunction, Raf-1/MEK/ERK downregulation, JNK activation, and apoptosis.	Acetylcysteine	28-46	Raf-1 proto-oncogene, serine/threonine kinase	Homo sapiens	110-115
14663554-7	2004	Furthermore, resveratrol, as well as the antioxidant N-acetyl-cysteine, decreased Ang II- or H2O2-increased protein synthesis, beta-MyHC promoter activity, and ERK phosphorylation.	Acetylcysteine	53-70	myosin heavy chain 7	Rattus norvegicus	127-136
14722249-7	2004	The distal CYP2B1 enhancer region conferred gene activation by PM, repression of PM-dependent activation by EGF, and enhancement of activation by the antioxidant N-acetylcysteine (NAC).	Acetylcysteine	162-178	cytochrome P450 2B1	Rattus norvegicus	11-17
14722249-7	2004	The distal CYP2B1 enhancer region conferred gene activation by PM, repression of PM-dependent activation by EGF, and enhancement of activation by the antioxidant N-acetylcysteine (NAC).	Acetylcysteine	180-183	cytochrome P450 2B1	Rattus norvegicus	11-17
14577570-0	2003	Reactive oxygen species play roles on B cell surface receptor CD40-mediated proximal and distal signaling events: effects of an antioxidant, N-acetyl-L-cysteine treatment.	Acetylcysteine	141-160	CD40 antigen	Mus musculus	62-66
14577570-4	2003	CD40-mediated proximal events, which include protein serine phosphorylation, protein translocation between membranes and cytosol, as well as receptor complex formation, were inhibited after the pre-incubation of cells with an antioxidant N-acetyl-L-cysteine (NAC).	Acetylcysteine	238-257	CD40 antigen	Mus musculus	0-4
14577570-4	2003	CD40-mediated proximal events, which include protein serine phosphorylation, protein translocation between membranes and cytosol, as well as receptor complex formation, were inhibited after the pre-incubation of cells with an antioxidant N-acetyl-L-cysteine (NAC).	Acetylcysteine	259-262	CD40 antigen	Mus musculus	0-4
14577570-5	2003	Additionally, B cell responses after long-term ligation of CD40, such as protein expression, nuclear transcription factor kappaB (NFkappaB) activation, and cell proliferation, were also affected when cells were treated with NAC.	Acetylcysteine	224-227	CD40 antigen	Mus musculus	59-63
12934647-5	2003	The antioxidant, N-acetyl-cysteine, also reduced the glutathione or catalase- attenuated COX-2 expressions in IL-1beta and TNF-alpha-treated cells.	Acetylcysteine	17-34	prostaglandin-endoperoxide synthase 2	Rattus norvegicus	89-94
12818576-8	2003	Furthermore, NAC blocked AngII-induced increase in myocardial oxidative stress, decreased the expression of ANF and myosin light chain-2v, and inhibited the re-organization of cytoskeletal proteins, desmin and alpha-actinin.	Acetylcysteine	13-16	desmin	Rattus norvegicus	199-205
12754095-0	2003	N-Acetylcysteine enhances UV-mediated caspase-3 activation, fragmentation of E2F-4, and apoptosis in human C8161 melanoma: inhibition by ectopic Bcl-2 expression.	Acetylcysteine	0-16	E2F transcription factor 4	Homo sapiens	77-82
12754095-5	2003	Compared to treatment with UV radiation alone, combination treatment with NAC doubled the ratio of activated caspase-3 to pro-caspase-3 and produced greater fragmentation of the retinoblastoma protein and the E2F-4 transcription factor without affecting the E2F-1 protein.	Acetylcysteine	74-77	E2F transcription factor 4	Homo sapiens	209-214
12754095-7	2003	To our knowledge, this report is the first to: (i) demonstrate a synergy between DNA-damaging agents, like UV radiation, and antioxidants, like NAC, and (ii) show that a Bcl-2-inhibitable E2F-4 fragmentation occurs concurrently with caspase-3 activation and apoptosis.	Acetylcysteine	144-147	E2F transcription factor 4	Homo sapiens	188-193
12699905-9	2003	The transcription levels of HO-1 and HSP72 in OE-DEP- and OE-UFP-exposed cells were also reduced by NAC.	Acetylcysteine	100-103	heat shock protein family A (Hsp70) member 1A	Rattus norvegicus	37-42
12466149-5	2003	Fibronectin and bFGF also significantly augmented invasion of myoblasts across a Matrigel barrier, and plasmin cotreatment potentiated whereas N-acetyl cysteine suppressed the effects of bFGF and fibronectin on myoblast migration and invasion.	Acetylcysteine	143-160	fibroblast growth factor 2	Mus musculus	187-191
12650928-2	2003	We show that Cu,Zn-superoxide dismutase (SOD1) plays a fundamental role in this adaptation process since under hyperosmosis SOD1 mutants lead to high protein oxidation levels and show a sensitive phenotype, which is reversed by the addition of N-acetylcysteine to the medium.	Acetylcysteine	244-260	superoxide dismutase SOD1	Saccharomyces cerevisiae S288C	41-45
12650928-2	2003	We show that Cu,Zn-superoxide dismutase (SOD1) plays a fundamental role in this adaptation process since under hyperosmosis SOD1 mutants lead to high protein oxidation levels and show a sensitive phenotype, which is reversed by the addition of N-acetylcysteine to the medium.	Acetylcysteine	244-260	superoxide dismutase SOD1	Saccharomyces cerevisiae S288C	124-128
12565201-0	2003	Astroglial CYP1B1 up-regulation in inflammatory/oxidative toxic conditions: IL-1beta effect and protection by N-acetylcysteine.	Acetylcysteine	110-126	cytochrome P450 family 1 subfamily B member 1	Homo sapiens	11-17
12631075-7	2003	Aminoguanidine and N-acetyl-l-cysteine inhibited the MG-induced p38 MAPK activation, as well as apoptosis in rat mesangial cells, suggesting the involvement of oxidative stress in these phenomena.	Acetylcysteine	19-38	mitogen activated protein kinase 14	Rattus norvegicus	64-67
17219914-4	2003	An elevated level of urinary thioether (mercapturic acid derivatives) a significant elevation in the level of DNA SSB was found among exposed workers in comparison with control group (p &lt; 0.01).	Acetylcysteine	40-56	small RNA binding exonuclease protection factor La	Homo sapiens	114-117
12244106-6	2002	A thiol antioxidant, N-acetyl-l-cysteine, or overexpression of an H(2)O(2) scavenger, catalase, inhibited glucose deprivation-induced dissociation of GRX from ASK1.	Acetylcysteine	21-40	glutaredoxin	Homo sapiens	150-153
12437967-7	2002	Fidarestat, a newly developed AR inhibitor, and N-acetylcysteine, an antioxidant, completely prevented these deleterious effects of SDH overexpression on pericytes.	Acetylcysteine	48-64	sorbitol dehydrogenase	Rattus norvegicus	132-135
12117417-4	2002	Oocytes expressing LAT1-4F2hc or LAT2-4F2hc demonstrated enhanced uptake of [(14)C]MeHg when administered as the L-cysteine or D,L-homocysteine complexes, but not when administered as the D-cysteine, N -acetyl-L-cysteine, penicillamine or GSH complexes.	Acetylcysteine	200-220	linker for activation of T cells family member 2	Homo sapiens	33-37
12372563-6	2002	Of these compounds, only CoQ(10) or NAC was able to restore the numbers of mature myelin basic protein-positive cells and the ability of the oligodendrocytes to form membrane sheets.	Acetylcysteine	36-39	myelin basic protein	Homo sapiens	82-102
12184631-4	2002	This increase in CD13/APN expression was suppressed by treatment with N-acetylcysteine.	Acetylcysteine	70-86	alanyl aminopeptidase, membrane	Homo sapiens	17-21
12184631-4	2002	This increase in CD13/APN expression was suppressed by treatment with N-acetylcysteine.	Acetylcysteine	70-86	alanyl aminopeptidase, membrane	Homo sapiens	22-25
12006557-3	2002	IFN-gamma-induced HLA-DRA expression was inhibited by nitric oxide (NO) and antioxidants such as superoxide dismutase, catalase, pyrrolidine dithiocarbamate, and N-acetylcysteine.	Acetylcysteine	162-178	major histocompatibility complex, class II, DR alpha	Homo sapiens	18-25
11997384-0	2002	N-acetylcysteine and celecoxib lessen cadmium cytotoxicity which is associated with cyclooxygenase-2 up-regulation in mouse neuronal cells.	Acetylcysteine	0-16	prostaglandin-endoperoxide synthase 2	Mus musculus	84-100
11997384-6	2002	The thiol-reducing antioxidant N-acetylcysteine, and, to a lesser extent, the COX-2 inhibitor celecoxib, attenuated the loss of cell viability induced by cadmium demonstrating that oxidative stress and COX-2 activation contribute to cadmium cytotoxicity.	Acetylcysteine	31-47	prostaglandin-endoperoxide synthase 2	Mus musculus	202-207
12006386-4	2002	Antioxidants, N-acetyl-L-cysteine, glutathione monoester, or alpha -tocopherol, inhibited ERK1/2 activation by lysoPC.	Acetylcysteine	14-33	mitogen activated protein kinase 3	Rattus norvegicus	90-96
11909699-4	2002	Simultaneous incubation with the thiol antioxidant N-acetylcysteine (NAC) inhibited indomethacin-mediated increases in GCLC mRNA, suggesting that increases in GCLC message were triggered by changes in intracellular oxidation/reduction (redox) reactions.	Acetylcysteine	51-67	glutamate-cysteine ligase catalytic subunit	Homo sapiens	119-123
11909699-4	2002	Simultaneous incubation with the thiol antioxidant N-acetylcysteine (NAC) inhibited indomethacin-mediated increases in GCLC mRNA, suggesting that increases in GCLC message were triggered by changes in intracellular oxidation/reduction (redox) reactions.	Acetylcysteine	51-67	glutamate-cysteine ligase catalytic subunit	Homo sapiens	159-163
12061835-3	2002	We thus studied the effect of reduced glutathione (GSH) and N-acetyl-cysteine (NAC) on IL-12 p75 production by human THP-1 cell stimulated with IFN-gamma and Staphylococcus aureus Cowan strain I (SAC), using ELISAs specific for IL-12 p75 or the p40 subunit.	Acetylcysteine	79-82	interleukin 2 receptor subunit beta	Homo sapiens	93-96
12061835-4	2002	NAC and GSH, but not cystine, at concentrations of 5-10 mM inhibited production of IL-12 p75 but not of the p40 subunit.	Acetylcysteine	0-3	interleukin 2 receptor subunit beta	Homo sapiens	89-92
12061835-6	2002	The effect of NAC was specific for IL-12 p75, as NAC did not affect induction of MHC class II expression by IFN-gamma-stimulated THP-1 cells.	Acetylcysteine	14-17	interleukin 2 receptor subunit beta	Homo sapiens	41-44
11716513-3	2001	Tyrosine phosphorylation of PKC delta was prevented by a radical scavenger, N-acetyl-l-cysteine, and by a tyrosine kinase inhibitor, genistein, in the ultraviolet-irradiated keratinocyte cell line.	Acetylcysteine	76-95	protein kinase C delta	Homo sapiens	28-37
11673494-7	2001	The L-PAM-induced accumulation of IFN-beta mRNA was mimicked with H(2)O(2) and was prevented with the antioxidant N-acetyl-L-cysteine, indicating that reactive oxygen species are involved in the transcriptional regulation of L-PAM-induced IFN-beta gene expression.	Acetylcysteine	114-133	peptidylglycine alpha-amidating monooxygenase	Mus musculus	6-9
11673494-7	2001	The L-PAM-induced accumulation of IFN-beta mRNA was mimicked with H(2)O(2) and was prevented with the antioxidant N-acetyl-L-cysteine, indicating that reactive oxygen species are involved in the transcriptional regulation of L-PAM-induced IFN-beta gene expression.	Acetylcysteine	114-133	peptidylglycine alpha-amidating monooxygenase	Mus musculus	227-230
11761336-3	2001	Pretreatment of cells with thiol antioxidants, N-acetylcysteine or alpha-lipoic acid attenuated MAPK phosphorylation induced by a 3-min incubation with HGF.	Acetylcysteine	47-63	hepatocyte growth factor	Homo sapiens	152-155
2437551-0	1987	Acetylcysteine in rats: inhibition of activation of prekallikrein and factor XII--protection against dextran-induced blood pressure fall.	Acetylcysteine	0-14	coagulation factor XII	Rattus norvegicus	70-80
2437551-4	1987	Also the activation of factor XII to factor XIIa, assayed as prekallikrein activator, was strongly inhibited in AC-treated rats.	Acetylcysteine	112-114	coagulation factor XII	Rattus norvegicus	23-33
11389684-6	2001	This effect was insensitive to pargyline (an MAO inhibitor), but was inhibited by semicarbazide (an SSAO inhibitor) and by N-acetylcysteine (an antioxidant agent), suggesting the involvement of the H(2)O(2) generated during SSAO-dependent amine oxidation.	Acetylcysteine	123-139	amine oxidase, copper containing 3	Mus musculus	224-228
6813467-1	1982	Twelve patients with adverse hematologic reactions to chrysotherapy received intravenous N-acetylcysteine (IV NAC) to achieve removal and/or redistribution of gold.	Acetylcysteine	89-105	synuclein alpha	Homo sapiens	110-113
11264281-5	2001	N-Acetylcysteine could reliably decrease inducible MnSOD expression by TNF-alpha, but not IL-1, linking reactive oxygen species (ROS) to the TNF-alpha signaling pathway.	Acetylcysteine	0-16	superoxide dismutase 2	Homo sapiens	51-56
11353799-8	2001	In primary hepatocyte cultures transfected with a CYP2B1 promoter-luciferase construct containing approximately 2.7 kilobase pairs of the native CYP2B1 promoter sequence, PB-dependent reporter gene activation was repressed by AT and stimulated by N-acetylcysteine.	Acetylcysteine	247-263	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	50-56
7011834-1	1980	The mucolytic activity of acetylcysteine (NAC) was evaluated in a double-blind, placebo controlled, clinical trial performed in three pneumology centres and involving a total of 215 patients with the following diagnoses: 84 acute bronchitis, 95 superinfections of chronic bronchitis, 36 complicated bronchitis in patients with severe chronic respiratory insufficiency.	Acetylcysteine	26-40	synuclein alpha	Homo sapiens	42-45
11353799-8	2001	In primary hepatocyte cultures transfected with a CYP2B1 promoter-luciferase construct containing approximately 2.7 kilobase pairs of the native CYP2B1 promoter sequence, PB-dependent reporter gene activation was repressed by AT and stimulated by N-acetylcysteine.	Acetylcysteine	247-263	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	145-151
33647387-3	2021	Reactive oxygen species (ROS) scavenger NAC (N-acetyl-L-cysteine) and palmitoylation inhibitor 2-bromopalmitate (2-BP) disturbed the nuclear shifting associated with the correlative up-regulation of PAC1 significantly, and PAC1-R mutant (M-PAC1-R) on Cys25/Ala25 displayed the significant decreased nuclear trafficking efficiency.	Acetylcysteine	40-43	ADCYAP receptor type I	Homo sapiens	199-203
11353799-9	2001	Furthermore, a 263-base pair CYP2B1 promoter fragment encompassing the phenobarbital-responsive enhancer module conferred suppression of PB-dependent luciferase expression by AT and activation by NAC in a heterologous SV40-promoter construct.	Acetylcysteine	196-199	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	29-35
33647387-3	2021	Reactive oxygen species (ROS) scavenger NAC (N-acetyl-L-cysteine) and palmitoylation inhibitor 2-bromopalmitate (2-BP) disturbed the nuclear shifting associated with the correlative up-regulation of PAC1 significantly, and PAC1-R mutant (M-PAC1-R) on Cys25/Ala25 displayed the significant decreased nuclear trafficking efficiency.	Acetylcysteine	40-43	ADCYAP receptor type I	Homo sapiens	223-229
33647387-3	2021	Reactive oxygen species (ROS) scavenger NAC (N-acetyl-L-cysteine) and palmitoylation inhibitor 2-bromopalmitate (2-BP) disturbed the nuclear shifting associated with the correlative up-regulation of PAC1 significantly, and PAC1-R mutant (M-PAC1-R) on Cys25/Ala25 displayed the significant decreased nuclear trafficking efficiency.	Acetylcysteine	45-64	ADCYAP receptor type I	Homo sapiens	199-203
11385283-9	2001	Inhibitors of NF-kappa B activation such as N-acetylcysteine or N-tosyl-L-phenylalanine chloromethyl ketone can suppress Fc epsilon RI-induced TNF-alpha and MCP-1 release.	Acetylcysteine	44-60	Fc epsilon receptor Ia	Homo sapiens	121-134
33647387-3	2021	Reactive oxygen species (ROS) scavenger NAC (N-acetyl-L-cysteine) and palmitoylation inhibitor 2-bromopalmitate (2-BP) disturbed the nuclear shifting associated with the correlative up-regulation of PAC1 significantly, and PAC1-R mutant (M-PAC1-R) on Cys25/Ala25 displayed the significant decreased nuclear trafficking efficiency.	Acetylcysteine	45-64	ADCYAP receptor type I	Homo sapiens	223-229
11226137-6	2001	We conclude: first, that the biphasic changes recorded in mitochondrial inner membrane potential by the effect of cocaine, were parallel to apoptosis; second, that caspase-3 activity and cleavage to it p20 subunit increased sharply in parallel to the translocation of cytochrome c from mitochondria to cytosol; and third, that the antioxidants, NAC or DFO exerted a noticeable protective role in counteracting the cytotoxicity of cocaine, these effects being more pronounced in the case of DFO than NAC.	Acetylcysteine	345-348	caspase 3	Rattus norvegicus	164-173
11159825-7	2001	Inhibition of nuclear factor-kappaB activation by N-acetyl-cysteine and SN50 suppressed Xiap protein expression and enhanced apoptosis induced by TNFalpha.	Acetylcysteine	50-67	X-linked inhibitor of apoptosis	Rattus norvegicus	88-92
11139434-5	2000	LMS (2 mmol l(-1))-induced apoptosis was inhibited by glutathione (-50%) and N-Acetylcysteine (-36%), which also counteracted reduction by Levamisole of pRb expression, suggesting reactive oxygen species and pRb play a role in these processes.	Acetylcysteine	77-93	RB transcriptional corepressor 1	Homo sapiens	153-156
33402029-8	2021	In addition, NAC reactivated the Wnt/beta-catenin pathway in osteoblasts under high-fat stimulation.	Acetylcysteine	13-16	wingless-type MMTV integration site family, member 3A	Mus musculus	33-36
33978073-5	2021	RESULTS: Data showed a reduction in malondialdehyde (MDA), myeloperoxidase (MPO), and TNF-alpha in the animals pretreated with NAC or MEL when compared to those treated with SS+iIR (p<0.05).	Acetylcysteine	127-130	myeloperoxidase	Rattus norvegicus	59-74
33978073-5	2021	RESULTS: Data showed a reduction in malondialdehyde (MDA), myeloperoxidase (MPO), and TNF-alpha in the animals pretreated with NAC or MEL when compared to those treated with SS+iIR (p<0.05).	Acetylcysteine	127-130	myeloperoxidase	Rattus norvegicus	76-79
33247942-13	2021	In all NAC treatment groups, levels of serum IL-6, neuronal apoptosis and brain NFkB, nNOS, Caspase 3, TNF-alpha, IL-6 and IL-1beta protein levels were significantly reduced compared to NEC group.	Acetylcysteine	7-10	RELA proto-oncogene, NF-kB subunit	Rattus norvegicus	80-84
33247942-14	2021	The most pronounced decrease was demonstrated within the NAC-NEC-NAC group CONCLUSIONS: NAC treatment can attenuate newborn inflammatory response syndrome and decrease offspring brain neuro apoptosis and inflammation in a rat model of NEC by inhibition of NFkB, nNOS and Caspase 3 pathways.	Acetylcysteine	57-60	RELA proto-oncogene, NF-kB subunit	Rattus norvegicus	256-260
11329937-7	2000	Cyclin D1 expression of carcinoma cells treated with NAC decreased remarkably compared with cells without NAC treatment.	Acetylcysteine	53-56	cyclin D1	Homo sapiens	0-9
33744595-14	2021	NAC (N-acetylcysteine), a reducer reversed valtrate-induced the depletion of Stat3, p-Stat3, c-Myc, and Cyclin B1.	Acetylcysteine	0-3	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	93-98
33744595-14	2021	NAC (N-acetylcysteine), a reducer reversed valtrate-induced the depletion of Stat3, p-Stat3, c-Myc, and Cyclin B1.	Acetylcysteine	0-3	cyclin B1	Homo sapiens	104-113
33902598-13	2021	The Inhibition of AKT/mTOR signaling pathways and the activation of autophagy induced by FLC could be efficiently reversed by pretreatment of NAC.	Acetylcysteine	142-145	mechanistic target of rapamycin kinase	Mus musculus	22-26
33919218-7	2021	Treating C2C12 cells with antioxidant N-acetylcysteine also promoted osteoblast differentiation, and upregulated Runx2/Osterix/Dlx5, while ROS generator antimycin A treatment performed the opposite.	Acetylcysteine	38-54	runt related transcription factor 2	Mus musculus	113-118
3288330-9	1988	In addition, the loss of ADPRT was not observed after the first cycle, but delayed to the end of the second, indicating that NAC exerts a protective effect on DNA and on ADPRT.	Acetylcysteine	125-128	poly (ADP-ribose) polymerase 1	Rattus norvegicus	25-30
3288330-9	1988	In addition, the loss of ADPRT was not observed after the first cycle, but delayed to the end of the second, indicating that NAC exerts a protective effect on DNA and on ADPRT.	Acetylcysteine	125-128	poly (ADP-ribose) polymerase 1	Rattus norvegicus	170-175
11329937-7	2000	Cyclin D1 expression of carcinoma cells treated with NAC decreased remarkably compared with cells without NAC treatment.	Acetylcysteine	106-109	cyclin D1	Homo sapiens	0-9
10906152-8	2000	The flavoprotein inhibitor diphenylene iodinium, as well as the antioxidant N-acetylcysteine, prevented AngII-induced p44/42 MAP kinase phosphorylation, indicating involvement of reactive oxygen species generated by membrane-bound NAD(P)H oxidase.	Acetylcysteine	76-92	interferon induced protein 44	Homo sapiens	118-121
10842199-8	2000	The addition of either ALA or NAC into cultures of PBMC isolated from cancer patients significantly increased the percentage of cells expressing CD25 as well as those expressing CD95.	Acetylcysteine	30-33	interleukin 2 receptor subunit alpha	Homo sapiens	145-149
2851201-5	1988	All the evidence points to conjugation of 4-hydroxyestradiol with glutathione or N-acetylcysteine at C-2 but not C-1 of this highly reactive catechol estrogen.	Acetylcysteine	81-97	complement C2	Rattus norvegicus	101-104
33544267-3	2021	Here we demonstrated the additive geroprotective effect of combined genetic and pharmacological interventions to the hydrogen sulfide biosynthesis system by overexpression of cystathionine-beta-synthase and cystathionine-gamma-lyase genes and treatment with precursors of H2S synthesis cysteine (Cys) and N-acetyl-L-cysteine (NAC).	Acetylcysteine	305-324	Cystathionine beta-synthase	Drosophila melanogaster	175-202
33544267-3	2021	Here we demonstrated the additive geroprotective effect of combined genetic and pharmacological interventions to the hydrogen sulfide biosynthesis system by overexpression of cystathionine-beta-synthase and cystathionine-gamma-lyase genes and treatment with precursors of H2S synthesis cysteine (Cys) and N-acetyl-L-cysteine (NAC).	Acetylcysteine	326-329	Cystathionine beta-synthase	Drosophila melanogaster	175-202
33551189-10	2021	After adding 3mM N-Acetylcysteine to HGK cultures, increased fluorescence intensity and protein amounts of Involucrin and Filaggrin indicated enhanced differentiation (p<0.05).	Acetylcysteine	17-33	filaggrin	Homo sapiens	122-131
10692565-6	2000	AP-1 and NF-kappaB activation were blocked by the thiol antioxidant N-acetylcysteine and by nordihydroguaiaretic acid, an antioxidant and lipooxygenase inhibitor and an inhibitor of the epoxygenase activity of CYP1A1, and did not take place in c35, c37, or in Ah nuclear translator-deficient c4 cells.	Acetylcysteine	68-84	jun proto-oncogene	Mus musculus	0-4
33649207-8	2021	ROS scavenging by N-acetylcysteine reverted the Ido1 -/-Gr-1+CD11b+ composition and function to an MDSC state, as well as improved the survival of GVHD hosts with Ido1 -/- BM.	Acetylcysteine	18-34	indoleamine 2,3-dioxygenase 1	Homo sapiens	48-52
33649207-8	2021	ROS scavenging by N-acetylcysteine reverted the Ido1 -/-Gr-1+CD11b+ composition and function to an MDSC state, as well as improved the survival of GVHD hosts with Ido1 -/- BM.	Acetylcysteine	18-34	indoleamine 2,3-dioxygenase 1	Homo sapiens	163-167
33495825-5	2021	NAC treatment in the drinking water for 12 weeks decreased the size of the atherosclerotic lesion, which was associated with a reduction in MG-dicarbonyl stress and oxidative stress, as indicated by decreased serum malondialdehyde levels, and increased superoxide dismutase-1 and glutathione peroxidase-1 levels in the diabetic aorta.	Acetylcysteine	0-3	glutathione peroxidase 1	Mus musculus	280-304
3307787-10	1987	It is concluded that mercapturic acids are deacetylated to the corresponding cysteine conjugates by cytosolic (N-Ac-PCBC, N-Ac-TCVC and N-Ac-DCVC) and bacterial enzymes (N-Ac-TCVC and N-Ac-DCVC) and further cleaved to reactive and mutagenic intermediates by mammalian and/or bacterial beta-lyase.	Acetylcysteine	21-38	EPH receptor B2	Homo sapiens	116-120
10775561-0	2000	N-Acetyl-L-cysteine potentiates interleukin-1beta induction of nitric oxide synthase : role of p44/42 mitogen-activated protein kinases.	Acetylcysteine	0-19	mitogen activated protein kinase 3	Rattus norvegicus	95-98
3965363-1	1985	Plasma glutathione S-transferase (GST) measurements have been used to study early changes in hepatocellular integrity after paracetamol overdose and treatment with N-acetylcysteine (NAC).	Acetylcysteine	164-180	glutathione S-transferase kappa 1	Homo sapiens	7-32
10775561-2	2000	The present study compares the effect of N-acetyl-L-cysteine with other antioxidants and tested the possibility that N-acetyl-L-cysteine potentiates iNOS induction by a mechanism involving activation of p44/42 mitogen-activated protein kinases (MAPKs).	Acetylcysteine	117-136	mitogen activated protein kinase 3	Rattus norvegicus	203-206
3965363-1	1985	Plasma glutathione S-transferase (GST) measurements have been used to study early changes in hepatocellular integrity after paracetamol overdose and treatment with N-acetylcysteine (NAC).	Acetylcysteine	164-180	glutathione S-transferase kappa 1	Homo sapiens	34-37
3965363-1	1985	Plasma glutathione S-transferase (GST) measurements have been used to study early changes in hepatocellular integrity after paracetamol overdose and treatment with N-acetylcysteine (NAC).	Acetylcysteine	182-185	glutathione S-transferase kappa 1	Homo sapiens	7-32
33359712-11	2021	Additionally, the expression levels of Wnt and p-beta-catenin, apoptosis of GCs decreased after NAC treatment.	Acetylcysteine	96-99	catenin beta 1	Rattus norvegicus	49-61
10775561-4	2000	Interleukin-1beta activated p44/42 MAPK, and this activation was enhanced in the presence of N-acetyl-L-cysteine.	Acetylcysteine	93-112	mitogen activated protein kinase 3	Rattus norvegicus	28-31
33504419-12	2021	While ROS scavenger N-acetyl-L-cysteine (NAC) inhibited the silica-induced release of ROS, and then inhibited the expression of ABC protein and Wnt/beta-catenin signal activity.	Acetylcysteine	20-39	catenin beta 1	Homo sapiens	148-160
33504419-12	2021	While ROS scavenger N-acetyl-L-cysteine (NAC) inhibited the silica-induced release of ROS, and then inhibited the expression of ABC protein and Wnt/beta-catenin signal activity.	Acetylcysteine	41-44	catenin beta 1	Homo sapiens	148-160
3965363-1	1985	Plasma glutathione S-transferase (GST) measurements have been used to study early changes in hepatocellular integrity after paracetamol overdose and treatment with N-acetylcysteine (NAC).	Acetylcysteine	182-185	glutathione S-transferase kappa 1	Homo sapiens	34-37
10775561-4	2000	Interleukin-1beta activated p44/42 MAPK, and this activation was enhanced in the presence of N-acetyl-L-cysteine.	Acetylcysteine	93-112	mitogen activated protein kinase 3	Rattus norvegicus	35-39
10775561-5	2000	Inhibition of p44/42 MAPK phosphorylation by the selective inhibitor PD98059 clearly inhibited iNOS expression induced by interleukin-1beta either in the absence or in the presence of N-acetyl-L-cysteine.	Acetylcysteine	184-203	mitogen activated protein kinase 3	Rattus norvegicus	14-17
6548620-0	1984	Urinary excretion of the N-acetyl cysteine conjugate of cis-1,3-dichloropropene by exposed individuals.	Acetylcysteine	25-42	suppressor of cytokine signaling 1	Homo sapiens	56-61
33246336-1	2021	STUDY QUESTION: Can antioxidant treatment with N-acetylcysteine (NAC) protect ovarian follicles from ischemia-reperfusion injury in xenotransplanted human ovarian tissue?	Acetylcysteine	47-63	synuclein alpha	Homo sapiens	65-68
10775561-5	2000	Inhibition of p44/42 MAPK phosphorylation by the selective inhibitor PD98059 clearly inhibited iNOS expression induced by interleukin-1beta either in the absence or in the presence of N-acetyl-L-cysteine.	Acetylcysteine	184-203	mitogen activated protein kinase 3	Rattus norvegicus	21-25
6548620-1	1984	A gas chromatographic-mass spectrometric assay was developed to identify and measure the N-acetyl cysteine conjugate of cis-1,3-dichloropropene.	Acetylcysteine	89-106	suppressor of cytokine signaling 1	Homo sapiens	120-125
10775561-6	2000	These observations, combined with previous results, indicate that p44/42 MAPK activation is required for interleukin-1beta induction of iNOS and that N-acetyl-L-cysteine may act as a reducing agent and facilitate interleukin-1beta-induced iNOS expression through a reduction/oxidation-related mechanism involving potentiation of cytokine activation of the p44/42 MAPK signaling pathway.	Acetylcysteine	150-169	mitogen activated protein kinase 3	Rattus norvegicus	356-359
10775561-6	2000	These observations, combined with previous results, indicate that p44/42 MAPK activation is required for interleukin-1beta induction of iNOS and that N-acetyl-L-cysteine may act as a reducing agent and facilitate interleukin-1beta-induced iNOS expression through a reduction/oxidation-related mechanism involving potentiation of cytokine activation of the p44/42 MAPK signaling pathway.	Acetylcysteine	150-169	mitogen activated protein kinase 3	Rattus norvegicus	363-367
10727516-7	2000	Pretreatment of the cells with N-acetyl-L-cysteine significantly suppressed the SNAP-induced up-regulation of AR mRNA.	Acetylcysteine	31-50	aldo-keto reductase family 1 member B1	Rattus norvegicus	110-112
7210465-1	1980	N-acetylcysteine was adsorbed by activated charcoal, lending in vitro support to previous clinical of activated charcoal for NAC in biologic fluid was significantly greater than in nonbiologic fluid and has important clinical implications.	Acetylcysteine	0-16	synuclein alpha	Homo sapiens	125-128
33446631-5	2021	The elimination of ROS using N-acetylcysteine (NAC) and inhibition of oxidative phosphorylation using carbonyl cyanide m-chlorophenyl hydrazone (CCCP) and rotenone inhibited the ARNT and PDK1 deficiency-induced cell migration and invasion.	Acetylcysteine	29-45	aryl hydrocarbon receptor nuclear translocator	Mus musculus	178-182
33446631-7	2021	Intriguingly, CCCP and NAC dramatically inhibited ARNT and PDK1 deficiency-induced tumor cell extravasation in mouse models.	Acetylcysteine	23-26	aryl hydrocarbon receptor nuclear translocator	Mus musculus	50-54
10734236-3	2000	This dephosphorylation (i) is very fast, being observed already 5 min after the exposure of the cells to DEM, (ii) is dependent on the prooxidant effects of DEM, being prevented by the treatment with N-acetylcysteine and (iii) is completely reversible, since the rephosphorylation of pRb is promptly obtained upon the removal of the glutathione-depleting agent from the culture medium.	Acetylcysteine	200-216	RB transcriptional corepressor 1	Homo sapiens	284-287
33530839-13	2021	Interestingly, NAC+CsA treatment improved histological alterations, cytochrome c, and 3-nitrotyrosine immunoreactivities and liver GSH, serum AST/ALT levels caused by APAP.	Acetylcysteine	15-18	solute carrier family 17 (anion/sugar transporter), member 5	Mus musculus	142-145
33530839-13	2021	Interestingly, NAC+CsA treatment improved histological alterations, cytochrome c, and 3-nitrotyrosine immunoreactivities and liver GSH, serum AST/ALT levels caused by APAP.	Acetylcysteine	15-18	glutamic pyruvic transaminase, soluble	Mus musculus	146-149
33130472-15	2021	N-acetyl-L-cysteine (NAC) not only revered ROS generation triggered by LCA but also restored IFN-gamma-induced expression of PD-L1.	Acetylcysteine	21-24	CD274 molecule	Homo sapiens	125-130
33130472-16	2021	Both the inhibition of 4EBP1 phosphorylation (Ser 65) and activation of PERK-eIF2alpha axis triggered by LCA was restored by co-treatment with NAC.	Acetylcysteine	143-146	eukaryotic translation initiation factor 4E binding protein 1	Homo sapiens	23-28
33130472-16	2021	Both the inhibition of 4EBP1 phosphorylation (Ser 65) and activation of PERK-eIF2alpha axis triggered by LCA was restored by co-treatment with NAC.	Acetylcysteine	143-146	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	72-76
33146789-10	2021	In addition, using the ROS inhibitor N-acetyl-L-cysteine (NAC), we observed abrogated mRNA expression of several ARPs and production of inflammatory cytokines/chemokines (IL-6, IL-8, MCP-1, and CCL-5) in the CSE-challenged cells suggesting an important role of ROS in regulating CSE-induced autophagy.	Acetylcysteine	37-56	C-C motif chemokine ligand 2	Homo sapiens	183-188
33961949-8	2021	Finally, antioxidant N-acetyl-L-cysteine (NAC) inhibited p53 activation upon PBDEQ exposure, and then ameliorated PBDEQ-induced DNA damage, cell cycle arrest and apoptosis, which illustrated that PBDEQ-induced DNA damage and p53 activation were mediated by reactive oxygen species (ROS).	Acetylcysteine	21-40	transformation related protein 53, pseudogene	Mus musculus	57-60
33961949-8	2021	Finally, antioxidant N-acetyl-L-cysteine (NAC) inhibited p53 activation upon PBDEQ exposure, and then ameliorated PBDEQ-induced DNA damage, cell cycle arrest and apoptosis, which illustrated that PBDEQ-induced DNA damage and p53 activation were mediated by reactive oxygen species (ROS).	Acetylcysteine	21-40	transformation related protein 53, pseudogene	Mus musculus	225-228
33961949-8	2021	Finally, antioxidant N-acetyl-L-cysteine (NAC) inhibited p53 activation upon PBDEQ exposure, and then ameliorated PBDEQ-induced DNA damage, cell cycle arrest and apoptosis, which illustrated that PBDEQ-induced DNA damage and p53 activation were mediated by reactive oxygen species (ROS).	Acetylcysteine	42-45	transformation related protein 53, pseudogene	Mus musculus	57-60
33146789-10	2021	In addition, using the ROS inhibitor N-acetyl-L-cysteine (NAC), we observed abrogated mRNA expression of several ARPs and production of inflammatory cytokines/chemokines (IL-6, IL-8, MCP-1, and CCL-5) in the CSE-challenged cells suggesting an important role of ROS in regulating CSE-induced autophagy.	Acetylcysteine	58-61	C-C motif chemokine ligand 2	Homo sapiens	183-188
33961949-8	2021	Finally, antioxidant N-acetyl-L-cysteine (NAC) inhibited p53 activation upon PBDEQ exposure, and then ameliorated PBDEQ-induced DNA damage, cell cycle arrest and apoptosis, which illustrated that PBDEQ-induced DNA damage and p53 activation were mediated by reactive oxygen species (ROS).	Acetylcysteine	42-45	transformation related protein 53, pseudogene	Mus musculus	225-228
10746948-6	2000	PARP inhibitors (niacinamide, 3-aminobenzamide, 6(5H)-phenanthridinone), and two sulfhydryl-group donors (N-acetylcysteine, WR-1065) were found to be effective in preventing HN2-induced metabolic dysfunction when added in immediate or delayed treatment with HN2.	Acetylcysteine	106-122	MT-RNR2 like 2 (pseudogene)	Homo sapiens	174-177
33951536-6	2021	N-acetyl cysteine, a thiol repletion agent that supports neuronal glutathione metabolism, suppressed the PFF - induced redox stress and c-Abl activation in the wild-type neurons, and likewise suppressed alpha-synuclein aggregation.	Acetylcysteine	0-17	synuclein, alpha	Mus musculus	203-218
33951536-7	2021	Parallel findings were observed in mouse brain: PFF-induced alpha-synuclein aggregation in the substantia nigra was associated with redox stress, c-Abl activation, and dopaminergic neuronal loss, along with microglial activation and motor impairment, all of which were attenuated with oral N-acetyl cysteine.	Acetylcysteine	290-307	synuclein, alpha	Mus musculus	60-75
32810585-11	2020	Further investigation of the underlying mechanisms revealed that the ROS scavenger N-acetyl-l-cysteine inhibited CRS-induced JNK activation.	Acetylcysteine	83-102	mitogen-activated protein kinase 8	Rattus norvegicus	125-128
32868342-8	2020	In addition, compared to SS2-infected STEC, PCV2/SS2 coinfection and pretreatment of STEC with NAC prior to SS2 infection both down-regulated the expression of inflammatory cytokines IL-6, TNF-alpha and IL-1beta.	Acetylcysteine	95-98	interleukin 1 alpha	Homo sapiens	203-211
32438104-4	2020	RESULTS: Pretreatment of NAC significantly alleviated pathologic damage of kidney tissues in septic rats; decreased the levels of serum creatinine, blood urea nitrogen, plasma neutrophil gelatinase-associated lipocalin, and kidney injury molecule-1; and reduced the expression of tumor necrosis factor a, interleukin [IL]-1beta, IL-6, and IL-8.	Acetylcysteine	25-28	hepatitis A virus cellular receptor 1	Rattus norvegicus	224-248
32438104-6	2020	Moreover, pretreatment of NAC reduced the number of apoptosis in kidney tissues induced by CLP, decreased the mRNA levels of caspase-3, caspase-9, cytochrome c, and poly ADP-ribose polymerase, and increased mitochondrial membrane activity in renal cortical cells (complex I/II/III/IV).	Acetylcysteine	26-29	poly (ADP-ribose) polymerase 1	Rattus norvegicus	165-191
32945495-9	2020	Furthermore, NAC reduced the expression of ASC, NLRP3, caspase-1 and TXNIP, but enhanced that of TRX.	Acetylcysteine	13-16	thioredoxin	Homo sapiens	97-100
32945495-10	2020	To conclude, NAC had anti-inflammatory effects on LPS-stimulated BMSCs, which was closely associated with the TXNIP/NLRP3/IL-1beta signaling pathway.	Acetylcysteine	13-16	interleukin 1 alpha	Homo sapiens	122-130
33162896-9	2020	The pretreatments of antioxidant N-acetylcysteine (NAC) and apocynin (APO) abolished the drop of the levels of PP2Ac Tyr307 and eNOS Ser1177 induced by AngII in HUVECs.	Acetylcysteine	33-49	protein phosphatase 2 catalytic subunit alpha	Homo sapiens	111-116
33118390-8	2021	Moreover, in western blot analysis, expression of anti-apoptotic proteins (thioredoxin1, peroxiredoxin-1, Bcl-2, and Bcl-xL) in I3C-treated cells was evidently downregulated and pro-apoptotic proteins (active ASK1 and cleaved PARP) were upregulated compared to cells co-treated with NAC.	Acetylcysteine	283-286	peroxiredoxin 1	Homo sapiens	89-104
10746948-6	2000	PARP inhibitors (niacinamide, 3-aminobenzamide, 6(5H)-phenanthridinone), and two sulfhydryl-group donors (N-acetylcysteine, WR-1065) were found to be effective in preventing HN2-induced metabolic dysfunction when added in immediate or delayed treatment with HN2.	Acetylcysteine	106-122	MT-RNR2 like 2 (pseudogene)	Homo sapiens	258-261
33162896-9	2020	The pretreatments of antioxidant N-acetylcysteine (NAC) and apocynin (APO) abolished the drop of the levels of PP2Ac Tyr307 and eNOS Ser1177 induced by AngII in HUVECs.	Acetylcysteine	51-54	protein phosphatase 2 catalytic subunit alpha	Homo sapiens	111-116
10746948-7	2000	Only N-acetylcysteine, however, was found to prevent cell death induced by HN2, though it must be present at the time of the HN2 challenge.	Acetylcysteine	5-21	MT-RNR2 like 2 (pseudogene)	Homo sapiens	75-78
10746948-8	2000	Flow cytometric measurements of intracellular sulfhydryl levels strongly suggested that N-acetylcysteine and WR-1065 are preventive in alkylation of cellular compounds, mainly by direct extracellular interaction with HN2.	Acetylcysteine	88-104	MT-RNR2 like 2 (pseudogene)	Homo sapiens	217-220
33760106-6	2021	The ROS scavenger NAC and ER stress inhibitor 4-PBA were found to reduce ER stress-associated protein expression and MUC5AC production and secretion.	Acetylcysteine	18-21	mucin 5AC, oligomeric mucus/gel-forming	Homo sapiens	117-123
10694352-11	2000	N-acetylcysteine reduced basal activity of both matrix metalloproteinase 9 and matrix metalloproteinase 2 to 20%.	Acetylcysteine	0-16	matrix metallopeptidase 2	Homo sapiens	79-105
33744595-14	2021	NAC (N-acetylcysteine), a reducer reversed valtrate-induced the depletion of Stat3, p-Stat3, c-Myc, and Cyclin B1.	Acetylcysteine	5-21	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	93-98
33744595-14	2021	NAC (N-acetylcysteine), a reducer reversed valtrate-induced the depletion of Stat3, p-Stat3, c-Myc, and Cyclin B1.	Acetylcysteine	5-21	cyclin B1	Homo sapiens	104-113
32891167-7	2020	The pretreatment of ROS inhibitor N-acetyl-L-cysteine (NAC) significantly attenuated N. caninum-induced ROS production, LDH release, IL-1beta secretion and NLRP3 expression, whereas N. caninum proliferation was notably increased.	Acetylcysteine	34-53	interleukin 1 alpha	Mus musculus	133-141
32891167-7	2020	The pretreatment of ROS inhibitor N-acetyl-L-cysteine (NAC) significantly attenuated N. caninum-induced ROS production, LDH release, IL-1beta secretion and NLRP3 expression, whereas N. caninum proliferation was notably increased.	Acetylcysteine	34-53	NLR family, pyrin domain containing 3	Mus musculus	156-161
32891167-7	2020	The pretreatment of ROS inhibitor N-acetyl-L-cysteine (NAC) significantly attenuated N. caninum-induced ROS production, LDH release, IL-1beta secretion and NLRP3 expression, whereas N. caninum proliferation was notably increased.	Acetylcysteine	55-58	interleukin 1 alpha	Mus musculus	133-141
32891167-7	2020	The pretreatment of ROS inhibitor N-acetyl-L-cysteine (NAC) significantly attenuated N. caninum-induced ROS production, LDH release, IL-1beta secretion and NLRP3 expression, whereas N. caninum proliferation was notably increased.	Acetylcysteine	55-58	NLR family, pyrin domain containing 3	Mus musculus	156-161
33879035-4	2021	Inhibition of vitamin K epoxide reductase (VKOR) by acetaminophen and NAC in chronic applications has been reported, however, detailed knowledge of the molecular mechanism and binding sites are not clear.	Acetylcysteine	70-73	vitamin K epoxide reductase complex subunit 1	Homo sapiens	14-41
10573084-4	1999	N-Acetylcysteine (NAC) is an antioxidant that inhibits the B7-1/CD28 expression in vitro, and it may contrabalance the effects of free radicals and oxidative stress; it has been tested in eight patients with steroid-resistant acute GVHD.	Acetylcysteine	0-16	CD80 molecule	Homo sapiens	59-63
33879035-4	2021	Inhibition of vitamin K epoxide reductase (VKOR) by acetaminophen and NAC in chronic applications has been reported, however, detailed knowledge of the molecular mechanism and binding sites are not clear.	Acetylcysteine	70-73	vitamin K epoxide reductase complex subunit 1	Homo sapiens	43-47
33879035-5	2021	Herein, we built the homology model of human VKOR (hVKOR) using ITASSER server, confirmed, and applied it for docking analysis of its interaction with acetaminophen and its metabolite, N-acetyl-p-benzoquinone imine (NAPQI), and NAC.	Acetylcysteine	228-231	vitamin K epoxide reductase complex subunit 1	Homo sapiens	45-49
33879035-5	2021	Herein, we built the homology model of human VKOR (hVKOR) using ITASSER server, confirmed, and applied it for docking analysis of its interaction with acetaminophen and its metabolite, N-acetyl-p-benzoquinone imine (NAPQI), and NAC.	Acetylcysteine	228-231	vitamin K epoxide reductase complex subunit 1	Homo sapiens	51-56
33879035-7	2021	Our analysis showed that NAPQI and NAC, but not acetaminophen, bind strongly to the similar sites in hVKOR via both hydrogen and van der Waals bonding; particularly with Cys135.	Acetylcysteine	35-38	vitamin K epoxide reductase complex subunit 1	Homo sapiens	101-106
32683902-12	2020	N-acetylcysteine treatment reduced cardiac oxidative stress and attenuated cardiac hypertrophy in NOX5 trangenic.	Acetylcysteine	0-16	NADPH oxidase 5	Homo sapiens	98-102
32548987-8	2020	At the mRNA level, NAC can inhibit AMPK and activate mTOR expression.	Acetylcysteine	19-22	mechanistic target of rapamycin kinase	Mus musculus	53-57
10479653-2	1999	In rat aortic smooth muscle cells, the antioxidants N-acetyl-L-cysteine (5 mmol/L) and pyrrolidine dithiocarbamate (100 micromol/L) completely inhibited angiotensin II-stimulated increases in IGF-1R mRNA and protein levels, suggesting the involvement of reactive oxygen species.	Acetylcysteine	52-71	insulin-like growth factor 1 receptor	Rattus norvegicus	192-198
32548987-9	2020	The results indicate that NAC might regulate autophagy in RAW264.7 cells through the AMPK/mTOR pathway.	Acetylcysteine	26-29	mechanistic target of rapamycin kinase	Mus musculus	90-94
32548987-21	2020	At the mRNA level, NAC can inhibit AMPK and activate mTOR expression.	Acetylcysteine	19-22	mechanistic target of rapamycin kinase	Mus musculus	53-57
32548987-22	2020	The results indicate that NAC might regulate autophagy in RAW264.7 cells through the AMPK/mTOR pathway.	Acetylcysteine	26-29	mechanistic target of rapamycin kinase	Mus musculus	90-94
33610944-6	2021	After MC-LR exposure, ASK1 expression in mouse ovarian granulosa cells was increased at the protein and mRNA levels, and decreased following pretreatment by antioxidant N-acetylcysteine, suggesting that MC-LR-induced oxidative stress has a regulatory role in ASK1 expression.	Acetylcysteine	169-185	mitogen-activated protein kinase kinase kinase 5	Mus musculus	22-26
33610944-6	2021	After MC-LR exposure, ASK1 expression in mouse ovarian granulosa cells was increased at the protein and mRNA levels, and decreased following pretreatment by antioxidant N-acetylcysteine, suggesting that MC-LR-induced oxidative stress has a regulatory role in ASK1 expression.	Acetylcysteine	169-185	mitogen-activated protein kinase kinase kinase 5	Mus musculus	259-263
10533675-6	1999	In contrast, the glutathione precursor N-acetyl-l-cysteine (NAC) prevented PDTC-dependent increase in GSSG/GSH ratio, inhibition of SP-A and -B mRNAs, and induction of apoJ.	Acetylcysteine	39-58	surfactant protein A1	Homo sapiens	132-143
33825597-9	2021	More importantly, the treatment with NAC even inhibited the expression of p53.	Acetylcysteine	37-40	transformation related protein 53, pseudogene	Mus musculus	74-77
32559414-5	2020	Adding N-acetyl-cysteine or inhibiting FA shuttling into mitochondria decreased ROS and cell death induced by DGAT1 inhibition.	Acetylcysteine	7-24	diacylglycerol O-acyltransferase 1	Homo sapiens	110-115
10533675-6	1999	In contrast, the glutathione precursor N-acetyl-l-cysteine (NAC) prevented PDTC-dependent increase in GSSG/GSH ratio, inhibition of SP-A and -B mRNAs, and induction of apoJ.	Acetylcysteine	39-58	clusterin	Homo sapiens	168-172
32779379-8	2021	Incubation of hNECs with N-acetyl-L-cysteine (NAC) significantly attenuated BC +- pollen-induced expression of ROS, NLRP3, and IL-1beta.	Acetylcysteine	25-44	interleukin 1 alpha	Homo sapiens	127-135
32779379-8	2021	Incubation of hNECs with N-acetyl-L-cysteine (NAC) significantly attenuated BC +- pollen-induced expression of ROS, NLRP3, and IL-1beta.	Acetylcysteine	46-49	interleukin 1 alpha	Homo sapiens	127-135
10533675-6	1999	In contrast, the glutathione precursor N-acetyl-l-cysteine (NAC) prevented PDTC-dependent increase in GSSG/GSH ratio, inhibition of SP-A and -B mRNAs, and induction of apoJ.	Acetylcysteine	60-63	surfactant protein A1	Homo sapiens	132-143
33453249-7	2021	Podocytes treatment with NAC reversed Nox4, Col4a1, Acta2, and Tgfb1 increased expression but did not abrogate the reduced expression of nephrin.	Acetylcysteine	25-28	actin alpha 2, smooth muscle	Rattus norvegicus	52-57
10533675-6	1999	In contrast, the glutathione precursor N-acetyl-l-cysteine (NAC) prevented PDTC-dependent increase in GSSG/GSH ratio, inhibition of SP-A and -B mRNAs, and induction of apoJ.	Acetylcysteine	60-63	clusterin	Homo sapiens	168-172
33712045-12	2021	After IR exposure, IGFBP3-induced NF-kappaB activation was inhibited by the ROS scavenger N-acetyl-L-cysteine (NAC).	Acetylcysteine	90-109	insulin-like growth factor binding protein 3	Mus musculus	19-25
32402895-9	2020	Dietary NAC supplementation significantly reversed back the activity of antioxidant enzymes in arsenite fed rats towards normalcy and also sustained the normal reproductive cyclicity, utero-ovarian histo-morphology and estradiol receptor alpha (ER-alpha) expression in these reproductive organs.	Acetylcysteine	8-11	estrogen receptor 1	Rattus norvegicus	245-253
10533675-7	1999	Insufficiency of SP-A and -B, which occurs in inflammatory lung diseases, may result from the exposure of the pulmonary epithelium to oxidant stress and may be reversed by the antioxidant NAC.	Acetylcysteine	188-191	surfactant protein A1	Homo sapiens	17-28
32402895-10	2020	Dietary NAC exerted its positive action against arsenic intoxication by up-regulation of Bcl-2 gene expression along with the suppression of pro-apoptotic Bax gene and p53 gene.	Acetylcysteine	8-11	BCL2 associated X, apoptosis regulator	Rattus norvegicus	155-158
33712045-12	2021	After IR exposure, IGFBP3-induced NF-kappaB activation was inhibited by the ROS scavenger N-acetyl-L-cysteine (NAC).	Acetylcysteine	111-114	insulin-like growth factor binding protein 3	Mus musculus	19-25
32402895-10	2020	Dietary NAC exerted its positive action against arsenic intoxication by up-regulation of Bcl-2 gene expression along with the suppression of pro-apoptotic Bax gene and p53 gene.	Acetylcysteine	8-11	Wistar clone pR53P1 p53 pseudogene	Rattus norvegicus	168-171
10428064-5	1999	Activation of caspase-3 induced by hypoxia was also inhibited by either GSH or NAC.	Acetylcysteine	79-82	caspase 3	Rattus norvegicus	14-23
32722598-7	2020	Treatment of cancer cell lines with the antioxidant N-acetylcysteine reduces the extent of membrane dysfunction and the expression of both CHOP-DR5 and miR-425-PTEN axes, attenuating PAM/TRAIL-induced cancer cell apoptosis.	Acetylcysteine	52-68	TNF receptor superfamily member 10b	Homo sapiens	144-147
32722598-7	2020	Treatment of cancer cell lines with the antioxidant N-acetylcysteine reduces the extent of membrane dysfunction and the expression of both CHOP-DR5 and miR-425-PTEN axes, attenuating PAM/TRAIL-induced cancer cell apoptosis.	Acetylcysteine	52-68	phosphatase and tensin homolog	Homo sapiens	160-164
33707964-10	2021	Furthermore, N-acetylcysteine (NAC), an ROS scavenger, inhibited the LPS/ATP-stimulated activation of NLRP3 inflammasome mediated inflammation and pyroptosis.	Acetylcysteine	13-29	NLR family, pyrin domain containing 3	Mus musculus	102-107
33707964-10	2021	Furthermore, N-acetylcysteine (NAC), an ROS scavenger, inhibited the LPS/ATP-stimulated activation of NLRP3 inflammasome mediated inflammation and pyroptosis.	Acetylcysteine	31-34	NLR family, pyrin domain containing 3	Mus musculus	102-107
10428064-6	1999	NAC but not GSH inhibited caspase-3 activation induced by C2-ceramide.	Acetylcysteine	0-3	caspase 3	Rattus norvegicus	26-35
33574492-5	2021	However, with N-acetylcysteine treatment, the level of oxidative stress was decreased, accompanied by significant increases in antioxidant enzyme activities and the mRNA levels of SOD, CAT, GSTCD, and GSTO1.	Acetylcysteine	14-30	glutathione S-transferase omega-1	Pelodiscus sinensis	201-206
32708634-4	2020	CBD-induced HO-1 expression was not decreased by antagonists of cannabinoid-activated receptors (CB1, CB2, transient receptor potential vanilloid 1), but by the reactive oxygen species (ROS) scavenger N-acetyl-L-cysteine (NAC).	Acetylcysteine	201-220	heme oxygenase 1	Homo sapiens	12-16
32708634-4	2020	CBD-induced HO-1 expression was not decreased by antagonists of cannabinoid-activated receptors (CB1, CB2, transient receptor potential vanilloid 1), but by the reactive oxygen species (ROS) scavenger N-acetyl-L-cysteine (NAC).	Acetylcysteine	222-225	heme oxygenase 1	Homo sapiens	12-16
10051436-3	1999	Attempts to characterize the signalling pathway from PDTC exposure to increases in the expression of the GCS catalytic and regulatory subunit genes demonstrated that induction by PDTC could be partially blocked by treatment with the thiol agent N-acetylcysteine and by the copper chelator bathocuproine disulphonic acid.	Acetylcysteine	245-261	glutamate-cysteine ligase catalytic subunit	Homo sapiens	105-108
32724493-11	2020	Finally, N-acetyl-cysteine (NAC) was added and its regulatory effect on the MAPK-NF-kappaB-MUC5B pathway was examined in PQ-induced cell inflammation.	Acetylcysteine	9-26	mucin 5, subtype B, tracheobronchial	Mus musculus	91-96
32724493-11	2020	Finally, N-acetyl-cysteine (NAC) was added and its regulatory effect on the MAPK-NF-kappaB-MUC5B pathway was examined in PQ-induced cell inflammation.	Acetylcysteine	28-31	mucin 5, subtype B, tracheobronchial	Mus musculus	91-96
32724493-15	2020	As expected, the addition of NAC efficiently suppresses the TNF-alpha and IL-6 secretion stimulated from PQ and also downregulated ERK, JNK, and p65 phosphorylation (ERK/JNK MAPK and NF-kappaB pathways) as well as MUC5B expression.	Acetylcysteine	29-32	v-rel reticuloendotheliosis viral oncogene homolog A (avian)	Mus musculus	145-148
32724493-15	2020	As expected, the addition of NAC efficiently suppresses the TNF-alpha and IL-6 secretion stimulated from PQ and also downregulated ERK, JNK, and p65 phosphorylation (ERK/JNK MAPK and NF-kappaB pathways) as well as MUC5B expression.	Acetylcysteine	29-32	mucin 5, subtype B, tracheobronchial	Mus musculus	214-219
32724493-17	2020	NAC can attenuate PQ-induced cell inflammation at least in part by suppressing the MAPK-NF-kappaB-MUC5B pathway.	Acetylcysteine	0-3	mucin 5, subtype B, tracheobronchial	Mus musculus	98-103
32347295-6	2020	However, in the groups of HG-N, DM, HG-N+I/R and DM+I/R, NAC can significantly reduce oxidative stress injury and apoptosis rate of myocytes, promote the Bcl-2 and DJ-1 molecules, inhibit BAX and c-caspase-3 protein and PTEN/Akt pathway.	Acetylcysteine	57-60	Parkinsonism associated deglycase	Homo sapiens	164-168
32347295-6	2020	However, in the groups of HG-N, DM, HG-N+I/R and DM+I/R, NAC can significantly reduce oxidative stress injury and apoptosis rate of myocytes, promote the Bcl-2 and DJ-1 molecules, inhibit BAX and c-caspase-3 protein and PTEN/Akt pathway.	Acetylcysteine	57-60	BCL2 associated X, apoptosis regulator	Rattus norvegicus	188-191
32347295-7	2020	Compared with HG-N+I/R+NAC and DM+I/R+NAC groups, the oxidative stress injury, apoptosis rate of myocardial cells and heart tissues increased after the knockdown of DJ-1, the expression of Bcl-2 and DJ-1 were inhibited, the BAX and c-caspase-3 expression was increased, and PTEN/Akt pathway was activated.	Acetylcysteine	23-26	Parkinsonism associated deglycase	Homo sapiens	165-169
32347295-7	2020	Compared with HG-N+I/R+NAC and DM+I/R+NAC groups, the oxidative stress injury, apoptosis rate of myocardial cells and heart tissues increased after the knockdown of DJ-1, the expression of Bcl-2 and DJ-1 were inhibited, the BAX and c-caspase-3 expression was increased, and PTEN/Akt pathway was activated.	Acetylcysteine	38-41	Parkinsonism associated deglycase	Homo sapiens	165-169
32347295-8	2020	Taken together, the findings suggest that NAC can reduce ischemia reperfusion injury in diabetic myocardium by up-regulating the PTEN/Akt pathway through the level of DJ-1.	Acetylcysteine	42-45	Parkinsonism associated deglycase	Homo sapiens	167-171
33560400-8	2021	Notably, an antioxidant, N-acetyl-l-cysteine, rescued HSC and lymphoid progenitor cell depletion, indicating a causal impact of OXPHOS-mediated ROS generation upon Jmjd6 deletion.	Acetylcysteine	25-44	fucosyltransferase 1 (H blood group)	Homo sapiens	54-57
33560400-8	2021	Notably, an antioxidant, N-acetyl-l-cysteine, rescued HSC and lymphoid progenitor cell depletion, indicating a causal impact of OXPHOS-mediated ROS generation upon Jmjd6 deletion.	Acetylcysteine	25-44	jumonji domain containing 6, arginine demethylase and lysine hydroxylase	Homo sapiens	164-169
33613826-8	2021	Additionally, dosing with N-acetylcysteine (NAC) effectively mitigated bone loss and normalized expression of ALP, Runx2, and OPN.	Acetylcysteine	26-42	runt related transcription factor 2	Mus musculus	115-120
33613826-8	2021	Additionally, dosing with N-acetylcysteine (NAC) effectively mitigated bone loss and normalized expression of ALP, Runx2, and OPN.	Acetylcysteine	44-47	runt related transcription factor 2	Mus musculus	115-120
33454892-0	2021	N-Acetylcysteine Reduces miR-146a and NF-kappaB p65 Inflammatory Signaling Following Cadmium Hepatotoxicity in Rats.	Acetylcysteine	0-16	microRNA 146a	Rattus norvegicus	25-33
10037708-7	1999	Surprisingly, a remarkable loss of both IRE binding and aconitase activities of IRP-1 follows treatment with MSB for 1-2 h. These effects do not result from alterations in IRP-1 half-life, can be antagonized by the antioxidant N-acetylcysteine, and regulate IRE-containing mRNAs; the capacity of iron-starved MSB-treated cells to increase transferrin receptor mRNA levels is inhibited, and MSB increases the translation of a human growth hormone indicator mRNA bearing an IRE in its 5"-untranslated region.	Acetylcysteine	227-243	aconitase 1	Homo sapiens	80-85
33454892-1	2021	We performed a thorough screening and analysis of the impact of cadmium chloride (CdCl2) and N-acetylcysteine (NAC) on the miR146a/NF-kappaB p65 inflammatory pathway and mitochondrial biogenesis dysfunction in male albino rats.	Acetylcysteine	93-109	microRNA 146a	Rattus norvegicus	123-130
33454892-1	2021	We performed a thorough screening and analysis of the impact of cadmium chloride (CdCl2) and N-acetylcysteine (NAC) on the miR146a/NF-kappaB p65 inflammatory pathway and mitochondrial biogenesis dysfunction in male albino rats.	Acetylcysteine	111-114	microRNA 146a	Rattus norvegicus	123-130
33454892-5	2021	Decreased miR146a and NF-kappaB p65 were also found after treatment with NAC and CdCl2 compared with CdCl2 treatment alone.	Acetylcysteine	73-76	microRNA 146a	Rattus norvegicus	10-17
33183638-4	2021	In this study, a novel N-acetyl-L-cysteine and arginine modified hydroxypropyl-beta-cyclodextrin (NAC-HP-beta-CD-Arg) was successfully synthesized and characterized.	Acetylcysteine	23-42	synuclein alpha	Homo sapiens	98-101
33188856-7	2021	The genes (ApoE/TET1/TIMP2/TIMP3) suppressed by Cd were further suppressed by hydroquinone (HQ; a reactive oxygen species [ROS] producer), whereas N-acetyl-L-cysteine (NAC; a ROS scavenger) prevented the suppression of their expression by HQ.	Acetylcysteine	168-171	tet methylcytosine dioxygenase 1	Rattus norvegicus	16-20
33188856-7	2021	The genes (ApoE/TET1/TIMP2/TIMP3) suppressed by Cd were further suppressed by hydroquinone (HQ; a reactive oxygen species [ROS] producer), whereas N-acetyl-L-cysteine (NAC; a ROS scavenger) prevented the suppression of their expression by HQ.	Acetylcysteine	168-171	TIMP metallopeptidase inhibitor 2	Rattus norvegicus	21-26
32546031-7	2021	TDI exposure led to significantly increased levels of interleukin 4 (IL-4) and IL-5, which were also suppressed by NAC.	Acetylcysteine	115-118	interleukin 4	Mus musculus	69-73
32337800-8	2020	NAC treatment or AON overexpression effectively prevented HFD-induced intracellular ROS production and reduction of BM lin- /CD117+ population.	Acetylcysteine	0-3	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	125-130
9990127-10	1999	LAO-induced apoptosis can be protected by the antioxidant N-acetylcysteine or the free radical scavenger melatonin, while H2O2-induced apoptotic cell death is not protected.	Acetylcysteine	58-74	interleukin 4 induced 1	Homo sapiens	0-3
32229256-6	2020	Out of many antioxidant candidates, N-acetyl-L-cysteine (a prodrug of L-cysteine) (NAC) is a potent antioxidant as the bioavailability of the parent drug, L-cysteine, determines the production of glutathione; the universal antioxidant that regulates ROS.	Acetylcysteine	36-55	synuclein alpha	Homo sapiens	83-86
33439409-15	2021	It was revealed by Western blotting analysis that NAC promoted Bcl-2 signaling and decreased p53 signaling.	Acetylcysteine	50-53	Wistar clone pR53P1 p53 pseudogene	Rattus norvegicus	93-96
9809995-5	1998	In addition, the p36 MBP kinase activation and apoptotic DNA fragmentation were inhibited by antioxidants such as N-acetylcysteine and reduced-form glutathione.	Acetylcysteine	114-130	myelin basic protein	Homo sapiens	21-24
33321464-6	2021	Conversely, exposures to antioxidant N-acetylcysteine (bolsters GSH pools; 100 muM; 48-72 hpf) or sulforaphane (activates Nrf2a; 20 muM; 48-72 hpf) significantly increased islet areas.	Acetylcysteine	37-53	nfe2 like bZIP transcription factor 2a	Danio rerio	122-127
33035499-7	2020	In striatum and cortex, NAC prevented glial cells activation (GFAP and Iba-1), decreased NGF, Bcl-2 and NeuN, the increase of lipid peroxidation and PARP induced by GA in both ages.	Acetylcysteine	24-27	glial fibrillary acidic protein	Mus musculus	62-66
33035499-7	2020	In striatum and cortex, NAC prevented glial cells activation (GFAP and Iba-1), decreased NGF, Bcl-2 and NeuN, the increase of lipid peroxidation and PARP induced by GA in both ages.	Acetylcysteine	24-27	induction of brown adipocytes 1	Mus musculus	71-76
32432042-9	2020	These data are confirmed by treatments with either N-acetylcysteine (NAC) or AMD3100 or NF-kappaB inhibitor IkappaB-alpha which revert the FtH-silenced K562 invasive phenotype.	Acetylcysteine	51-67	ferritin heavy chain 1	Homo sapiens	139-142
32432042-9	2020	These data are confirmed by treatments with either N-acetylcysteine (NAC) or AMD3100 or NF-kappaB inhibitor IkappaB-alpha which revert the FtH-silenced K562 invasive phenotype.	Acetylcysteine	69-72	ferritin heavy chain 1	Homo sapiens	139-142
31895126-6	2020	mTOR inhibition via rapamycin and N-acetylcysteine, and blockade of glucose utilization show clinical efficacy in both mouse models and clinical trials, such as systemic lupus erythematosus.	Acetylcysteine	34-50	mechanistic target of rapamycin kinase	Mus musculus	0-4
9781735-12	1998	Insufficient evidence exists to support the beneficial effects of nitric oxide donors or blockers, pentoxifylline, or N-acetylcysteine on pHi.	Acetylcysteine	118-134	glucose-6-phosphate isomerase	Homo sapiens	138-141
32071301-7	2020	Furthermore, MAPK signaling pathway activation contributed to BD-induced cell proliferation inhibition and NAC could eliminate p-ERK and p-JNK upregulation.	Acetylcysteine	107-110	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	127-132
31838118-11	2020	Furthermore, NAC improved redox and inflammatory status; decreased levels of RIPK3, MLKL, NLRP3, IL-18; down-regulated ASC, iNOS, GFAP and MMP-9 expression; and decreased myeloperoxidase activity in cerebral cortex.	Acetylcysteine	13-16	interleukin 18	Rattus norvegicus	97-102
32684241-8	2020	Upregulation of RRAGC was limited by the reactive oxygen species (ROS) scavenger N-acetyl cysteine (NAC), suggesting that ROS are involved in EHMT2-mediated transcriptional regulation of stress-response genes in HCC cells.	Acetylcysteine	81-98	Ras related GTP binding C	Homo sapiens	16-21
32684241-8	2020	Upregulation of RRAGC was limited by the reactive oxygen species (ROS) scavenger N-acetyl cysteine (NAC), suggesting that ROS are involved in EHMT2-mediated transcriptional regulation of stress-response genes in HCC cells.	Acetylcysteine	100-103	Ras related GTP binding C	Homo sapiens	16-21
31838118-11	2020	Furthermore, NAC improved redox and inflammatory status; decreased levels of RIPK3, MLKL, NLRP3, IL-18; down-regulated ASC, iNOS, GFAP and MMP-9 expression; and decreased myeloperoxidase activity in cerebral cortex.	Acetylcysteine	13-16	myeloperoxidase	Rattus norvegicus	171-186
9668619-9	1998	IRP seems a direct target of ROS; in fact, in vivo inhibition can be prevented by the antioxidant N-acetylcysteine and by interleukin-1 receptor antagonist.	Acetylcysteine	98-114	Wnt family member 2	Homo sapiens	0-3
31631367-17	2020	NAC or DEX administration can attenuate ALI by rebalancing Th1/Th2/Th17 cytokines.	Acetylcysteine	0-3	heart and neural crest derivatives expressed 2	Mus musculus	63-66
31669540-11	2020	N-acetyl-l-cysteine treatment attenuated the 15-keto PGE2-induced phosphorylation of GSK3beta, transcriptional activity of Nrf2, and subsequently HO-1 expression.	Acetylcysteine	0-19	heme oxygenase 1	Homo sapiens	146-150
31756635-6	2020	The elevation of Drp1 phosphorylation was partly dependent on the reactive oxygen species (ROS)-mediated activation of c-Jun-N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (MAPK), as N-acetyl-l-cysteine (NAC) pretreatment inhibited the activation of JNK and p38 MAPK while attenuating Drp1 phosphorylation in acetaldehyde-treated cells.	Acetylcysteine	201-220	dynamin 1 like	Homo sapiens	17-21
31756635-6	2020	The elevation of Drp1 phosphorylation was partly dependent on the reactive oxygen species (ROS)-mediated activation of c-Jun-N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (MAPK), as N-acetyl-l-cysteine (NAC) pretreatment inhibited the activation of JNK and p38 MAPK while attenuating Drp1 phosphorylation in acetaldehyde-treated cells.	Acetylcysteine	222-225	dynamin 1 like	Homo sapiens	17-21
33224008-10	2020	The acetylcysteine treatment did not cause a significant change of blood parameters, but significantly decreased 24-hour elimination of CysC and KIM-1 with urine, and accounted for alleviation of the histopathological abnormalities of urinary bladders, with no significant effects on the structure of the kidneys.	Acetylcysteine	4-18	cystatin C	Rattus norvegicus	136-140
9618303-4	1998	Pretreatment of cells with antioxidants N-acetylcysteine (NAC) and glutathione (GSH) almost completely blocked tyrosine phosphorylations of Syk, Fc gamma receptor(s) and PLC gamma 2.	Acetylcysteine	40-56	phospholipase C gamma 2	Homo sapiens	170-181
32083315-8	2020	Treatment using the ROS inhibitor N-acetyl- l-cysteine abrogated the increase in mitochondrial membrane potential after EGF treatment.	Acetylcysteine	34-54	epidermal growth factor	Homo sapiens	120-123
32945495-0	2020	N-acetyl cysteine inhibits the lipopolysaccharide-induced inflammatory response in bone marrow mesenchymal stem cells by suppressing the TXNIP/NLRP3/IL-1beta signaling pathway.	Acetylcysteine	0-17	interleukin 1 alpha	Homo sapiens	149-157
32945475-14	2020	Changes in the expression of PCNA, and Bcl-xL and in the levels of cleaved-caspase 3 were partly reversed by N-acetyl-L-cysteine, a reactive oxygen species (ROS) scavenger.	Acetylcysteine	109-128	proliferating cell nuclear antigen	Homo sapiens	29-33
32819581-7	2020	Our results showed that third-passage RSCs from WT mice had good stemness; Bmi-1 deficiency led to the decreased stemness, and the increased apoptosis for RSCs; NAC treatment or p16/p53 deletion ameliorated the decreased self-renewal of RSCs in Bmi-1 deficiency mice by maintaining redox balance or inhibiting cell cycle arrest respectively; Oxidative stress (OS) could negatively feedback regulate the mRNA expressions of Bmi-1, p16 and p53.	Acetylcysteine	161-164	transformation related protein 53, pseudogene	Mus musculus	438-441
31790150-7	2019	The ATP7B increase in TMEM16A-overexpressing cells was reversed by suppression of NADPH oxidase 2 (NOX2), by the antioxidant N-Acetyl-Cysteine (NAC) and by copper chelation using cuprizone and bathocuproine sulphonate (BCS).	Acetylcysteine	125-142	anoctamin 1	Homo sapiens	22-29
31790150-7	2019	The ATP7B increase in TMEM16A-overexpressing cells was reversed by suppression of NADPH oxidase 2 (NOX2), by the antioxidant N-Acetyl-Cysteine (NAC) and by copper chelation using cuprizone and bathocuproine sulphonate (BCS).	Acetylcysteine	144-147	anoctamin 1	Homo sapiens	22-29
9618303-4	1998	Pretreatment of cells with antioxidants N-acetylcysteine (NAC) and glutathione (GSH) almost completely blocked tyrosine phosphorylations of Syk, Fc gamma receptor(s) and PLC gamma 2.	Acetylcysteine	58-61	phospholipase C gamma 2	Homo sapiens	170-181
31404677-8	2019	RESULTS: mRNAs of PAI-1, HO-1, and p21 were upregulated after photoirradiation of HEK293, which was suppressed by N-acetyl-L-cysteine, a reactive oxygen species (ROS) scavenger.	Acetylcysteine	114-133	serpin family E member 1	Homo sapiens	18-23
33061803-7	2020	The activation of p38-MAPK/HSP27 induced by the p38-MAPK activator Anisomycin enhanced the apoptosis of lung SCC cells, while the ROS inhibitor N-acetyl-L-cysteine (NAC) and the p38-MAPK inhibitor SB203580 both attenuated dioscin-mediated cell apoptosis.	Acetylcysteine	144-163	heat shock protein family B (small) member 1	Homo sapiens	27-32
33061803-7	2020	The activation of p38-MAPK/HSP27 induced by the p38-MAPK activator Anisomycin enhanced the apoptosis of lung SCC cells, while the ROS inhibitor N-acetyl-L-cysteine (NAC) and the p38-MAPK inhibitor SB203580 both attenuated dioscin-mediated cell apoptosis.	Acetylcysteine	165-168	heat shock protein family B (small) member 1	Homo sapiens	27-32
33061803-8	2020	Moreover, NAC suppressed the activation of p38-MAPK/HSP27 that induced by dioscin.	Acetylcysteine	10-13	heat shock protein family B (small) member 1	Homo sapiens	52-57
32098455-8	2020	Treatment with NAC or dexamethasone decreased the OVA-induced increase in interleukin-1alpha protein levels.	Acetylcysteine	15-18	interleukin 1 alpha	Mus musculus	74-92
32534099-5	2020	While SFN significantly (p < 0.05) induced NRF2, KEAP1 and BACH1, NAC attenuated SFN-induced NRF2, KEAP1 and BACH1.	Acetylcysteine	66-69	BTB and CNC homology 1, basic leucine zipper transcription factor 1	Mus musculus	109-114
31404677-8	2019	RESULTS: mRNAs of PAI-1, HO-1, and p21 were upregulated after photoirradiation of HEK293, which was suppressed by N-acetyl-L-cysteine, a reactive oxygen species (ROS) scavenger.	Acetylcysteine	114-133	heme oxygenase 1	Homo sapiens	25-29
31404677-8	2019	RESULTS: mRNAs of PAI-1, HO-1, and p21 were upregulated after photoirradiation of HEK293, which was suppressed by N-acetyl-L-cysteine, a reactive oxygen species (ROS) scavenger.	Acetylcysteine	114-133	H3 histone pseudogene 16	Homo sapiens	35-38
9633518-4	1998	Here we show that other oxidant compounds, such as hydrogen peroxide, also induce a rapid downmodulation of membrane TfR and that pretreatment of cells with the antioxidant, thiol supplier, N-acetylcysteine inhibits the downmodulation of these receptors elicited by either menadione or hydrogen peroxide.	Acetylcysteine	190-206	transferrin receptor	Homo sapiens	117-120
31654686-3	2019	Besides the use of antibiotics, the mucolytic agent N-acetylcysteine (NAC) is recommended to be co-administered in the treatment of CF.	Acetylcysteine	52-68	synuclein alpha	Homo sapiens	70-73
31827678-10	2019	Lastly, we discuss the possibility of using small molecule antioxidants, such as N-acetyl cysteine, resveratrol, and curcumin, to augment HSC function and improve the therapeutic efficacy of BM transplantation.	Acetylcysteine	81-98	fucosyltransferase 1 (H blood group)	Homo sapiens	138-141
32684991-2	2020	N-acetylcysteine (NAC 0.2% w/v) was added as an antioxidant, preventing the oxidation of NDGA to toxic quinones.	Acetylcysteine	0-16	synuclein alpha	Homo sapiens	18-21
32353423-10	2020	Application of N-acetylcysteine blocked AKT/FOXO3a/Bim signaling.	Acetylcysteine	15-31	BCL2 like 11	Homo sapiens	51-54
32347295-3	2020	This research is to investigate whether the antioxidant N-acetylcysteine (NAC) could alleviating diabetic myocardial ischemia reperfusion (I/R) injury by the protective molecule DJ-1.	Acetylcysteine	56-72	Parkinsonism associated deglycase	Homo sapiens	178-182
32347295-3	2020	This research is to investigate whether the antioxidant N-acetylcysteine (NAC) could alleviating diabetic myocardial ischemia reperfusion (I/R) injury by the protective molecule DJ-1.	Acetylcysteine	74-77	Parkinsonism associated deglycase	Homo sapiens	178-182
9603460-6	1998	Treatment of SF T cells with N-acetylcysteine, an antioxidant and replenisher of GSH, selectively improved CD3-induced responses, while leaving CD28 responsiveness unaffected.	Acetylcysteine	29-45	CD28 molecule	Homo sapiens	144-148
32560255-0	2020	N-Acetylcysteine Reduces Skeletal Muscles Oxidative Stress and Improves Grip Strength in Dysferlin-Deficient Bla/J Mice.	Acetylcysteine	0-16	dysferlin	Mus musculus	89-98
32560255-7	2020	By using the Kondziela"s inverted screen test, we further demonstrated that NAC improved grip strength in dysferlin deficient animals, as compared with non-treated Bla/J mice, without affecting body mass.	Acetylcysteine	76-79	dysferlin	Mus musculus	106-115
31699096-14	2019	The ROS scavenger N-acetylcysteine (NAC) did not affect SiO2 NP-induced ER stress, but inhibited SiO2 NP-induced activation of the NF-kappaB and MAPK pathways, expression of inflammatory cytokines, SiO2 NP-induced serine phosphorylation of IRS1, and SiO2 NP-induced elevations of blood glucose.	Acetylcysteine	18-34	insulin receptor substrate 1	Mus musculus	240-244
31699096-14	2019	The ROS scavenger N-acetylcysteine (NAC) did not affect SiO2 NP-induced ER stress, but inhibited SiO2 NP-induced activation of the NF-kappaB and MAPK pathways, expression of inflammatory cytokines, SiO2 NP-induced serine phosphorylation of IRS1, and SiO2 NP-induced elevations of blood glucose.	Acetylcysteine	36-39	insulin receptor substrate 1	Mus musculus	240-244
31419475-6	2019	Importantly, TCE exposure resulted in the activation of hepatic inflammasome (NLRP3 and caspase-1) and up-regulation of pro-inflammatory cytokine IL-1beta, and these changes were attenuated by NAC supplementation.	Acetylcysteine	193-196	NLR family, pyrin domain containing 3	Mus musculus	78-83
32526845-5	2020	In the group treated with NAC, reductions in inflammatory infiltration; AST (aspartate aminotransferase), nitrite, and TBARS levels; GPx (gutathione peroxidase) activity; cytokines synthesis; and number of apoptotic cells were observed while the GR (glutathione reductase) activity was increased.	Acetylcysteine	26-29	solute carrier family 17 (anion/sugar transporter), member 5	Mus musculus	72-75
32526845-5	2020	In the group treated with NAC, reductions in inflammatory infiltration; AST (aspartate aminotransferase), nitrite, and TBARS levels; GPx (gutathione peroxidase) activity; cytokines synthesis; and number of apoptotic cells were observed while the GR (glutathione reductase) activity was increased.	Acetylcysteine	26-29	solute carrier family 17 (anion/sugar transporter), member 5	Mus musculus	77-103
9566715-7	1998	The nucleotide depletion likely reflected the action of ROS, since the nucleotide depletion caused by TNF or oxidants such as menadione or H2O2 in cells with active c-Myc was partly inhibited by the anti-oxidant N-acetylcysteine.	Acetylcysteine	212-228	MYC proto-oncogene, bHLH transcription factor	Rattus norvegicus	165-170
9518260-11	1998	In addition, provision of the GSH precursor, N-acetylcysteine during TNF-alpha challenge only diminished MnSOD activity and mitochondrial compartmentalization in the AIDS-KS cells, a finding that likely reflects the lower levels of reduced thiols in this cellular population.	Acetylcysteine	45-61	superoxide dismutase 2	Homo sapiens	105-110
9484648-11	1998	The rat alveolar macrophage cell line (NR8383) also showed increased MIP-1 alpha mRNA levels in response to LPS (10 micrograms/ml) with a maximal increase after 6-8 h. The induction of MIP-1 alpha mRNA expression by LPS in NR8383 cells was attenuated by cotreatment with the antioxidants N-acetylcysteine and dimethylsulfoxide, suggesting that the induction of MIP-1 alpha mRNA by LPS is mediated via the generation of reactive oxygen species.	Acetylcysteine	288-304	C-C motif chemokine ligand 3	Rattus norvegicus	69-80
32378169-11	2020	There was decline of IKK-beta and NF-kappaB-P65 and elevation of IkappaB-alpha in the N-acetylcysteine group, which was even significantly in the Budesonide group (P < 0.01).	Acetylcysteine	86-102	conserved helix-loop-helix ubiquitous kinase	Mus musculus	21-29
32346830-2	2020	N,S,P co-doped carbon dots (N,S,P-CDs) and N-acetyl-L-cysteine functionalized gold nanoclusters (NAC-AuNCs) are used in the FRET system, which serve as energy donor and acceptor, respectively.	Acetylcysteine	43-62	synuclein alpha	Homo sapiens	97-100
31368586-11	2019	Similarly, NAC pretreatment increased p-mTOR and decreased LC3B-II protein expression.	Acetylcysteine	11-14	mechanistic target of rapamycin kinase	Mus musculus	40-44
31368586-12	2019	Moreover, NAC decreased mitophagy related mRNA Pink1 and Parkin expression.	Acetylcysteine	10-13	PTEN induced putative kinase 1	Mus musculus	47-52
31310363-4	2019	The effects of H2 O2 and N-acetylcysteine (NAC) on the levels of HIF1-alpha and HIF2-alpha after overexpression of GPX3 were studied.	Acetylcysteine	43-46	endothelial PAS domain protein 1	Homo sapiens	80-90
31310363-12	2019	The addition of H2 O2 increased while NAC reduced the protein levels of HIF1-alpha and HIF2-alpha in the cells overexpressing GPX3.	Acetylcysteine	38-41	endothelial PAS domain protein 1	Homo sapiens	87-97
31454652-10	2019	Pretreatment with the antioxidant N-acetyl-L-cysteine prevented SFN-induced apoptosis in CL1-0 cells and production of gammaH2AX in both CL1-0 and CL1-5 cells.	Acetylcysteine	34-53	adhesion G protein-coupled receptor L1	Homo sapiens	89-92
31454652-10	2019	Pretreatment with the antioxidant N-acetyl-L-cysteine prevented SFN-induced apoptosis in CL1-0 cells and production of gammaH2AX in both CL1-0 and CL1-5 cells.	Acetylcysteine	34-53	adhesion G protein-coupled receptor L1	Homo sapiens	137-140
31578304-4	2019	Here, we investigated chronic NAC treatment in aging mice displaying lung oxidative stress and cell senescence due to inactivation of the transcription factor JunD, which is downregulated in diseased human lungs.	Acetylcysteine	30-33	jun D proto-oncogene	Mus musculus	159-163
32398966-10	2020	By using ROS scavenger N-acetyl-cysteine (NAC) could reverse the effects of nicotine by down-regulation the phosphorylation of p38MAPK and JNK pathways, and pretreatment of specific inhibitors of p38MAPK and JNK could restore the autophagy impairment and cardiomyocytes hypertrophy induced by nicotine.	Acetylcysteine	23-40	mitogen-activated protein kinase 8	Rattus norvegicus	139-142
9484648-11	1998	The rat alveolar macrophage cell line (NR8383) also showed increased MIP-1 alpha mRNA levels in response to LPS (10 micrograms/ml) with a maximal increase after 6-8 h. The induction of MIP-1 alpha mRNA expression by LPS in NR8383 cells was attenuated by cotreatment with the antioxidants N-acetylcysteine and dimethylsulfoxide, suggesting that the induction of MIP-1 alpha mRNA by LPS is mediated via the generation of reactive oxygen species.	Acetylcysteine	288-304	C-C motif chemokine ligand 3	Rattus norvegicus	185-196
32398966-10	2020	By using ROS scavenger N-acetyl-cysteine (NAC) could reverse the effects of nicotine by down-regulation the phosphorylation of p38MAPK and JNK pathways, and pretreatment of specific inhibitors of p38MAPK and JNK could restore the autophagy impairment and cardiomyocytes hypertrophy induced by nicotine.	Acetylcysteine	23-40	mitogen-activated protein kinase 8	Rattus norvegicus	208-211
32398966-10	2020	By using ROS scavenger N-acetyl-cysteine (NAC) could reverse the effects of nicotine by down-regulation the phosphorylation of p38MAPK and JNK pathways, and pretreatment of specific inhibitors of p38MAPK and JNK could restore the autophagy impairment and cardiomyocytes hypertrophy induced by nicotine.	Acetylcysteine	42-45	mitogen-activated protein kinase 8	Rattus norvegicus	139-142
31432125-13	2019	The antioxidant N-acetylcysteine was identified to antagonize 2,5-HD-stimulated cleaved-caspase-3 and Bax upregulation, and Bcl-2 downregulation.	Acetylcysteine	16-32	BCL2 associated X, apoptosis regulator	Rattus norvegicus	102-105
9484648-11	1998	The rat alveolar macrophage cell line (NR8383) also showed increased MIP-1 alpha mRNA levels in response to LPS (10 micrograms/ml) with a maximal increase after 6-8 h. The induction of MIP-1 alpha mRNA expression by LPS in NR8383 cells was attenuated by cotreatment with the antioxidants N-acetylcysteine and dimethylsulfoxide, suggesting that the induction of MIP-1 alpha mRNA by LPS is mediated via the generation of reactive oxygen species.	Acetylcysteine	288-304	C-C motif chemokine ligand 3	Rattus norvegicus	185-196
32398966-10	2020	By using ROS scavenger N-acetyl-cysteine (NAC) could reverse the effects of nicotine by down-regulation the phosphorylation of p38MAPK and JNK pathways, and pretreatment of specific inhibitors of p38MAPK and JNK could restore the autophagy impairment and cardiomyocytes hypertrophy induced by nicotine.	Acetylcysteine	42-45	mitogen-activated protein kinase 8	Rattus norvegicus	208-211
21528327-3	1997	In this study, we have examined the ability of dietary N-acetylcysteine (NAG) to inhibit the formation of cigarette smoke-related DNA adducts in various tissues of rats.	Acetylcysteine	55-71	sodium voltage-gated channel alpha subunit 7	Rattus norvegicus	73-76
31251971-6	2019	Treatment with the antioxidants N-acetyl-L-cysteine (NAC) and superoxide dismutase (SOD) prevented PCB118-induced effects on PKM2, cell proliferation and glycolysis.	Acetylcysteine	32-51	pyruvate kinase M1/2	Homo sapiens	125-129
9227460-9	1997	Similarly, feeding N-acetylcysteine to CuA rats increased hepatic GSH levels 2.5-fold, and this was accompanied by a significant induction in FAS expression.	Acetylcysteine	19-35	fatty acid synthase	Rattus norvegicus	142-145
31553952-5	2019	In parallel, ROS scavenger N-acetyl cysteine (NAC) abrogated the effects of downregulated LncRNA-XIST on NSCLC cell pyroptosis.	Acetylcysteine	46-49	X inactive specific transcript	Homo sapiens	97-101
31396402-8	2019	Inhibition of ROS with N-acetyl cysteine (NAC) significantly decreased pristimerin-induced cell death by inhibiting the phosphorylation of ASK1 and JNK.	Acetylcysteine	23-40	mitogen-activated protein kinase kinase kinase 5	Homo sapiens	139-143
31396402-8	2019	Inhibition of ROS with N-acetyl cysteine (NAC) significantly decreased pristimerin-induced cell death by inhibiting the phosphorylation of ASK1 and JNK.	Acetylcysteine	42-45	mitogen-activated protein kinase kinase kinase 5	Homo sapiens	139-143
31594390-4	2020	AuNP + NAC association decreased MPO activity and pro-inflammatory cytokines production, being more effective than NAC or AuNP isolated treatment.	Acetylcysteine	7-10	myeloperoxidase	Rattus norvegicus	33-36
32108165-8	2020	Treatment of KrasG12D/+;Trp53fl/fl mice with 5E1 and N-acetylcysteine, as a ROS scavenger, decreased tumor DNA damage, inhibited tumor growth and prolonged mouse survival.	Acetylcysteine	53-69	transformation related protein 53	Mus musculus	24-29
31172724-4	2019	RESULTS: In A549 cells, the levels of reactive oxygen species (ROS) and thymic stromal lymphopoietin (TSLP) were significantly increased by GCE treatment, but were suppressed by PAR2-antagonist (PAR2-ant) or N-acetylcysteine (NAC) treatment.	Acetylcysteine	208-224	coagulation factor II (thrombin) receptor-like 1	Mus musculus	178-182
31172724-4	2019	RESULTS: In A549 cells, the levels of reactive oxygen species (ROS) and thymic stromal lymphopoietin (TSLP) were significantly increased by GCE treatment, but were suppressed by PAR2-antagonist (PAR2-ant) or N-acetylcysteine (NAC) treatment.	Acetylcysteine	208-224	coagulation factor II (thrombin) receptor-like 1	Mus musculus	195-199
8908200-9	1996	N-acetylcysteine did not affect the LPS-stimulated cytotoxicity but resulted in an early and transient reduction in induction of the MnSOD gene.	Acetylcysteine	0-16	superoxide dismutase [Mn], mitochondrial	Bos taurus	133-138
31172724-4	2019	RESULTS: In A549 cells, the levels of reactive oxygen species (ROS) and thymic stromal lymphopoietin (TSLP) were significantly increased by GCE treatment, but were suppressed by PAR2-antagonist (PAR2-ant) or N-acetylcysteine (NAC) treatment.	Acetylcysteine	226-229	coagulation factor II (thrombin) receptor-like 1	Mus musculus	178-182
31172724-4	2019	RESULTS: In A549 cells, the levels of reactive oxygen species (ROS) and thymic stromal lymphopoietin (TSLP) were significantly increased by GCE treatment, but were suppressed by PAR2-antagonist (PAR2-ant) or N-acetylcysteine (NAC) treatment.	Acetylcysteine	226-229	coagulation factor II (thrombin) receptor-like 1	Mus musculus	195-199
32109512-9	2020	With 4 h posttreatment in vivo, minocycline and minocycline plus NAC decreased ALT and necrosis by ~20% and ~50%, respectively, but NAC alone was not effective.	Acetylcysteine	65-68	glutamic pyruvic transaminase, soluble	Mus musculus	79-82
31724279-7	2020	N-acetyl-L-cysteine, an ROS inhibitor, prevented p,p"-DDT-induced promotion of aerobic glycolysis, ERK1/2 activation, upregulation, and nucleus translocation of PKM2.	Acetylcysteine	0-19	pyruvate kinase M1/2	Homo sapiens	161-165
8953175-2	1996	A sensitive, rapid method for determining reduced N-acetylcysteine (NAC) concentration in biological samples has been developed which uses a modified reversed-phase high-performance liquid chromatography (HPLC) technique in conjunction with the derivatizing agent N-(1-pyrenyl)maleimide (NPM).	Acetylcysteine	50-66	nucleophosmin 1	Homo sapiens	288-291
31631367-0	2020	Co-administration of N-acetylcysteine and dexmedetomidine plays a synergistic effect on protection of LPS-induced acute lung injury via correcting Th1/Th2/Th17 cytokines imbalance.	Acetylcysteine	21-37	heart and neural crest derivatives expressed 2	Mus musculus	151-154
31556775-13	2020	Two-hit induced hippocampal alterations in females, namely expression of GPER-1, alpha7-nAChR and parvalbumin, were prevented by NAC.	Acetylcysteine	129-132	G protein-coupled estrogen receptor 1	Rattus norvegicus	73-79
8953175-2	1996	A sensitive, rapid method for determining reduced N-acetylcysteine (NAC) concentration in biological samples has been developed which uses a modified reversed-phase high-performance liquid chromatography (HPLC) technique in conjunction with the derivatizing agent N-(1-pyrenyl)maleimide (NPM).	Acetylcysteine	68-71	nucleophosmin 1	Homo sapiens	288-291
8953175-3	1996	The NAC-NPM adduct was analyzed by HPLC with fluorescence detection.	Acetylcysteine	4-7	nucleophosmin 1	Homo sapiens	8-11
8760145-3	1996	Pretreatment of human pulmonary adenocarcinoma cells H441 with the antioxidants N-acetyl-L-cysteine (NAC) and nordihydroguaiaretic acid (NDGA) blocked MnSOD induction by TNF-alpha, implicating ROS as a signaling agent in this pathway.	Acetylcysteine	101-104	superoxide dismutase 2	Homo sapiens	151-156
31948545-4	2020	We describe a procedure for the differentiation of TCF-1+ stem-like CD8+ memory T cells from peripheral blood naive precursors that takes advantage of the use of antioxidants, in particular N-acetylcysteine (NAC), in combination with T cell receptor stimulation and proinflammatory cytokines.	Acetylcysteine	190-206	transcription factor 7	Homo sapiens	51-56
8723482-0	1996	N-acetylcysteine inhibits germination of conidia and growth of Aspergillus spp.	Acetylcysteine	0-16	histocompatibility minor 13	Homo sapiens	75-78
31714069-3	2019	It was discovered that HTF-1 dose dependently induced overproduction of ROS in HeLa cells, and the cell viability can be rescued when adding ROS scavenger N-acetyl-l-cysteine (NAC).	Acetylcysteine	155-174	zinc finger protein 85	Homo sapiens	23-28
31714069-3	2019	It was discovered that HTF-1 dose dependently induced overproduction of ROS in HeLa cells, and the cell viability can be rescued when adding ROS scavenger N-acetyl-l-cysteine (NAC).	Acetylcysteine	176-179	zinc finger protein 85	Homo sapiens	23-28
8929261-3	1996	It has been suggested that N-acetylcysteine (NAC) breaks disulphide bonds in Lp(a) as well as between homocysteine and plasma proteins.	Acetylcysteine	27-43	lipoprotein(a)	Homo sapiens	77-82
31867003-6	2019	Using the HSG cell line, our results showed that both ICAM-1 and PD-L1 are induced by ROS through pSTAT3, and that this activation pathway is reversed by the use of JAK inhibitors, AG490 and ruxolitinib, as well as by N-acetylcysteine, which is a direct inhibitor of ROS.	Acetylcysteine	218-234	CD274 molecule	Homo sapiens	65-70
8929261-3	1996	It has been suggested that N-acetylcysteine (NAC) breaks disulphide bonds in Lp(a) as well as between homocysteine and plasma proteins.	Acetylcysteine	45-48	lipoprotein(a)	Homo sapiens	77-82
7967350-10	1994	However, BSO reversed the increased mRNA levels for collagen I, IV and TGF-beta seen in the presence of NAC.	Acetylcysteine	104-107	transforming growth factor, beta 1	Mus musculus	71-79
31871537-8	2019	In H9c2 cells pretreated with ROS scavenger N-acetylcysteine, or transfected with miR-15b mimic and inhibitor, fructose-induced cardiac ROS overload could drive Pitx2c-mediated miR-15b low expression, then cause p-p53-activated TGF-beta1/Smads signaling and CTGF induction in myocardial fibrosis.	Acetylcysteine	44-60	paired-like homeodomain 2	Rattus norvegicus	161-167
8042190-3	1994	Purified Lp(a) was subjected to variable concentrations (0.01-10 mM) of various sulfhydryl compounds: DTT, 2-mercapto-ethanol (BME), N-acetylcysteine (NAC) and homocysteine (HCys).	Acetylcysteine	133-149	lipoprotein(a)	Homo sapiens	9-14
30535793-6	2019	Treatment with NAC significantly increased jejunal superoxide dismutase activity, reduced glutathione: oxidized glutathione ratio, and the mRNA abundance of nuclear respiratory factor 2, heme oxygenase 1, and superoxide dismutase 2 in the IUGR-NAC piglets compared with the IUGR-CON piglets.	Acetylcysteine	15-18	GA binding protein transcription factor subunit beta 1	Homo sapiens	157-185
30535793-6	2019	Treatment with NAC significantly increased jejunal superoxide dismutase activity, reduced glutathione: oxidized glutathione ratio, and the mRNA abundance of nuclear respiratory factor 2, heme oxygenase 1, and superoxide dismutase 2 in the IUGR-NAC piglets compared with the IUGR-CON piglets.	Acetylcysteine	15-18	heme oxygenase 1	Homo sapiens	187-203
8042190-3	1994	Purified Lp(a) was subjected to variable concentrations (0.01-10 mM) of various sulfhydryl compounds: DTT, 2-mercapto-ethanol (BME), N-acetylcysteine (NAC) and homocysteine (HCys).	Acetylcysteine	151-154	lipoprotein(a)	Homo sapiens	9-14
1430195-0	1992	Modulation of transforming growth factor-beta 1 antiproliferative effects on endothelial cells by cysteine, cystine, and N-acetylcysteine.	Acetylcysteine	121-137	transforming growth factor beta 1	Bos taurus	14-47
31780643-6	2019	The antioxidant N-acetylcysteine increased the nuclear area in schizophrenia interneurons, increased NLGN2 expression and rescued synaptic deficits.	Acetylcysteine	16-32	neuroligin 2	Homo sapiens	101-106
31518877-7	2019	In vitro experiments showed that high glucose induced the accumulation of reactive oxygen species and activated NLRP3 inflammasomes, which was significantly suppressed by treatment with metformin or antioxidant N-acetyl-L-cysteine.	Acetylcysteine	211-230	NLR family, pyrin domain containing 3	Mus musculus	112-117
1430195-3	1992	Additions of 2 mM cysteine, 1 mM cystine, or 2 mM N-acetylcysteine at the time of the initial addition of TGF-beta 1 blocked the inhibitory effect of TGF-beta 1 on [3H]-thymidine labeling when this was assessed after 72-96 h, but not at earlier times.	Acetylcysteine	50-66	transforming growth factor beta 1	Bos taurus	106-116
1430195-3	1992	Additions of 2 mM cysteine, 1 mM cystine, or 2 mM N-acetylcysteine at the time of the initial addition of TGF-beta 1 blocked the inhibitory effect of TGF-beta 1 on [3H]-thymidine labeling when this was assessed after 72-96 h, but not at earlier times.	Acetylcysteine	50-66	transforming growth factor beta 1	Bos taurus	150-160
33802941-8	2021	The PA-induced oxidation of HDAC2 was attenuated by N-acetyl-L-cysteine and siRNA specific for Pkc delta, Sphk2, and Nox4.	Acetylcysteine	52-71	NADPH oxidase 4	Mus musculus	117-121
32009631-12	2019	The administration of NAC in both groups 2 and 3 also resulted in a decrease of concentrations in urine and a reduction in 24-hour excretion with urine of all assessed proteins (CysC, KIM-1 and nephrin).	Acetylcysteine	22-25	cystatin C	Rattus norvegicus	178-182
32009631-12	2019	The administration of NAC in both groups 2 and 3 also resulted in a decrease of concentrations in urine and a reduction in 24-hour excretion with urine of all assessed proteins (CysC, KIM-1 and nephrin).	Acetylcysteine	22-25	hepatitis A virus cellular receptor 1	Rattus norvegicus	184-189
32009631-12	2019	The administration of NAC in both groups 2 and 3 also resulted in a decrease of concentrations in urine and a reduction in 24-hour excretion with urine of all assessed proteins (CysC, KIM-1 and nephrin).	Acetylcysteine	22-25	NPHS1 adhesion molecule, nephrin	Rattus norvegicus	194-201
31577702-1	2019	BACKGROUND: The aim of this study was to investigate the role of n-acetyl cysteine (NAC) in the lipopolysaccharide (LPS)-mediated induction of tumor necrosis factor-alpha (TNF-alpha) and interleukin-1beta (IL-1beta) synthesis by human periodontal ligament fibroblast cells (hPDLFs).	Acetylcysteine	65-82	interleukin 1 alpha	Homo sapiens	206-214
31577702-1	2019	BACKGROUND: The aim of this study was to investigate the role of n-acetyl cysteine (NAC) in the lipopolysaccharide (LPS)-mediated induction of tumor necrosis factor-alpha (TNF-alpha) and interleukin-1beta (IL-1beta) synthesis by human periodontal ligament fibroblast cells (hPDLFs).	Acetylcysteine	84-87	interleukin 1 alpha	Homo sapiens	206-214
31577702-2	2019	In addition, we aimed to determine the involvement of the nuclear factor-kappa B (NF-kappaB) pathway in any changes in IL-1beta and TNF-alpha expression observed in response to LPS and NAC.	Acetylcysteine	185-188	interleukin 1 alpha	Homo sapiens	119-127
31577702-13	2019	CONCLUSION: NAC inhibits the LPS-mediated synthesis of tumor TNF-alpha and IL-1beta in hPDLFs, through the NF-kappaB pathway.	Acetylcysteine	12-15	interleukin 1 alpha	Homo sapiens	75-83
32890923-10	2020	In addition, NAC pretreatment promoted the phagocytic activity of Cd-exposed chicken peritoneal macrophages, and significantly inhibited expression of pro-inflammatory factors (IL-1beta, IL-6 and TNF-alpha) in both Cd-exposed macrophages and Cd-treated cells in response to LPS stimuli.	Acetylcysteine	13-16	lipopolysaccharide induced TNF factor	Gallus gallus	196-205
31583053-5	2019	Pretreatment with the antioxidant N-acetylcysteine (NAC) attenuated hyperglycemia-induced reduction of Cav-3 expression and Akt and STAT3 activation and restored RPC-mediated cardioprotection in diabetes, which was abolished by cardiac-specific knockdown of Cav-3 by AAV9-shRNA-Cav-3, PI3K/Akt inhibitor wortmannin, or JAK2/STAT3 inhibitor AG490, respectively.	Acetylcysteine	34-50	signal transducer and activator of transcription 3	Rattus norvegicus	132-137
31583053-5	2019	Pretreatment with the antioxidant N-acetylcysteine (NAC) attenuated hyperglycemia-induced reduction of Cav-3 expression and Akt and STAT3 activation and restored RPC-mediated cardioprotection in diabetes, which was abolished by cardiac-specific knockdown of Cav-3 by AAV9-shRNA-Cav-3, PI3K/Akt inhibitor wortmannin, or JAK2/STAT3 inhibitor AG490, respectively.	Acetylcysteine	34-50	signal transducer and activator of transcription 3	Rattus norvegicus	324-329
31583053-5	2019	Pretreatment with the antioxidant N-acetylcysteine (NAC) attenuated hyperglycemia-induced reduction of Cav-3 expression and Akt and STAT3 activation and restored RPC-mediated cardioprotection in diabetes, which was abolished by cardiac-specific knockdown of Cav-3 by AAV9-shRNA-Cav-3, PI3K/Akt inhibitor wortmannin, or JAK2/STAT3 inhibitor AG490, respectively.	Acetylcysteine	52-55	signal transducer and activator of transcription 3	Rattus norvegicus	132-137
31583053-5	2019	Pretreatment with the antioxidant N-acetylcysteine (NAC) attenuated hyperglycemia-induced reduction of Cav-3 expression and Akt and STAT3 activation and restored RPC-mediated cardioprotection in diabetes, which was abolished by cardiac-specific knockdown of Cav-3 by AAV9-shRNA-Cav-3, PI3K/Akt inhibitor wortmannin, or JAK2/STAT3 inhibitor AG490, respectively.	Acetylcysteine	52-55	signal transducer and activator of transcription 3	Rattus norvegicus	324-329
21156189-8	2011	In cultured human or mouse HSC, production of CTGF, alpha-SMA and/or collagen was increased by ethanol treatment, an effect mimicked by acetaldehyde and blocked by 4-methylpyrazole (4-MP) or N-acetylcysteine (NAC).	Acetylcysteine	191-207	cellular communication network factor 2	Mus musculus	46-50
31266772-6	2019	Reduced expression of HIF2alpha inhibited the self-renewal of Sca-1+ cells; this effect was blocked through suppression of ROS by N-acetyl cysteine or the knockdown of p53, Nanog, or Sox2.	Acetylcysteine	130-147	endothelial PAS domain protein 1	Homo sapiens	22-31
21156189-8	2011	In cultured human or mouse HSC, production of CTGF, alpha-SMA and/or collagen was increased by ethanol treatment, an effect mimicked by acetaldehyde and blocked by 4-methylpyrazole (4-MP) or N-acetylcysteine (NAC).	Acetylcysteine	209-212	cellular communication network factor 2	Mus musculus	46-50
31175120-3	2019	Genomic disruption of xCT via CRISPR-Cas9 was achieved in two PDAC cell lines, MiaPaCa-2 and Capan-2, and xCT-KO clones were cultivated in the presence of N-acetylcysteine.	Acetylcysteine	155-171	solute carrier family 7 member 11	Homo sapiens	22-25
34861471-11	2022	Furthermore, c-Jun NH2-terminal kinase inhibition reduced Nix and Bax cleavage, and both signaling pathways were suppressed by N-acetylcysteine treatment.	Acetylcysteine	127-143	BCL2 interacting protein 3 like	Homo sapiens	58-61
31447555-5	2019	NAC can effectively mitigate iron-induced oxidative injury of cardiomyocytes, evidenced by reduced production of MDA, 8-iso-PGF2alpha, and 8-OHDG and maintained concentrations of SOD, CAT, GSH-Px, and GSH in ELISA and biochemical tests; downregulated expression of CHOP, GRP78, p62, and LC3-II proteins in Western Blot, and less cardiomyocytes apoptosis in flow cytometric analysis.	Acetylcysteine	0-3	DNA-damage inducible transcript 3	Rattus norvegicus	265-269
34687772-6	2021	Removal of ROS by N-acetylcysteine significantly reduced ER stress in prostate cancer cells, followed by the decrease of Smad3 phosphorylation and expression of nuclear Snail, resulting in the inhibition of EMT and malignant phenotypic changes of prostate cancer cells.	Acetylcysteine	18-34	SMAD family member 3	Homo sapiens	121-126
34619980-10	2021	Mechanistically, NAC treatment resulted in plasma NAC concentrations ranging from 75.5 to 449.2 ng/ml, which was sufficient to block free thiol labeling of plasma proteins and reduce active TGF-beta1 levels without substantially affecting reactive oxygen species-modified products in valvular cells.	Acetylcysteine	17-20	transforming growth factor, beta 1	Mus musculus	190-199
30825206-9	2019	Moreover, NAC blocked cholesterol-induced phosphorylation of IkappaBalpha and p65.	Acetylcysteine	10-13	v-rel reticuloendotheliosis viral oncogene homolog A (avian)	Mus musculus	78-81
34619980-10	2021	Mechanistically, NAC treatment resulted in plasma NAC concentrations ranging from 75.5 to 449.2 ng/ml, which was sufficient to block free thiol labeling of plasma proteins and reduce active TGF-beta1 levels without substantially affecting reactive oxygen species-modified products in valvular cells.	Acetylcysteine	50-53	transforming growth factor, beta 1	Mus musculus	190-199
34619980-11	2021	CONCLUSIONS: Short-term treatment with NAC inhibits AS progression, by inhibiting WSS-induced TGF-beta1 activation in the LDLR mouse model of AS, motivating a clinical trial of NAC and/or other thiol-reactive agent(s) as a potential therapy for AS.	Acetylcysteine	39-42	transforming growth factor, beta 1	Mus musculus	94-103
34794237-10	2021	TGF-beta-induced upregulation of KCa2.3, KCa3.1, collagen, and alpha-smooth muscle actin and downregulation of catalase were reversed by modafinil, polyethylene glycol catalase, N-acetylcysteine, siRNA against KCa2.3 or KCa3.1, and Epac inhibitors.	Acetylcysteine	178-194	transforming growth factor alpha	Homo sapiens	0-8
31004932-7	2019	Whereas N-acetylcysteine suppressed the elevated m6A level and its methyltransferases in human keratinocytes exposed to arsenite.	Acetylcysteine	8-24	methyltransferase 3, N6-adenosine-methyltransferase complex catalytic subunit	Homo sapiens	49-52
34794237-10	2021	TGF-beta-induced upregulation of KCa2.3, KCa3.1, collagen, and alpha-smooth muscle actin and downregulation of catalase were reversed by modafinil, polyethylene glycol catalase, N-acetylcysteine, siRNA against KCa2.3 or KCa3.1, and Epac inhibitors.	Acetylcysteine	178-194	potassium calcium-activated channel subfamily N member 4	Homo sapiens	41-47
34425375-7	2021	The mechanistic analysis further demonstrated that N-acetylcysteine pretreatment attenuated the decreased expression of target genes (UBC and PPP2CA) induced by PQ.	Acetylcysteine	51-67	protein phosphatase 2 (formerly 2A), catalytic subunit, alpha isoform	Mus musculus	142-148
31317129-1	2019	Background: Acetylcysteine (NAC) is effective at preventing liver injury after paracetamol overdose.	Acetylcysteine	12-26	synuclein alpha	Homo sapiens	28-31
34544266-10	2021	NAC/AAP also improved the population doubling time of MSCs (first 6-days post isolation) and significantly downregulated the expression of 2 genes (Nox1 and Rag2) associated with oxidative stress compared to placebo treatment.	Acetylcysteine	0-3	NADPH oxidase 1	Mus musculus	148-152
30977273-2	2019	The protective antioxidant activity of acetylcysteine (NAC) against toxicity due to cisplatin has been reported in experimental models; however, its efficacy in patients has not been elucidated.	Acetylcysteine	39-53	synuclein alpha	Homo sapiens	55-58
34850077-5	2021	Changes in other molecular factors after NAC treatment were also observed in the placenta exposed to DHT and insulin, such as increased glutathione peroxidase 4 protein level.	Acetylcysteine	41-44	glutathione peroxidase 4	Rattus norvegicus	136-160
34850077-8	2021	Finally, we demonstrated that NAC selectively normalized uterine leukemia inhibitory factor, osteopontin/secreted phosphoprotein 1, progesterone receptor, and homeobox A11 mRNA expression and placental estrogen related receptor beta and trophoblast specific protein alpha mRNA expression.	Acetylcysteine	30-33	secreted phosphoprotein 1	Rattus norvegicus	93-104
34850077-8	2021	Finally, we demonstrated that NAC selectively normalized uterine leukemia inhibitory factor, osteopontin/secreted phosphoprotein 1, progesterone receptor, and homeobox A11 mRNA expression and placental estrogen related receptor beta and trophoblast specific protein alpha mRNA expression.	Acetylcysteine	30-33	secreted phosphoprotein 1	Rattus norvegicus	105-130
30851366-5	2019	CPT simultaneously increased Nrf2 expression and the level of intracellular reactive oxygen species (ROS), whereas pretreatment with the antioxidants N-acetyl-cysteine (NAC) or glutathione (GSH) strongly attenuated ROS production, which was accompanied by hTERT downregulation.	Acetylcysteine	150-167	telomerase reverse transcriptase	Homo sapiens	256-261
34850077-8	2021	Finally, we demonstrated that NAC selectively normalized uterine leukemia inhibitory factor, osteopontin/secreted phosphoprotein 1, progesterone receptor, and homeobox A11 mRNA expression and placental estrogen related receptor beta and trophoblast specific protein alpha mRNA expression.	Acetylcysteine	30-33	trophoblast specific protein alpha	Rattus norvegicus	237-271
30614543-9	2019	Moreover, high levels of reactive oxygen species (ROS) were detected in sRBC-DCs, and treatment with N-acetylcysteine simultaneously decreased the lymph node-homing ability of DCs and phosphorylation of RhoA, ROCK1, and cortactin.	Acetylcysteine	101-117	cortactin	Mus musculus	220-229
34942984-6	2021	The ROS inhibitors diphenyleneiodonium and N-acetyl cysteine suppressed apoptosis and excessive ER stress by inhibiting Nox4 in JI017-treated breast cancer cells.	Acetylcysteine	43-60	NADPH oxidase 4	Homo sapiens	120-124
31049140-11	2019	Phosphorylated ASK1 and p38 levels were significantly higher in the 1000 nM dexamethasone group, which NAC or DPI markedly attenuated.	Acetylcysteine	103-106	mitogen-activated protein kinase kinase kinase 5	Mus musculus	15-19
30911326-13	2019	Furthermore, SKN/PTX-induced downregulation of PKM2 (a key enzyme in glycolysis) and the suppression of its activity were inhibited by a ROS scavenger N-acetyl cysteine (NAC), suggesting that the synergy of the SKN/PTX combination may be not rely on PKM2 suppression.	Acetylcysteine	151-168	pyruvate kinase M1/2	Homo sapiens	47-51
30911326-13	2019	Furthermore, SKN/PTX-induced downregulation of PKM2 (a key enzyme in glycolysis) and the suppression of its activity were inhibited by a ROS scavenger N-acetyl cysteine (NAC), suggesting that the synergy of the SKN/PTX combination may be not rely on PKM2 suppression.	Acetylcysteine	151-168	pyruvate kinase M1/2	Homo sapiens	250-254
34830376-6	2021	Pretreatment with ROS scavenger- N-acetylcysteine (NAC) reserved the viability loss and forced activation of mTORC1 kinase revived the neurite outgrowth in AZOX treated neurons.	Acetylcysteine	31-49	CREB regulated transcription coactivator 1	Mus musculus	109-115
30911326-13	2019	Furthermore, SKN/PTX-induced downregulation of PKM2 (a key enzyme in glycolysis) and the suppression of its activity were inhibited by a ROS scavenger N-acetyl cysteine (NAC), suggesting that the synergy of the SKN/PTX combination may be not rely on PKM2 suppression.	Acetylcysteine	170-173	pyruvate kinase M1/2	Homo sapiens	47-51
30911326-13	2019	Furthermore, SKN/PTX-induced downregulation of PKM2 (a key enzyme in glycolysis) and the suppression of its activity were inhibited by a ROS scavenger N-acetyl cysteine (NAC), suggesting that the synergy of the SKN/PTX combination may be not rely on PKM2 suppression.	Acetylcysteine	170-173	pyruvate kinase M1/2	Homo sapiens	250-254
30508555-6	2019	alphaNF also induced accumulation of reactive oxygen species (ROS) and an antioxidant, N-acetylcysteine, reduced alphaNF-induced MAPK phosphorylation, CHOP expression, and cell death.	Acetylcysteine	87-103	DNA-damage inducible transcript 3	Mus musculus	151-155
30633982-9	2019	Simultaneously, NAC pretreatment downregulated XBP1 splicing, reduced JNK phosphorylation and further blocked cleavage of caspase-3, all these might contribute to the inhibition of testicular cell apoptosis.	Acetylcysteine	16-19	X-box binding protein 1	Rattus norvegicus	47-51
30633982-9	2019	Simultaneously, NAC pretreatment downregulated XBP1 splicing, reduced JNK phosphorylation and further blocked cleavage of caspase-3, all these might contribute to the inhibition of testicular cell apoptosis.	Acetylcysteine	16-19	mitogen-activated protein kinase 8	Rattus norvegicus	70-73
31359699-3	2019	Due to the poor stability,low solubility,poor absorption and low bioavailability of curcumin,N-acetyl-L-cysteine( NAC) was used as an absorption enhancer and mixed with curcumin to improve the absorption of curcumin in the body.	Acetylcysteine	93-112	synuclein alpha	Homo sapiens	114-117
30633982-10	2019	Collectively, the present results suggested that prolonged administration of NAC preserved testicular function and normalized sex hormonal disruption induced by NaF via the inhibition of Nrf2-associated oxidative damage and Ire1alpha-JNK-mediated apoptosis in rat testis.	Acetylcysteine	77-80	mitogen-activated protein kinase 8	Rattus norvegicus	234-237
34830376-6	2021	Pretreatment with ROS scavenger- N-acetylcysteine (NAC) reserved the viability loss and forced activation of mTORC1 kinase revived the neurite outgrowth in AZOX treated neurons.	Acetylcysteine	51-54	CREB regulated transcription coactivator 1	Mus musculus	109-115
34447990-5	2021	On the other hand, treatment with the antioxidant N-acetylcysteine (NAC) increased glutathione concentration, decreased basal H2O2 production, p53 levels and sensitivity to AA treatment in the XPC-null back to the levels found in XPC-wt cells.	Acetylcysteine	50-66	XPC complex subunit, DNA damage recognition and repair factor	Homo sapiens	193-196
34447990-5	2021	On the other hand, treatment with the antioxidant N-acetylcysteine (NAC) increased glutathione concentration, decreased basal H2O2 production, p53 levels and sensitivity to AA treatment in the XPC-null back to the levels found in XPC-wt cells.	Acetylcysteine	68-71	XPC complex subunit, DNA damage recognition and repair factor	Homo sapiens	193-196
34753902-6	2021	RESULTS: The inclusion of NAC increased the activity of mitochondrial complexes I and II + III as well as decreased the concentration of interleukin-1beta, tumor necrosis factor alpha, and caspase-3, but only in the parotid glands of rats with hyperglycemia compared to the HFD group.	Acetylcysteine	26-29	caspase 3	Rattus norvegicus	189-198
30559295-7	2019	We observed similar antioxidant effects in WT mice: N-acetylcysteine blunted beta3-AR stimulation-induced browning of white adipose tissue and reduced mitochondrial activity in brown adipose tissue even in the absence of beta3-AR stimulation.	Acetylcysteine	52-68	adrenergic receptor, beta 3	Mus musculus	77-85
31030296-5	2019	Subjective "readiness" was lowered by prior exhaustive exercise from PT-1 to PT-2 (P = 0.012) in both PLA and NAC.	Acetylcysteine	110-113	zinc finger protein 77	Homo sapiens	69-81
30559295-8	2019	Furthermore, N-acetylcysteine increased the levels of peroxiredoxin 3 and superoxide dismutase 2 in adipose tissue, indicating increased mitochondrial oxidative stress.	Acetylcysteine	13-29	peroxiredoxin 3	Mus musculus	54-69
34627931-8	2021	TQ increased the levels of reactive oxygen species (ROS), whereas pretreatment with N-acetyl cysteine (NAC), a ROS scavenger, prevented the suppressive effect of TQ on Jak2/STAT3 activation and protected SK-MEL-28 cells from TQ-induced apoptosis.	Acetylcysteine	84-101	Janus kinase 2	Homo sapiens	168-172
30746371-14	2019	CONCLUSION: The efficacies of split-dose indomethacin and combined administration (N-acetylcysteine with indomethacin) for preventing PEP were similar to that of the standard regimen.	Acetylcysteine	83-99	progestagen associated endometrial protein	Homo sapiens	134-137
30796177-6	2019	And ROS scavenger N-acetyl-cysteine attenuated the activation of caspase-1 induced by MST1 and the effect of MST1 in PDAC cell death, proliferation, migration, and invasion.	Acetylcysteine	18-35	macrophage stimulating 1	Homo sapiens	86-90
30796177-6	2019	And ROS scavenger N-acetyl-cysteine attenuated the activation of caspase-1 induced by MST1 and the effect of MST1 in PDAC cell death, proliferation, migration, and invasion.	Acetylcysteine	18-35	macrophage stimulating 1	Homo sapiens	109-113
30700808-5	2019	We then analysed the expression patterns of the top 10 altered genes, and found that NAC markedly stimulated HMGCS3 and LDHC expression in IPEC-J2 cells.	Acetylcysteine	85-88	lactate dehydrogenase C	Sus scrofa	120-124
34627931-8	2021	TQ increased the levels of reactive oxygen species (ROS), whereas pretreatment with N-acetyl cysteine (NAC), a ROS scavenger, prevented the suppressive effect of TQ on Jak2/STAT3 activation and protected SK-MEL-28 cells from TQ-induced apoptosis.	Acetylcysteine	103-106	Janus kinase 2	Homo sapiens	168-172
34420083-7	2021	Delayed NAC treatment had no effect on APAP-induced liver injury at 24 h but reduced the decline of plasma ALT activities and prevented the shrinkage of the areas of necrosis at 48 h. This effect correlated with down-regulation of key activators of mitochondrial biogenesis (AMPK, PGC-1alpha, Nrf1/2, TFAM) and reduced expression of Tom 20 (mitochondrial mass) and PCNA (cell proliferation).	Acetylcysteine	8-11	peroxisome proliferative activated receptor, gamma, coactivator 1 alpha	Mus musculus	281-291
34420083-7	2021	Delayed NAC treatment had no effect on APAP-induced liver injury at 24 h but reduced the decline of plasma ALT activities and prevented the shrinkage of the areas of necrosis at 48 h. This effect correlated with down-regulation of key activators of mitochondrial biogenesis (AMPK, PGC-1alpha, Nrf1/2, TFAM) and reduced expression of Tom 20 (mitochondrial mass) and PCNA (cell proliferation).	Acetylcysteine	8-11	transcription factor A, mitochondrial	Mus musculus	301-305
30641904-7	2019	Chemical inhibition of PPARalpha- and reactive oxygen species (ROS)-dependent pathways by GW6471 and N-acetyl-L-cysteine, respectively, had no effect on cell sensitivity to combined DCX/FF treatment.	Acetylcysteine	101-120	peroxisome proliferator activated receptor alpha	Homo sapiens	23-32
30992317-8	2019	Furthermore, when reactive oxygen species (ROS) generation was suppressed by antioxidant N-acetyl-l-cysteine (L-NAC) pretreatment, EBSS-induced autophagy was inhibited, and the chloride current was unable to be activated.	Acetylcysteine	89-108	synuclein alpha	Homo sapiens	112-115
34414459-8	2021	The ROS inhibitor, N-acetyl-l-cysteine, exerted a protective effect on the UA-induced apoptosis of tubular epithelial cells by reducing excess ROS production, which significantly inhibited NEK7 and NLRP3 inflammasome activation.	Acetylcysteine	19-38	NIMA-related kinase 7	Rattus norvegicus	189-193
29364751-6	2018	Furthermore, HG could promote the generation of reactive oxygen species (ROS), while N-acetyl cysteine, a ROS scavenger, had an inhibitory effect on the expression of TNF-alpha, IL-6 and PAI-1 in HG-treated cells.	Acetylcysteine	85-102	serpin family E member 1	Homo sapiens	187-192
34343907-12	2021	The antioxidant N-acetylcysteine (NAC) also efficiently blocked CYP2E1-and NOX4-mediated induction of autophagy.	Acetylcysteine	16-32	NADPH oxidase 4	Homo sapiens	75-79
29964331-7	2018	Moreover, inhibition of reactive oxygen species by N-acetyl-L-cysteine efficiently blocked BIX-01294-induced DR5 upregulation by inhibiting ATF4/CHOP expression, leading to diminished sensitization to TRAIL.	Acetylcysteine	51-70	TNF receptor superfamily member 10b	Homo sapiens	109-112
30315252-14	2019	Consistently, pretreatment with N-acetyl-L-cysteine (NAC) significantly attenuated TMX-induced increase in ALT and AST activities.	Acetylcysteine	32-51	glutamic pyruvic transaminase, soluble	Mus musculus	107-110
30315252-14	2019	Consistently, pretreatment with N-acetyl-L-cysteine (NAC) significantly attenuated TMX-induced increase in ALT and AST activities.	Acetylcysteine	32-51	solute carrier family 17 (anion/sugar transporter), member 5	Mus musculus	115-118
30315252-14	2019	Consistently, pretreatment with N-acetyl-L-cysteine (NAC) significantly attenuated TMX-induced increase in ALT and AST activities.	Acetylcysteine	53-56	glutamic pyruvic transaminase, soluble	Mus musculus	107-110
34343907-12	2021	The antioxidant N-acetylcysteine (NAC) also efficiently blocked CYP2E1-and NOX4-mediated induction of autophagy.	Acetylcysteine	34-37	NADPH oxidase 4	Homo sapiens	75-79
30315252-14	2019	Consistently, pretreatment with N-acetyl-L-cysteine (NAC) significantly attenuated TMX-induced increase in ALT and AST activities.	Acetylcysteine	53-56	solute carrier family 17 (anion/sugar transporter), member 5	Mus musculus	115-118
30416532-5	2018	Additionally, exposure of bone marrow stromal cells (HS-5) to NAC increased adiponectin, PPARgamma, HO-1, and SIRT-1 and increased beta-oxidation markers such as PPARalpha and PPARdelta mRNA levels.	Acetylcysteine	62-65	heme oxygenase 1	Homo sapiens	100-104
34343907-13	2021	Finally, specific and non-toxic production of H2O2 by the GOX/CAT system as evidenced by elevated peroxiredoxin (Prx-2) also induced LC3B which was efficiently blocked by NAC.	Acetylcysteine	171-174	paired related homeobox 2	Mus musculus	113-118
30416532-5	2018	Additionally, exposure of bone marrow stromal cells (HS-5) to NAC increased adiponectin, PPARgamma, HO-1, and SIRT-1 and increased beta-oxidation markers such as PPARalpha and PPARdelta mRNA levels.	Acetylcysteine	62-65	peroxisome proliferator activated receptor alpha	Homo sapiens	162-171
30951973-8	2019	NAC and LA supplementation prevented GSH and total non-enzymatic antioxidants depletion as well as restored GPx and GR activities, TNF-alpha, IL6 and cholesterol in OVX rats.	Acetylcysteine	0-3	glutathione-disulfide reductase	Rattus norvegicus	116-118
34343907-13	2021	Finally, specific and non-toxic production of H2O2 by the GOX/CAT system as evidenced by elevated peroxiredoxin (Prx-2) also induced LC3B which was efficiently blocked by NAC.	Acetylcysteine	171-174	microtubule associated protein 1 light chain 3 beta	Homo sapiens	133-137
34417577-6	2022	Additionally, inhibition of TFEB activation by ROS scavenger N-acetyl cysteine or inhibition of protein synthesis by cycloheximide effectively compromises ATF4 upregulation and apoptosis in response to 15d-PGJ2.	Acetylcysteine	61-78	transcription factor EB	Homo sapiens	28-32
30633472-10	2019	Bax protein expression was reduced in the cyclophosphamide (20%) and cyclophosphamide+N-acetylcysteine (20%) groups when compared with the Control (50%) and N-acetylcysteine (50%) groups.	Acetylcysteine	86-102	BCL2 associated X, apoptosis regulator	Rattus norvegicus	0-3
30633472-10	2019	Bax protein expression was reduced in the cyclophosphamide (20%) and cyclophosphamide+N-acetylcysteine (20%) groups when compared with the Control (50%) and N-acetylcysteine (50%) groups.	Acetylcysteine	157-173	BCL2 associated X, apoptosis regulator	Rattus norvegicus	0-3
31341611-2	2019	The development of antidotes followed within 10 years, and by 1980 acetylcysteine (NAC) was acknowledged as the optimal therapy available.	Acetylcysteine	67-81	synuclein alpha	Homo sapiens	83-86
30349652-6	2018	Instead, the CBD-mediated increase in HO-1 protein was reversed by the glutathione precursor N-acetylcysteine, indicating the participation of reactive oxygen species (ROS) signaling; this was confirmed by flow cytometry-based ROS detection.	Acetylcysteine	93-109	heme oxygenase 1	Homo sapiens	38-42
29884989-8	2018	When reactive oxygen species (ROS) generation was inhibited by the antioxidant N-acetyl-L-cysteine (L-NAC), ZA-induced apoptosis and chloride current were blocked accordingly, suggesting that ZA induces apoptosis through promoting ROS production and subsequently activating chloride channel.	Acetylcysteine	79-98	synuclein alpha	Homo sapiens	102-105
34262291-17	2021	Mechanistically, tumor cell death induced by Stattic-mediated GSR inhibition was ROS-dependent, since the ROS scavengers GSH and N-acetyl cysteine (NAC) reversed the effect of Stattic.	Acetylcysteine	129-146	gutter shaped root	Mus musculus	62-65
29982513-4	2018	Oral administration of N-acetyl cysteine, a GHS precursor, led to a marked improvement of GHS content, a decrease in oxidative stress markers including protein carbonyls and an improvement of left ventricular structure and function in a model of LMNA cardiomyopathy.	Acetylcysteine	23-40	lamin A	Mus musculus	246-250
30975143-0	2019	Effect of N-acetylcysteine on exacerbations of bronchiectasis (BENE): a randomized controlled trial.	Acetylcysteine	10-26	mal, T cell differentiation protein like	Homo sapiens	63-67
34262291-17	2021	Mechanistically, tumor cell death induced by Stattic-mediated GSR inhibition was ROS-dependent, since the ROS scavengers GSH and N-acetyl cysteine (NAC) reversed the effect of Stattic.	Acetylcysteine	148-151	gutter shaped root	Mus musculus	62-65
30692122-7	2019	Platelet and VWF signals in ponatinib-treated mice were significantly reduced by N-acetylcysteine and completely eliminated by recombinant ADAMTS13.	Acetylcysteine	81-97	Von Willebrand factor	Mus musculus	13-16
34203104-7	2021	Our results showed that the high NAC dose stimulated cFOS expression in the NAcc, and that this effect was suppressed in the presence of MTEP, thus suggesting the implication of mGluR5.	Acetylcysteine	33-36	glutamate receptor, ionotropic, kainate 1	Mus musculus	178-184
30197667-11	2018	However, the SCE-induced cytotoxic effects and the increased expression of proapoptotic proteins, including p53 and p21, and reduced Bcl-2/Bax ratio, could be attenuated by N-acetyl cysteine, an ROS inhibitor.	Acetylcysteine	173-190	transformation related protein 53, pseudogene	Mus musculus	108-111
30217943-9	2018	The levels of TNF-alpha, IL-8, CC16, and ICAM-1 in EBC were significantly lower, and SOD activity was higher, at T2 in the NAC group; similar data were found in serum at T2, T3, and T4.	Acetylcysteine	123-126	secretoglobin family 1A member 1	Homo sapiens	31-35
34257541-7	2021	Moreover, pre-incubation of cells with ROS inhibitor N-acetyl-L-cysteine (NAC) significantly reversed beta-elemene-mediated apoptosis effect and down-regulation of JAK2/Src-STAT3 signaling pathway.	Acetylcysteine	53-72	Janus kinase 2	Homo sapiens	164-168
30771458-3	2019	The human RALBP1 gene encodes a 76-kDa splice variant protein, RLIP (ral-binding protein1, RalBP1), a stress-protective mercapturic acid pathway (MAP) transporter protein, that also plays a key role in regulating clathrin-dependent endocytosis (CDE) as a Ral effector.	Acetylcysteine	120-136	ralA binding protein 1	Homo sapiens	10-16
30771458-3	2019	The human RALBP1 gene encodes a 76-kDa splice variant protein, RLIP (ral-binding protein1, RalBP1), a stress-protective mercapturic acid pathway (MAP) transporter protein, that also plays a key role in regulating clathrin-dependent endocytosis (CDE) as a Ral effector.	Acetylcysteine	120-136	ralA binding protein 1	Homo sapiens	91-97
29768044-8	2018	Furthermore, N-acety-l-cysteine, a pharmacological inhibitor of ROS, also abolished CoCl2-induced expression of Drp1 and protected against CoCl2-induced PDLSC dysfunction, as shown by restored mitochondrial membrane potential, ATP level, inhibited mitochondrial fission, and decreased apoptosis.	Acetylcysteine	13-31	dynamin 1 like	Homo sapiens	112-116
34257541-7	2021	Moreover, pre-incubation of cells with ROS inhibitor N-acetyl-L-cysteine (NAC) significantly reversed beta-elemene-mediated apoptosis effect and down-regulation of JAK2/Src-STAT3 signaling pathway.	Acetylcysteine	74-77	Janus kinase 2	Homo sapiens	164-168
29698568-11	2018	Inflammatory markers tumor necrosis factor-alpha, interferon-gamma, and interleukin-6 were significantly decreased in serum and callus following NAC treatment.	Acetylcysteine	145-148	interferon gamma	Rattus norvegicus	50-66
35462185-10	2022	Acetylcysteine, clavulanic acid and homovanillic acid were identified as potential lead compounds for the SARS-CoV-2 helicase.	Acetylcysteine	0-14	helicase for meiosis 1	Homo sapiens	117-125
29565452-8	2018	Furthermore, pretreatment of Caki cells with ROS scavengers (N-acetylcysteine and glutathione) prevented the downregulation of cFLIP(L), the upregulation of cFLIP(S) and apoptosis induced by FasL.	Acetylcysteine	61-77	Fas ligand	Homo sapiens	191-195
29429900-5	2018	We provide evidence suggesting the possibility that sulfane sulfur species produced by 3-mercaptopyruvate sulfurtransferase and sulfide:quinone oxidoreductase are the actual mediators of the immediate antioxidative and cytoprotective effects provided by NAC.	Acetylcysteine	254-257	crystallin zeta	Homo sapiens	136-158
30832310-6	2019	Treatment with an ROS scavenger (N-acetylcysteine, NAC), an NADPH oxidase inhibitor (apocynin), or an activating protein (AP)-1 inhibitor (tanshinone IIA) attenuated leptin-mediated cPLA2alpha/COX-2 expression and leukocyte recruitment in the lung.	Acetylcysteine	33-49	leptin	Mus musculus	166-172
30496017-9	2019	Expressions of Brca2, Xpc, Mlh3, Rad51, Xrcc2, Hus1, Rad9a, Cdkn1a, Gadd45a which are the DNA-repair genes were found to be significantly higher in NAC + ALC + IR group than those in individual treatment of ALC or NAC.	Acetylcysteine	214-217	HUS1 checkpoint clamp component	Homo sapiens	47-51
35449013-9	2022	The phosphorylated levels of focal adhesion kinase (FAK) and formation of the focal adhesion complex were significantly increased in ambient PM or PAH-treated VSMCs, and these effects were blocked by administration of NAC or alpha-NF, an inhibitor of AhR, the receptor that allows PAH uptake.	Acetylcysteine	218-221	protein tyrosine kinase 2	Homo sapiens	29-50
30597356-8	2019	N-acetylcysteine, a well-known antioxidant, abrogated D-glucose-induced NFkappaB and Egr1 activation in BV2 cells.	Acetylcysteine	0-16	early growth response 1	Mus musculus	85-89
30633982-0	2019	N-acetylcysteine alleviates fluoride-induced testicular apoptosis by modulating IRE1alpha/JNK signaling and nuclear Nrf2 activation.	Acetylcysteine	0-16	mitogen-activated protein kinase 8	Rattus norvegicus	90-93
29692782-9	2018	Scavenging of ROS by N-acetyl-cysteine also attenuated NLRP3 inflammasome activation and liver inflammation, indicating that the essential role of ROS in mediating NLRP3 inflammasome activation in ConA-induced hepatitis.	Acetylcysteine	21-38	NLR family, pyrin domain containing 3	Mus musculus	55-60
29396710-9	2018	This suggests a model in which NAC through PI3K/Akt activation suppresses Foxo1 expression, thereby impacting its transcriptional targets EOMES, PD-1, and granzyme B.	Acetylcysteine	31-34	granzyme B	Homo sapiens	155-165
35449013-9	2022	The phosphorylated levels of focal adhesion kinase (FAK) and formation of the focal adhesion complex were significantly increased in ambient PM or PAH-treated VSMCs, and these effects were blocked by administration of NAC or alpha-NF, an inhibitor of AhR, the receptor that allows PAH uptake.	Acetylcysteine	218-221	protein tyrosine kinase 2	Homo sapiens	52-55
29463639-0	2018	Bet 1: A slower rate of initial N-acetylcysteine infusion in the treatment of acute paracetamol overdose to reduce adverse reactions.	Acetylcysteine	32-48	Bet1 golgi vesicular membrane trafficking protein	Homo sapiens	0-5
31160972-7	2019	Furthermore, co-treatment with N-Acetyl-Cysteine (NAC) rescues the effects of DEHP on OS, ROS, beta-galactosidase levels and gene expression activities.	Acetylcysteine	31-48	galactosidase, beta 1	Rattus norvegicus	95-113
31160972-7	2019	Furthermore, co-treatment with N-Acetyl-Cysteine (NAC) rescues the effects of DEHP on OS, ROS, beta-galactosidase levels and gene expression activities.	Acetylcysteine	50-53	galactosidase, beta 1	Rattus norvegicus	95-113
35449013-9	2022	The phosphorylated levels of focal adhesion kinase (FAK) and formation of the focal adhesion complex were significantly increased in ambient PM or PAH-treated VSMCs, and these effects were blocked by administration of NAC or alpha-NF, an inhibitor of AhR, the receptor that allows PAH uptake.	Acetylcysteine	218-221	aryl hydrocarbon receptor	Homo sapiens	251-254
30289994-9	2019	N-acetylcysteine combined with sildenafil decreased MMP-2 and MMP-9 activity and NO consumption and inhibited apoptosis of pulmonary arterial endothelial cells.	Acetylcysteine	0-16	72 kDa type IV collagenase	Oryctolagus cuniculus	52-57
29962570-4	2018	Aims: To examine the efficacy of add-on NAC (1200 mg) in treating negative symptoms measured using Scale for the Assessment of Negative Symptoms (SANS) and clinical global impression (CGI) at baseline and 24 weeks.	Acetylcysteine	40-43	USH1 protein network component sans	Homo sapiens	146-150
35065167-9	2022	Further studies revealed that beneficial effects of NAC is through targeting the mitochondrial autophagy via regulating the GSK-3beta/Drp1mediated mitochondrial fission and inhibiting the expression of beclin-1 and conversion of LC3, as well as activating the p-Akt pro-survival pathway.	Acetylcysteine	52-55	glycogen synthase kinase 3 alpha	Rattus norvegicus	124-133
29962570-10	2018	Results: NAC augmentation showed a significantly greater improvement in negative symptoms on total SANS and CGI scores at 24 weeks.	Acetylcysteine	9-12	USH1 protein network component sans	Homo sapiens	99-103
29353375-4	2018	A dual inhibitor of the biosynthetic enzymes for H2S, cystathionine beta-synthase (CBS) and cystathionine gamma-lyase (CSE), amino-oxyacetic acid (AOA; 3 mM) reversed the inhibitory responses caused by GYY 4137, L-cysteine and N-acetylcysteine on K+-evoked [3H]D-aspartate release.	Acetylcysteine	227-243	cystathionine gamma-lyase	Bos taurus	92-117
30641872-7	2019	The benefits of NAC were associated with enhanced AMPK-PGC-1alpha-SIRT3 signaling protein expressions, which led to decreased acetylation of superoxide dismutase 2 (SOD2) and increased expression of mitochondrial antioxidant manganese superoxide dismutase (MnSOD).	Acetylcysteine	16-19	sirtuin 3	Rattus norvegicus	66-71
30641872-8	2019	The findings demonstrate the efficacy of NAC in protecting BPA-induced kidney and liver injury, which, in part, is mediated by activating SIRT3 and improving mitochondrial function, dynamics, and oxidative imbalance.	Acetylcysteine	41-44	sirtuin 3	Rattus norvegicus	138-143
35065167-9	2022	Further studies revealed that beneficial effects of NAC is through targeting the mitochondrial autophagy via regulating the GSK-3beta/Drp1mediated mitochondrial fission and inhibiting the expression of beclin-1 and conversion of LC3, as well as activating the p-Akt pro-survival pathway.	Acetylcysteine	52-55	beclin 1	Rattus norvegicus	202-210
35065167-9	2022	Further studies revealed that beneficial effects of NAC is through targeting the mitochondrial autophagy via regulating the GSK-3beta/Drp1mediated mitochondrial fission and inhibiting the expression of beclin-1 and conversion of LC3, as well as activating the p-Akt pro-survival pathway.	Acetylcysteine	52-55	annexin A3	Rattus norvegicus	229-232
29294389-9	2018	Given that NAC inhibits Snail-mediated EMT, this may be a potential therapeutic intervention for FECD.	Acetylcysteine	11-14	collagen type VIII alpha 2 chain	Homo sapiens	97-101
35065167-10	2022	CONCLUSION: Our results suggest that NAC exerts neuroprotective effects to inhibit the altered mitochondrial changes and cell death in I/R injury via regulation of p-GSK-3beta mediated Drp-1 translocation to the mitochondria.	Acetylcysteine	37-40	glycogen synthase kinase 3 alpha	Rattus norvegicus	166-175
35156537-9	2022	Meanwhile, RPN2 upregulation increased the levels of p-PI3K/PI3K and p-Akt/Akt, which were attenuated by N-acetyl-L-cysteine (NAC), an ROS inhibitor.	Acetylcysteine	105-124	ribophorin II	Homo sapiens	11-15
30580562-10	2019	NF-kappaB antagonist SN50 or antioxidant N-acetyl-L-cysteine partially abrogated the exacerbating effects of SM22alpha silencing on AAA formation.	Acetylcysteine	41-60	transgelin	Mus musculus	109-118
30387809-7	2019	The results revealed that the reduced form of Trx1 was markedly increased, and the oxidized forms of Prx1, GSR and PTEN were decreased following NAC pretreatment.	Acetylcysteine	145-148	peroxiredoxin 1	Rattus norvegicus	101-105
35156537-9	2022	Meanwhile, RPN2 upregulation increased the levels of p-PI3K/PI3K and p-Akt/Akt, which were attenuated by N-acetyl-L-cysteine (NAC), an ROS inhibitor.	Acetylcysteine	126-129	ribophorin II	Homo sapiens	11-15
31168028-8	2019	The antioxidant N-acetylcysteine reduced the expression of phosphorylated ATM and H2AX, and the ATM inhibitor, caffeine, inhibited p53 activation.	Acetylcysteine	16-32	ATM serine/threonine kinase	Homo sapiens	74-77
29134467-9	2018	In addition, we found that both the decreased cell viability and the increased pAkt/pERK levels could be rescued by the antioxidant NAC, suggesting a central role for reactive oxygen species (ROS) in the mechanism of action of C4.	Acetylcysteine	132-135	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	84-88
35156537-10	2022	Both NAC and PI3K inhibitor LY294002 could reverse the effects of RPN2 overexpression on the malignant phenotypes of LSCC cells.	Acetylcysteine	5-8	ribophorin II	Homo sapiens	66-70
29207099-9	2018	Three weeks after obstruction relief, UUO+iohexol+NAC rats exhibited a lower apoptosis rate, lower Bax mRNA expression, higher expression of Bcl-2 mRNA and higher ratio of Bcl-2/Bax (all P&lt;0.05) compared with day 1 following drug administration.	Acetylcysteine	50-53	BCL2 associated X, apoptosis regulator	Rattus norvegicus	99-102
35086548-8	2022	Neutralization of ROS with N-acetyl-L-cysteine (NAC) increased the levels of miR-155-5p in tumor exosomes that were taken up by macrophages, leading to reduction of macrophage migration and tumor spheroid infiltration.	Acetylcysteine	27-46	microRNA 155	Mus musculus	77-84
29207099-9	2018	Three weeks after obstruction relief, UUO+iohexol+NAC rats exhibited a lower apoptosis rate, lower Bax mRNA expression, higher expression of Bcl-2 mRNA and higher ratio of Bcl-2/Bax (all P&lt;0.05) compared with day 1 following drug administration.	Acetylcysteine	50-53	BCL2 associated X, apoptosis regulator	Rattus norvegicus	178-181
29207099-10	2018	The prophylactic use of NAC reduced the apoptotic rate of renal tubular cells following contrast exposition, which was accompanied by changes in the expression of Bcl-2/Bax mRNA.	Acetylcysteine	24-27	BCL2 associated X, apoptosis regulator	Rattus norvegicus	169-172
30243219-1	2018	N-acetylcysteine modified hyaluronic acid-paclitaxel (NAC-HA-PTX) conjugate was designed to improve the water solubility and oral bioavailability of PTX through mucosal bioadhesion ability.	Acetylcysteine	0-16	synuclein alpha	Homo sapiens	54-57
35086548-8	2022	Neutralization of ROS with N-acetyl-L-cysteine (NAC) increased the levels of miR-155-5p in tumor exosomes that were taken up by macrophages, leading to reduction of macrophage migration and tumor spheroid infiltration.	Acetylcysteine	48-51	microRNA 155	Mus musculus	77-84
29278702-8	2018	Finally, the role of the ROS-TXNIP axis in mediating the activation of the NLRP3 inflammasome and cell death was characterized by pretreating with the ROS scavenger N-acetylcysteine (NAC) and performing TXNIP knockdown experiments in MIN6.	Acetylcysteine	165-181	NLR family, pyrin domain containing 3	Mus musculus	75-80
29278702-8	2018	Finally, the role of the ROS-TXNIP axis in mediating the activation of the NLRP3 inflammasome and cell death was characterized by pretreating with the ROS scavenger N-acetylcysteine (NAC) and performing TXNIP knockdown experiments in MIN6.	Acetylcysteine	183-186	NLR family, pyrin domain containing 3	Mus musculus	75-80
30993256-8	2019	A decrease in interferon gamma, tumor necrosis factor alpha, interleukin 1alpha, and other type 1 diabetes-associated proinflammatory cytokines was found in mice supplemented with NAC in adulthood or during early life compared with control NOD mice.	Acetylcysteine	180-183	interleukin 1 alpha	Mus musculus	61-79
2582614-6	1989	Patients in whom the concentration of GST exceeded 10 micrograms/L on admission subsequently went on to develop moderate or severe liver damage, despite treatment with N-acetylcysteine.	Acetylcysteine	168-184	glutathione S-transferase kappa 1	Homo sapiens	38-41
30340029-10	2018	Antioxidant N-acetyl cysteine can reverse the nuclear to cytoplasmic ratio of PME-1 proteins and dem-p-PP2Ac after H2O2 exposure.	Acetylcysteine	12-29	protein phosphatase methylesterase 1	Homo sapiens	78-83
30340029-10	2018	Antioxidant N-acetyl cysteine can reverse the nuclear to cytoplasmic ratio of PME-1 proteins and dem-p-PP2Ac after H2O2 exposure.	Acetylcysteine	12-29	protein phosphatase 2 catalytic subunit alpha	Homo sapiens	103-108
29423685-4	2018	Catalase, superoxide dismutase, and acetylcholinesterase activities were increased by Cys and NAC.	Acetylcysteine	94-97	acetylcholinesterase	Rattus norvegicus	36-56
30222967-5	2018	These effects were rescued by re-expression of LKB1 or pre-treatment with the anti-oxidant and GSH replenisher N-acetyl cysteine.	Acetylcysteine	111-128	serine/threonine kinase 11	Homo sapiens	47-51
30249712-0	2018	BET 1: In paracetamol overdose, is oral N-acetylcysteine as effective as intravenous N-acetylcysteine?	Acetylcysteine	40-56	Bet1 golgi vesicular membrane trafficking protein	Homo sapiens	0-5
30249712-0	2018	BET 1: In paracetamol overdose, is oral N-acetylcysteine as effective as intravenous N-acetylcysteine?	Acetylcysteine	85-101	Bet1 golgi vesicular membrane trafficking protein	Homo sapiens	0-5
30025894-9	2018	Besides, administration of the antioxidant N-acetyl-l-cysteine (NAC) normalized the increased ROS levels in FoxO1-deficient osteoblasts, restoring the decreased osteoblasts differentiation, suppressing apoptosis-related caspase-3 activity, and promoting the expression of osteogenic markers in FoxO1-deficient osteoblasts.	Acetylcysteine	43-62	forkhead box O1	Mus musculus	108-113
30025894-9	2018	Besides, administration of the antioxidant N-acetyl-l-cysteine (NAC) normalized the increased ROS levels in FoxO1-deficient osteoblasts, restoring the decreased osteoblasts differentiation, suppressing apoptosis-related caspase-3 activity, and promoting the expression of osteogenic markers in FoxO1-deficient osteoblasts.	Acetylcysteine	43-62	forkhead box O1	Mus musculus	294-299
30025894-9	2018	Besides, administration of the antioxidant N-acetyl-l-cysteine (NAC) normalized the increased ROS levels in FoxO1-deficient osteoblasts, restoring the decreased osteoblasts differentiation, suppressing apoptosis-related caspase-3 activity, and promoting the expression of osteogenic markers in FoxO1-deficient osteoblasts.	Acetylcysteine	64-67	forkhead box O1	Mus musculus	108-113
30025894-9	2018	Besides, administration of the antioxidant N-acetyl-l-cysteine (NAC) normalized the increased ROS levels in FoxO1-deficient osteoblasts, restoring the decreased osteoblasts differentiation, suppressing apoptosis-related caspase-3 activity, and promoting the expression of osteogenic markers in FoxO1-deficient osteoblasts.	Acetylcysteine	64-67	forkhead box O1	Mus musculus	294-299
30060081-8	2018	Furthermore, N-acetyl-L-cysteine, a ROS inhibitor, decreased NLRP3 expression, and rotenone, a robust ROS inducer, partially reversed the inhibitory effect of INK128 on NLRP3.	Acetylcysteine	13-32	NLR family, pyrin domain containing 3	Mus musculus	61-66
29940243-10	2018	Yet, H2O2-induced oxidative stress had no obvious effect on PHLPP1 expression of NRVMs at early stage but N-acetylcysteine (NAC) pretreatment increased PHLPP1 levels after 4 h H2O2 stimulation.	Acetylcysteine	106-122	PH domain and leucine rich repeat protein phosphatase 1	Rattus norvegicus	152-158
29940243-10	2018	Yet, H2O2-induced oxidative stress had no obvious effect on PHLPP1 expression of NRVMs at early stage but N-acetylcysteine (NAC) pretreatment increased PHLPP1 levels after 4 h H2O2 stimulation.	Acetylcysteine	124-127	PH domain and leucine rich repeat protein phosphatase 1	Rattus norvegicus	152-158
30131715-6	2018	Furthermore, NAC pretreatment partly inhibited MC-LR-induced ERs and autophagy via the PERK/ATG12 and XBP1/Beclin1 pathways.	Acetylcysteine	13-16	autophagy related 12	Mus musculus	92-97
30131715-6	2018	Furthermore, NAC pretreatment partly inhibited MC-LR-induced ERs and autophagy via the PERK/ATG12 and XBP1/Beclin1 pathways.	Acetylcysteine	13-16	beclin 1, autophagy related	Mus musculus	107-114
29989329-9	2018	RESULTS: Iron overload induced M1 polarization by increasing ROS production and inducing p53 acetylation in RAW cells, and reduction in ROS levels by NAC repressed M1 polarization and p53 acetylation.	Acetylcysteine	150-153	transformation related protein 53, pseudogene	Mus musculus	184-187
29679867-10	2018	In addition, NAC significantly attenuated MCLR-triggered testicular eIF2s1 and MAPK8 activation, indicating that NAC counteracts MCLR-induced unfolded protein response (UPR) in testes.	Acetylcysteine	13-16	eukaryotic translation initiation factor 2, subunit 1 alpha a	Danio rerio	68-74
29679867-10	2018	In addition, NAC significantly attenuated MCLR-triggered testicular eIF2s1 and MAPK8 activation, indicating that NAC counteracts MCLR-induced unfolded protein response (UPR) in testes.	Acetylcysteine	13-16	mitogen-activated protein kinase 8b	Danio rerio	79-84
29679867-10	2018	In addition, NAC significantly attenuated MCLR-triggered testicular eIF2s1 and MAPK8 activation, indicating that NAC counteracts MCLR-induced unfolded protein response (UPR) in testes.	Acetylcysteine	113-116	eukaryotic translation initiation factor 2, subunit 1 alpha a	Danio rerio	68-74
29679867-10	2018	In addition, NAC significantly attenuated MCLR-triggered testicular eIF2s1 and MAPK8 activation, indicating that NAC counteracts MCLR-induced unfolded protein response (UPR) in testes.	Acetylcysteine	113-116	mitogen-activated protein kinase 8b	Danio rerio	79-84
29668110-8	2018	Pre-incubation with ROS scavenger N-acetyl-l-cysteine preserved AR and PSA abundance, markedly reduced ISC-4-induced apoptosis and attenuated p53 Ser phosphorylation, p21Cip1, and p-H2A.X.	Acetylcysteine	34-53	kallikrein related peptidase 3	Homo sapiens	71-74
30011295-6	2018	Pre-treatment with the antioxidant, N-acetylcysteine, prevented the actions of arecoline on cell viability, G2/M growth arrest, reactive oxygen species (ROS) production, and the levels of CDK1, p21, p27, p53, cyclin B1, and phospho-AMPK proteins.	Acetylcysteine	36-52	cyclin dependent kinase 1	Homo sapiens	188-192
30011295-6	2018	Pre-treatment with the antioxidant, N-acetylcysteine, prevented the actions of arecoline on cell viability, G2/M growth arrest, reactive oxygen species (ROS) production, and the levels of CDK1, p21, p27, p53, cyclin B1, and phospho-AMPK proteins.	Acetylcysteine	36-52	interferon alpha inducible protein 27	Homo sapiens	199-202
30011295-6	2018	Pre-treatment with the antioxidant, N-acetylcysteine, prevented the actions of arecoline on cell viability, G2/M growth arrest, reactive oxygen species (ROS) production, and the levels of CDK1, p21, p27, p53, cyclin B1, and phospho-AMPK proteins.	Acetylcysteine	36-52	cyclin B1	Homo sapiens	209-218
29907654-9	2018	Vascular contractile responses in Nox5 mice were normalized by N-acetylcysteine and inhibitors of calcium channels, calmodulin, and endoplasmic reticulum ryanodine receptors, but not by GKT137831 (Nox1/4 inhibitor).	Acetylcysteine	63-79	NADPH oxidase 5	Homo sapiens	34-38
29904431-1	2018	The aim of the present study was to investigate the impact of N-acetylcysteine (NAC) on the expression of activin receptor-like kinase-1 (ALK-1) and mothers against decapentaplegic homolog 1 (Smad1) in the pulmonary artery of rats with pulmonary arterial hypertension (PAH), and to explore the possible mechanisms underlying its effects on pulmonary vascular remodeling (PVR).	Acetylcysteine	62-78	activin A receptor like type 1	Rattus norvegicus	106-136
29904431-1	2018	The aim of the present study was to investigate the impact of N-acetylcysteine (NAC) on the expression of activin receptor-like kinase-1 (ALK-1) and mothers against decapentaplegic homolog 1 (Smad1) in the pulmonary artery of rats with pulmonary arterial hypertension (PAH), and to explore the possible mechanisms underlying its effects on pulmonary vascular remodeling (PVR).	Acetylcysteine	62-78	activin A receptor like type 1	Rattus norvegicus	138-143
29904431-1	2018	The aim of the present study was to investigate the impact of N-acetylcysteine (NAC) on the expression of activin receptor-like kinase-1 (ALK-1) and mothers against decapentaplegic homolog 1 (Smad1) in the pulmonary artery of rats with pulmonary arterial hypertension (PAH), and to explore the possible mechanisms underlying its effects on pulmonary vascular remodeling (PVR).	Acetylcysteine	80-83	activin A receptor like type 1	Rattus norvegicus	106-136
29904431-1	2018	The aim of the present study was to investigate the impact of N-acetylcysteine (NAC) on the expression of activin receptor-like kinase-1 (ALK-1) and mothers against decapentaplegic homolog 1 (Smad1) in the pulmonary artery of rats with pulmonary arterial hypertension (PAH), and to explore the possible mechanisms underlying its effects on pulmonary vascular remodeling (PVR).	Acetylcysteine	80-83	activin A receptor like type 1	Rattus norvegicus	138-143
29904431-7	2018	In addition, NAC reduced the MCT-induced PVR, pulmonary inflammation score and upregulation of ALK-1 and Smad1.	Acetylcysteine	13-16	activin A receptor like type 1	Rattus norvegicus	95-100
29904431-8	2018	These results indicate that ALK-1 and Smad1 participate in the formation of PAH and the process of PVR, and suggest that NAC may inhibit PAH by inhibiting the expression of ALK-1 and Smad1 in the pulmonary artery.	Acetylcysteine	121-124	activin A receptor like type 1	Rattus norvegicus	28-33
29904431-8	2018	These results indicate that ALK-1 and Smad1 participate in the formation of PAH and the process of PVR, and suggest that NAC may inhibit PAH by inhibiting the expression of ALK-1 and Smad1 in the pulmonary artery.	Acetylcysteine	121-124	activin A receptor like type 1	Rattus norvegicus	173-178
29178427-7	2018	CD38 and a set of IFN-stimulated genes (ISGs) were inhibited by the anti-oxidant N-acetyl cysteine.	Acetylcysteine	81-98	CD38 molecule	Homo sapiens	0-4
29436612-6	2018	Furthermore, blocking ROS with NAC inhibited SW-induced ER stress, as evidenced by the downregulation of GRP78, phosphorylated (p)-protein kinase R-like ER kinase (PERK), p-inositol-requiring kinase 1alpha (IRE1alpha), p-50 activating transcription factor 6alpha and CHOP.	Acetylcysteine	31-34	DNA-damage inducible transcript 3	Rattus norvegicus	267-271
29544934-9	2018	NAC restored the ability of PKA to modulate myofilament Ca2+ sensitivity and prevented cardiac dysfunction observed in HSE animals.	Acetylcysteine	0-3	protein kinase cAMP-activated catalytic subunit alpha	Rattus norvegicus	28-31
29522769-7	2018	Finally, NAC-treated MSG rats retained normal liver glucokinase and fructokinase activities, and Srebp1c, Fas and Gpat (lipogenic genes) expression levels.	Acetylcysteine	9-12	glycerol-3-phosphate acyltransferase, mitochondrial	Rattus norvegicus	114-118
29327381-16	2018	N-Acetyl-cysteine or tempol prevented the decreases in the LC3 II/I ratio and Beclin1 and Atg5 expression and attenuated the increases in LV wall thickness, myocyte diameter and brain natriuretic peptide expression in AAC rats.	Acetylcysteine	0-17	autophagy related 5	Rattus norvegicus	90-94
29432840-5	2018	Pre-treatment of the cells with the antioxidant N-acetyl-cysteine markedly suppressed T-2 toxin-induced neurotoxicity and caspase activation.	Acetylcysteine	48-65	brachyury 2	Mus musculus	86-89
29397791-9	2018	Furthermore, N-acetyl cysteine (NAC), an ROS scavenger, enhanced the effects of GLRX3 knockdown on Notch-dependent EMT.	Acetylcysteine	13-30	glutaredoxin 3	Homo sapiens	80-85
29397791-9	2018	Furthermore, N-acetyl cysteine (NAC), an ROS scavenger, enhanced the effects of GLRX3 knockdown on Notch-dependent EMT.	Acetylcysteine	32-35	glutaredoxin 3	Homo sapiens	80-85
29193259-7	2018	The suppressive effects of PM2.5LL on proliferation and interleukin-2 production in splenocytes were rescued by the antioxidant N-acetylcysteine.	Acetylcysteine	128-144	interleukin 2	Mus musculus	56-69
29113965-9	2018	Furthermore, treatment of atherosclerotic-MSCs with the reactive oxygen species scavenger N-acetyl-l-cysteine reduced the levels of interleukin-6, interleukin-8/C-X-C motif chemokine ligand 8, and monocyte chemoattractant protein-1/chemokine ligand 2 in the MSC secretome and improved MSCs immunosuppressive capacity (P=0.03).	Acetylcysteine	90-109	C-C motif chemokine ligand 2	Homo sapiens	197-231
29315209-8	2018	Pin-activated ERK/JNK were significantly reduced after the administration of NAC; however, the inhibition of ERK/JNK failed to change the Pin-induced ROS production.	Acetylcysteine	77-80	mitogen-activated protein kinase 8	Rattus norvegicus	18-21
29223047-5	2018	Standard IMITC-NAC was synthesized and its structure confirmed by NMR and MS. IMITC-NAC was identified in extracts of Brussels sprouts chopped in the presence of N-acetylcysteine.	Acetylcysteine	162-178	synuclein alpha	Homo sapiens	15-18
29223047-5	2018	Standard IMITC-NAC was synthesized and its structure confirmed by NMR and MS. IMITC-NAC was identified in extracts of Brussels sprouts chopped in the presence of N-acetylcysteine.	Acetylcysteine	162-178	synuclein alpha	Homo sapiens	84-87
29383185-7	2017	Here we found that the increased Egr-1 expression was a consequence of G-1-mediated ROS-dependent ERK activation that were promptly reversed by the presence of the antioxidant n-acetyl-cysteine.	Acetylcysteine	176-193	early growth response 1	Homo sapiens	33-38
29233977-6	2017	In vivo treatment with an inhibitor of MCJ expression protects liver from acetaminophen-induced liver injury at a time when N-acetylcysteine, the standard therapy, has no efficacy.	Acetylcysteine	124-140	DnaJ heat shock protein family (Hsp40) member C15	Homo sapiens	39-42
29125538-3	2017	CYP1A1 is mediated by aryl hydrocarbon receptor signaling, while induction of HO-1 is regulated by oxidative stress, and suppressed by N-acetylcysteine treatment.	Acetylcysteine	135-151	heme oxygenase 1	Homo sapiens	78-82
29123322-3	2017	In this study, using the antioxidant N-acetylcysteine (NAC), we show that hypoxia-induced reactive oxygen species (ROS) in MDA-MB-468 breast cancer cells, selectively regulate hypoxia-induced increases in N-cadherin and SERPINE1, two proteins involved in cell adhesion.	Acetylcysteine	37-53	serpin family E member 1	Homo sapiens	220-228
29123322-3	2017	In this study, using the antioxidant N-acetylcysteine (NAC), we show that hypoxia-induced reactive oxygen species (ROS) in MDA-MB-468 breast cancer cells, selectively regulate hypoxia-induced increases in N-cadherin and SERPINE1, two proteins involved in cell adhesion.	Acetylcysteine	55-58	serpin family E member 1	Homo sapiens	220-228
28901448-7	2017	Pretreatment of cells with an antioxidant, N-acetyl cysteine (NAC), prior to plasma exposure suppressed the formation of 8-oxoG and restored the expression levels of OGG1 and Nrf2.	Acetylcysteine	43-60	8-oxoguanine DNA glycosylase	Homo sapiens	166-170
28901448-7	2017	Pretreatment of cells with an antioxidant, N-acetyl cysteine (NAC), prior to plasma exposure suppressed the formation of 8-oxoG and restored the expression levels of OGG1 and Nrf2.	Acetylcysteine	62-65	8-oxoguanine DNA glycosylase	Homo sapiens	166-170
28715732-6	2017	MG132 treatment generated ROS, and the cleavage of HSP90 was blocked by a ROS scavenger, N-acetylcysteine (NAC).	Acetylcysteine	89-105	heat shock protein 90 alpha family class A member 1	Homo sapiens	51-56
28715732-6	2017	MG132 treatment generated ROS, and the cleavage of HSP90 was blocked by a ROS scavenger, N-acetylcysteine (NAC).	Acetylcysteine	107-110	heat shock protein 90 alpha family class A member 1	Homo sapiens	51-56
28715732-7	2017	MG132 activated several caspases, and the activation was reduced by pretreatment with NAC.	Acetylcysteine	86-89	caspase 10	Homo sapiens	24-32
31457864-1	2017	We have combined results from several spectroscopic techniques to investigate the aerobic reactions of Rh2(AcO)4 (AcO- = CH3COO-) with l-cysteine (H2Cys) and its derivatives d-penicillamine (3,3"-dimethylcysteine, H2Pen), with steric hindrance at the thiol group, and N-acetyl-l-cysteine (H2NAC), with its amino group blocked.	Acetylcysteine	268-287	Rh associated glycoprotein	Homo sapiens	103-112
28705740-5	2017	Especially, the glutamine metabolic process related molecules, GPX1, GPX3, SMS, GGCT, GSTK1, NFkappaB, GSTT2, SOD1 and GCLM, are involved in the switching process from oxidized glutathione (GSSG) conversion to the reduced glutathione (GSH) by glutathione, mercapturic acid and arginine metabolism process.	Acetylcysteine	256-272	glutathione S-transferase kappa 1	Homo sapiens	86-91
28705740-5	2017	Especially, the glutamine metabolic process related molecules, GPX1, GPX3, SMS, GGCT, GSTK1, NFkappaB, GSTT2, SOD1 and GCLM, are involved in the switching process from oxidized glutathione (GSSG) conversion to the reduced glutathione (GSH) by glutathione, mercapturic acid and arginine metabolism process.	Acetylcysteine	256-272	glutathione S-transferase theta 2 (gene/pseudogene)	Homo sapiens	103-108
28743626-3	2017	However, NAC significantly inhibited production of NO and ROS and markedly suppressed expression of iNOS and COX-2 protein in LPS-stimulated zebrafish embryos.	Acetylcysteine	9-12	cytochrome c oxidase II, mitochondrial	Danio rerio	109-114
28580603-7	2017	In addition, high glucose-stimulated melatonin receptor 1B (MTNR1B) mRNA and PINK1 expressions were reversed by ROS scavenger N-acetyl cysteine pretreatment.	Acetylcysteine	126-143	melatonin receptor 1B	Homo sapiens	60-66
28522564-8	2017	In both primary bronchial epithelial cells and BEAS-2B cells, CSE decreased PTEN protein, which was reversed by N-acetyl cysteine treatment.	Acetylcysteine	112-129	phosphatase and tensin homolog	Homo sapiens	76-80
28512265-3	2017	In this study, we show that the dying myeloma cells treated with chaetocin resulted in the induction of heat shock protein (HSP) 90, which was inhibited by antioxidant N-acetyl cysteine, and showed an increase in the expression of MAGE-A3 and MAGE-C1/CT7.	Acetylcysteine	168-185	heat shock protein 90 alpha family class A member 1	Homo sapiens	104-131
28438466-2	2017	N-acetylcysteine (NAC) is a glutathione precursor with potent antioxidant, pro-neurogenesis and anti-inflammatory properties and a favourable safety profile.	Acetylcysteine	0-16	synuclein alpha	Homo sapiens	18-21
28380464-7	2017	N-Acetyl-L-Cysteine was shown to inhibit ROS generation, suppress permeabilization of lysosomal membranes, decrease levels of cathepsin B and cytochrome C in the cytosol, and inhibit Bax/Bcl2 ratio, caspase-9 and caspase-3 activity both in vitro and in vivo.	Acetylcysteine	0-19	caspase 9	Homo sapiens	199-208
28388573-6	2017	What is more, when detect the function of alphaMSH in ROS-induced apoptosis, similar inhibitory trend was found with the oxidative stress inhibitor N-acetyl-L-cysteine (NAC) in ROS-induced adipocyte apoptosis and this trend is alphaMSH receptor melanocortin 5 receptor (MC5R) depended, while an opposite trend was found between alphaMSH and Foxo1, which is a known positive regulator of adipocyte apoptosis.	Acetylcysteine	169-172	forkhead box O1	Mus musculus	341-346
28630426-6	2017	The down-regulation of SLC7A11 markedly enhanced ROS induced P-gp over-expression and drug resistance in MCF-7 cells; a combination of either an inhibited/silenced SLC7A11 or cystine deprivation and increased ROS dramatically promoted P-gp expression, which could be reversed by N-acetylcysteine.	Acetylcysteine	279-295	solute carrier family 7 member 11	Homo sapiens	23-30
30263604-6	2017	Gene knockdown experiments revealed that the effect of NAC is not dependent on SKN-1, a protein-sensing DR status, whereas DAF-16, a transcription factor regulating stress-responsive genes, is required for lifespan extension by NAC.	Acetylcysteine	228-231	Fork-head domain-containing protein;Forkhead box protein O	Caenorhabditis elegans	123-129
30263604-8	2017	Our results show that NAC mimics the effect of DR on lifespan, possibly through the induction of DAF-16 nuclear localization and may retard the incidence of AD.	Acetylcysteine	22-25	Fork-head domain-containing protein;Forkhead box protein O	Caenorhabditis elegans	97-103
28506985-6	2017	Intraperitoneal injection of the antioxidant N-acetylcysteine rescued defective follicle and oocyte development resulting from Kat8 deficiency.	Acetylcysteine	45-61	K(lysine) acetyltransferase 8	Mus musculus	127-131
29248134-14	2017	CONCLUSIONS: NAC as a single agent reduces MCT4 stromal expression, which is a marker of glycolysis in breast cancer with reduced carcinoma cell proliferation.	Acetylcysteine	13-16	solute carrier family 16 member 3	Homo sapiens	43-47
28264926-7	2017	Treatment with N-acetyl-L-cysteine, a ROS scavenger, prevented senescence induced by PRODH overexpression.	Acetylcysteine	15-34	proline dehydrogenase 1	Homo sapiens	85-90
28231391-5	2017	Moreover, N-acetyl-cysteine treatment rescues the vascular defects in prdx1 morphants.	Acetylcysteine	10-27	peroxiredoxin 1	Danio rerio	70-75
28011677-4	2017	N-acetylcysteine (NAC), an FDA-approved anti-mucolytic agent, is a possible new treatment strategy for TTP, as it was demonstrated to reduce disulfide bonds in VWF, thereby decreasing VWF multimers size and hence their prothrombotic potential.	Acetylcysteine	0-16	Von Willebrand factor	Mus musculus	160-163
28011677-4	2017	N-acetylcysteine (NAC), an FDA-approved anti-mucolytic agent, is a possible new treatment strategy for TTP, as it was demonstrated to reduce disulfide bonds in VWF, thereby decreasing VWF multimers size and hence their prothrombotic potential.	Acetylcysteine	0-16	Von Willebrand factor	Mus musculus	184-187
28011677-4	2017	N-acetylcysteine (NAC), an FDA-approved anti-mucolytic agent, is a possible new treatment strategy for TTP, as it was demonstrated to reduce disulfide bonds in VWF, thereby decreasing VWF multimers size and hence their prothrombotic potential.	Acetylcysteine	18-21	Von Willebrand factor	Mus musculus	160-163
28011677-4	2017	N-acetylcysteine (NAC), an FDA-approved anti-mucolytic agent, is a possible new treatment strategy for TTP, as it was demonstrated to reduce disulfide bonds in VWF, thereby decreasing VWF multimers size and hence their prothrombotic potential.	Acetylcysteine	18-21	Von Willebrand factor	Mus musculus	184-187
27929749-8	2017	In addition, ROS scavenger (N-acetyl-L-cysteine, NAC) and NOX4 inhibitor GKT137831 reduced ROS generation and alleviated activation of Xbp1 and RIPK1-related NF-kappaB signaling.	Acetylcysteine	28-47	X-box binding protein 1	Rattus norvegicus	135-139
27929749-8	2017	In addition, ROS scavenger (N-acetyl-L-cysteine, NAC) and NOX4 inhibitor GKT137831 reduced ROS generation and alleviated activation of Xbp1 and RIPK1-related NF-kappaB signaling.	Acetylcysteine	49-52	X-box binding protein 1	Rattus norvegicus	135-139
28769003-7	2017	Further, blue LED light-induced decreasing of S-opsin levels and altered rhodopsin localization, which were suppressed by NAC.	Acetylcysteine	122-125	opsin 1 (cone pigments), short-wave-sensitive (color blindness, tritan)	Mus musculus	46-53
28769003-7	2017	Further, blue LED light-induced decreasing of S-opsin levels and altered rhodopsin localization, which were suppressed by NAC.	Acetylcysteine	122-125	rhodopsin	Mus musculus	73-82
28535537-10	2017	The effect of exemestane (40 microg/ml) on annexin-V-binding was significantly blunted by antioxidant N-acetylcysteine (1mM), but was not significantly modified by removal or increase of extracellular Ca2+, by p38 kinase inhibitor SB203580 (2 microM), casein kinase inhibitor D4476 (10 microM) and caspase inhibitor zVAD (10 microM).	Acetylcysteine	104-118	annexin A5	Homo sapiens	43-52
27941930-8	2016	Furthermore, suppression of ASIC1-mediated generation of reactive oxygen species (ROS) by ROS scavengers, such as glutathione or N-acetyl-cysteine causes a decrease in ERK phosphorylation and degradation of IkappaBalpha.	Acetylcysteine	129-146	acid sensing ion channel subunit 1	Homo sapiens	28-33
26822174-6	2016	Antioxidant N-acetyl-L-cysteine (NAC) and c-Jun NH2-terminal kinase (JNK) inhibitor SP600125 inhibited PEITC-induced DR4 and DR5 expression.	Acetylcysteine	33-36	TNF receptor superfamily member 10b	Homo sapiens	125-128
27989750-6	2016	We further demonstrate that the radical scavenger N-acetyl-L-cysteine reverts hnRNPA2/B1 and PKM2 inhibition by genipin indicating a role for reactive oxygen species in the metabolic reprogramming of cancer cells mediated by UCP2.	Acetylcysteine	50-69	pyruvate kinase M1/2	Homo sapiens	93-97
27590200-5	2016	Apocynin, Akt inhibitor SH-5, Bay 11-7085 and N-acetylcysteine each attenuated the lipopolysaccharide-induced production of cytokines, PGE2, and chemokines, changes in the levels of Toll-like receptor-4, p-Akt, mTOR, and NF-kappaB, and production of reactive oxygen species in keratinocytes.	Acetylcysteine	46-62	toll like receptor 4	Homo sapiens	182-202
27897258-5	2016	Analysis of the underlying mechanisms revealed that STZ + EDA-/- mice show increased oxidative stress as demonstrated by enhanced aortic superoxide anion, nitrotyrosine levels and expression of NADPH oxidase NOX4 and TGF-beta1, the last two being reverted by treatment with the antioxidant n-acetylcysteine.	Acetylcysteine	290-306	ectodysplasin-A	Mus musculus	58-61
27725188-11	2016	Although N-acetyl cysteine (NAC) significantly decreased H2O2 levels in OM-treated cells, we observed that OM further increased HO-1 mRNA and protein expression in NAC-pretreated compared to vehicle-pretreated cells, suggesting that OM induces HO-1 via H2O2-independent mechanisms.	Acetylcysteine	164-167	heme oxygenase 1	Homo sapiens	128-132
27725188-11	2016	Although N-acetyl cysteine (NAC) significantly decreased H2O2 levels in OM-treated cells, we observed that OM further increased HO-1 mRNA and protein expression in NAC-pretreated compared to vehicle-pretreated cells, suggesting that OM induces HO-1 via H2O2-independent mechanisms.	Acetylcysteine	164-167	heme oxygenase 1	Homo sapiens	244-248
27484511-12	2016	Finally, the employment of NAC and MAPK inhibitors (U0126, SP600125 and SB203580) remarkably blocked the S phase arrest, apoptosis and down-regulation of P-gp induced by Z5.	Acetylcysteine	27-30	phosphoglycolate phosphatase	Homo sapiens	154-158
27544755-8	2016	It inhibited nuclear factor erythroid 2-related factor 2 and glutathione S-transferase P in cisplatin-resistant HNC cells, resulting in increased ROS accumulation in HNC cells, an effect that could be blocked by the antioxidant N-acetyl-L-cysteine.	Acetylcysteine	228-247	glutathione S-transferase pi 1	Homo sapiens	61-88
27325640-10	2016	This was abrogated by N-acetylcysteine (NAC) treatment, indicating that Abeta-induced ROS generation is the main cause of suppression of proliferation.	Acetylcysteine	22-38	amyloid beta (A4) precursor protein	Mus musculus	72-77
27325640-10	2016	This was abrogated by N-acetylcysteine (NAC) treatment, indicating that Abeta-induced ROS generation is the main cause of suppression of proliferation.	Acetylcysteine	40-43	amyloid beta (A4) precursor protein	Mus musculus	72-77
27325640-11	2016	NAC also restored Abeta-induced annexin V/PI-positive cell populations.	Acetylcysteine	0-3	amyloid beta (A4) precursor protein	Mus musculus	18-23
27643875-4	2016	Combined inhibition of GSH and Trx metabolism enhanced cancer cell clonogenic killing and radiation responses in human breast and pancreatic cancer cells via a mechanism that could be inhibited by N-acetylcysteine (NAC).	Acetylcysteine	197-213	thioredoxin	Homo sapiens	31-34
27643875-4	2016	Combined inhibition of GSH and Trx metabolism enhanced cancer cell clonogenic killing and radiation responses in human breast and pancreatic cancer cells via a mechanism that could be inhibited by N-acetylcysteine (NAC).	Acetylcysteine	215-218	thioredoxin	Homo sapiens	31-34
27161488-7	2016	NAC treatment significantly lowered HFD-induced macrophage infiltration, and enhanced adiponectin gene expression, resulting in reduced hyperglycemia and hyperinsulinemia, and improvement of insulin resistance.	Acetylcysteine	0-3	adiponectin, C1Q and collagen domain containing	Mus musculus	86-97
27183920-9	2016	Moreover, it was shown in vitro that GSTs can strongly increase the efficiency of GSH to protect against the alkylation of the model thiol N-acetylcysteine by reactive diclofenac metabolites.	Acetylcysteine	139-155	glutathione S-transferase kappa 1	Homo sapiens	37-41
27179791-9	2016	Furthermore, NAC was able to rescue changes in key glutamate receptor proteins related to excitotoxicity in HD, including NMDAR2B.	Acetylcysteine	13-16	glutamate receptor, ionotropic, NMDA2B (epsilon 2)	Mus musculus	122-129
27220372-9	2016	The in vitro experiments demonstrated that Ang II upregulated the expression levels of periostin and alpha-SMA compared with the control, whereas, pretreatment with NAC inhibited oxidative stress, periostin and alpha-SMA expression in fibroblasts.	Acetylcysteine	165-168	actin gamma 2, smooth muscle	Rattus norvegicus	101-110
27220372-9	2016	The in vitro experiments demonstrated that Ang II upregulated the expression levels of periostin and alpha-SMA compared with the control, whereas, pretreatment with NAC inhibited oxidative stress, periostin and alpha-SMA expression in fibroblasts.	Acetylcysteine	165-168	actin gamma 2, smooth muscle	Rattus norvegicus	211-220
27083693-5	2016	Both NAC and enoxaparin led to a significant reduction in ovarian tissue 8-OHdG (P = 0.004 and P = 0.01, respectively) and MPO (P = 0.013 and P = 0.023, respectively) concentrations compared with I/R group, indicating a protective effect against I/R oxidative damage.	Acetylcysteine	5-8	myeloperoxidase	Rattus norvegicus	123-126
27010086-11	2016	Furthermore, the expressions of NF-kappaB p65/RelA and phospho-NF-kappaB p65/RelA (Ser536) were suppressed after 2,5-HD exposure and restored by NAC pretreatment.	Acetylcysteine	145-148	RELA proto-oncogene, NF-kB subunit	Rattus norvegicus	46-50
27010086-11	2016	Furthermore, the expressions of NF-kappaB p65/RelA and phospho-NF-kappaB p65/RelA (Ser536) were suppressed after 2,5-HD exposure and restored by NAC pretreatment.	Acetylcysteine	145-148	RELA proto-oncogene, NF-kB subunit	Rattus norvegicus	77-81
27105530-10	2016	This increased ROS levels resulting in defective CD34+ cells, an effect partially reversed by N-acetyl-L-cysteine.	Acetylcysteine	94-113	CD34 antigen	Mus musculus	49-53
26206603-8	2016	The ROS increase and OCT4 downregulation after BDE-209 exposure could be reversed partly by antioxidant N-acetylcysteine supplement.	Acetylcysteine	104-120	POU class 5 homeobox 1	Homo sapiens	21-25
26934645-7	2016	Moreover, N-acetylcysteine (reactive oxygen species scavenger) blocked the SK inhibitor-induced increase in p21 and p53 expression but had no effect on the proteasomal degradation of SK1a.	Acetylcysteine	10-26	H3 histone pseudogene 16	Homo sapiens	108-111
26836389-9	2016	HUA exposure directly increased the phospho-IRS1 (Ser307) response to insulin and inhibited that of phospho-Akt in H9C2 cardiomyocytes, which was blocked by NAC.	Acetylcysteine	157-160	insulin receptor substrate 1	Mus musculus	44-48
26577769-7	2016	Overexpression of the anti-apoptotic protein Bcl-xL or pre-incubation with N-acetyl cysteine reduced the intracellular level of ROS and increased resistance to hLf, confirming a ROS-mediated mitochondrial cell death process.	Acetylcysteine	75-92	HLF transcription factor, PAR bZIP family member	Homo sapiens	160-163
27003169-6	2016	Furthermore, NAC blocked the decrease of B-cell lymphoma 2/Bcl-2 associated X protein (Bcl-2/Bax) ratio, release of cytochrome c, cleavage of caspase-3 and poly(ADP-ribose) polymerase (PARP), and nuclear translocation of apoptosis-inducing factor (AIF) and endonuclease G (Endo G).	Acetylcysteine	13-16	BCL2 associated X, apoptosis regulator	Rattus norvegicus	93-96
27003169-6	2016	Furthermore, NAC blocked the decrease of B-cell lymphoma 2/Bcl-2 associated X protein (Bcl-2/Bax) ratio, release of cytochrome c, cleavage of caspase-3 and poly(ADP-ribose) polymerase (PARP), and nuclear translocation of apoptosis-inducing factor (AIF) and endonuclease G (Endo G).	Acetylcysteine	13-16	poly (ADP-ribose) polymerase 1	Rattus norvegicus	156-183
27003169-6	2016	Furthermore, NAC blocked the decrease of B-cell lymphoma 2/Bcl-2 associated X protein (Bcl-2/Bax) ratio, release of cytochrome c, cleavage of caspase-3 and poly(ADP-ribose) polymerase (PARP), and nuclear translocation of apoptosis-inducing factor (AIF) and endonuclease G (Endo G).	Acetylcysteine	13-16	poly (ADP-ribose) polymerase 1	Rattus norvegicus	185-189
25941092-10	2016	Furthermore, NAC increased the GSH level and SOD and GST activities, which decreased in ulcerous stomach tissues.	Acetylcysteine	13-16	hematopoietic prostaglandin D synthase	Rattus norvegicus	53-56
25941092-11	2016	Only MPO activity increased in both IND and NAC groups when compared to healthy rat group.	Acetylcysteine	44-47	myeloperoxidase	Rattus norvegicus	5-8
27119348-15	2016	In contrast, both NAC and PFT-alpha treatment inhibited GA-induced p53 expression in mouse tumors.	Acetylcysteine	18-21	transformation related protein 53, pseudogene	Mus musculus	67-70
27184952-9	2016	High-mobility group box 1 (HMGB1) was rapidly released and associated with TLR4 after TNF-alpha stimulation with a peak at 5 min, which was prevented by N-acetylcysteine, an antioxidant.	Acetylcysteine	153-169	toll like receptor 4	Homo sapiens	75-79
27957238-6	2016	NAC led to a decrease in hydrogen peroxide (H2O2), malondialdehyde (MDA) levels, and myeloperoxidase activity.	Acetylcysteine	0-3	myeloperoxidase	Rattus norvegicus	85-100
27807451-3	2016	In this study, we determined whether this low calcium K-NAC medium with antioxidants (N-acetyl-L-cysteine and L-ascorbic acid-2-phosphate) is a better medium to grow human breast epithelial cells.	Acetylcysteine	86-105	synuclein alpha	Homo sapiens	56-59
26343184-9	2015	The observed HIF stabilization, MMP-1 expression and migration under hypoxia are dependent on increases in intracellular ROS, as these effects are attenuated by treatment with the antioxidant N-acetyl-L-cysteine.	Acetylcysteine	192-211	matrix metallopeptidase 1	Homo sapiens	32-37
26431905-11	2015	NAC decreased SIRT1 phosphorylation and formation of the autophagy marker LC3II, which resulted in an increase in the apoptosis mediators gammaH2AX and cleaved/activated caspase-3.	Acetylcysteine	0-3	sirtuin 1	Mus musculus	14-19
26498924-6	2015	Further in vitro experiments revealed that Nur77 expression was rapidly increased in the VSMCs following stimulation with PDGF and H2O2, whereas treatment with N-acetyl cysteine (NAC, a ROS scavenger) reversed the increase in the protein level of Nur77 induced by H2O2.	Acetylcysteine	160-177	nuclear receptor subfamily 4, group A, member 1	Mus musculus	247-252
26498924-6	2015	Further in vitro experiments revealed that Nur77 expression was rapidly increased in the VSMCs following stimulation with PDGF and H2O2, whereas treatment with N-acetyl cysteine (NAC, a ROS scavenger) reversed the increase in the protein level of Nur77 induced by H2O2.	Acetylcysteine	179-182	nuclear receptor subfamily 4, group A, member 1	Mus musculus	43-48
26498924-6	2015	Further in vitro experiments revealed that Nur77 expression was rapidly increased in the VSMCs following stimulation with PDGF and H2O2, whereas treatment with N-acetyl cysteine (NAC, a ROS scavenger) reversed the increase in the protein level of Nur77 induced by H2O2.	Acetylcysteine	179-182	nuclear receptor subfamily 4, group A, member 1	Mus musculus	247-252
26498383-6	2015	Antioxidant N-acetyl-cysteine (1mM) treatment prevented GSH decrease and N-cadherin and alpha-catenin up-regulation induced by MEHP.	Acetylcysteine	12-29	cadherin 2	Rattus norvegicus	73-83
29116368-10	2018	Decreased IL-10 in the LPS, MA and LPS + MA animals, and increased TNF-alpha in the LPS and MA animals, was reversed with NAC.	Acetylcysteine	122-125	interleukin 10	Rattus norvegicus	10-15
29242562-4	2017	Treatment of HCT116 cells with the oxidant tert-butyl hydroperoxide (tBHP) induced apoptosis and reduced NHLRC2 protein levels, whereas pretreatment with the antioxidant N-acetyl-L-cysteine prevented apoptosis and the decrease in NHLRC2 protein levels seen in tBHP-treated cells.	Acetylcysteine	170-189	NHL repeat containing 2	Homo sapiens	105-111
29242562-4	2017	Treatment of HCT116 cells with the oxidant tert-butyl hydroperoxide (tBHP) induced apoptosis and reduced NHLRC2 protein levels, whereas pretreatment with the antioxidant N-acetyl-L-cysteine prevented apoptosis and the decrease in NHLRC2 protein levels seen in tBHP-treated cells.	Acetylcysteine	170-189	NHL repeat containing 2	Homo sapiens	230-236
31618189-3	2017	We report a retrospective cohort study evaluating the role of N-acetylcysteine (NAC) in the development of colistin (COL) associated nephrotoxicity.	Acetylcysteine	62-78	synuclein alpha	Homo sapiens	80-83
28271166-8	2017	The adverse effects of LPS on porcine intestinal function and redox status were mitigated by NAC supplementation through the activation of multiple signaling pathways involving PI3K/Akt/mTOR, EGFR, TLR4/NF-kappaB, AMPK, and type I IFN.	Acetylcysteine	93-96	toll like receptor 4	Homo sapiens	198-202
28966297-7	2017	In addition, NAC (N-acetylcysteine, a reactive oxygen species (ROS) scavenger) treatment dramatically decreased ROS generation in H1299 cells; both of NAC and 4-PBA (4-phenylbutyrate, a specific endoplasmic reticulum (ER) stress inhibitor) administration impaired apoptosis and expression levels of ATF4, CHOP and caspase-4 in G-Rh2 incubated H1299 cells.	Acetylcysteine	18-34	synuclein alpha	Homo sapiens	13-16
28966297-7	2017	In addition, NAC (N-acetylcysteine, a reactive oxygen species (ROS) scavenger) treatment dramatically decreased ROS generation in H1299 cells; both of NAC and 4-PBA (4-phenylbutyrate, a specific endoplasmic reticulum (ER) stress inhibitor) administration impaired apoptosis and expression levels of ATF4, CHOP and caspase-4 in G-Rh2 incubated H1299 cells.	Acetylcysteine	18-34	synuclein alpha	Homo sapiens	151-154
28966297-7	2017	In addition, NAC (N-acetylcysteine, a reactive oxygen species (ROS) scavenger) treatment dramatically decreased ROS generation in H1299 cells; both of NAC and 4-PBA (4-phenylbutyrate, a specific endoplasmic reticulum (ER) stress inhibitor) administration impaired apoptosis and expression levels of ATF4, CHOP and caspase-4 in G-Rh2 incubated H1299 cells.	Acetylcysteine	18-34	Rh associated glycoprotein	Homo sapiens	329-332
28804952-8	2017	Most significantly, propofol induced apoptotic effects by decreasing Bcl-2 but increasing Bax, cleaved caspase-9/caspase-3 levels, which were partially reversed by NAC.	Acetylcysteine	164-167	caspase 9	Homo sapiens	103-112
28739487-9	2017	Notably, treatment with the ROS scavenger N-acetylcysteine (NAC) markedly blocked 27HC-induced ROS production and activation of IL-6/STAT3 signaling pathway.	Acetylcysteine	42-58	signal transducer and activator of transcription 3	Rattus norvegicus	133-138
28739487-9	2017	Notably, treatment with the ROS scavenger N-acetylcysteine (NAC) markedly blocked 27HC-induced ROS production and activation of IL-6/STAT3 signaling pathway.	Acetylcysteine	60-63	signal transducer and activator of transcription 3	Rattus norvegicus	133-138
28986255-7	2017	Analysis of mTORC2, the complex responsible for phosphorylating Akt at S473, reveals increased cysteine oxidation of Rictor in Prdx3 KD cells that can be rescued with NAC.	Acetylcysteine	167-170	RPTOR independent companion of MTOR complex 2	Homo sapiens	117-123
28807874-9	2017	N-Acetyl-l-cysteine, a ROS scavenger, abrogated the DHA-induced increases in Akt phosphorylation, Nrf2 nuclear accumulation, and OSGIN1 expression.	Acetylcysteine	0-19	oxidative stress induced growth inhibitor 1	Homo sapiens	129-135
28987348-1	2017	The electrooxidation of N-acetylcysteine (N-AC) was studied by a novel Ni(II) complex modified ZrO2 nanoparticle carbon paste electrode [Ni(II)/ZrO2/NPs/CPE] using voltammetric methods.	Acetylcysteine	24-40	carboxypeptidase E	Homo sapiens	153-156
28987348-2	2017	The results showed that Ni(II)/ZrO2/NPs/CPE had high electrocatalytic activity for the electrooxidation of N-AC in aqueous buffer solution (pH = 7.0).	Acetylcysteine	107-111	carboxypeptidase E	Homo sapiens	40-43
28987348-6	2017	Finally, Ni(II)/ZrO2/NPs/CPE was also examined as an ultrasensitive electrochemical sensor for the determination of N-AC in real samples such as tablet and urine.	Acetylcysteine	116-120	carboxypeptidase E	Homo sapiens	25-28
28979696-9	2017	In addition, the expression of Bax increased after the ACN treatment, and the induction of Bax was abolished by NAC.	Acetylcysteine	112-115	BCL2 associated X, apoptosis regulator	Rattus norvegicus	31-34
28979696-9	2017	In addition, the expression of Bax increased after the ACN treatment, and the induction of Bax was abolished by NAC.	Acetylcysteine	112-115	BCL2 associated X, apoptosis regulator	Rattus norvegicus	91-94
28814068-5	2017	The expression levels of the NLRP3-inflammasome and caspase-1 were upregulated in RAW 264.7 cells by stimulation with CSE and DEPs and were inhibited by NAC.	Acetylcysteine	153-156	NLR family, pyrin domain containing 3	Mus musculus	29-34
28814068-9	2017	NLRP3-inflammasome expression as determined by immunohistochemistry was increased by CSE and DEPs in both the normal and elastin-induced emphysema groups, and was suppressed by NAC.	Acetylcysteine	177-180	NLR family, pyrin domain containing 3	Mus musculus	0-5
28814068-10	2017	CONCLUSIONS: The NLRP3-inf lammasome is activated by DEPs in ex vivo tissue explants from elastase-induced emphysema animal model, and this activation is inhibited by NAC.	Acetylcysteine	167-170	NLR family, pyrin domain containing 3	Mus musculus	17-22
28819639-3	2017	Here, we investigated whether the glutathione precursor N-acetyl cysteine (NAC) can prevent changes in synaptic transmission at pyramidal cells and PVIs that result from developmental NMDAR blockade and how these changes are related to mitochondrial dysfunction in the PFCs of mice.	Acetylcysteine	56-73	glutamate receptor, ionotropic, NMDA1 (zeta 1)	Mus musculus	184-189
28819639-3	2017	Here, we investigated whether the glutathione precursor N-acetyl cysteine (NAC) can prevent changes in synaptic transmission at pyramidal cells and PVIs that result from developmental NMDAR blockade and how these changes are related to mitochondrial dysfunction in the PFCs of mice.	Acetylcysteine	75-78	glutamate receptor, ionotropic, NMDA1 (zeta 1)	Mus musculus	184-189
28487393-4	2017	In the present study, we postulated that NAC might cleave the VWF multimers inside occlusive thrombi, thereby leading to their dissolution and arterial recanalization.	Acetylcysteine	41-44	Von Willebrand factor	Mus musculus	62-65
28487393-10	2017	Through in vitro and in vivo experiments, we provide evidence that the molecular target underlying the thrombolytic effects of NAC is principally the VWF that cross-link platelets in arterial thrombi.	Acetylcysteine	127-130	Von Willebrand factor	Mus musculus	150-153
28505249-7	2017	More importantly, the antioxidant, oral N-acetylcysteine led to amelioration of the muscle atrophy and weakness in Gne mutant mice.	Acetylcysteine	40-56	glucosamine (UDP-N-acetyl)-2-epimerase/N-acetylmannosamine kinase	Mus musculus	115-118
27884591-8	2017	The antioxidant drug, NAC also reduced the TSLP-production in fibroblasts stimulated with poly(I:C).	Acetylcysteine	22-25	thymic stromal lymphopoietin	Homo sapiens	43-47
28394319-11	2017	We found Hcy-induced NLRP3 inflammasome activation was abolished by NAC.	Acetylcysteine	68-71	NLR family, pyrin domain containing 3	Mus musculus	21-26
28394319-12	2017	Treatment with NAC in HHcy mice also suppressed NLRP3 inflammasome activation and improved HHcy-induced atherosclerosis.	Acetylcysteine	15-18	NLR family, pyrin domain containing 3	Mus musculus	48-53
28353032-11	2017	Co-treatment with N-acetyl-L-cysteine was sufficient to attenuate and abolish the alpha-Syn x Cd-induced cytotoxicity.	Acetylcysteine	18-37	synuclein alpha	Homo sapiens	82-91
28499986-11	2017	The decrease in SYN, MAP2 and GFAP expressions were also prevented by NAC and PHY treatments.	Acetylcysteine	70-73	glial fibrillary acidic protein	Mus musculus	30-34
28163174-8	2017	The areas positive for both C4bp and C3d were increased in the presence of N-acetylcysteine.	Acetylcysteine	75-91	endogenous retrovirus group K member 13	Homo sapiens	37-40
28108410-7	2017	The antioxidant, N-acetyl-l-cysteine, significantly ameliorated all of these endothelial injuries caused by A/R, suggesting that antioxidant activities might play a key role in PSG-1-induced endothelial protection.	Acetylcysteine	17-36	pregnancy specific beta-1-glycoprotein 1	Homo sapiens	177-182
27943387-5	2017	Results showed that ovariectomy resulted in bone loss with increased osteoclast surface, increased ROS levels, T cell activation, and increased TNF and RANKL levels in serum and in CD4 T cells; NAC supplementation largely prevented these alterations.	Acetylcysteine	194-197	tumor necrosis factor (ligand) superfamily, member 11	Mus musculus	152-157
28335600-8	2017	The study found that the morphology as well as the expression of microgliosis marker Iba-1 of the cells treated with NAC-NPs and LPS were close to those of control cells, indicating that NAC-NPs can inhibit the activation of microglia stimulated by LPS.	Acetylcysteine	117-120	allograft inflammatory factor 1	Homo sapiens	85-90
28335600-8	2017	The study found that the morphology as well as the expression of microgliosis marker Iba-1 of the cells treated with NAC-NPs and LPS were close to those of control cells, indicating that NAC-NPs can inhibit the activation of microglia stimulated by LPS.	Acetylcysteine	187-190	allograft inflammatory factor 1	Homo sapiens	85-90
28529596-8	2017	N-acetyl cysteine prevented andrographolide-mediated DR5 induction and the apoptotic effect induced by the combination of rhTRAIL and andrographolide.	Acetylcysteine	0-17	TNF receptor superfamily member 10b	Homo sapiens	53-56
28496415-9	2017	The intracellular Ca2+ responses to both CSE types were also totally prevented by NAC, AMTB (a TRPM8 antagonist), or EGTA (an extracellular Ca2+ chelator).	Acetylcysteine	82-85	choreoathetosis/spasticity, episodic (paroxysmal choreoathetosis/spasticity)	Homo sapiens	41-44
28496415-10	2017	The activation of the MAPK/NF-kappaB signaling and induction of IL-8 to both CSE types were suppressed to similar levels by NAC, AMTB, or EGTA.	Acetylcysteine	124-127	choreoathetosis/spasticity, episodic (paroxysmal choreoathetosis/spasticity)	Homo sapiens	77-80
28469982-9	2017	No early antioxidant action of 17beta-E2 has been found but the estrogen effect is similar to N-acetylcysteine which, by increasing the intracellular redox state, maintains JNK bound to GSTP1-1.	Acetylcysteine	94-110	glutathione S-transferase, pi 1	Mus musculus	186-193
27770431-4	2017	Plasma from patients treated with acetylcysteine (NAC) for a single APAP overdose was analyzed from discovery (n = 116) and validation (n = 150) patient cohorts.	Acetylcysteine	34-48	synuclein alpha	Homo sapiens	50-53
28187322-7	2017	N-acetylcysteine prevented the aspartame-induced liver injury and the increase in plasma ALT activity as well as the decrease in GSH, gamma-GC, cysteine, SAM and SAH levels and GCLc protein levels.	Acetylcysteine	0-16	glutamic pyruvic transaminase, soluble	Mus musculus	89-92
28223539-10	2017	Furthermore, H2O2 treatment increased the phosphorylation of p65 and IkappaBalpha, which were decreased when treated with N-acetyl cysteine or thymol.	Acetylcysteine	122-139	v-rel reticuloendotheliosis viral oncogene homolog A (avian)	Mus musculus	61-64
28011677-7	2017	This in vivo finding was supported by in vitro data demonstrating the VWF multimer-reducing properties of NAC in solution.	Acetylcysteine	106-109	Von Willebrand factor	Mus musculus	70-73
28011677-9	2017	Failure to improve clinical outcome occurred even though a reduction in VWF multimers was observed, demonstrating that NAC was efficient in reducing disulfide bonds in circulating VWF multimers.	Acetylcysteine	119-122	Von Willebrand factor	Mus musculus	72-75
28011677-9	2017	Failure to improve clinical outcome occurred even though a reduction in VWF multimers was observed, demonstrating that NAC was efficient in reducing disulfide bonds in circulating VWF multimers.	Acetylcysteine	119-122	Von Willebrand factor	Mus musculus	180-183
27654302-7	2017	Meanwhile, fucoidan treatment increased the generation of intracellular ROS, whereas the over-elimination of ROS by N-acetylcysteine, an anti-oxidant, attenuated fucoidan-induced apoptosis, inhibition of hTERT, c-myc, and Sp1 expression, and reversed fucoidan-induced inactivation of the PI3K/Akt signaling pathway.	Acetylcysteine	116-132	telomerase reverse transcriptase	Homo sapiens	204-209
27654302-7	2017	Meanwhile, fucoidan treatment increased the generation of intracellular ROS, whereas the over-elimination of ROS by N-acetylcysteine, an anti-oxidant, attenuated fucoidan-induced apoptosis, inhibition of hTERT, c-myc, and Sp1 expression, and reversed fucoidan-induced inactivation of the PI3K/Akt signaling pathway.	Acetylcysteine	116-132	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	211-216
27886758-2	2017	In this study, we report the recognition of tyrosine (Tyr) enantiomers by chiral N-acetyl-L-cysteine (L-NAC) capped CdSe/CdS quantum dots (QDs) under alkaline experimental condition.	Acetylcysteine	81-100	synuclein alpha	Homo sapiens	104-107
28116245-6	2017	Pre-incubation of the cells with NAC suppressed the 7KCHO-induced upregulation of CHOP, but not GRP78.	Acetylcysteine	33-36	DNA-damage inducible transcript 3	Mus musculus	82-86
27514995-5	2016	Efficiency of NAC administration was evaluated by following outcome parameters: cell viability, apoptosis rate, anabolic/catabolic gene expression, secretion and activity of matrix metalloproteinases (MMPs) and proteoglycan (PG) release.	Acetylcysteine	14-17	matrix metallopeptidase 1	Homo sapiens	201-205
27514995-9	2016	Moreover, NAC inhibited proteolytic activity of MMPs and reduced PG release.	Acetylcysteine	10-13	matrix metallopeptidase 1	Homo sapiens	48-52
27742673-5	2016	Notably, treatment with the antioxidant N-acetyl cysteine (NAC) significantly reduced upregulation of the DNA damage marker gammaH2AX, subsequent ATM activation, and cell death.	Acetylcysteine	40-57	ATM serine/threonine kinase	Homo sapiens	146-149
27742673-5	2016	Notably, treatment with the antioxidant N-acetyl cysteine (NAC) significantly reduced upregulation of the DNA damage marker gammaH2AX, subsequent ATM activation, and cell death.	Acetylcysteine	59-62	ATM serine/threonine kinase	Homo sapiens	146-149
27633119-7	2016	Finally, we found that pretreatment with NAC prevented the JNK, p53, caspase-9 and -3 protein phosphorylation induced by the polysaccharide, however, pretreatment with SP600125 did not affect the generation of ROS, suggesting that ROS is upstream of JNK.	Acetylcysteine	41-44	caspase 9	Homo sapiens	69-85
27557522-6	2016	In addition, Ca2+ levels and the expression of the Ca2+ channels, RyR1, SERCA, CACNA1S, TRPC1, and TRPC3 were recovered to normal levels by N-acetyl-L-cysteine (NAC) treatment compared with SelW knockdown cells.	Acetylcysteine	140-159	ryanodine receptor 1	Gallus gallus	66-70
27557522-6	2016	In addition, Ca2+ levels and the expression of the Ca2+ channels, RyR1, SERCA, CACNA1S, TRPC1, and TRPC3 were recovered to normal levels by N-acetyl-L-cysteine (NAC) treatment compared with SelW knockdown cells.	Acetylcysteine	140-159	ATPase sarcoplasmic/endoplasmic reticulum Ca2+ transporting 3	Gallus gallus	72-77
27557522-6	2016	In addition, Ca2+ levels and the expression of the Ca2+ channels, RyR1, SERCA, CACNA1S, TRPC1, and TRPC3 were recovered to normal levels by N-acetyl-L-cysteine (NAC) treatment compared with SelW knockdown cells.	Acetylcysteine	140-159	calcium voltage-gated channel subunit alpha1 S	Gallus gallus	79-86
27557522-6	2016	In addition, Ca2+ levels and the expression of the Ca2+ channels, RyR1, SERCA, CACNA1S, TRPC1, and TRPC3 were recovered to normal levels by N-acetyl-L-cysteine (NAC) treatment compared with SelW knockdown cells.	Acetylcysteine	161-164	ryanodine receptor 1	Gallus gallus	66-70
27557522-6	2016	In addition, Ca2+ levels and the expression of the Ca2+ channels, RyR1, SERCA, CACNA1S, TRPC1, and TRPC3 were recovered to normal levels by N-acetyl-L-cysteine (NAC) treatment compared with SelW knockdown cells.	Acetylcysteine	161-164	ATPase sarcoplasmic/endoplasmic reticulum Ca2+ transporting 3	Gallus gallus	72-77
27557522-6	2016	In addition, Ca2+ levels and the expression of the Ca2+ channels, RyR1, SERCA, CACNA1S, TRPC1, and TRPC3 were recovered to normal levels by N-acetyl-L-cysteine (NAC) treatment compared with SelW knockdown cells.	Acetylcysteine	161-164	calcium voltage-gated channel subunit alpha1 S	Gallus gallus	79-86
27363620-11	2016	Body temperature in animals treated with anti-IL-10+NAC/LPS was 38.28+-0.12 C vs. 37.73+-0.06 C in IgG+NAC/LPS rats (p&lt;0.001) and 38.31+-0.20 C in NaCl/LPS-treated animals (n.s.).	Acetylcysteine	103-106	interleukin 10	Rattus norvegicus	46-51
27363620-12	2016	Based on these data, we conclude that NAC acts as an antipyretic via IL-10 stimulation.	Acetylcysteine	38-41	interleukin 10	Rattus norvegicus	69-74
27235905-8	2016	NAC also decreased malonaldehyde (MDA) in liver, increased glutathione S-transferase (GST) activity in plasma, up-regulated mRNA expression of Superoxide dismutase (SOD) and GPx in liver and headkidney.	Acetylcysteine	0-3	superoxide dismutase [Mn], mitochondrial	Oreochromis niloticus	143-163
27235905-8	2016	NAC also decreased malonaldehyde (MDA) in liver, increased glutathione S-transferase (GST) activity in plasma, up-regulated mRNA expression of Superoxide dismutase (SOD) and GPx in liver and headkidney.	Acetylcysteine	0-3	superoxide dismutase [Mn], mitochondrial	Oreochromis niloticus	165-168
27071802-6	2016	Further study revealed that N-acetyl cysteine (NAC) markedly prevented Cd-induced proliferation of MRC-5 cells, ROS generation, and the increasing protein level of HMGA2.	Acetylcysteine	28-45	high mobility group AT-hook 2	Homo sapiens	164-169
27071802-6	2016	Further study revealed that N-acetyl cysteine (NAC) markedly prevented Cd-induced proliferation of MRC-5 cells, ROS generation, and the increasing protein level of HMGA2.	Acetylcysteine	47-50	high mobility group AT-hook 2	Homo sapiens	164-169
27005845-6	2016	Furthermore, we found that these inhibitory effects of SSBb were associated with reduced reactive oxygen species (ROS) because pretreating cells with N-acetyl-L-cysteine and NADPH oxidase inhibitor diphenyleneiodonium (DPI) inhibited LPS-induced TLR4 recruitment into lipid rafts and NF-kappaB activation.	Acetylcysteine	150-169	toll like receptor 4	Homo sapiens	246-250
27108714-2	2016	Currently, the antidote acetylcysteine (NAC) is administered at a dose determined only by body weight without regard for the body burden of paracetamol.	Acetylcysteine	24-38	synuclein alpha	Homo sapiens	40-43
26968795-7	2016	In addition, the PI-mediated induction of HO-1 was abolished by N-acetyl-l-cysteine and rotenone.	Acetylcysteine	64-83	heme oxygenase 1	Homo sapiens	42-46
27084536-9	2016	Interestingly, pretreatment of MB cells with NAC or the pan-caspase inhibitor zVAD-fmk abrogated TQ-induced apoptosis, loss of cyclin B1 and NF-kappaB activity, suggesting that these TQ-mediated effects are oxidative stress- and caspase-dependent.	Acetylcysteine	45-48	cyclin B1	Homo sapiens	127-136
26945724-7	2016	To elucidate these findings, it was found that PEITC-induced HO-1 upregulation can be inhibited with thiol antioxidants (glutathione and N-acetylcysteine).	Acetylcysteine	137-153	heme oxygenase 1	Homo sapiens	61-65
26923123-6	2016	NAC preconditioning improved cell viability, decreased lactate dehydrogenase release, beta-galactosidase activity, and Annexin-V-positive cells.	Acetylcysteine	0-3	galactosidase, beta 1	Mus musculus	86-104
26908203-0	2016	Induction of IL-8(CXCL8) and MCP-1(CCL2) with oxidative stress and its inhibition with N-acetyl cysteine (NAC) in cell culture model using HK-2 cell.	Acetylcysteine	106-109	C-C motif chemokine ligand 2	Homo sapiens	35-39
26908203-12	2016	Pre-incubation of the cells with the anti-oxidant N-acetyl cysteine (NAC) strongly suppressed the induction of both IL-8 and MCP-1 when stimulated with hydrogen peroxide and IL-1beta.	Acetylcysteine	50-67	C-C motif chemokine ligand 2	Homo sapiens	125-130
26908203-12	2016	Pre-incubation of the cells with the anti-oxidant N-acetyl cysteine (NAC) strongly suppressed the induction of both IL-8 and MCP-1 when stimulated with hydrogen peroxide and IL-1beta.	Acetylcysteine	69-72	C-C motif chemokine ligand 2	Homo sapiens	125-130
26844631-8	2016	Pretreatment with N-acetyl-L-cysteine, a reactive oxygen species scavenger, and cyanidem-chlorophenylhydrazone, an uncoupler of OXPHOS, suppressed CTRP3-induced ROS production, PGC-1alpha expression and ATP synthesis.	Acetylcysteine	18-37	PPARG coactivator 1 alpha	Sus scrofa	177-187
26851027-4	2016	The specificity of ROS-mediated ATM-JNK activation was confirmed by treatment with N-acetylcysteine, a ROS scavenger.	Acetylcysteine	83-99	ATM serine/threonine kinase	Homo sapiens	32-35
26724531-11	2016	The farnesylation inhibitors pravastatin and FTI-277, or the antioxidant N-acetyl cysteine, partly restored ZMPSTE24 expression, and concomitantly decreased oxidative stress, inflammation, senescence, and calcification of PI-treated VSCMs.	Acetylcysteine	73-90	zinc metallopeptidase STE24	Homo sapiens	108-116
26719856-5	2016	We demonstrated that high glucose levels induced the production of reactive oxygen species (ROS) in MC3T3-E1 cells, and this production was inhibited by treatment with uncarboxylated osteocalcin and N-acetyl-L-cysteine (NAC), a ROS scavenger.	Acetylcysteine	220-223	bone gamma-carboxyglutamate protein 2	Mus musculus	183-194
26783539-6	2016	N-Acetylcysteine remarkably increased cardiac p-STAT3 which was further enhanced by sevo-postC.	Acetylcysteine	0-16	signal transducer and activator of transcription 3	Rattus norvegicus	48-53
26783539-9	2016	N-Acetylcysteine restored Sevo-postC cardioprotection in diabetes possibly through enhancing cardiac p-STAT3 and adiponectin and reducing Fox1 and CD36.	Acetylcysteine	0-16	signal transducer and activator of transcription 3	Rattus norvegicus	103-108
26895214-8	2016	PDTC and NAC markedly decreased the protein expression of IL-1beta (p &lt; 0.01) and increased the protein expression of DIO1 (p &lt; 0.01), respectively.	Acetylcysteine	9-12	iodothyronine deiodinase 1	Rattus norvegicus	121-125
26407525-7	2015	Inhibition of ROS generation by the antioxidant N-acetylcysteine (NAC) restored a normal expression level of p53.	Acetylcysteine	48-64	transformation related protein 53, pseudogene	Mus musculus	109-112
26407525-7	2015	Inhibition of ROS generation by the antioxidant N-acetylcysteine (NAC) restored a normal expression level of p53.	Acetylcysteine	66-69	transformation related protein 53, pseudogene	Mus musculus	109-112
26694382-3	2015	N-acetyl-l-cysteine (the active form) (NAC) is being studied in diseases characterized by increased OS or decreased glutathione (GSH) level.	Acetylcysteine	0-19	synuclein alpha	Homo sapiens	39-42
26674585-0	2015	Effect of oral N-acetylcysteine on COPD patients with microsatellite polymorphism in the heme oxygenase-1 gene promoter.	Acetylcysteine	15-31	heme oxygenase 1	Homo sapiens	89-105
26670322-7	2015	In addition, the induction of HO-1 was also confirmed in normal fibroblasts following incubation with 10-100 micromol/L NAC for 4 h. RESULTS: Following NAC therapy we observed an increase in expression of the antioxidants HO-1 (~4-fold) and its effector ferritin (~160-fold) in patient samples as compared with baseline.	Acetylcysteine	120-123	heme oxygenase 1	Homo sapiens	30-34
26670322-7	2015	In addition, the induction of HO-1 was also confirmed in normal fibroblasts following incubation with 10-100 micromol/L NAC for 4 h. RESULTS: Following NAC therapy we observed an increase in expression of the antioxidants HO-1 (~4-fold) and its effector ferritin (~160-fold) in patient samples as compared with baseline.	Acetylcysteine	120-123	heme oxygenase 1	Homo sapiens	222-226
26670322-7	2015	In addition, the induction of HO-1 was also confirmed in normal fibroblasts following incubation with 10-100 micromol/L NAC for 4 h. RESULTS: Following NAC therapy we observed an increase in expression of the antioxidants HO-1 (~4-fold) and its effector ferritin (~160-fold) in patient samples as compared with baseline.	Acetylcysteine	152-155	heme oxygenase 1	Homo sapiens	30-34
26670322-7	2015	In addition, the induction of HO-1 was also confirmed in normal fibroblasts following incubation with 10-100 micromol/L NAC for 4 h. RESULTS: Following NAC therapy we observed an increase in expression of the antioxidants HO-1 (~4-fold) and its effector ferritin (~160-fold) in patient samples as compared with baseline.	Acetylcysteine	152-155	heme oxygenase 1	Homo sapiens	222-226
26670322-8	2015	We also observed that NAC exposure significantly increased HO-1 expression in fibroblasts.	Acetylcysteine	22-25	heme oxygenase 1	Homo sapiens	59-63
26670322-9	2015	CONCLUSION: Our data suggest that HO-1 is a possible target protein of NAC and a mediator of its cytoprotective effects in these patients.	Acetylcysteine	71-74	heme oxygenase 1	Homo sapiens	34-38
26436984-7	2015	In the presence of TAC, scavenging of reactive oxygen species with N-acetylcysteine reduced eNOS S-glutathionylation, eNOS monomer and NOS-dependent superoxide levels in eNOS-Tg mice to wildtype levels.	Acetylcysteine	67-83	nitric oxide synthase 3, endothelial cell	Mus musculus	92-96
26436984-7	2015	In the presence of TAC, scavenging of reactive oxygen species with N-acetylcysteine reduced eNOS S-glutathionylation, eNOS monomer and NOS-dependent superoxide levels in eNOS-Tg mice to wildtype levels.	Acetylcysteine	67-83	nitric oxide synthase 3, endothelial cell	Mus musculus	118-122
26436984-7	2015	In the presence of TAC, scavenging of reactive oxygen species with N-acetylcysteine reduced eNOS S-glutathionylation, eNOS monomer and NOS-dependent superoxide levels in eNOS-Tg mice to wildtype levels.	Acetylcysteine	67-83	nitric oxide synthase 3, endothelial cell	Mus musculus	118-122
26436984-8	2015	Accordingly, N-acetylcysteine improved cardiac function in eNOS-Tg but not in wildtype mice with TAC.	Acetylcysteine	13-29	nitric oxide synthase 3, endothelial cell	Mus musculus	59-63
26680088-6	2015	RESULTS: NAC, ATOR, and NAC+ATOR in rats showed lower MPO (P &lt; .05) and higher GPx activity (P &lt; .05) versus control; SOD activity was lower in NAC versus ATOR (P &lt; .05).	Acetylcysteine	9-12	myeloperoxidase	Rattus norvegicus	54-57
26680088-6	2015	RESULTS: NAC, ATOR, and NAC+ATOR in rats showed lower MPO (P &lt; .05) and higher GPx activity (P &lt; .05) versus control; SOD activity was lower in NAC versus ATOR (P &lt; .05).	Acetylcysteine	24-27	myeloperoxidase	Rattus norvegicus	54-57
26680088-6	2015	RESULTS: NAC, ATOR, and NAC+ATOR in rats showed lower MPO (P &lt; .05) and higher GPx activity (P &lt; .05) versus control; SOD activity was lower in NAC versus ATOR (P &lt; .05).	Acetylcysteine	24-27	myeloperoxidase	Rattus norvegicus	54-57
26341012-12	2015	Plumbagin increased TrxR-1 and heme oxygenase (HO)-1 expression and pretreatment with NAC significantly attenuated the plumbagin-induced increase of TrxR-1 and HO-1 expression in HepG2 cells, LLC cells and SiHa cells.	Acetylcysteine	86-89	heme oxygenase 1	Homo sapiens	160-164
26408691-4	2015	Treatment of tumor cells with the antioxidant N-acetylcysteine was able to prevent Zn(2+)-induced apoptosis, as well as the increase of p53 and FAS ligand protein induced by zinc.	Acetylcysteine	46-62	Fas ligand	Homo sapiens	144-154
26622517-9	2015	Pretreatment of H9c2 cells with N-acetyl-L-cysteine (NAC), a scavenger of ROS, prior to exposure to DOX dramatically increased the phosphorylation of FoxO3a and led to a marked reduction in Prx III expression in the H9c2 cells.	Acetylcysteine	32-51	peroxiredoxin 3	Rattus norvegicus	190-197
26622517-9	2015	Pretreatment of H9c2 cells with N-acetyl-L-cysteine (NAC), a scavenger of ROS, prior to exposure to DOX dramatically increased the phosphorylation of FoxO3a and led to a marked reduction in Prx III expression in the H9c2 cells.	Acetylcysteine	53-56	peroxiredoxin 3	Rattus norvegicus	190-197
26296767-5	2015	The HCV-induced increase in the Bim mRNA and protein levels was significantly counteracted by treatment with NAC or SP600125, suggesting that the ROS/JNK signalling pathway is involved in Bim upregulation.	Acetylcysteine	109-112	BCL2 like 11	Homo sapiens	32-35
26296767-5	2015	The HCV-induced increase in the Bim mRNA and protein levels was significantly counteracted by treatment with NAC or SP600125, suggesting that the ROS/JNK signalling pathway is involved in Bim upregulation.	Acetylcysteine	109-112	BCL2 like 11	Homo sapiens	188-191
26116162-10	2015	The inhibitory effects of celastrol on LPS binding to MD2 were reversed by thiol donors (N-acetyl-L-cysteine and dithiothreitol), suggesting that the thiol reactivity of celastrol contributes to its inhibitory effects on TLR4 activation in macrophages.	Acetylcysteine	89-108	lymphocyte antigen 96	Mus musculus	54-57
26093296-3	2015	In this study, we found that angiotensin II dose-dependently increased the expression of Col1a1, Col3a1 and alpha-smooth muscle actin, which were blocked by ROS (reactive oxygen species) scavenger N-acetyl cysteine (NAC).	Acetylcysteine	197-214	collagen type III alpha 1 chain	Homo sapiens	97-103
26093296-3	2015	In this study, we found that angiotensin II dose-dependently increased the expression of Col1a1, Col3a1 and alpha-smooth muscle actin, which were blocked by ROS (reactive oxygen species) scavenger N-acetyl cysteine (NAC).	Acetylcysteine	216-219	collagen type III alpha 1 chain	Homo sapiens	97-103
25940980-6	2015	Among potential lifespan-promoting substances, mannose-binding lectin and N-acetylcysteine were found to increase daf-16 expression.	Acetylcysteine	74-90	Fork-head domain-containing protein;Forkhead box protein O	Caenorhabditis elegans	114-120
26218392-0	2015	Effect of N-Acetylcysteine on Adipose-Derived Stem Cell and Autologous Fat Graft Survival in a Mouse Model.	Acetylcysteine	10-26	WD and tetratricopeptide repeats 1	Mus musculus	30-37
26218392-2	2015	The authors examined whether a widely available, clinically safe antioxidant, N-acetylcysteine, could improve adipose-derived stem cell survival and graft take when added to tumescent solution during fat harvest.	Acetylcysteine	78-94	WD and tetratricopeptide repeats 1	Mus musculus	110-117
26218392-7	2015	RESULTS: In culture, N-acetylcysteine protected adipose-derived stem cells from oxidative stress and improved cell survival following hydrogen peroxide treatment.	Acetylcysteine	21-37	WD and tetratricopeptide repeats 1	Mus musculus	48-55
26218392-8	2015	Combined exposure to both N-acetylcysteine and hydrogen peroxide led to a 200-fold increase in adipose-derived stem cell proliferation, significantly higher than with either agent alone.	Acetylcysteine	26-42	WD and tetratricopeptide repeats 1	Mus musculus	95-102
26218392-9	2015	N-Acetylcysteine decreased differentiation of adipose-derived stem cells into mature adipocytes, as evidenced by decreased transcription of adipocyte differentiation markers and reduced Oil Red-O staining.	Acetylcysteine	0-16	WD and tetratricopeptide repeats 1	Mus musculus	46-53
26114584-3	2015	Consistent with TAK1 inhibition being causally related to thiol-mediated oxidative stress, 10mM N-acetylcysteine (NAC) partially reversed the growth inhibitory effects of 5Z-7-oxozeaenol.	Acetylcysteine	96-112	mitogen-activated protein kinase kinase kinase 7	Homo sapiens	16-20
26114584-3	2015	Consistent with TAK1 inhibition being causally related to thiol-mediated oxidative stress, 10mM N-acetylcysteine (NAC) partially reversed the growth inhibitory effects of 5Z-7-oxozeaenol.	Acetylcysteine	114-117	mitogen-activated protein kinase kinase kinase 7	Homo sapiens	16-20
26057728-7	2015	We identified enhancement of STAT1 activity as a potential strategy to treat EGFR-hyperactive cancers and PTEN as a target of the antioxidant, N-acetylcysteine.	Acetylcysteine	143-159	phosphatase and tensin homolog	Homo sapiens	106-110
26122524-9	2015	Expression levels of mature brain-derived neurotrophic factor (BDNF) and phosphorylated cAMP response element binding protein (CREB) were significantly enhanced by treatment with either PMC-12 or NAC.	Acetylcysteine	196-199	brain derived neurotrophic factor	Mus musculus	28-61
26122524-9	2015	Expression levels of mature brain-derived neurotrophic factor (BDNF) and phosphorylated cAMP response element binding protein (CREB) were significantly enhanced by treatment with either PMC-12 or NAC.	Acetylcysteine	196-199	brain derived neurotrophic factor	Mus musculus	63-67
26104799-14	2015	N-acetyl-cysteine, a scavenger of reactive oxygen species (ROS), inhibited Cu(II)-Abeta-elicited microglial release of TNF-alpha and nitric oxide as well as the microglia-mediated neurotoxic effect.	Acetylcysteine	0-17	amyloid beta (A4) precursor protein	Mus musculus	82-87
26073647-9	2015	Experiments using HepG2 cells and N-acetylcysteine-pretreated mice showed a discernible effect of IGFBP-3 on reactive oxygen species generation.	Acetylcysteine	34-50	insulin-like growth factor binding protein 3	Mus musculus	98-105
26018652-10	2015	Inhibition of intracellular ROS production by N-acetyl-L-cysteine (NAC) can alleviate NF-kappaB activation and restore the insulin secretion mediated by FTO overexpression.	Acetylcysteine	46-65	fat mass and obesity associated	Mus musculus	153-156
26018652-10	2015	Inhibition of intracellular ROS production by N-acetyl-L-cysteine (NAC) can alleviate NF-kappaB activation and restore the insulin secretion mediated by FTO overexpression.	Acetylcysteine	67-70	fat mass and obesity associated	Mus musculus	153-156
26008229-8	2015	The up-regulation of annexin-V-binding following nelfinavir treatment was significantly blunted, but not abolished by either addition of the antioxidant N-acetylcysteine (1 mM) or removal of extracellular Ca2+.	Acetylcysteine	153-169	annexin A5	Homo sapiens	21-30
24612076-0	2015	Glutamate transporter GLT-1 mediates N-acetylcysteine inhibition of cocaine reinstatement.	Acetylcysteine	37-53	solute carrier family 1 member 3	Rattus norvegicus	0-21
24756473-4	2015	RESULTS: GSH supplementation with 2 mM N-acetyl cysteine (NAC) or 0.1 mM ursodeoxycholic acid (UDCA) increased the viability, GSH level and the GSH-dependent glyoxalase I activity in 50 mM glucose-treated VL-17A cells.	Acetylcysteine	39-56	glyoxalase I	Homo sapiens	158-170
24756473-4	2015	RESULTS: GSH supplementation with 2 mM N-acetyl cysteine (NAC) or 0.1 mM ursodeoxycholic acid (UDCA) increased the viability, GSH level and the GSH-dependent glyoxalase I activity in 50 mM glucose-treated VL-17A cells.	Acetylcysteine	58-61	glyoxalase I	Homo sapiens	158-170
25607831-8	2015	Pretreatment with N-acetyl-cysteine (NAC), the inhibitor of ROS, or with SP600125, the inhibitor of JNK, prevented the apoptosis and the high expression of p-JNK, p53, caspase-9 and caspase-3 in CDK5RAP1-deficient MCF-7 cells.	Acetylcysteine	18-35	caspase 9	Homo sapiens	168-177
25607831-8	2015	Pretreatment with N-acetyl-cysteine (NAC), the inhibitor of ROS, or with SP600125, the inhibitor of JNK, prevented the apoptosis and the high expression of p-JNK, p53, caspase-9 and caspase-3 in CDK5RAP1-deficient MCF-7 cells.	Acetylcysteine	37-40	caspase 9	Homo sapiens	168-177
25226206-8	2015	Treatment of mESCs with AA and NAC led to a dose-dependent decrease in Sox17 and Foxa2 expression.	Acetylcysteine	31-34	SRY (sex determining region Y)-box 17	Mus musculus	71-76
25096201-9	2015	NAC significantly protected against MDMA-induced apoptosis and the up- and down-regulation of Bax and Bcl-2, respectively.	Acetylcysteine	0-3	BCL2 associated X, apoptosis regulator	Rattus norvegicus	94-97
25176316-8	2015	Moreover, inhibition of oxLDL uptake and subsequent redox signalling by anti-CD36 and anti-LOX-1 receptor antibodies and by N-acetylcysteine, respectively, blocked SPHK1 activation and tube formation.	Acetylcysteine	124-140	sphingosine kinase 1	Homo sapiens	164-169
25256574-5	2015	NAC led to STAT5 dephosphorylation and cell apoptosis at clinically achievable concentrations in DND-41 cells, and Ba/F3 cells transformed by an IL7R-mutant construct containing a cysteine insertion.	Acetylcysteine	0-3	signal transducer and activator of transcription 5A	Homo sapiens	11-16
25256574-6	2015	The apoptotic effects of NAC could be rescued in part by a constitutively active allele of STAT5.	Acetylcysteine	25-28	signal transducer and activator of transcription 5A	Homo sapiens	91-96
25463279-11	2015	Moreover, TNF-alpha-enhanced IKK-beta activity was also inhibited by (polyethylene glycol) PEG-catalase, N-acetylcysteine (NAC), and vitamin E. In conclusion, these results suggest that AR reduces VCAM-1 and ICAM-1 expression through NADPH oxidase-dependent IKK/NF-kappaB pathways in TNF-alpha-induced HUVECs, which finally suppress monocyte-HUVECs adhesion.	Acetylcysteine	105-121	inhibitor of nuclear factor kappa B kinase subunit beta	Homo sapiens	29-37
25463279-11	2015	Moreover, TNF-alpha-enhanced IKK-beta activity was also inhibited by (polyethylene glycol) PEG-catalase, N-acetylcysteine (NAC), and vitamin E. In conclusion, these results suggest that AR reduces VCAM-1 and ICAM-1 expression through NADPH oxidase-dependent IKK/NF-kappaB pathways in TNF-alpha-induced HUVECs, which finally suppress monocyte-HUVECs adhesion.	Acetylcysteine	123-126	inhibitor of nuclear factor kappa B kinase subunit beta	Homo sapiens	29-37
25302047-5	2014	In human and mouse cells that are deficient in p53, the frequency of MN-gamma-H2AX (+) is significantly elevated, but can be attenuated by antioxidant N-acetylcysteine (NAC).	Acetylcysteine	151-167	transformation related protein 53, pseudogene	Mus musculus	47-50
25302047-5	2014	In human and mouse cells that are deficient in p53, the frequency of MN-gamma-H2AX (+) is significantly elevated, but can be attenuated by antioxidant N-acetylcysteine (NAC).	Acetylcysteine	169-172	transformation related protein 53, pseudogene	Mus musculus	47-50
25305669-22	2014	Despite diminishing ABCA-1, NAC increases ABCG-1 that counteracts the reduction in apo A-I-mediated cholesterol efflux.	Acetylcysteine	28-31	apolipoprotein A1	Rattus norvegicus	83-90
25063220-3	2014	Treatment with Ang IIinduced RANKL expression in a dose- and time-dependent manner in osteoblasts, which was attenuated by pre-treatment with an AT1 receptor antagonist (olmesartan), ROS scavenger (N-acetylcysteine, NAC), or the ERK inhibitor (U0126), but not with AT2R antagonist (PD123319).	Acetylcysteine	198-214	tumor necrosis factor (ligand) superfamily, member 11	Mus musculus	29-34
24894197-2	2014	We previously found that antioxidant administration (N-acetylcysteine) in the Nkx3.1 knockout mouse model promoted prostate epithelial proliferation, suggesting that NKX3.1 activity modifies the effect of antioxidant administration on prostate carcinogenesis.	Acetylcysteine	53-69	NK3 homeobox 1	Mus musculus	78-84
24894197-2	2014	We previously found that antioxidant administration (N-acetylcysteine) in the Nkx3.1 knockout mouse model promoted prostate epithelial proliferation, suggesting that NKX3.1 activity modifies the effect of antioxidant administration on prostate carcinogenesis.	Acetylcysteine	53-69	NK3 homeobox 1	Mus musculus	166-172
24628121-5	2014	Pre-treatment with the antioxidant N-Acetyl-L-Cysteine (NAC) resulted in a significant inhibition in PAF-induced enhancement of CK2 activity, phosphorylation and protein expression in vivo as well as in vitro.	Acetylcysteine	35-54	PCNA clamp associated factor	Homo sapiens	101-104
24628121-5	2014	Pre-treatment with the antioxidant N-Acetyl-L-Cysteine (NAC) resulted in a significant inhibition in PAF-induced enhancement of CK2 activity, phosphorylation and protein expression in vivo as well as in vitro.	Acetylcysteine	56-59	PCNA clamp associated factor	Homo sapiens	101-104
24974374-6	2014	To investigate whether mustard feeding is coupled with evolution in the mercapturic acid pathway, we profiled functional and molecular evolutionary changes in the enzyme glutathione S-transferase D1 (GSTD1), which catalyzes the first step of the mercapturic acid pathway and is induced by mustard defense products in Scaptomyza.	Acetylcysteine	72-88	Glutathione S transferase D1	Drosophila melanogaster	170-198
24974374-6	2014	To investigate whether mustard feeding is coupled with evolution in the mercapturic acid pathway, we profiled functional and molecular evolutionary changes in the enzyme glutathione S-transferase D1 (GSTD1), which catalyzes the first step of the mercapturic acid pathway and is induced by mustard defense products in Scaptomyza.	Acetylcysteine	72-88	Glutathione S transferase D1	Drosophila melanogaster	200-205
24974374-6	2014	To investigate whether mustard feeding is coupled with evolution in the mercapturic acid pathway, we profiled functional and molecular evolutionary changes in the enzyme glutathione S-transferase D1 (GSTD1), which catalyzes the first step of the mercapturic acid pathway and is induced by mustard defense products in Scaptomyza.	Acetylcysteine	246-262	Glutathione S transferase D1	Drosophila melanogaster	170-198
24974374-6	2014	To investigate whether mustard feeding is coupled with evolution in the mercapturic acid pathway, we profiled functional and molecular evolutionary changes in the enzyme glutathione S-transferase D1 (GSTD1), which catalyzes the first step of the mercapturic acid pathway and is induced by mustard defense products in Scaptomyza.	Acetylcysteine	246-262	Glutathione S transferase D1	Drosophila melanogaster	200-205
24732633-7	2014	In vitro, gemcitabine activated MST1 through reactive oxygen species (ROS) production, which was prevented by antioxidant n-acetyl-cysteine (NAC).	Acetylcysteine	122-139	macrophage stimulating 1	Homo sapiens	32-36
24732633-7	2014	In vitro, gemcitabine activated MST1 through reactive oxygen species (ROS) production, which was prevented by antioxidant n-acetyl-cysteine (NAC).	Acetylcysteine	141-144	macrophage stimulating 1	Homo sapiens	32-36
24836981-14	2014	NAC also down-regulated both increases in NLRP3, ASC, caspase-1 and IL-1beta mRNA levels, along with their immunostaining.	Acetylcysteine	0-3	NLR family, pyrin domain containing 3	Mus musculus	42-47
24892995-9	2014	Remarkably, NAC supplementation not only ameliorated TCE-induced nitrosative stress as evident from decreased iNOS, NT, nitrated proteins, NF-kappaB p65 activation and increased GSH levels, but also the markers of autoimmunity, as evident from decreased levels of autoantibodies in the sera.	Acetylcysteine	12-15	v-rel reticuloendotheliosis viral oncogene homolog A (avian)	Mus musculus	149-152
24662196-9	2014	Moreover, treatment with valsartan or NAC suppressed the induction of c-fos (a component of the AP-1 transcription factor) and the upregulation of fasl (a proapoptotic molecule whose transcript is regulated downstream of AP-1).	Acetylcysteine	38-41	FBJ osteosarcoma oncogene	Mus musculus	70-75
24661543-6	2014	RESULTS: Signaling studies showed TSH increased NADPH oxidase activity, and either diphenyleneiodonium (oxidase inhibitor) or N-acetyl cysteine (scavenger of reactive oxygen species) reduced IKKbeta phosphorylation.	Acetylcysteine	126-143	inhibitor of nuclear factor kappa B kinase subunit beta	Homo sapiens	191-198
24825887-9	2014	Consistently, ROS-suppressing antioxidant chemicals, such as butylated hydroxyanisole and N-acetylcysteine, inhibited cold- or cAMP-induced Ucp1 expression as well.	Acetylcysteine	90-106	uncoupling protein 1	Homo sapiens	140-144
26350099-5	2015	Furthermore, with the addition of N-acetylcysteine, a scavenger of reactive oxygen species (ROS), it was found that NGAL depletion was sufficient to cause apoptosis of lung adenocarcinoma cells by generating ROS through the inhibition of the nuclear factor E2-related factor 2/heme oxygenase-1 anti-oxidant pathway.	Acetylcysteine	34-50	heme oxygenase 1	Homo sapiens	277-293
26291278-6	2015	Conversely, arsenite-induced H3S10 phosphorylation and HO-1 expression were blocked by N-acetylcysteine (NAC), the c-Jun N-terminal kinase (JNK) inhibitor SP600125, and JNK knockdown (siJNK).	Acetylcysteine	87-103	heme oxygenase 1	Homo sapiens	55-59
26291278-6	2015	Conversely, arsenite-induced H3S10 phosphorylation and HO-1 expression were blocked by N-acetylcysteine (NAC), the c-Jun N-terminal kinase (JNK) inhibitor SP600125, and JNK knockdown (siJNK).	Acetylcysteine	105-108	heme oxygenase 1	Homo sapiens	55-59
26206453-5	2015	RESULTS: Treatment with NAC inhibited apoptosis of penile tissue, the expressions of ERS-related products: BIP, CHOP, caspase12, and Bax, NO, and endothelial NOS.	Acetylcysteine	24-27	DNA-damage inducible transcript 3	Rattus norvegicus	112-116
26206453-5	2015	RESULTS: Treatment with NAC inhibited apoptosis of penile tissue, the expressions of ERS-related products: BIP, CHOP, caspase12, and Bax, NO, and endothelial NOS.	Acetylcysteine	24-27	BCL2 associated X, apoptosis regulator	Rattus norvegicus	133-136
26206453-7	2015	CONCLUSION: Our results show that pre-CIH NAC administration ameliorates the ED following CIH partly by alleviating CIH-induced ERS and cell apoptosis via regulating the expressions of BIP, CHOP, caspase12, and Bax.	Acetylcysteine	42-45	DNA-damage inducible transcript 3	Rattus norvegicus	190-194
26206453-7	2015	CONCLUSION: Our results show that pre-CIH NAC administration ameliorates the ED following CIH partly by alleviating CIH-induced ERS and cell apoptosis via regulating the expressions of BIP, CHOP, caspase12, and Bax.	Acetylcysteine	42-45	BCL2 associated X, apoptosis regulator	Rattus norvegicus	211-214
26337463-7	2015	When HSP27 was overexpressed, pretreatment of HUVECs with the antioxidant, apocynin, or N-acetyl cysteine, suppressed apoptosis.	Acetylcysteine	88-105	heat shock protein family B (small) member 1	Homo sapiens	5-10
25971793-5	2015	Parthenolide, Akt inhibitor, Bay 11-7085, and N-acetylcysteine each attenuated the lipopolysaccharide-induced production of IL-1beta and PGE2, increase in the levels of cyclooxygenase, formation of reactive oxygen species, increase in the levels of Toll-like receptor-4, and activation of the Akt/mTOR and NF-kappaB in keratinocytes.	Acetylcysteine	46-62	toll like receptor 4	Homo sapiens	249-269
26317351-7	2015	We found that GSH-AITC and NAC-AITC effectively inhibit adipogenic differentiation of 3T3-L1 preadipocytes and suppress expression of PPAR-gamma, C/EBPalpha, and FAS, which are up-regulated during adipogenesis.	Acetylcysteine	27-30	CCAAT/enhancer binding protein alpha	Rattus norvegicus	146-156
26105008-9	2015	Whereas p-mTOR was not significantly decreased by NAC after EX or REC, phosphorylation of the downstream protein synthesis target kinase p70S6K was blunted by 48% at PI with NAC compared with CON (P &lt; 0.05).	Acetylcysteine	174-177	ribosomal protein S6 kinase B1	Homo sapiens	137-143
25155877-6	2015	At the molecular levels, under glutathione-deficit conditions induced by short hairpin RNA targeting the key glutathione synthesis enzyme, oligodendrocyte progenitors showed a decreased proliferation mediated by an upregulation of Fyn kinase activity, reversed by either the antioxidant N-acetylcysteine or Fyn kinase inhibitors.	Acetylcysteine	287-303	FYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	231-234
25263448-3	2015	Cells lacking LKB1 exhibit markedly increased intracellular ROS levels, excessive oxidation of DNA, increased mutation rates and accumulation of DNA damage, which are effectively prevented by ectopic expression of LKB1 and by incubation with antioxidant N-acetylcysteine.	Acetylcysteine	254-270	serine/threonine kinase 11	Homo sapiens	14-18
26100173-10	2015	In addition, treatment with N-acetylcysteine, an antioxidant, inhibited the CSE-augmented phosphorylation of ERK and MUC5AC.	Acetylcysteine	28-44	mucin 5AC, oligomeric mucus/gel-forming	Homo sapiens	117-123
24819505-4	2014	Overexpression of Nrf2 or HO-1 resulted in upregulation of TP in NCI-H292 cells, an effect mimicked by treatment with an antioxidant N-acetylcysteine and partially reversed by HO-1 knockdown.	Acetylcysteine	133-149	heme oxygenase 1	Homo sapiens	26-30
24601883-9	2014	N-acetylcysteine prevented indoxyl sulfate-induced phosphorylation of Stat3 in proximal tubular cells.	Acetylcysteine	0-16	signal transducer and activator of transcription 3	Rattus norvegicus	70-75
26023321-7	2015	An anti-oxidant, N-acetylcysteine completely blocked insulin-induced up-regulation of SGLT2 as well as increase in glucose absorption by tubular cells.	Acetylcysteine	17-33	solute carrier family 5 member 2	Homo sapiens	86-91
3307787-1	1987	The metabolism of the mercapturic acids S-pentachlorobutadienyl-N-acetylcysteine (N-Ac-PCBC), S-trichlorovinyl-N-acetylcysteine (N-Ac-TCVC) and S-dichlorovinyl-N-acetylcysteine (N-Ac-DCVC) by subcellular fractions from male rat liver and kidney homogenates was studied.	Acetylcysteine	22-39	EPH receptor B2	Homo sapiens	87-91
25955698-9	2015	The decrease in IGF-1R and increase in IGFBP-3, as well as apoptosis, were also antagonized by pre-treatment with the antioxidant agents, N-acetylcysteine, dexrazoxane, and carvedilol.	Acetylcysteine	138-154	insulin like growth factor binding protein 3	Homo sapiens	39-46
24556569-6	2014	In addition, NAC significantly attenuated MSG-induced endoplasmic reticulum (ER) stress markers, such as XBP1 splicing and CHOP, PERK, and GRP78 up-regulation.	Acetylcysteine	13-16	X-box binding protein 1	Homo sapiens	105-109
3666282-9	1987	The hearts perfused with 1 mM acetylcysteine after 15 min of perfusion with t-butylhydroperoxide recovered almost completely the initial ODC activity.	Acetylcysteine	30-44	ornithine decarboxylase 1	Rattus norvegicus	137-140
24574456-6	2014	Treatment of cells with intracellular ROS scavenger N-acetyl-l-cysteine also inhibits AGP-induced activation of ASK1, as well as apoptosis.	Acetylcysteine	52-71	mitogen-activated protein kinase kinase kinase 5	Homo sapiens	112-116
24412704-9	2014	MSI suppression by N-acetylcysteine appears to be mediated through reduction of oxidative frameshift mutations in the coding microsatellite of hMSH6 and protection of hMSH6 and other MMR protein levels from being decreased by H2O2.	Acetylcysteine	19-35	mutS homolog 6	Homo sapiens	143-148
24412704-9	2014	MSI suppression by N-acetylcysteine appears to be mediated through reduction of oxidative frameshift mutations in the coding microsatellite of hMSH6 and protection of hMSH6 and other MMR protein levels from being decreased by H2O2.	Acetylcysteine	19-35	mutS homolog 6	Homo sapiens	167-172
25769956-7	2015	Pretreatment with the ROS inhibitor N-acetylcysteine abrogated the phosphorylation of p38 and JNK induced by high glucose.	Acetylcysteine	36-52	mitogen-activated protein kinase 8	Rattus norvegicus	94-97
25572853-6	2015	ROS generation promoted caveolin-1 phosphorylation on tyrosine-14 that was abrogated by the anti-oxidant N-acetylcysteine or the incubation with the Src-family kinase inhibitor, PP2 (4-amino-5-(4-chlorophenyl)-7(dimethylethyl)pyrazolo[3,4-d]pyrimidine).	Acetylcysteine	105-121	caveolin 1, caveolae protein	Mus musculus	24-34
2880383-9	1986	At the doses employed, glutathione and N-acetylcysteine induce early stimulation of glutathione-S-transferase, had little effect on the loss of glucose-6-phosphatase activity and scanty influence on the net increase in gamma-glutamyltranspeptidase activity.	Acetylcysteine	39-55	hematopoietic prostaglandin D synthase	Rattus norvegicus	84-109
24961937-5	2015	RESULTS: The data indicate that 1-month treatment of N-acetylcysteine or hydrogen-rich saline significantly ameliorated systemic and splanchnic hyperdynamic circulation, corrected hepatic endothelial dysfunction, and decreased intrahepatic resistance and mesenteric angiogenesis by inhibiting inflammatory cytokines, nitric oxide, VEGF and reducing mesenteric oxidative stress in cirrhotic rats.	Acetylcysteine	53-69	vascular endothelial growth factor A	Rattus norvegicus	331-335
24355171-9	2014	TQ also generated reactive oxygen species (ROS) and pretreatment with N-acetyl cysteine (NAC) abrogated TQ-induced ROS accumulation, Akt and AMPKalpha activation, Nrf2 nuclear localization, the ARE-luciferase activity, and HO-1 expression in HaCaT cells.	Acetylcysteine	70-87	heme oxygenase 1	Homo sapiens	223-227
24355171-9	2014	TQ also generated reactive oxygen species (ROS) and pretreatment with N-acetyl cysteine (NAC) abrogated TQ-induced ROS accumulation, Akt and AMPKalpha activation, Nrf2 nuclear localization, the ARE-luciferase activity, and HO-1 expression in HaCaT cells.	Acetylcysteine	89-92	heme oxygenase 1	Homo sapiens	223-227
24434148-10	2014	NADPH oxidase inhibitor Apocynin and superoxide scavenger N-acetyl-cysteine (NAC) significantly attenuated EI-stimulated expression of OKL38 and HO-1.	Acetylcysteine	58-75	oxidative stress induced growth inhibitor 1	Homo sapiens	135-140
24434148-10	2014	NADPH oxidase inhibitor Apocynin and superoxide scavenger N-acetyl-cysteine (NAC) significantly attenuated EI-stimulated expression of OKL38 and HO-1.	Acetylcysteine	58-75	heme oxygenase 1	Homo sapiens	145-149
26170769-1	2015	OBJECTIVE: Conventionally, intravenous N-acetylcysteine (IV-NAC) administration is a 3-bag regimen administered over the course of 21 hours, which increases the risk of reconstitution and administration errors.	Acetylcysteine	39-55	synuclein alpha	Homo sapiens	60-63
24434148-10	2014	NADPH oxidase inhibitor Apocynin and superoxide scavenger N-acetyl-cysteine (NAC) significantly attenuated EI-stimulated expression of OKL38 and HO-1.	Acetylcysteine	77-80	oxidative stress induced growth inhibitor 1	Homo sapiens	135-140
2859259-7	1985	N-acetylcysteine was administered to AT-125 treated rats in an attempt to supply cysteine to the brain in the face of gamma-GTP inhibition.	Acetylcysteine	0-16	gamma-glutamyltransferase 1	Rattus norvegicus	118-127
24434148-10	2014	NADPH oxidase inhibitor Apocynin and superoxide scavenger N-acetyl-cysteine (NAC) significantly attenuated EI-stimulated expression of OKL38 and HO-1.	Acetylcysteine	77-80	heme oxygenase 1	Homo sapiens	145-149
24451478-7	2014	The induction of autophagy caused by PFKFB3 inhibition required an increase in reactive oxygen species since N-acetyl-cysteine blocked both the conversion of LC3-I to LC3-II and the increase in acridine orange fluorescence in acidic vesicles after exposure of HCT-116 cells to 3PO.	Acetylcysteine	109-126	6-phosphofructo-2-kinase/fructose-2,6-biphosphatase 3	Homo sapiens	37-43
25724285-7	2015	Pre-treatment of EUK-134 or NAC alone altered the level of total free radical generation, LPO, GSH content and catalytic activity of MPO, SOD, GR and GPx and the expression of metallothionein I and II towards normalcy.	Acetylcysteine	28-31	myeloperoxidase	Rattus norvegicus	133-136
25724285-7	2015	Pre-treatment of EUK-134 or NAC alone altered the level of total free radical generation, LPO, GSH content and catalytic activity of MPO, SOD, GR and GPx and the expression of metallothionein I and II towards normalcy.	Acetylcysteine	28-31	glutathione-disulfide reductase	Rattus norvegicus	143-145
25724285-9	2015	Catalytic activity/expression of GSTA4-4 remained unchanged in the PMNs of EUK-134 or NAC treated rats.	Acetylcysteine	86-89	glutathione S-transferase alpha 4	Rattus norvegicus	33-40
6238023-8	1984	Its reaction with myosin SH1 was about 30 times faster than that with N-acetylcysteine (NAC).	Acetylcysteine	70-86	myosin heavy chain 14	Homo sapiens	18-24
25681429-8	2015	The reactive oxygen species (ROS) inhibitors N-acetylcysteine (NAC), diphenyleneiodonium (DPI), and Tempol also diminished MCP-1 upregulation and JNK activation induced by ADP.	Acetylcysteine	45-61	C-C motif chemokine ligand 2	Rattus norvegicus	123-128
25681429-8	2015	The reactive oxygen species (ROS) inhibitors N-acetylcysteine (NAC), diphenyleneiodonium (DPI), and Tempol also diminished MCP-1 upregulation and JNK activation induced by ADP.	Acetylcysteine	45-61	mitogen-activated protein kinase 8	Rattus norvegicus	146-149
25681429-8	2015	The reactive oxygen species (ROS) inhibitors N-acetylcysteine (NAC), diphenyleneiodonium (DPI), and Tempol also diminished MCP-1 upregulation and JNK activation induced by ADP.	Acetylcysteine	63-66	C-C motif chemokine ligand 2	Rattus norvegicus	123-128
25681429-8	2015	The reactive oxygen species (ROS) inhibitors N-acetylcysteine (NAC), diphenyleneiodonium (DPI), and Tempol also diminished MCP-1 upregulation and JNK activation induced by ADP.	Acetylcysteine	63-66	mitogen-activated protein kinase 8	Rattus norvegicus	146-149
24161787-7	2014	Moreover, the andrographolide-induced Hsp90 cleavage, Src degradation, inhibition of transformation, and induction of apoptosis were abolished by a ROS inhibitor, N-acetyl-cysteine.	Acetylcysteine	163-180	heat shock protein 90 alpha family class A member 1	Homo sapiens	38-43
24713665-10	2014	The expression levels of NF-kappaB-regulated inflammatory cytokines, namely TNF-alpha, IL-6 and IL-1beta, were markedly increased after BHBA treatment, while significantly decreased after NAC treatment.	Acetylcysteine	188-191	tumor necrosis factor	Bos taurus	76-85
24162829-4	2014	GA activated calcium/calmodulin-dependent protein kinase II (CaMKII), c-Jun N-terminal kinase (JNK) and P38; but these activating effects were attenuated by pretreatment with N-acetyl-L-cysteine, a ROS inhibitor.	Acetylcysteine	175-194	mitogen-activated protein kinase 8	Rattus norvegicus	70-93
6238023-8	1984	Its reaction with myosin SH1 was about 30 times faster than that with N-acetylcysteine (NAC).	Acetylcysteine	88-91	myosin heavy chain 14	Homo sapiens	18-24
6312894-3	1983	For small molecules, such as cysteine, N-acetylcysteine, glutathione, and 2-mercaptoethanol, the spectrum is that of a freely rotating nitroxide while for the proteins, bovine serum albumin and myosin, the spectrum is characteristic of a strongly immobilized nitroxide spin label rigidly attached to the protein.	Acetylcysteine	39-55	myosin heavy chain 14	Homo sapiens	194-200
25359386-12	2014	Significantly increased expressions of GRP78 and CHOP were observed in the NRK-52E cells exposed to iopromide for 4 h; NAC attenuated iopromide-induced NRK-52E cell apoptosis by inhibiting the overproduction of intracellular ROS and subsequently suppressing the overexpression of GRP78 and CHOP.	Acetylcysteine	119-122	DNA-damage inducible transcript 3	Rattus norvegicus	49-53
25359386-12	2014	Significantly increased expressions of GRP78 and CHOP were observed in the NRK-52E cells exposed to iopromide for 4 h; NAC attenuated iopromide-induced NRK-52E cell apoptosis by inhibiting the overproduction of intracellular ROS and subsequently suppressing the overexpression of GRP78 and CHOP.	Acetylcysteine	119-122	DNA-damage inducible transcript 3	Rattus norvegicus	290-294
25660312-0	2015	Glutathione, N-acetylcysteine and lipoic acid down-regulate starvation-induced apoptosis, RANKL/OPG ratio and sclerostin in osteocytes: involvement of JNK and ERK1/2 signalling.	Acetylcysteine	13-29	tumor necrosis factor (ligand) superfamily, member 11	Mus musculus	90-95
24436257-7	2015	Pretreatment with antioxidant N-acetyl-L-cysteine, c-Jun NH2-terminal kinase inhibitor SP600125, and extracellular signal-regulated kinase inhibitor PD98059 significantly reduced arecoline-induced Egr-1 synthesis.	Acetylcysteine	30-49	early growth response 1	Homo sapiens	197-202
6131667-2	1982	The enzymes glutathione S-transferase, gamma-glutamyl peptidyltransferase and dipeptidase, which participate in the detoxification pathway through mercapturic acid production, were measured in rat mammary gland during pregnancy and lactation.	Acetylcysteine	147-163	hematopoietic prostaglandin D synthase	Rattus norvegicus	12-37
25668756-8	2015	Interestingly, treatment with the antioxidant N-acetyl-l-cysteine significantly suppressed 4-ClBQ-induced increase in CYP1A1 expression.	Acetylcysteine	46-65	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	118-124
23891589-3	2013	The results showed that (1) UVB caused PDCD4 inhibition in JB6 cells; (2) exposure of cells to UVB caused a significant increase of miR-21, the upstream regulator of PDCD4, expression; (3) both inhibition of ERKs with U0126 and inhibition of p38 with SB203580 significantly reversed UVB-induced PDCD4 inhibition; (4) ROS scavenger, N-acetyl-l-cysteine reversed the inhibitory effect of UVB on PDCD4 expression.	Acetylcysteine	332-351	microRNA 21	Homo sapiens	132-138
24036416-10	2013	In the corpus callosum, MINO plus NAC decreased CD68 expression yet increased overall microglial activation as measured by Iba-1.	Acetylcysteine	34-37	allograft inflammatory factor 1	Rattus norvegicus	123-128
24036416-11	2013	MINO plus NAC acted synergistically to increase Iba-1 expression since MINO alone suppressed expression and NAC alone had no effect.	Acetylcysteine	10-13	allograft inflammatory factor 1	Rattus norvegicus	48-53
24036416-11	2013	MINO plus NAC acted synergistically to increase Iba-1 expression since MINO alone suppressed expression and NAC alone had no effect.	Acetylcysteine	108-111	allograft inflammatory factor 1	Rattus norvegicus	48-53
25619390-12	2015	Incubation in a high-glucose medium induced oxidative stress and activation of TLR-4/MyD-88 signaling in cultured myocytes in vitro, which were significantly attenuated by pretreatment with N-acetylcysteine.	Acetylcysteine	190-206	MYD88, innate immune signal transduction adaptor	Rattus norvegicus	85-91
7097475-4	1982	The mercapturic acids were identified as N-acetyl-S-(1-phenyl-2-hydroxyethyl)cysteine (MA-1) and N-acetyl-S-(2-phenyl-2-hydroxyethyl)cysteine (MA-2).	Acetylcysteine	4-21	Activity QTL 1	Rattus norvegicus	87-91
25652258-5	2015	METHODS: We retrospectively identified cases of patients hospitalized for acute APAP poisoning by querying the pharmacy database of all patients treated with acetylcysteine (NAC) from January 1, 2001 to March 19, 2013.	Acetylcysteine	158-172	synuclein alpha	Homo sapiens	174-177
25666878-8	2015	Neutrophil lipid peroxidation, apoptosis, caspase-3, caspase-9, cytosolic reactive oxygen species production, and mitochondrial membrane depolarization values were decreased by NAC treatment although neutrophil glutathione peroxidase and reduced glutathione levels were increased by the NAC treatment.	Acetylcysteine	177-180	caspase 9	Homo sapiens	53-62
25581570-12	2015	Furthermore, AGE- or MGO-induced increased expression of VEGF and MCP-1 was significantly reduced in the presence of NAC or SB203580.	Acetylcysteine	117-120	C-C motif chemokine ligand 2	Homo sapiens	66-71
23911883-7	2013	Pre-incubation with thiol antioxidants glutathione or N-acetyl-cysteine(NAC) almost abolished the cytotoxicity of PHII-7.	Acetylcysteine	54-71	synuclein alpha	Homo sapiens	72-75
24098483-0	2013	N-acetyl-L-cysteine prevents stress-induced desmin aggregation in cellular models of desminopathy.	Acetylcysteine	0-19	desmin	Homo sapiens	44-50
7097475-8	1982	The mercapturic acid, MA-1, was excreted at higher rate than the isomer, MA-2, on the administration of styrene and the phenyloxiranes.	Acetylcysteine	4-20	Activity QTL 1	Rattus norvegicus	22-26
1262-1	1975	The initial enzymic step in mercapturic acid formation is catalyzed by glutathione S-transferase.	Acetylcysteine	28-44	glutathione S-transferase kappa 1	Homo sapiens	71-96
22532030-11	2013	Collectively, these results indicate that dietary NAC supplementation alleviates LPS-induced intestinal inflammation via regulating redox, EGF, and TLR4 signaling.	Acetylcysteine	50-53	epidermal growth factor	Homo sapiens	139-142
22532030-11	2013	Collectively, these results indicate that dietary NAC supplementation alleviates LPS-induced intestinal inflammation via regulating redox, EGF, and TLR4 signaling.	Acetylcysteine	50-53	toll like receptor 4	Homo sapiens	148-152
23666527-6	2013	In a therapeutic trial of short-term NAC administration to NPC1 patients, no significant effects on oxidative stress in these patients were identified other than moderate improvement of the fraction of reduced CoQ10, suggesting limited efficacy of NAC monotherapy.	Acetylcysteine	37-40	NPC intracellular cholesterol transporter 1	Homo sapiens	59-63
24015194-12	2013	These findings suggest that N-acetylcysteine protects ventricular arrhythmias by attenuating reduced connexin43 expression and function via both PKA- and Epac-dependent pathways, which converge through the inactivation of glycogen synthase kinase-3beta.	Acetylcysteine	28-44	protein kinase cAMP-activated catalytic subunit alpha	Rattus norvegicus	145-148
25534136-11	2015	Treatment with the antioxidant N-acetylcysteine prior to oxidative stress rescued S326C-OGG1 activity, demonstrated by in vitro and cellular repair assays.	Acetylcysteine	31-47	8-oxoguanine DNA glycosylase	Homo sapiens	88-92
23500899-8	2013	Lowering the serum homocysteine level by a simultaneous supplementation with N-acetylcysteine improved OPG and FOXO1 expression and partially antagonized RANKL and proresorptive cytokine synthesis in the bone milieu.	Acetylcysteine	77-93	TNF receptor superfamily member 11B	Rattus norvegicus	103-106
32291602-8	2021	Further in vitro studies show that CD21 (20 muM) strongly enhanced the Msr1 mRNA and MSR1 protein levers in RAW264.7 cells and PRX1 internalization in cellular lysosomes, which were significantly reversed by N-acetylcysteine treatment.	Acetylcysteine	208-224	peroxiredoxin 1	Mus musculus	127-131
26390620-0	2015	[ROLE OF NEUTRAL SPHINGOMYELINASE IN AGE-DEPENDENT MUSCLE INSULIN RESISTANCE DEVELOPMENT AND ITS IMPROVEMENT WITH N-ACETYLCYSTEINE].	Acetylcysteine	114-130	sphingomyelin phosphodiesterase 2	Rattus norvegicus	9-33
26390620-4	2015	N-acetylcysteine as well as specific neutral sphingomyelinase (nSMase) inhibitor--GW4869, decreases ceramide content and increases GSH level, and enhances the insulin-induced [3H-D-glucose uptake in the "aged" tissue.	Acetylcysteine	0-16	sphingomyelin phosphodiesterase 2	Rattus norvegicus	63-69
34052344-9	2021	H2O2 induced cellular injury and inflammation, excessive ROS production, mitochondrial abnormalities, and increased expression of p-Drp1 and Drp1 in hPDLCs, which could be reversed by NAC and Mdivi-1.	Acetylcysteine	184-187	dynamin 1 like	Homo sapiens	132-136
26119951-5	2015	In addition, levels of mature BDNF expression and CREB phosphorylation were increased by combined treatment with WEPM, NAC, and intracellular Ca (2+) inhibitor BAPTA compared to other treatment groups.	Acetylcysteine	119-122	brain derived neurotrophic factor	Mus musculus	30-34
34052344-9	2021	H2O2 induced cellular injury and inflammation, excessive ROS production, mitochondrial abnormalities, and increased expression of p-Drp1 and Drp1 in hPDLCs, which could be reversed by NAC and Mdivi-1.	Acetylcysteine	184-187	dynamin 1 like	Homo sapiens	141-145
25896065-9	2015	High-mobility group box-1 (HMGB-1), an endogenous activator of TLR4, rapidly increased in TLR4 immunoprecipitates upon high glucose stimulation, and this association was reduced by N-acetylcysteine, an antioxidant.	Acetylcysteine	181-197	toll like receptor 4	Homo sapiens	63-67
23796398-12	2013	Similarly, numerous crystals with Gly-I inactivation and elevated oxidative stress seen in the rats (EG-VD3) were also significantly prevented with NAC supplement.	Acetylcysteine	148-151	glyoxalase I	Canis lupus familiaris	34-39
25896065-9	2015	High-mobility group box-1 (HMGB-1), an endogenous activator of TLR4, rapidly increased in TLR4 immunoprecipitates upon high glucose stimulation, and this association was reduced by N-acetylcysteine, an antioxidant.	Acetylcysteine	181-197	toll like receptor 4	Homo sapiens	90-94
33980809-9	2021	Inhibition or promotion of ROS production with N-acetyl-L-cysteine or H2O2 not only upregulated or downregulated beta-catenin expression, but also prevented or promoted DNA damage, rescued or impeded sphere formation, respectively.	Acetylcysteine	47-66	catenin beta 1	Homo sapiens	113-125
25553484-8	2015	The effects of NAC are associated with some intestinal cell signaling pathways, such as EGFR, TLR4, apoptosis and tight junction signaling.	Acetylcysteine	15-18	toll like receptor 4	Homo sapiens	94-98
23765110-8	2013	Concomitant treatment of CsA and NAC translocated FoxO1 from the cytoplasm to the nucleus, implicating dephosphorylation of FoxO1 by NAC in p-AKT/p-FoxO1 pathway.	Acetylcysteine	33-36	forkhead box O1	Mus musculus	50-55
23765110-8	2013	Concomitant treatment of CsA and NAC translocated FoxO1 from the cytoplasm to the nucleus, implicating dephosphorylation of FoxO1 by NAC in p-AKT/p-FoxO1 pathway.	Acetylcysteine	33-36	forkhead box O1	Mus musculus	124-129
23765110-8	2013	Concomitant treatment of CsA and NAC translocated FoxO1 from the cytoplasm to the nucleus, implicating dephosphorylation of FoxO1 by NAC in p-AKT/p-FoxO1 pathway.	Acetylcysteine	33-36	forkhead box O1	Mus musculus	124-129
23765110-8	2013	Concomitant treatment of CsA and NAC translocated FoxO1 from the cytoplasm to the nucleus, implicating dephosphorylation of FoxO1 by NAC in p-AKT/p-FoxO1 pathway.	Acetylcysteine	133-136	forkhead box O1	Mus musculus	50-55
23765110-8	2013	Concomitant treatment of CsA and NAC translocated FoxO1 from the cytoplasm to the nucleus, implicating dephosphorylation of FoxO1 by NAC in p-AKT/p-FoxO1 pathway.	Acetylcysteine	133-136	forkhead box O1	Mus musculus	124-129
23765110-8	2013	Concomitant treatment of CsA and NAC translocated FoxO1 from the cytoplasm to the nucleus, implicating dephosphorylation of FoxO1 by NAC in p-AKT/p-FoxO1 pathway.	Acetylcysteine	133-136	forkhead box O1	Mus musculus	124-129
23765110-9	2013	CONCLUSION: NAC treatment preserves Klotho expression and modifies p-AKT/p-FoxO1 pathway in chronic CsA nephropathy.	Acetylcysteine	12-15	forkhead box O1	Mus musculus	75-80
23603059-6	2013	Finally, SA-induced AT1R expression was found to be prevented both by NAC and specific JNK inhibitor, SP6001325, strongly indicating that AT1R upregulation is a result of the ROS-mediated activation of the JNK signaling pathway.	Acetylcysteine	70-73	angiotensin II, type I receptor-associated protein	Mus musculus	20-24
25464205-5	2015	Scavenging of ROS by N-acetyl-L-cysteine (NAC) or acetyl-L-carnitine (ALC) rescued MMP and mitochondrial mass, and squelched PINK1 level, mitochondrial accumulation of Parkin and LC3-II/LC3-I ratio, suggesting that ROS were associated with Cd-induced mitophagy.	Acetylcysteine	42-45	PTEN induced putative kinase 1	Mus musculus	125-130
34016350-6	2021	In addition, NAC attenuated the activity of the Nf-kappaB pathway activated by heat stress and decreased the expression of the proinflammatory cytokines IL-6, IL-18, TNF-alpha, IKK, and IFN-gamma.	Acetylcysteine	13-16	interleukin 18	Gallus gallus	159-164
34016350-7	2021	In addition, NAC treatment regulated the expression of HO-1, GSH, SOD2 and PRDX3 by regulating the activity of Nrf2 at different time points to resist oxidative stress caused by heat exposure.	Acetylcysteine	13-16	peroxiredoxin 3	Gallus gallus	75-80
23660190-11	2013	Poly IC-induced upregulation of B7-H1 was attenuated by N-acetyl-L-cysteine, an antioxidant, or by oxypurinol, an inhibitor of xanthine oxidase.	Acetylcysteine	56-75	CD274 molecule	Homo sapiens	32-37
33921050-9	2021	NAC treatment upregulated ATG-5 (p < 0.0001), beclin-1 (p < 0.0001) and LC3-I to LC3-II (p < 0.0001) conversion, which was inhibited in the DA treatment group.	Acetylcysteine	0-3	beclin 1, autophagy related	Mus musculus	46-54
25560241-5	2015	Redox Western blot analysis of PC-3 cells also supported the conclusion that thioredoxin-1 (Trx-1) oxidation was enhanced by treatment DHEA+Au and inhibited by NAC.	Acetylcysteine	160-163	thioredoxin	Homo sapiens	77-90
25560241-5	2015	Redox Western blot analysis of PC-3 cells also supported the conclusion that thioredoxin-1 (Trx-1) oxidation was enhanced by treatment DHEA+Au and inhibited by NAC.	Acetylcysteine	160-163	thioredoxin	Homo sapiens	92-97
33740178-6	2022	NAC treatments significantly improved TAC and IL-10, but decreased MDA and TNF-alpha values in rats that were exposed to a single and continuous dose of Cd (p < 0.05).	Acetylcysteine	0-3	interleukin 10	Rattus norvegicus	46-51
23183129-7	2013	In addition, NAC-treated rats showed upregulated expression of NKCC2, AQP2, and UT-A1; elevated Klotho protein expression, low p53 expression, and few ED-1 positive cells.	Acetylcysteine	13-16	aquaporin 2	Rattus norvegicus	70-74
33712558-9	2021	As shown in our study, although ROS play a role in upregulating NOXA mRNA transcription, ROS scavenging in CRC cells by N-acetyl-L-cysteine (NAC) can significantly reduce CUL5 neddylation and extend the NOXA protein half-life.	Acetylcysteine	120-139	cullin 5	Homo sapiens	171-175
23183129-7	2013	In addition, NAC-treated rats showed upregulated expression of NKCC2, AQP2, and UT-A1; elevated Klotho protein expression, low p53 expression, and few ED-1 positive cells.	Acetylcysteine	13-16	Klotho	Rattus norvegicus	96-102
23183129-7	2013	In addition, NAC-treated rats showed upregulated expression of NKCC2, AQP2, and UT-A1; elevated Klotho protein expression, low p53 expression, and few ED-1 positive cells.	Acetylcysteine	13-16	Wistar clone pR53P1 p53 pseudogene	Rattus norvegicus	127-130
23183129-8	2013	In conclusion, we attribute these beneficial effects of NAC (the significant improvements in inulin clearance and in the expression of NKCC2, AQP2, and UT-A1) to its ability to decrease oxidative stress, inhibit p53 expression, minimize kidney inflammation, and stimulate Klotho expression.	Acetylcysteine	56-59	aquaporin 2	Rattus norvegicus	142-146
25437431-7	2014	Pretreatment of the cells with antioxidant N-acetylcysteine (NAC) decreased ROS generation and prevented BQ-induced PKM2 degradation, suggesting involvement of ROS in the PKM2 protein degradation in cellular response to BQ.	Acetylcysteine	43-59	pyruvate kinase M1/2	Homo sapiens	116-120
33712558-9	2021	As shown in our study, although ROS play a role in upregulating NOXA mRNA transcription, ROS scavenging in CRC cells by N-acetyl-L-cysteine (NAC) can significantly reduce CUL5 neddylation and extend the NOXA protein half-life.	Acetylcysteine	141-144	cullin 5	Homo sapiens	171-175
25437431-7	2014	Pretreatment of the cells with antioxidant N-acetylcysteine (NAC) decreased ROS generation and prevented BQ-induced PKM2 degradation, suggesting involvement of ROS in the PKM2 protein degradation in cellular response to BQ.	Acetylcysteine	43-59	pyruvate kinase M1/2	Homo sapiens	171-175
25437431-7	2014	Pretreatment of the cells with antioxidant N-acetylcysteine (NAC) decreased ROS generation and prevented BQ-induced PKM2 degradation, suggesting involvement of ROS in the PKM2 protein degradation in cellular response to BQ.	Acetylcysteine	61-64	pyruvate kinase M1/2	Homo sapiens	116-120
23183129-8	2013	In conclusion, we attribute these beneficial effects of NAC (the significant improvements in inulin clearance and in the expression of NKCC2, AQP2, and UT-A1) to its ability to decrease oxidative stress, inhibit p53 expression, minimize kidney inflammation, and stimulate Klotho expression.	Acetylcysteine	56-59	Wistar clone pR53P1 p53 pseudogene	Rattus norvegicus	212-215
23183129-8	2013	In conclusion, we attribute these beneficial effects of NAC (the significant improvements in inulin clearance and in the expression of NKCC2, AQP2, and UT-A1) to its ability to decrease oxidative stress, inhibit p53 expression, minimize kidney inflammation, and stimulate Klotho expression.	Acetylcysteine	56-59	Klotho	Rattus norvegicus	272-278
25437431-7	2014	Pretreatment of the cells with antioxidant N-acetylcysteine (NAC) decreased ROS generation and prevented BQ-induced PKM2 degradation, suggesting involvement of ROS in the PKM2 protein degradation in cellular response to BQ.	Acetylcysteine	61-64	pyruvate kinase M1/2	Homo sapiens	171-175
33495825-6	2021	Endothelial damage was also corrected by NAC, as indicated by an increase in the expression levels of phosphorylated (p-)Akt and p-endothelial nitric oxide synthase (eNOS) in the aorta, as well as nitric oxide (NO) in the serum.	Acetylcysteine	41-44	nitric oxide synthase 3, endothelial cell	Mus musculus	129-164
25134437-5	2014	N-acetylcysteine (a general antioxidant) attenuated the CSE-induced ASK-1 and p38 MAPK activation and cell apoptosis, suggesting a triggering role of ROS in ASK-1/p38 MAPK activation during apoptotic progression.	Acetylcysteine	0-16	mitogen-activated protein kinase kinase kinase 5	Homo sapiens	68-73
25134437-5	2014	N-acetylcysteine (a general antioxidant) attenuated the CSE-induced ASK-1 and p38 MAPK activation and cell apoptosis, suggesting a triggering role of ROS in ASK-1/p38 MAPK activation during apoptotic progression.	Acetylcysteine	0-16	mitogen-activated protein kinase kinase kinase 5	Homo sapiens	157-162
23357435-0	2013	In this issue/abstract thinking: NAC attack: is N-acetylcysteine ready for prime time in child and adolescent psychiatry?	Acetylcysteine	48-64	synuclein alpha	Homo sapiens	33-36
23124852-5	2013	After scavenging ROS with N-acetylcysteine, Wnt/beta-catenin signaling-induced MSC aging was significantly attenuated and the DNA damage and the expression of p16(INK4A), p53, and p21 were reduced in MSCs.	Acetylcysteine	26-42	catenin beta 1	Homo sapiens	48-60
23124852-5	2013	After scavenging ROS with N-acetylcysteine, Wnt/beta-catenin signaling-induced MSC aging was significantly attenuated and the DNA damage and the expression of p16(INK4A), p53, and p21 were reduced in MSCs.	Acetylcysteine	26-42	H3 histone pseudogene 16	Homo sapiens	180-183
33495825-6	2021	Endothelial damage was also corrected by NAC, as indicated by an increase in the expression levels of phosphorylated (p-)Akt and p-endothelial nitric oxide synthase (eNOS) in the aorta, as well as nitric oxide (NO) in the serum.	Acetylcysteine	41-44	nitric oxide synthase 3, endothelial cell	Mus musculus	166-170
25237784-15	2014	These concentrations were confirmed by using a previously reported GC-MS method and agree with those measured previously by HPLC-UV (334 nm) after nitrite conversion to S-nitroso-N-acetylcysteine (SNAC) by N-acetylcysteine (NAC).	Acetylcysteine	179-195	synuclein alpha	Homo sapiens	198-201
33495825-10	2021	Furthermore, NAC may offer protection against atherosclerotic development in DM by altering aortic and systemic responses via correcting GSH-dependent MG elimination, leading to decreased oxidative stress and restoration of the p-Akt/p-eNOS pathway in the aorta.	Acetylcysteine	13-16	nitric oxide synthase 3, endothelial cell	Mus musculus	236-240
25016575-11	2014	The decrease in the phosphorylation of JAK2 and JAK3, earlier in the process, could explain the downregulation of STAT3 and offer a hypothesis on the mechanism of action of NAC antioxidant properties which were confirmed by a decrease in the level of S-glutathionylation of proteins.	Acetylcysteine	173-176	Janus kinase 3	Homo sapiens	48-52
33498402-10	2021	Subchronic NAC administration protected against an acute pro-oxidant challenge, decreased KYNA levels, and lowered KAT II activity and improved memory both under basal conditions and after acute Kyn treatment.	Acetylcysteine	11-14	aminoadipate aminotransferase	Mus musculus	115-121
33441706-2	2021	The BPOFc/BMPF6/NiO-SWCNTs/CPE with high electrical conductivity showed two completely separate signals with oxidation potentials of 432 and 970 mV for the first time that is sufficient for the determination of N-acetylcysteine in the presence of theophylline.	Acetylcysteine	211-227	carboxypeptidase E	Homo sapiens	27-30
25008790-7	2014	Finally, B2-induced dynamin-related protein 1 (Drp1)-mediated mitochondrial fragmentation and cell death could be reversed by NAC and inhibitors of Drp1 and Mdivi in GF-1 cells.	Acetylcysteine	126-129	dynamin 1 like	Homo sapiens	47-51
22940466-5	2013	Pretreatment of the A549 cells with N-acetyl-cysteine (NAC), an antioxidant, decreased the effects of AgNPs on the reduced cell viability, change in the MMP and proportion of cells in the sub-G1population, but had no effect on the AgNP-mediated S phase arrest or down-regulation of PCNA.	Acetylcysteine	36-53	proliferating cell nuclear antigen	Homo sapiens	282-286
22940466-5	2013	Pretreatment of the A549 cells with N-acetyl-cysteine (NAC), an antioxidant, decreased the effects of AgNPs on the reduced cell viability, change in the MMP and proportion of cells in the sub-G1population, but had no effect on the AgNP-mediated S phase arrest or down-regulation of PCNA.	Acetylcysteine	55-58	proliferating cell nuclear antigen	Homo sapiens	282-286
23267148-5	2013	Likewise, NAC prevented the CDDO-Me-caused binding of fluorescein isothiocyanate (FITC)-tagged annexin V, cleavage of poly ADP-ribose polymerase-1 (PARP-1), procaspases-3, -8 and -9 and loss of mitochondrial membrane potential.	Acetylcysteine	10-13	annexin A5	Homo sapiens	95-104
33441706-3	2021	The BPOFc/BMPF6/NiO-SWCNTs/CPE showed linear dynamic ranges of 0.02-300.0 muM and 1.0-350.0 muM with the detection limit of ~ 8.0 nM and 0.6 muM for the measurement of N-acetylcysteine and theophylline, respectively.	Acetylcysteine	168-184	carboxypeptidase E	Homo sapiens	27-30
33441976-8	2021	Moreover, NAC increased the concentrations of citrulline and D-xylose in the plasma, as well as the expression of genes for aquaporin (AQP) 3, AQP4, peptide transporter 1 (PepT1), sodium/glucose co-transporter-1 (SGLT-1), potassium inwardly-rectifying channel, subfamily J, member 13 (KCNJ13), and solute carrier family 1 member 1 (SLC1A1) in the jejunum, demonstrating that NAC augmented intestinal metabolic activity and absorptive function.	Acetylcysteine	10-13	aquaporin 3 (Gill blood group)	Homo sapiens	124-141
33130472-15	2021	N-acetyl-L-cysteine (NAC) not only revered ROS generation triggered by LCA but also restored IFN-gamma-induced expression of PD-L1.	Acetylcysteine	0-19	CD274 molecule	Homo sapiens	125-130
23038752-8	2013	The antioxidant N-acetyl cysteine rescued myotube formation and atrophy gene induction in M-ERRgamma(-/-) myocytes.	Acetylcysteine	16-33	estrogen-related receptor gamma	Mus musculus	92-100
26461335-11	2014	Additionally, NAC caused an elevation in the glutathione peroxidase and glutathione reductase activities, total glutathione, ascorbic acid, and total reactive antioxidant potential levels, which were decreased in the kidney of aspartame-treated rats.	Acetylcysteine	14-17	glutathione-disulfide reductase	Rattus norvegicus	72-93
33371832-7	2021	Furthermore, NAC decreases TNF-alpha, IL-1beta, IL-6, IL-8, IL-10, and IL-17 serum levels in patients with sepsis, severe burns, acute liver failure, or peritoneal dialysis and may also reduce cytokine storm in COVID-19.	Acetylcysteine	13-16	interleukin 1 alpha	Homo sapiens	38-46
24734887-6	2014	We found that NAC significantly increased Nrf2 and downstream HO-1 expression.	Acetylcysteine	14-17	heme oxygenase 1	Homo sapiens	62-66
25264893-11	2014	RESULTS: We found that ALT, AST and pathological changes were significantly improved in the NAC group.	Acetylcysteine	92-95	glutamic pyruvic transaminase, soluble	Mus musculus	23-26
33354859-7	2021	Treatment augmentation with N-acetylcysteine showed a moderate effect size favoring NAC over placebo (d = 0.45, 95% C.I.	Acetylcysteine	28-44	synuclein alpha	Homo sapiens	84-87
25264893-11	2014	RESULTS: We found that ALT, AST and pathological changes were significantly improved in the NAC group.	Acetylcysteine	92-95	solute carrier family 17 (anion/sugar transporter), member 5	Mus musculus	28-31
25264893-12	2014	Western blotting analysis showed that the expression levels of Beclin 1 and LC3 were significantly decreased in NAC-treated mice.	Acetylcysteine	112-115	beclin 1, autophagy related	Mus musculus	63-71
25264893-12	2014	Western blotting analysis showed that the expression levels of Beclin 1 and LC3 were significantly decreased in NAC-treated mice.	Acetylcysteine	112-115	microtubule-associated protein 1 light chain 3 alpha	Mus musculus	76-79
25264893-13	2014	In addition, JNK, p-JNK, Bax, TNF-alpha, NF-kappaB, IL2, IL6 and levels were also decreased in NAC-treated mice.	Acetylcysteine	95-98	interleukin 2	Mus musculus	52-55
22986467-4	2013	ROS was scavenged by N-acetyl cysteine; NADPH oxidase, the major source of ROS, was inhibited by diphenyliodonium, apocynin or gp91-phox siRNA transfection; and protein kinase was inhibited by its specific inhibitor.	Acetylcysteine	21-38	paired Ig-like receptor B	Mus musculus	127-131
23115158-8	2013	Radiosensitization of U87MG-IDH1(R132H) cells was accompanied by increased apoptosis and accentuated ROS generation, and this effect was abrogated by the presence of the ROS scavenger N-acetyl-cysteine.	Acetylcysteine	184-201	isocitrate dehydrogenase (NADP(+)) 1	Homo sapiens	28-33
23181590-4	2013	Treating the cells with free radical scavenger N-acetylcysteine had no effect on VLA-4 expression, but did reduce the avidity between RAW264.7 cells and VCAM-1 to a similar level, independent of ionizing radiation dose.	Acetylcysteine	47-63	vascular cell adhesion molecule 1	Mus musculus	153-159
25002068-8	2014	N-acetylcysteine suppressed the augmentation of ROS levels and the enhanced expression of COQ2, COQ4, COQ7, and COQ9 induced by oligomycin, but did not modulate the changes in CoQ10 levels.	Acetylcysteine	0-16	coenzyme Q2, polyprenyltransferase	Homo sapiens	90-94
25002068-8	2014	N-acetylcysteine suppressed the augmentation of ROS levels and the enhanced expression of COQ2, COQ4, COQ7, and COQ9 induced by oligomycin, but did not modulate the changes in CoQ10 levels.	Acetylcysteine	0-16	coenzyme Q7, hydroxylase	Homo sapiens	102-106
33381272-5	2020	Antioxidant N-acetylcysteine (NAC) inhibited OLA-induced oxidative stress and p53 activation in vivo.	Acetylcysteine	12-28	transformation related protein 53, pseudogene	Mus musculus	78-81
25128474-3	2014	METHODS AND RESULTS: Acute recombinant angptl2 reduced (P&lt;0.05) acetylcholine-mediated vasodilation of isolated wild-type (WT) mouse femoral artery, an effect reversed (P&lt;0.05) by the antioxidant N-acetylcysteine.	Acetylcysteine	202-218	angiopoietin-like 2	Mus musculus	39-46
24398995-0	2013	Valproic acid substantially downregulated genes folr1, IGF2R, RGS2, COL6A3, EDNRB, KLF6, and pax-3, N-acetylcysteine alleviated most of the induced gene alterations in chicken embryo model.	Acetylcysteine	100-116	insulin like growth factor 2 receptor	Gallus gallus	55-60
24398995-0	2013	Valproic acid substantially downregulated genes folr1, IGF2R, RGS2, COL6A3, EDNRB, KLF6, and pax-3, N-acetylcysteine alleviated most of the induced gene alterations in chicken embryo model.	Acetylcysteine	100-116	paired box 3	Gallus gallus	93-98
22985912-6	2013	N-acetylcysteine prevented morphologic and oxidative derangements, and significantly reduced proinflammatory product secretion (P range&lt;0.0001 to&lt;0.00001 for TNFalpha, VCAM-1, MCP-1, and IL-6); rosuvastatin inhibited morphology and oxidative modifications only.	Acetylcysteine	0-16	C-C motif chemokine ligand 2	Homo sapiens	182-187
23085426-11	2012	Interestingly, RANKL expression was suppressed when the calvarial osteoblasts were treated with NAC before IR exposure.	Acetylcysteine	96-99	tumor necrosis factor (ligand) superfamily, member 11	Mus musculus	15-20
24718901-8	2014	WA demonstrated induction of N-acetyl-L-cysteine-repressible oxidative stress as measured directly and through a subsequent heat shock response with HSP32 and HSP70 upregulation and decreased HSF1.	Acetylcysteine	29-48	heme oxygenase 1	Homo sapiens	149-154
33381272-5	2020	Antioxidant N-acetylcysteine (NAC) inhibited OLA-induced oxidative stress and p53 activation in vivo.	Acetylcysteine	30-33	transformation related protein 53, pseudogene	Mus musculus	78-81
23085515-6	2012	The effect of TNF-alpha on MST1 activation was reversed by the reducing agent N-acetyl-l-cysteine.	Acetylcysteine	78-97	macrophage stimulating 1	Homo sapiens	27-31
32871518-7	2020	Moreover, NAC administration achieved its therapeutic effect by inhibiting ovarian apoptosis-induced by radiation through downregulating p53 and Bax levels by 33% and 16%, respectively while increasing the Bcl-2 mRNA expression by 135%.	Acetylcysteine	10-13	Wistar clone pR53P1 p53 pseudogene	Rattus norvegicus	137-140
23007278-8	2012	Pretreatment with the c-Jun N-terminal kinase (JNK) inhibitor SP600125 and the reactive oxygen species (ROS) scavenger N-acetylcysteine reduced the SVT and TRAIL-induced upregulation of DR4 and DR5 expression, expression of the apoptosis related protein such as caspase-3 and-9, as well as cell growth inhibitory effects.	Acetylcysteine	119-135	TNF receptor superfamily member 10b	Homo sapiens	194-197
32871518-7	2020	Moreover, NAC administration achieved its therapeutic effect by inhibiting ovarian apoptosis-induced by radiation through downregulating p53 and Bax levels by 33% and 16%, respectively while increasing the Bcl-2 mRNA expression by 135%.	Acetylcysteine	10-13	BCL2 associated X, apoptosis regulator	Rattus norvegicus	145-148
25027749-6	2014	Control group received all standard ICU therapies and NAC group received intravenous NAC 3 gr every 6 hours for 72 hours in addition to standard therapies.	Acetylcysteine	54-57	sodium voltage-gated channel alpha subunit 3	Homo sapiens	85-90
32871518-9	2020	Importantly, the anti-apoptotic property of NAC could be attributed to inactivation of MAPK signaling molecules; p38 and JNK, and enhancement of the ovarian vascular endothelial growth factor (VEGF) expression.	Acetylcysteine	44-47	mitogen-activated protein kinase 8	Rattus norvegicus	121-124
24085626-6	2014	CoCl2-induced increase of Bax/Bcl-2 ratio and Caspase-3 expression was attenuated by RA, NAC and SB203580 (p38MAPK inhibitor).	Acetylcysteine	89-92	BCL2 associated X, apoptosis regulator	Rattus norvegicus	26-29
22991071-1	2012	The present study aimed to investigate the influence of N-acetylcysteine (NAC) on cadmium (Cd) poisoning by evaluating Cd concentration in tissues, hematological indices as well as the activity of NTPDase, acetylcholinesterase (AChE) and butyrylcholinesterase (BChE) enzymes of rats exposed to Cd and co-treated with NAC.	Acetylcysteine	74-77	acetylcholinesterase	Rattus norvegicus	228-232
32871518-9	2020	Importantly, the anti-apoptotic property of NAC could be attributed to inactivation of MAPK signaling molecules; p38 and JNK, and enhancement of the ovarian vascular endothelial growth factor (VEGF) expression.	Acetylcysteine	44-47	vascular endothelial growth factor A	Rattus norvegicus	157-191
32871518-9	2020	Importantly, the anti-apoptotic property of NAC could be attributed to inactivation of MAPK signaling molecules; p38 and JNK, and enhancement of the ovarian vascular endothelial growth factor (VEGF) expression.	Acetylcysteine	44-47	vascular endothelial growth factor A	Rattus norvegicus	193-197
32871518-10	2020	Taken together, our results suggest that NAC can inhibit radiotherapy-induced POF while preserving ovarian function and structure through upregulating VEGF expression and suppressing NOX4/MAPK/p53 apoptotic signaling.	Acetylcysteine	41-44	vascular endothelial growth factor A	Rattus norvegicus	151-155
24681255-11	2014	When the cells were pretreated with N-acetyl-l-cysteine, the effect of DJ-1 knockdown on sensitizing HeLa/DHA cells to DHA was significantly attenuated.	Acetylcysteine	36-55	Parkinsonism associated deglycase	Homo sapiens	71-75
32871518-10	2020	Taken together, our results suggest that NAC can inhibit radiotherapy-induced POF while preserving ovarian function and structure through upregulating VEGF expression and suppressing NOX4/MAPK/p53 apoptotic signaling.	Acetylcysteine	41-44	Wistar clone pR53P1 p53 pseudogene	Rattus norvegicus	193-196
23513466-3	2012	MATERIAL AND METHOD: Cytotoxicity of NAC to human prostate cancer cells, DU145 and PC3, were determined by proliferation assay using the 3-(4, 5-dimethylthiazol, 2-yl)-2, 5-diphenyltetrazolium bromide (MTT) reagent.	Acetylcysteine	37-40	chromobox 8	Homo sapiens	83-86
23513466-6	2012	RESULTS: NAC could inhibit the growth of DU145 and PC3 cells.	Acetylcysteine	9-12	chromobox 8	Homo sapiens	51-54
33343802-5	2020	Here, we found that DDF time- and concentration-dependently induced HO-1 protein and mRNA expression, which was attenuated by pretreatment with reactive oxygen species (ROS) scavenger N-acetyl cysteine (NAC) in HCFs.	Acetylcysteine	184-201	heme oxygenase 1	Homo sapiens	68-72
22692000-6	2012	Pre-treatment with the scavenger for H(2)O(2), dimethylthiourea (DMTU) and antioxidant, N-acetyl cysteine (NAC), effectively inhibited the activities of caspase-3 and caspase-9, eventually blocked Cd-induced DNA fragmentation and the appearance of markers for apoptotic cell death.	Acetylcysteine	88-105	caspase 9	Homo sapiens	167-176
24500986-7	2014	In PRA, CYP2E1-induced suppression of GLUT4 expression was blocked by chlormethiazole (CYP2E1-specific inhibitor) and the antioxidants vitamin E and N-acetyl-l-cysteine.	Acetylcysteine	149-168	solute carrier family 2 member 4	Rattus norvegicus	38-43
22692000-6	2012	Pre-treatment with the scavenger for H(2)O(2), dimethylthiourea (DMTU) and antioxidant, N-acetyl cysteine (NAC), effectively inhibited the activities of caspase-3 and caspase-9, eventually blocked Cd-induced DNA fragmentation and the appearance of markers for apoptotic cell death.	Acetylcysteine	107-110	caspase 9	Homo sapiens	167-176
22932892-6	2012	The H(2)O(2)-mediated hepcidin induction requires STAT3 phosphorylation and is effectively blocked by siRNA-mediated STAT3 silencing, overexpression of SOCS3 (suppressor of cytokine signaling 3), and antioxidants such as N-acetylcysteine.	Acetylcysteine	221-237	hepcidin antimicrobial peptide	Homo sapiens	22-30
24357417-6	2014	Vitamin C, vitamin E analogue (Trolox), glutathione, and N-acetyl-L-cysteine inhibited the Nic-Cl-induced PCNA damage, implicating oxidation in PCNA damage.	Acetylcysteine	57-76	proliferating cell nuclear antigen	Homo sapiens	106-110
33343802-5	2020	Here, we found that DDF time- and concentration-dependently induced HO-1 protein and mRNA expression, which was attenuated by pretreatment with reactive oxygen species (ROS) scavenger N-acetyl cysteine (NAC) in HCFs.	Acetylcysteine	203-206	heme oxygenase 1	Homo sapiens	68-72
24357417-6	2014	Vitamin C, vitamin E analogue (Trolox), glutathione, and N-acetyl-L-cysteine inhibited the Nic-Cl-induced PCNA damage, implicating oxidation in PCNA damage.	Acetylcysteine	57-76	proliferating cell nuclear antigen	Homo sapiens	144-148
22800716-5	2012	Bay11-7085 (an inhibitor of NF-kappaB pathway) inhibited the up-regulation of HIF-2alpha, and N-acetyl-l-cysteine (a ROS scavenger) inhibited both the decrease of IkappaB-alpha and the up-regulation of HIF-2alpha.	Acetylcysteine	94-113	endothelial PAS domain protein 1	Mus musculus	202-212
33343802-11	2020	Moreover, DDF-induced HO-1 expression was mediated through Nrf2 phosphorylation and translocation into the nucleus which was attenuated by NAC or p38 siRNA.	Acetylcysteine	139-142	heme oxygenase 1	Homo sapiens	22-26
33343802-13	2020	Interaction between Nrf2 and the ARE-binding sites on the HO-1 promoter was revealed by chromatin immunoprecipitation assay, which was attenuated by NAC, GSH, or p38i VIII.	Acetylcysteine	149-152	heme oxygenase 1	Homo sapiens	58-62
22822083-5	2012	Citreoviridin-enhanced eIF2alpha phosphorylation could be reversed by siRNA-mediated attenuation of the UPR kinase PKR-like endoplasmic reticulum kinase (PERK) combined with treatment with the antioxidant N-acetylcysteine, establishing that reactive oxygen species (ROS) boost UPR after citreoviridin treatment.	Acetylcysteine	205-221	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	154-158
33262689-0	2020	N-Acetylcysteine Rescues Hippocampal Oxidative Stress-Induced Neuronal Injury via Suppression of p38/JNK Signaling in Depressed Rats.	Acetylcysteine	0-16	mitogen-activated protein kinase 8	Rattus norvegicus	101-104
33131013-7	2021	Treatment with N-acetylcysteine (NAC) blocked 27-HC-induced ROS generation and p38 signaling pathway activation, prevented beta-catenin from release from binding, and inhibited EndMT.	Acetylcysteine	15-31	catenin beta 1	Homo sapiens	123-135
24625211-9	2014	After collection by RO bleeding, serum miR-122 could be measured and this miRNA was substantially increased by paracetamol 24 h after exposure, an increase that was prevented by delayed (3 h poststart of paracetamol exposure) treatment with acetylcysteine.	Acetylcysteine	241-255	microRNA 122	Danio rerio	39-46
33131013-7	2021	Treatment with N-acetylcysteine (NAC) blocked 27-HC-induced ROS generation and p38 signaling pathway activation, prevented beta-catenin from release from binding, and inhibited EndMT.	Acetylcysteine	33-36	catenin beta 1	Homo sapiens	123-135
33123307-8	2020	ROS induced by iron overload promote necroptosis via a positive feedback mechanism, as on the one hand N-acetylcysteine attenuates the upregulation of RIPK1 and RIPK3 and phosphorylation of RIPK1, RIPK3, and MLKL and on the other hand Nec-1, siRIPK1, or siRIPK3 reduced ROS generation.	Acetylcysteine	103-119	receptor interacting serine/threonine kinase 1	Homo sapiens	151-156
22180025-12	2012	Moreover, NAC prevented the LPS-induced decrease in claudin-1 and occludin expression in the jejunal and ileal mucosae.	Acetylcysteine	10-13	claudin 1	Sus scrofa	52-61
22180025-12	2012	Moreover, NAC prevented the LPS-induced decrease in claudin-1 and occludin expression in the jejunal and ileal mucosae.	Acetylcysteine	10-13	occludin	Sus scrofa	66-74
33123307-8	2020	ROS induced by iron overload promote necroptosis via a positive feedback mechanism, as on the one hand N-acetylcysteine attenuates the upregulation of RIPK1 and RIPK3 and phosphorylation of RIPK1, RIPK3, and MLKL and on the other hand Nec-1, siRIPK1, or siRIPK3 reduced ROS generation.	Acetylcysteine	103-119	receptor interacting serine/threonine kinase 1	Homo sapiens	190-195
22710416-7	2012	NAC successfully blocked the inhibition             of HSP70 and HSP90 as well as the activation of caspase-3, suggesting that ROS             is essential in Cr(VI)-induced caspase-3 activation.	Acetylcysteine	0-3	heat shock protein 90 alpha family class A member 1	Homo sapiens	65-70
24704379-6	2014	GST activity and the GSH/GSSG ratio increased in saline-treated CCI rats, while the NAC treatment increased GST and GPx activities at day 10, with no significant change in the GSH/GSSG ratio.	Acetylcysteine	84-87	glutathione S-transferase kappa 1	Homo sapiens	108-111
33123307-8	2020	ROS induced by iron overload promote necroptosis via a positive feedback mechanism, as on the one hand N-acetylcysteine attenuates the upregulation of RIPK1 and RIPK3 and phosphorylation of RIPK1, RIPK3, and MLKL and on the other hand Nec-1, siRIPK1, or siRIPK3 reduced ROS generation.	Acetylcysteine	103-119	proprotein convertase subtilisin/kexin type 1	Homo sapiens	235-240
23156673-0	2012	N-acetylcysteine enhances neuronal differentiation of P19 embryonic stem cells via Akt and N-cadherin activation.	Acetylcysteine	0-16	interleukin 23 subunit alpha	Homo sapiens	54-57
33030315-16	2020	N-acetylcysteine also improved all these alterations, including p53 staining.	Acetylcysteine	0-16	Wistar clone pR53P1 p53 pseudogene	Rattus norvegicus	64-67
23156673-1	2012	We examined whether N-acetylcysteine (NAC) enhanced embryonic body (EB) formation and neuronal differentiation in terms of EB formation, neuronal marker (microtubule-associated protein 2; MAP-2) expression, and neuron maturation using P19 embryonic stem cells.	Acetylcysteine	20-36	interleukin 23 subunit alpha	Homo sapiens	235-238
23156673-1	2012	We examined whether N-acetylcysteine (NAC) enhanced embryonic body (EB) formation and neuronal differentiation in terms of EB formation, neuronal marker (microtubule-associated protein 2; MAP-2) expression, and neuron maturation using P19 embryonic stem cells.	Acetylcysteine	38-41	interleukin 23 subunit alpha	Homo sapiens	235-238
22534037-12	2012	OTC and NAC counteracted the effect of HEMA on GPx1/2, SOD1, and catalase expression.	Acetylcysteine	8-11	glutathione peroxidase 1	Mus musculus	47-53
24769205-5	2014	HepG2 cells were exposed to HUA treatment and N-acetylcysteine (NAC), reactive oxygen species scavenger; IRS1 and Akt phosphorylation was detected by Western blot analysis after insulin treatment.	Acetylcysteine	64-67	insulin receptor substrate 1	Homo sapiens	105-109
24769205-8	2014	HUA induced oxidative stress, and the antioxidant NAC blocked HUA-induced IRS1 activation and Akt inhibition in HepG2 cells.	Acetylcysteine	50-53	insulin receptor substrate 1	Homo sapiens	74-78
24668803-10	2014	In determining the cigarette smoke components responsible for changes in DICER, we found that N-acetylcysteine, an antioxidant and anti-aldehyde, protected DICER protein and activity from cigarette smoke extract.	Acetylcysteine	94-110	dicer 1, ribonuclease III	Homo sapiens	73-78
24668803-10	2014	In determining the cigarette smoke components responsible for changes in DICER, we found that N-acetylcysteine, an antioxidant and anti-aldehyde, protected DICER protein and activity from cigarette smoke extract.	Acetylcysteine	94-110	dicer 1, ribonuclease III	Homo sapiens	156-161
22129233-8	2012	RESULTS: Myocardin expression after hypoxia was inhibited by atorvastatin, RhoA/Rho kinase inhibitor (Y27632), extracellular signal-regulated kinase (ERK) small interfering RNA (siRNA)/ERK pathway inhibitor (PD98059), myocardin siRNA and NAC.	Acetylcysteine	238-241	myocardin	Rattus norvegicus	9-18
24456905-8	2014	Redox-sensitive PP2A and tyrosine protein phosphatase activities diminished in pancreatitis and this loss was abrogated by N-acetylcysteine.	Acetylcysteine	123-139	protein phosphatase 2 phosphatase activator	Homo sapiens	16-20
33224008-10	2020	The acetylcysteine treatment did not cause a significant change of blood parameters, but significantly decreased 24-hour elimination of CysC and KIM-1 with urine, and accounted for alleviation of the histopathological abnormalities of urinary bladders, with no significant effects on the structure of the kidneys.	Acetylcysteine	4-18	hepatitis A virus cellular receptor 1	Rattus norvegicus	145-150
22342303-9	2012	Furthermore, NAC treatment abrogated CSE-stimulated Src activation.	Acetylcysteine	13-16	choreoathetosis/spasticity, episodic (paroxysmal choreoathetosis/spasticity)	Homo sapiens	37-40
22745145-9	2012	CONCLUSION: short-term oral NAC treatment resulted in reduction of circulating PCT, IL-6, IL-1, C3, sICAM, hsCRP, and TNF- in CAPD patients.	Acetylcysteine	28-31	interleukin 1 alpha	Homo sapiens	90-94
32715490-7	2020	In addition, citbismine-E-induced apoptosis, decrease in mitochondrial membrane potential and caspase activation were significantly alleviated by pretreatment of the cells with antioxidant N-acetylcysteine (NAC).	Acetylcysteine	189-205	caspase 9	Homo sapiens	94-101
22294162-5	2012	N-acetylcysteine, a reactive oxygen species scavenger, not only blocked the oridonin-induced increase in hydrogen peroxide and glutathione depletion, but also blocked apoptosis and senescence induced by oridonin, as evidenced by the decrease in Annexin V and senescence-associated beta-galactosidase- positive cells and the inhibition of oridonin-induced upregulation of p53 and p16 and downregulation of c-Myc.	Acetylcysteine	0-16	annexin A5	Homo sapiens	245-254
22294162-5	2012	N-acetylcysteine, a reactive oxygen species scavenger, not only blocked the oridonin-induced increase in hydrogen peroxide and glutathione depletion, but also blocked apoptosis and senescence induced by oridonin, as evidenced by the decrease in Annexin V and senescence-associated beta-galactosidase- positive cells and the inhibition of oridonin-induced upregulation of p53 and p16 and downregulation of c-Myc.	Acetylcysteine	0-16	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	405-410
24486703-8	2014	Furthermore, SB203580 prevented the increase in p22(phox) expression, and NAC and DPI not only inhibited Hcy-induced phosphorylation of p38MAPK, but also prevented expression of p22(phox).	Acetylcysteine	74-77	calcineurin like EF-hand protein 1	Homo sapiens	178-181
24296245-9	2014	We observed that NAC pretreatment upregulated heat-shock protein 90 (Hsp90) expression and increased the interaction of Hsp90 with HIF-1alpha in ischemic brains.	Acetylcysteine	17-20	heat shock protein 90 alpha family class A member 1	Homo sapiens	46-67
24296245-9	2014	We observed that NAC pretreatment upregulated heat-shock protein 90 (Hsp90) expression and increased the interaction of Hsp90 with HIF-1alpha in ischemic brains.	Acetylcysteine	17-20	heat shock protein 90 alpha family class A member 1	Homo sapiens	69-74
24296245-9	2014	We observed that NAC pretreatment upregulated heat-shock protein 90 (Hsp90) expression and increased the interaction of Hsp90 with HIF-1alpha in ischemic brains.	Acetylcysteine	17-20	heat shock protein 90 alpha family class A member 1	Homo sapiens	120-125
24296245-11	2014	Moreover, Hsp90 inhibition attenuated NAC-induced HIF-1alpha protein accumulation and diminished NAC-induced neuroprotection in the MCAO model.	Acetylcysteine	38-41	heat shock protein 90 alpha family class A member 1	Homo sapiens	10-15
24296245-11	2014	Moreover, Hsp90 inhibition attenuated NAC-induced HIF-1alpha protein accumulation and diminished NAC-induced neuroprotection in the MCAO model.	Acetylcysteine	97-100	heat shock protein 90 alpha family class A member 1	Homo sapiens	10-15
22526207-9	2012	The addition of PD98059, NAC, herbimycin-A, SB203580, and LY294002 markedly inhibited the arecoline-induced beta-catenin expression (p &lt; 0.05).	Acetylcysteine	25-28	catenin beta 1	Homo sapiens	108-120
24504121-5	2014	On the other hand, we have found that short-time N-acetyl-L-cysteine treatment at low dose increases p53 expression, which inhibits expressions of proinflammatory cytokines.	Acetylcysteine	49-68	transformation related protein 53, pseudogene	Mus musculus	101-104
32715490-7	2020	In addition, citbismine-E-induced apoptosis, decrease in mitochondrial membrane potential and caspase activation were significantly alleviated by pretreatment of the cells with antioxidant N-acetylcysteine (NAC).	Acetylcysteine	207-210	caspase 9	Homo sapiens	94-101
22526207-12	2012	In addition, beta-catenin expression induced by arecoline is downregulated by PD98059, NAC, herbimycin-A, SB203580, and LY294002.	Acetylcysteine	87-90	catenin beta 1	Homo sapiens	13-25
24270669-5	2014	HSP70 and BiP levels were higher in cultures treated with PES for 24h, but this was blocked by NAC.	Acetylcysteine	95-98	heat shock protein family A (Hsp70) member 8b	Oncorhynchus mykiss	0-5
32504923-8	2020	NAC has also been shown to inhibit the NLRP3 inflammasome pathway (IL1beta and IL18) in vitro, and decrease plasma TNF-alpha in human clinical trials.	Acetylcysteine	0-3	interleukin 1 alpha	Homo sapiens	67-74
24270669-6	2014	As well, PES treatment caused HSP70, BiP and p53 to accumulate in the detergent-insoluble fraction, and this too was prevented by NAC.	Acetylcysteine	130-133	heat shock protein family A (Hsp70) member 8b	Oncorhynchus mykiss	30-35
32768617-5	2020	We report here that NAC, but not GSH, inhibits KAT II activity in brain tissue homogenates from rats and humans with IC50 values in the high micromolar to low millimolar range.	Acetylcysteine	20-23	aminoadipate aminotransferase	Homo sapiens	47-53
24762600-8	2014	Knock-down of SIRT3 induced increased production of ROS while decreased glucose uptake in both L6 and L6-IR cells, and these effects were reversed by N-acetyl-L-cysteine (NAC).	Acetylcysteine	150-169	sirtuin 3	Rattus norvegicus	14-19
22328136-10	2012	Moreover, the increased AChE activity is prevented by the coadministration of N-acetylcysteine and deferoxamine as antioxidants.	Acetylcysteine	78-94	acetylcholinesterase	Rattus norvegicus	24-28
32768617-7	2020	NAC was a competitive inhibitor of recombinant human KAT II (Ki: 450 muM).	Acetylcysteine	0-3	aminoadipate aminotransferase	Homo sapiens	53-59
24762600-8	2014	Knock-down of SIRT3 induced increased production of ROS while decreased glucose uptake in both L6 and L6-IR cells, and these effects were reversed by N-acetyl-L-cysteine (NAC).	Acetylcysteine	171-174	sirtuin 3	Rattus norvegicus	14-19
32768617-11	2020	Together, these results suggest that NAC exerts its neurobiological effects at least in part by reducing cerebral KYNA formation via KAT II inhibition.	Acetylcysteine	37-40	aminoadipate aminotransferase	Homo sapiens	133-139
32339879-7	2020	Furthermore, N-acetylcysteine was applied as an enhancer for ATP synthesis, which reversed the downregulation of ATP5F, NDUF, and COX7A, and consequently alleviated the elevation of RELA, CAPN1, and RIP3.	Acetylcysteine	13-29	calpain 1	Homo sapiens	188-193
24872935-8	2014	Hepatic malondialdehyde (MDA), myeloperoxidase (MPO), and nitric oxide (NO) activities were significantly increased after I/R injury, but they were decreased in the groups with NAC treatment.	Acetylcysteine	177-180	myeloperoxidase	Rattus norvegicus	31-46
32339879-7	2020	Furthermore, N-acetylcysteine was applied as an enhancer for ATP synthesis, which reversed the downregulation of ATP5F, NDUF, and COX7A, and consequently alleviated the elevation of RELA, CAPN1, and RIP3.	Acetylcysteine	13-29	myosin phosphatase Rho interacting protein	Homo sapiens	199-203
24872935-8	2014	Hepatic malondialdehyde (MDA), myeloperoxidase (MPO), and nitric oxide (NO) activities were significantly increased after I/R injury, but they were decreased in the groups with NAC treatment.	Acetylcysteine	177-180	myeloperoxidase	Rattus norvegicus	48-51
24145059-8	2013	SA-induced upregulation of LOX-1 protein expression was clearly prevented by treatment with an antioxidant, N-acetylcysteine (NAC), or an NF-kappaB inhibitor, caffeic acid phenethylester (CAPE).	Acetylcysteine	108-124	oxidized low density lipoprotein (lectin-like) receptor 1	Mus musculus	27-32
32334250-10	2020	We further found that N-acetylcysteine, a well-known antioxidant, obviously reversed Cd-downregulated 11beta-HSD2 protein expression by inhibiting p-PERK/p-eIF2alpha signaling in placental trophoblasts.	Acetylcysteine	22-38	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	149-153
24145059-8	2013	SA-induced upregulation of LOX-1 protein expression was clearly prevented by treatment with an antioxidant, N-acetylcysteine (NAC), or an NF-kappaB inhibitor, caffeic acid phenethylester (CAPE).	Acetylcysteine	126-129	oxidized low density lipoprotein (lectin-like) receptor 1	Mus musculus	27-32
24064383-7	2013	All these changes, including the intestinal histology and hepatic apoptosis, determined by TUNEL assay, were significantly reversed when WT-EtOH mice were treated with the specific inhibitor of CYP2E1 chlormethiazole and the antioxidant N-acetylcysteine, both of which suppressed oxidative markers including intestinal CYP2E1.	Acetylcysteine	237-253	cytochrome P450, family 2, subfamily e, polypeptide 1	Mus musculus	194-200
23975535-10	2013	NAC protected against MDMA-induced cell death and the up -regulation of Bax and Caspase-3, in addition to the down-regulation of Bcl-2.	Acetylcysteine	0-3	BCL2 associated X, apoptosis regulator	Rattus norvegicus	72-75
32640348-4	2020	Furthermore, RT-qPCR and immunofluorescence assay results indicated that NAC restored the expression of Gclc, reduced the expression of ATF4, JNK and Caspase-12, and decreased the expression of eNOS and IGF-1, in the placenta.	Acetylcysteine	73-76	nitric oxide synthase 3, endothelial cell	Mus musculus	194-198
24142350-6	2013	Similarly to ZNS effects, the treatment with N-acetyl-cysteine (100 muM) displayed significant protective effects against rotenone-induced ROS production and Deltapsim at 4 and 12 h respectively, reaching the maximal extent at 24 h. Additionally, ZNS displayed antiapoptotic effects, as demonstrated by flow cytometric analysis of annexin V/propidium iodide double staining, and significant attenuated rotenone-increased caspase 3 activity.	Acetylcysteine	45-62	annexin A5	Homo sapiens	331-340
32444367-5	2020	NAC treatment normalized HFD-induced maternal weight gain and oxidative stress, improved the maternal lipidome and prevented maternal leptin resistance.	Acetylcysteine	0-3	leptin	Mus musculus	134-140
23811485-2	2013	In this work, a ratiometric fluorescence sensor is developed based on fluorescence resonance energy transfer (FRET) with N-acetyl-L-cysteine functionalized quantum dots (NAC-QDs) as donor and Rhodamine 6G derivative-mercury conjugate (R6G-D-Hg) as acceptor.	Acetylcysteine	121-140	synuclein alpha	Homo sapiens	170-173
32583517-8	2020	Relative to Bmi-1-/- mice, the control and Bmi-1-/- +NAC mice showed significantly lower p16, p21, and p53 levels.	Acetylcysteine	53-56	transformation related protein 53, pseudogene	Mus musculus	103-106
24134840-4	2013	Meanwhile, curcumin induced reactive oxygen species (ROS) production in melanoma cells, and the ROS scavenger, N-acetyl-cysteine (NAC), almost blocked MST1 activation to suggest that ROS might be required for MST1 activation by curcumin.	Acetylcysteine	111-128	macrophage stimulating 1	Homo sapiens	151-155
24134840-4	2013	Meanwhile, curcumin induced reactive oxygen species (ROS) production in melanoma cells, and the ROS scavenger, N-acetyl-cysteine (NAC), almost blocked MST1 activation to suggest that ROS might be required for MST1 activation by curcumin.	Acetylcysteine	111-128	macrophage stimulating 1	Homo sapiens	209-213
24134840-4	2013	Meanwhile, curcumin induced reactive oxygen species (ROS) production in melanoma cells, and the ROS scavenger, N-acetyl-cysteine (NAC), almost blocked MST1 activation to suggest that ROS might be required for MST1 activation by curcumin.	Acetylcysteine	130-133	macrophage stimulating 1	Homo sapiens	151-155
32361974-5	2020	The presence of NAC antagonized the ROS production, expressions of IRE1alpha and p-IRE1alpha; however, STF-083010 could decrease the expression levels of GRP78, XBP1, NF-kappaB, and p-NF-kappaB and attenuate IL-1beta, IL-6, TNF-alpha, VCAM-1, and ET-1 release induced by endosulfan.	Acetylcysteine	16-19	interleukin 1 alpha	Homo sapiens	208-216
24134840-4	2013	Meanwhile, curcumin induced reactive oxygen species (ROS) production in melanoma cells, and the ROS scavenger, N-acetyl-cysteine (NAC), almost blocked MST1 activation to suggest that ROS might be required for MST1 activation by curcumin.	Acetylcysteine	130-133	macrophage stimulating 1	Homo sapiens	209-213
24134840-5	2013	c-Jun N-terminal protein kinase (JNK) activation by curcumin was dependent on MST1, since MST1 inhibition by RNAi or NAC largely inhibited curcumin-induced JNK activation.	Acetylcysteine	117-120	macrophage stimulating 1	Homo sapiens	78-82
32655795-4	2020	In addition, N-acetylcysteine (NAC) has been shown to effectively suppress HSC activation-dependent expression of alpha-smooth muscle actin in HSCs, suggesting that NAC could be a candidate for the clinical treatment of hepatic fibrosis.	Acetylcysteine	13-29	fucosyltransferase 1 (H blood group)	Homo sapiens	75-78
24134840-5	2013	c-Jun N-terminal protein kinase (JNK) activation by curcumin was dependent on MST1, since MST1 inhibition by RNAi or NAC largely inhibited curcumin-induced JNK activation.	Acetylcysteine	117-120	macrophage stimulating 1	Homo sapiens	90-94
32655795-4	2020	In addition, N-acetylcysteine (NAC) has been shown to effectively suppress HSC activation-dependent expression of alpha-smooth muscle actin in HSCs, suggesting that NAC could be a candidate for the clinical treatment of hepatic fibrosis.	Acetylcysteine	31-34	fucosyltransferase 1 (H blood group)	Homo sapiens	75-78
23558526-8	2013	Furthermore, NAC induced a marked decrease in splenomegaly with reduction in the frequency of the Jak2(V617F)-positive hematopoietic progenitors in BM and spleen.	Acetylcysteine	13-16	Janus kinase 2	Mus musculus	98-108
32655795-4	2020	In addition, N-acetylcysteine (NAC) has been shown to effectively suppress HSC activation-dependent expression of alpha-smooth muscle actin in HSCs, suggesting that NAC could be a candidate for the clinical treatment of hepatic fibrosis.	Acetylcysteine	165-168	fucosyltransferase 1 (H blood group)	Homo sapiens	75-78
32655795-7	2020	In addition, co-administration of NAC with everolimus further reduced the expression of fibrogenic genes and improved the characteristic of HSCs via blockage of HSC activation and up-regulation of fibrolytic gene.	Acetylcysteine	34-37	fucosyltransferase 1 (H blood group)	Homo sapiens	140-143
23475548-7	2013	RESULTS: Serum transaminases and tissue and serum MDA and tissue MPO were all increased in group 1 compared to control and were significantly decreased in the group treated with NAC.	Acetylcysteine	178-181	myeloperoxidase	Rattus norvegicus	65-68
31837856-8	2020	Incidentally, both CH and NAC attenuated the EOM-induced changes in the mRNA expression of genes involved in cardiac development (nkx2.5, sox9b), oxidative stress (nrf2a, nrf2b, gstp1, gstp2, sod2, ho1, cat) and apoptosis (p53, bax).	Acetylcysteine	26-29	glutathione S-transferase pi 1.1	Danio rerio	185-190
31837856-8	2020	Incidentally, both CH and NAC attenuated the EOM-induced changes in the mRNA expression of genes involved in cardiac development (nkx2.5, sox9b), oxidative stress (nrf2a, nrf2b, gstp1, gstp2, sod2, ho1, cat) and apoptosis (p53, bax).	Acetylcysteine	26-29	tumor protein p53	Danio rerio	223-226
23804706-9	2013	N-acetylcysteine blocked reduction in the levels of Mcl-1, c-FLIP, and intracellular GSH as well as apoptosis in HL-60 cells treated by either compound.	Acetylcysteine	0-16	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	52-57
24015194-0	2013	Both PKA and Epac pathways mediate N-acetylcysteine-induced Connexin43 preservation in rats with myocardial infarction.	Acetylcysteine	35-51	protein kinase cAMP-activated catalytic subunit alpha	Rattus norvegicus	5-8
24015194-10	2013	In an ex vivo study, enhanced connexin43 levels afforded by N-acetylcysteine were partially blocked by either H-89 (a PKA inhibitor) or brefeldin A (an Epac-signaling inhibitor) and completely blocked when H-89 and brefeldin A were given in combination.	Acetylcysteine	60-76	protein kinase cAMP-activated catalytic subunit alpha	Rattus norvegicus	118-121
31837856-8	2020	Incidentally, both CH and NAC attenuated the EOM-induced changes in the mRNA expression of genes involved in cardiac development (nkx2.5, sox9b), oxidative stress (nrf2a, nrf2b, gstp1, gstp2, sod2, ho1, cat) and apoptosis (p53, bax).	Acetylcysteine	26-29	BCL2 associated X, apoptosis regulator a	Danio rerio	228-231
32450865-10	2020	In the unfolded protein response (UPR) pathway, the expression of ECHS1, HSP60, and HSP70 was decreased in the HFD group (p < 0.05) and rescued by NAC therapy.	Acetylcysteine	147-150	heat shock protein 1 (chaperonin)	Mus musculus	73-78
32443749-8	2020	In turn, ROS inhibition by N-acetyl-L-cysteine (NAC) had no effect on T98G morphology, but considerably attenuated EGF-induced cell motility.	Acetylcysteine	27-46	epidermal growth factor	Homo sapiens	115-118
23860378-14	2013	NAC also blocked stromal induction of MCT4, indicating that NAC effectively functions as an "MCT4 inhibitor".	Acetylcysteine	0-3	solute carrier family 16 member 3	Homo sapiens	38-42
23860378-14	2013	NAC also blocked stromal induction of MCT4, indicating that NAC effectively functions as an "MCT4 inhibitor".	Acetylcysteine	0-3	solute carrier family 16 member 3	Homo sapiens	93-97
23860378-14	2013	NAC also blocked stromal induction of MCT4, indicating that NAC effectively functions as an "MCT4 inhibitor".	Acetylcysteine	60-63	solute carrier family 16 member 3	Homo sapiens	38-42
23867003-5	2013	NAC also induced the protein expression of PPARalpha.	Acetylcysteine	0-3	peroxisome proliferator activated receptor alpha	Homo sapiens	43-52
32443749-8	2020	In turn, ROS inhibition by N-acetyl-L-cysteine (NAC) had no effect on T98G morphology, but considerably attenuated EGF-induced cell motility.	Acetylcysteine	48-51	epidermal growth factor	Homo sapiens	115-118
23867003-6	2013	While PPARalpha ligand enhanced, PPARalpha antagonist and siRNA abrogated the effect of NAC on PDK1 promoter activity, protein expression and cell growth.	Acetylcysteine	88-91	peroxisome proliferator activated receptor alpha	Homo sapiens	33-42
23867003-8	2013	NAC induced p53 and reduced p65 protein expression through activation of PPARalpha.	Acetylcysteine	0-3	peroxisome proliferator activated receptor alpha	Homo sapiens	73-82
32432106-8	2020	In addition, suppressing ROS production by N-acetyl-L-cysteine down-regulated the number of intracellular autophagosomes and the expression of Beclin-1, ATG5, and cytokines IL-1beta, IL-6, and TNF-alpha.	Acetylcysteine	43-62	tumor necrosis factor	Ovis aries	193-202
23867003-10	2013	CONCLUSION: Our results show that NAC inhibits PDK1 expression through PPARalpha-mediated induction of p53 and inhibition of p65 protein expression.	Acetylcysteine	34-37	peroxisome proliferator activated receptor alpha	Homo sapiens	71-80
23867003-11	2013	PPARalpha ligand enhances the effect of NAC.	Acetylcysteine	40-43	peroxisome proliferator activated receptor alpha	Homo sapiens	0-9
31587481-8	2020	The NAC therapy considerably attenuated the exacerbated effects of BPA, which was associated with increased AMP-activated protein kinase (AMPK), PGC-1alpha, silent information regulator 3 or sirtuin 3 (SIRT3), and mitofusin 2 (MFN2) expressions but decreased Phosphorylated dynamin-related protein 1 (p-DRP1)/Dynamin-related protein 1 (DRP1), PTEN-induced putative kinase (PINK), and PARKIN expressions.	Acetylcysteine	4-7	sirtuin 3	Rattus norvegicus	191-200
23578993-15	2013	Keeping in view the biochemical and histopathological studies, it was concluded that CCl4 and TAA are strong hepatotoxic agents that produce liver fibrosis with close proximity to human etiology (micronodular cirrhosis) and NAC has a significant protective activity against CCl4 and TAA.	Acetylcysteine	224-227	C-C motif chemokine ligand 4	Homo sapiens	85-89
31587481-8	2020	The NAC therapy considerably attenuated the exacerbated effects of BPA, which was associated with increased AMP-activated protein kinase (AMPK), PGC-1alpha, silent information regulator 3 or sirtuin 3 (SIRT3), and mitofusin 2 (MFN2) expressions but decreased Phosphorylated dynamin-related protein 1 (p-DRP1)/Dynamin-related protein 1 (DRP1), PTEN-induced putative kinase (PINK), and PARKIN expressions.	Acetylcysteine	4-7	sirtuin 3	Rattus norvegicus	202-207
31587481-9	2020	These findings reveal the detrimental effect of repeated BPA exposure on the renal outcomes following the IR episode, and further demonstrate the protective efficacy of NAC by maintaining mitochondrial homeostasis, which is, partly, mediated through the AMPK-PGC-1alpha-SIRT3 axis.	Acetylcysteine	169-172	sirtuin 3	Rattus norvegicus	270-275
32144161-4	2020	Mechanistically, we found that the increased ULBP2/5 expression was dependent on oxidative stress and the antioxidants N-acetylcysteine and glutathione (GSH) abrogated ULBP2/5 upregulated by DMF.	Acetylcysteine	119-135	UL16 binding protein 2	Homo sapiens	45-50
32144161-4	2020	Mechanistically, we found that the increased ULBP2/5 expression was dependent on oxidative stress and the antioxidants N-acetylcysteine and glutathione (GSH) abrogated ULBP2/5 upregulated by DMF.	Acetylcysteine	119-135	UL16 binding protein 2	Homo sapiens	168-173
32104284-11	2020	In conclusion, tetrandrine combined with acetylcysteine can improve pulmonary function and exercise tolerance of patients with silicosis by inhibiting the expressions of TGF-beta1 and MMP-7, thus improving clinical efficacy.	Acetylcysteine	41-55	matrix metallopeptidase 7	Homo sapiens	184-189
31995555-8	2020	Notably, the triple treatment-induced cytotoxic effects and the elevated expression of p53 and p21 proteins as well as the increased Bax/Bcl-2 ratio, all could be alleviated by the ROS scavenger, N-acetyl-cysteine (NAC).	Acetylcysteine	196-213	H3 histone pseudogene 16	Homo sapiens	95-98
31995555-8	2020	Notably, the triple treatment-induced cytotoxic effects and the elevated expression of p53 and p21 proteins as well as the increased Bax/Bcl-2 ratio, all could be alleviated by the ROS scavenger, N-acetyl-cysteine (NAC).	Acetylcysteine	215-218	H3 histone pseudogene 16	Homo sapiens	95-98
31707343-7	2020	Furthermore, compared with control HaCaT cells, CNT-treated HaCaT cells produced more reactive oxygen species (ROS), but this effect was inhibited by the antioxidants N-acetyl-cysteine (NAC), diphenyleneiodonium chloride (DPI), and apocynin and the necroptosis inhibitor Nec-1.	Acetylcysteine	186-189	proprotein convertase subtilisin/kexin type 1	Homo sapiens	271-276
31707348-5	2020	In angiotensin II (Ang II)-treated cardiomyocytes, BRD4 decrease markedly blunted the prohypertrophic effect, which was further promoted by the combinational treatment of ROS scavenger (N-acetyl-cysteine, NAC).	Acetylcysteine	186-203	bromodomain containing 4	Mus musculus	51-55
32468750-8	2020	When this increase was compared between groups, the lowest increase in serum ALT and AST levels was observed in Nacetylcysteine and prazosin group with no significant difference.	Acetylcysteine	112-127	glutamic pyruvic transaminase, soluble	Mus musculus	77-80
32468750-8	2020	When this increase was compared between groups, the lowest increase in serum ALT and AST levels was observed in Nacetylcysteine and prazosin group with no significant difference.	Acetylcysteine	112-127	solute carrier family 17 (anion/sugar transporter), member 5	Mus musculus	85-88
31585350-0	2020	Osteogenesis enhancement of silk fibroin/ alpha-TCP cement by N-acetyl cysteine through Wnt/beta-catenin signaling pathway in vivo and vitro.	Acetylcysteine	62-79	Wnt family member 2	Rattus norvegicus	88-91
31585350-0	2020	Osteogenesis enhancement of silk fibroin/ alpha-TCP cement by N-acetyl cysteine through Wnt/beta-catenin signaling pathway in vivo and vitro.	Acetylcysteine	62-79	catenin beta 1	Rattus norvegicus	92-104
31751619-0	2020	N-acetylcysteine (NAC) alleviates the peripheral neuropathy associated with liver cirrhosis via modulation of neural MEG3/PAR2/ NF-kB axis.	Acetylcysteine	0-16	F2R like trypsin receptor 1	Rattus norvegicus	122-126
31751619-0	2020	N-acetylcysteine (NAC) alleviates the peripheral neuropathy associated with liver cirrhosis via modulation of neural MEG3/PAR2/ NF-kB axis.	Acetylcysteine	0-16	RELA proto-oncogene, NF-kB subunit	Rattus norvegicus	128-133
31751619-0	2020	N-acetylcysteine (NAC) alleviates the peripheral neuropathy associated with liver cirrhosis via modulation of neural MEG3/PAR2/ NF-kB axis.	Acetylcysteine	18-21	F2R like trypsin receptor 1	Rattus norvegicus	122-126
31751619-0	2020	N-acetylcysteine (NAC) alleviates the peripheral neuropathy associated with liver cirrhosis via modulation of neural MEG3/PAR2/ NF-kB axis.	Acetylcysteine	18-21	RELA proto-oncogene, NF-kB subunit	Rattus norvegicus	128-133
31751619-3	2020	We aimed to investigate the role of this axis in cirrhotic neuropathy and whether an antioxidant compound such as N-acetylcysteine (NAC) could improve the peripheral nerve function through repression of MEG3/PAR2.	Acetylcysteine	114-130	F2R like trypsin receptor 1	Rattus norvegicus	208-212
31751619-3	2020	We aimed to investigate the role of this axis in cirrhotic neuropathy and whether an antioxidant compound such as N-acetylcysteine (NAC) could improve the peripheral nerve function through repression of MEG3/PAR2.	Acetylcysteine	132-135	F2R like trypsin receptor 1	Rattus norvegicus	208-212
31751619-11	2020	CONCLUSIONS: NAC could improve the peripheral neuropathy in cirrhotic rat through suppression of MEG3/PAR2 expression.	Acetylcysteine	13-16	F2R like trypsin receptor 1	Rattus norvegicus	102-106
31751620-10	2020	The antidepressive-like and procognitive effects of NAC was associated with normalization of volume loss in CA1, dentate gyrus (DG) and hilar subfields of the hippocampus.	Acetylcysteine	52-55	carbonic anhydrase 1	Rattus norvegicus	108-111
31655538-14	2019	Interestingly, NAC elevated MPO and HMGB-1 levels significantly.	Acetylcysteine	15-18	myeloperoxidase	Rattus norvegicus	28-31
31842349-9	2019	The reactive oxygen species (ROS) scavengers N-acetyl cysteine (NAC) and reduced glutathione (GSH) partially attenuated apoptosis in the HCT116 p53-/- cell line but had no obvious effect on the p53+/+ cell line.	Acetylcysteine	45-62	transformation related protein 53, pseudogene	Mus musculus	144-147
31842349-9	2019	The reactive oxygen species (ROS) scavengers N-acetyl cysteine (NAC) and reduced glutathione (GSH) partially attenuated apoptosis in the HCT116 p53-/- cell line but had no obvious effect on the p53+/+ cell line.	Acetylcysteine	64-67	transformation related protein 53, pseudogene	Mus musculus	144-147
31430466-7	2019	Consistent with these morphologic improvements, placentas from HFD dams treated with NAC had decreased mRNA and immunostaining of IL-1beta and monocyte chemoattractant protein-1, decreased mRNA of inflammatory genes, and increased mRNA of Vegfa.	Acetylcysteine	85-88	interleukin 1 alpha	Mus musculus	130-138
22274925-8	2012	Additionally, H(2)O(2) treatment inhibited the nuclear localization and expression of RUNX3, which was abolished by NAC treatment.	Acetylcysteine	116-119	RUNX family transcription factor 3	Homo sapiens	86-91
22166790-5	2012	Pre-treatment with antioxidant vitamin E or N-acetylcysteine (NAC) completely abolished the I6-induced generation of ROS, loss of MMP, release of cytochrome c, activation of caspase-9 and caspase-3, and cleavage of PARP.	Acetylcysteine	44-60	poly (ADP-ribose) polymerase 1	Rattus norvegicus	215-219
22166790-5	2012	Pre-treatment with antioxidant vitamin E or N-acetylcysteine (NAC) completely abolished the I6-induced generation of ROS, loss of MMP, release of cytochrome c, activation of caspase-9 and caspase-3, and cleavage of PARP.	Acetylcysteine	62-65	poly (ADP-ribose) polymerase 1	Rattus norvegicus	215-219
31272005-10	2019	N-acetylcysteine antagonized arsenite-mediated induction of HMOX1 expression as well as reduction of neuronal and oligodendrocyte differentiation in hNPC suggesting involvement of oxidative stress in arsenite DNT.	Acetylcysteine	0-16	heme oxygenase 1	Homo sapiens	60-65
20673252-10	2012	The content of muscle-derived ROS, TBARS, EBD and MPO activity in both gastrocnemius and soleus muscles were also decreased by NAC pre-treatment.	Acetylcysteine	127-130	myeloperoxidase	Rattus norvegicus	50-53
22078209-6	2012	The NAC-induced homoaggregation phenotype is paralleled with increased expressions of CD54, CD11a, CD27 and CD38.	Acetylcysteine	4-7	CD27 molecule	Homo sapiens	99-103
22078209-6	2012	The NAC-induced homoaggregation phenotype is paralleled with increased expressions of CD54, CD11a, CD27 and CD38.	Acetylcysteine	4-7	CD38 molecule	Homo sapiens	108-112
31666108-12	2019	Furthermore, the antioxidant agent N-acetylcysteine and NRF2 inhibitor brusatol effectively suppressed the growth of Gstz1-knockout HepG2 cells and HCC progression in Gstz1-/- mice.	Acetylcysteine	35-51	glutathione S-transferase zeta 1	Homo sapiens	117-122
22530011-7	2012	N-acetylcysteine (NAC), a pharmacological antioxidant, increased T-cell proliferation and IL-2 production by TCR and ConA stimulated splenocytes but had no effect on the response to PHA in primary porcine splenocytes confirming that PHA-induced T-cell activation is insensitive to the redox status.	Acetylcysteine	0-16	T cell receptor beta variable 20/OR9-2 (non-functional)	Homo sapiens	109-112
22530011-7	2012	N-acetylcysteine (NAC), a pharmacological antioxidant, increased T-cell proliferation and IL-2 production by TCR and ConA stimulated splenocytes but had no effect on the response to PHA in primary porcine splenocytes confirming that PHA-induced T-cell activation is insensitive to the redox status.	Acetylcysteine	18-21	T cell receptor beta variable 20/OR9-2 (non-functional)	Homo sapiens	109-112
22019925-9	2011	In addition, DNA strand breaks were attenuated when cells were pre-treated with N-acetyl-l-cysteine (NAC) and oxidative base modifications were revealed when a lesion specific endonuclease, human 8-hydroxyguanine DNA glycosylase 1 (hOGG1) was introduced into the comet assay.	Acetylcysteine	80-99	8-oxoguanine DNA glycosylase	Homo sapiens	232-237
31666108-12	2019	Furthermore, the antioxidant agent N-acetylcysteine and NRF2 inhibitor brusatol effectively suppressed the growth of Gstz1-knockout HepG2 cells and HCC progression in Gstz1-/- mice.	Acetylcysteine	35-51	glutathione S-transferase zeta 1	Homo sapiens	167-172
31640182-8	2019	NAC also mitigated the abnormalities in mitochondrial functions, dynamics, mitophagy, and ultrastructure of the liver by improving the mitochondrial homeostasis regulatory signaling AMPK-PGC-1alpha-SIRT3.	Acetylcysteine	0-3	sirtuin 3	Rattus norvegicus	198-203
21667118-9	2011	Combined treatment with N-acetyl-L: -cysteine and/or desferrioxamine mesylate attenuated the stimulating effect of ascorbic acid on tyrosinase activation in the cells.	Acetylcysteine	24-45	tyrosinase	Mus musculus	132-142
21843499-3	2011	We found that pretreatment of SP600125, an inhibitor of c-Jun N-terminal kinase (JNK), or an anti-oxidant, N-acetylcysteine (NAC), could not only prevent Daxx from trafficking but also increase the number of the surviving CA1 pyramidal cells of hippocampus at 5days of reperfusion.	Acetylcysteine	107-123	carbonic anhydrase 1	Rattus norvegicus	222-225
21843499-3	2011	We found that pretreatment of SP600125, an inhibitor of c-Jun N-terminal kinase (JNK), or an anti-oxidant, N-acetylcysteine (NAC), could not only prevent Daxx from trafficking but also increase the number of the surviving CA1 pyramidal cells of hippocampus at 5days of reperfusion.	Acetylcysteine	125-128	carbonic anhydrase 1	Rattus norvegicus	222-225
21843499-5	2011	We found the treatment of SP600125 or NAC could decrease the activation of Ask1 during ischemia/reperfusion and suppress the assembly of the Fas Daxx Ask1 signaling module, and in succession inhibit JNK activation and c-Jun phosphorylation.	Acetylcysteine	38-41	mitogen-activated protein kinase 8	Rattus norvegicus	199-202
21854768-8	2011	Interestingly, pretreatment with an antioxidant, N-acetylcysteine (NAC), inhibited not only CHOP and DR5 up-regulation but also the cell death induced by acrolein plus TRAIL.	Acetylcysteine	49-65	TNF receptor superfamily member 10b	Homo sapiens	101-104
21854768-8	2011	Interestingly, pretreatment with an antioxidant, N-acetylcysteine (NAC), inhibited not only CHOP and DR5 up-regulation but also the cell death induced by acrolein plus TRAIL.	Acetylcysteine	67-70	TNF receptor superfamily member 10b	Homo sapiens	101-104
23640483-8	2013	Treatment of THP-1 cells with an antioxidant, N-acetyl cysteine, suppressed the above HNE-induced responses and negated the HNE-mediated increase in TF activity.	Acetylcysteine	46-63	coagulation factor III, tissue factor	Homo sapiens	149-151
31649499-12	2019	These effects of AF on ARPE-19 are inhibited by antioxidant N-acetylcysteine (5 mM, NAC) and significantly by a combination of SS31 (mitochondrial antioxidant) and anti-inflammatory drugs (amlexanox and tranilast).	Acetylcysteine	60-76	synuclein alpha	Homo sapiens	84-87
23731375-11	2013	Leukocyte GST activities decreased significantly after treatment in workers receiving 200 mg of NAC by 34%, while LPS levels decreased significantly in workers receiving 200, 400, and 800 mg of NAC compared to those in baseline by 5%, 15%, and 13%, respectively.	Acetylcysteine	96-99	glutathione S-transferase kappa 1	Homo sapiens	10-13
22126012-5	2011	First two rate limiting enzymes of the mercapturic acid pathway, GSTs that conjugate HNE to glutathione (GSH), and RLIP76 that excludes GHS-HNE conjugate from cells, regulate the intracellular concentration of HNE.	Acetylcysteine	39-55	ralA binding protein 1	Homo sapiens	115-121
22126012-8	2011	A major outcome of these findings is that by blocking the mercapturic acid pathway mediated detoxification of HNE through the inhibition of RLIP76 catalyzed transport of GS-HNE, a complete remission of many human cancer xenografts in mice can be achieved.	Acetylcysteine	58-74	ralA binding protein 1	Homo sapiens	140-146
21954051-6	2011	Overall, the proteomic results support the notion that NAC may be beneficial for increasing cellular stress responses in WT mice and for influencing the levels of energy- and mitochondria-related proteins in APP/PS-1 mice.	Acetylcysteine	55-58	presenilin 1	Mus musculus	212-216
31581464-9	2019	Maternal treatment with sapropterin, a cofactor of eNOS, and antioxidants such as N-acetylcysteine, vitamin E, and glutathione as well as maternal exercise have been shown to improve eNOS function, reduce oxidative stress, and lower the incidence CHDs in the offspring of mice with pregestational diabetes.	Acetylcysteine	82-98	nitric oxide synthase 3, endothelial cell	Mus musculus	183-187
21864514-7	2011	Presence of the antioxidant N-acetylcysteine (1.0mM) attenuated intracellular ROS and prevented cell death induction in both SH-SY5Y and FS2 cells, indicating that the cytotoxicity of ribosylated beta(2)M aggregates depends on a ROS-mediated pathway in both cell lines.	Acetylcysteine	28-44	beta-2-microglobulin	Homo sapiens	196-204
23840457-4	2013	The antioxidant N-acetylcysteine (NAC) was recently shown to prevent Hif-1alpha stabilization under hypoxia, and has been identified as a potential alternative method to target the hypoxic response in tumors.	Acetylcysteine	16-32	hypoxia inducible factor 1, alpha subunit	Mus musculus	69-79
23840457-4	2013	The antioxidant N-acetylcysteine (NAC) was recently shown to prevent Hif-1alpha stabilization under hypoxia, and has been identified as a potential alternative method to target the hypoxic response in tumors.	Acetylcysteine	34-37	hypoxia inducible factor 1, alpha subunit	Mus musculus	69-79
23840457-6	2013	While NAC prevented Hif-1alpha stabilization under hypoxia in vitro and increased levels of glutathione in the blood of mice in vivo, this did not translate to a difference in tumor growth or the hypoxic state of the tumor compared to untreated control mice.	Acetylcysteine	6-9	hypoxia inducible factor 1, alpha subunit	Mus musculus	20-30
31288199-7	2019	In conclusion, NAC exhibits dual and antagonistic effects on Cd2+ cytotoxicity in human leukemia cells.	Acetylcysteine	15-18	CD2 molecule	Homo sapiens	61-64
23604711-7	2013	In addition, the strain-mediated induction of HO-1 and activation of Nrf2 was abolished by the antioxidant N-acetyl-l-cysteine.	Acetylcysteine	107-126	heme oxygenase 1	Homo sapiens	46-50
21762691-8	2011	We then showed that luteolin induced accumulation of reactive oxygen species and that the anti-oxidant N-acetylcysteine reduced luteolin-induced cell death and expression of CHOP and GRP78.	Acetylcysteine	103-119	DNA-damage inducible transcript 3	Mus musculus	174-178
21544615-6	2011	The TNF-alpha-induced upregulation of LOX-1 was also attenuated by the NF-kappaB inhibitor N-acetyl-L-cysteine.	Acetylcysteine	91-110	oxidized low density lipoprotein (lectin-like) receptor 1	Mus musculus	38-43
31332969-6	2019	The ROS inhibitor N-acetylcysteine and MAPK inhibitors significantly reduced the expression of IL-6 and IL-24 induced by T. forsythia.	Acetylcysteine	18-34	interleukin 24	Homo sapiens	104-109
24278567-8	2011	Pretreatment of antioxidants, N-acetylcysteine (NAC) and sulforaphane restored decreased viability of N990-treated A-10 cells, and N-acetylcysteine, but not sulforaphane, attenuated N990-induced ROS generation in A-10 cells.	Acetylcysteine	30-46	immunoglobulin kappa variable 6D-21 (non-functional)	Homo sapiens	115-119
24278567-8	2011	Pretreatment of antioxidants, N-acetylcysteine (NAC) and sulforaphane restored decreased viability of N990-treated A-10 cells, and N-acetylcysteine, but not sulforaphane, attenuated N990-induced ROS generation in A-10 cells.	Acetylcysteine	48-51	immunoglobulin kappa variable 6D-21 (non-functional)	Homo sapiens	115-119
24278567-8	2011	Pretreatment of antioxidants, N-acetylcysteine (NAC) and sulforaphane restored decreased viability of N990-treated A-10 cells, and N-acetylcysteine, but not sulforaphane, attenuated N990-induced ROS generation in A-10 cells.	Acetylcysteine	131-147	immunoglobulin kappa variable 6D-21 (non-functional)	Homo sapiens	213-217
23454206-7	2013	Furthermore, exposure to the ROS scavenger N acetylcysteine (NAC)prevents CRA-induced apoptosis, suggesting a role for ROS in CRA-induced apoptosis.	Acetylcysteine	43-59	synuclein alpha	Homo sapiens	61-64
31553952-5	2019	In parallel, ROS scavenger N-acetyl cysteine (NAC) abrogated the effects of downregulated LncRNA-XIST on NSCLC cell pyroptosis.	Acetylcysteine	27-44	X inactive specific transcript	Homo sapiens	97-101
21252047-10	2011	Both N-acetyl cysteine and diphenylene iodonium, a NADP(H) inhibitor, inhibited the expression of HIF-1alpha and VEGF stimulated by leptin or PDGF.	Acetylcysteine	5-22	leptin	Homo sapiens	132-138
31583053-6	2019	Similarly, NAC could restore RPC protection from high glucose and hypoxia/reoxygenation-induced injury evidenced by decreased levels of LDH release, 15-F2t-isoprostane, O2 -, and JC-1 monomeric cells, which were reversed by caveolae disrupter methyl-beta-cyclodextrin, wortmannin, or AG490 in isolated primary cardiomyocytes or siRNAs of Cav-3, Akt, or STAT3 in H9C2 cells.	Acetylcysteine	11-14	signal transducer and activator of transcription 3	Rattus norvegicus	353-358
23375450-7	2013	Notably, in a translational setting of therapeutic treatment 2 hours after APAP, IL-22 supported protection in the context of suboptimal N-acetylcysteine dosing.	Acetylcysteine	137-153	interleukin 22	Mus musculus	81-86
31583053-10	2019	Antioxidant treatment with NAC could restore RPC-induced cardioprotection in diabetes by improving Cav-3-dependent Akt and STAT3 activation and by facilitating the cross talk between PI3K/Akt and JAK2/STAT3 signaling pathways.	Acetylcysteine	27-30	signal transducer and activator of transcription 3	Rattus norvegicus	123-128
21358671-5	2011	SirT3 knockdown increases tumorigenesis in xenograft models, and this is abolished by giving mice the anti-oxidant N-acetyl cysteine.	Acetylcysteine	115-132	sirtuin 3	Mus musculus	0-5
31583053-10	2019	Antioxidant treatment with NAC could restore RPC-induced cardioprotection in diabetes by improving Cav-3-dependent Akt and STAT3 activation and by facilitating the cross talk between PI3K/Akt and JAK2/STAT3 signaling pathways.	Acetylcysteine	27-30	signal transducer and activator of transcription 3	Rattus norvegicus	201-206
21536676-6	2011	15(S)-HETE induced the production of H(2)O(2) via an NADPH oxidase-dependent manner and its scavengers, N-acetyl cysteine (NAC) and catalase suppressed 15(S)-HETE-stimulated EGFR, Src, Jak2, and STAT3 phosphorylation and MCP-1 expression.	Acetylcysteine	104-121	epidermal growth factor receptor	Mus musculus	174-178
23313378-7	2013	Mechanistically, it was determined that the induced levels of GADD45gamma mRNA resulting from (-)-xanthatin exposures were stabilized by coordinately produced ROS, and that the consequent induction of GADD45gamma mRNA, GADD45gamma protein and ROS generation were abrogated by co-treatment with N-acetyl-l-cysteine.	Acetylcysteine	294-313	growth arrest and DNA damage inducible gamma	Homo sapiens	62-73
31311721-17	2019	Keratin-18 and ccK18 increased in the NAC alone group more than with calmangafodipir (baseline to 20 h fold change, NAC + calmangafodipir (5 mumol/kg) compared to NAC alone: 0.48 (95%CI 0.28-0.83)).	Acetylcysteine	38-41	keratin 18	Homo sapiens	0-10
23353715-10	2013	Interestingly, NAC almost completely prevented the Cd-induced elevation of C/EBP homologous protein (CHOP) and phosphorylation of c-Jun N-terminal kinase (JNK), two components of the ER stress-mediated apoptotic pathway.	Acetylcysteine	15-18	DNA-damage inducible transcript 3	Mus musculus	75-99
23353715-10	2013	Interestingly, NAC almost completely prevented the Cd-induced elevation of C/EBP homologous protein (CHOP) and phosphorylation of c-Jun N-terminal kinase (JNK), two components of the ER stress-mediated apoptotic pathway.	Acetylcysteine	15-18	DNA-damage inducible transcript 3	Mus musculus	101-105
23113536-7	2013	The effect of SKi on androgen receptor expression was reversed by N-acetylcysteine, which was used to scavenge reactive oxygen species.	Acetylcysteine	66-82	SKI proto-oncogene	Homo sapiens	14-17
21536676-6	2011	15(S)-HETE induced the production of H(2)O(2) via an NADPH oxidase-dependent manner and its scavengers, N-acetyl cysteine (NAC) and catalase suppressed 15(S)-HETE-stimulated EGFR, Src, Jak2, and STAT3 phosphorylation and MCP-1 expression.	Acetylcysteine	104-121	Rous sarcoma oncogene	Mus musculus	180-183
21536676-6	2011	15(S)-HETE induced the production of H(2)O(2) via an NADPH oxidase-dependent manner and its scavengers, N-acetyl cysteine (NAC) and catalase suppressed 15(S)-HETE-stimulated EGFR, Src, Jak2, and STAT3 phosphorylation and MCP-1 expression.	Acetylcysteine	104-121	Janus kinase 2	Mus musculus	185-189
23159886-8	2013	Conversely, MB and/or PQ-induced GSTA4-4 expression/activity was further increased by NAC/SIL and glutathione reductase activity was also increased.	Acetylcysteine	86-89	glutathione S-transferase alpha 4	Rattus norvegicus	33-40
21406724-5	2011	Oxidative stress contributed to DDR activation, and our results showed impaired PVR levels in the presence of the reactive oxygen species (ROS) scavenger N-acetyl-cysteine (NAC), being monocytes the main ROS source needed for optimal PVR expression on activated T cells.	Acetylcysteine	154-171	PVR cell adhesion molecule	Homo sapiens	80-83
30793306-10	2019	Furthermore, N-acetyl- l-cysteine markedly abrogated VEGF-A-increased ROS production, IRE-1, GRP78/Bip, beclin-1 expression, and LC3-II/LC3-I in the HUVECs.	Acetylcysteine	13-33	endoplasmic reticulum (ER) to nucleus signalling 2	Mus musculus	86-91
21406724-5	2011	Oxidative stress contributed to DDR activation, and our results showed impaired PVR levels in the presence of the reactive oxygen species (ROS) scavenger N-acetyl-cysteine (NAC), being monocytes the main ROS source needed for optimal PVR expression on activated T cells.	Acetylcysteine	154-171	PVR cell adhesion molecule	Homo sapiens	234-237
21406724-5	2011	Oxidative stress contributed to DDR activation, and our results showed impaired PVR levels in the presence of the reactive oxygen species (ROS) scavenger N-acetyl-cysteine (NAC), being monocytes the main ROS source needed for optimal PVR expression on activated T cells.	Acetylcysteine	173-176	PVR cell adhesion molecule	Homo sapiens	80-83
21406724-5	2011	Oxidative stress contributed to DDR activation, and our results showed impaired PVR levels in the presence of the reactive oxygen species (ROS) scavenger N-acetyl-cysteine (NAC), being monocytes the main ROS source needed for optimal PVR expression on activated T cells.	Acetylcysteine	173-176	PVR cell adhesion molecule	Homo sapiens	234-237
23841333-4	2013	The coordination of Cd2+ with those groups was supported by the application of auxiliary molecules (D-penicillamine, glycine, cysteine and glutamic acid dipeptides, mercaptosuccinic acid and N-acetyl-L-cysteine).	Acetylcysteine	191-210	CD2 molecule	Homo sapiens	20-23
30793306-10	2019	Furthermore, N-acetyl- l-cysteine markedly abrogated VEGF-A-increased ROS production, IRE-1, GRP78/Bip, beclin-1 expression, and LC3-II/LC3-I in the HUVECs.	Acetylcysteine	13-33	beclin 1, autophagy related	Mus musculus	104-112
23319318-10	2013	TNF-alpha-induced MCP-1 mRNA expression was inhibited by N-acetylcysteine (NAC), Syk inhibitor, Syk-siRNA and MPA.	Acetylcysteine	57-73	C-C motif chemokine ligand 2	Homo sapiens	18-23
21237301-9	2011	Eugenol and N-acetylcysteine were found to down regulate the Th1 cytokines in nicotine treated macrophages with concurrent activation of Th2 responses.	Acetylcysteine	12-28	heart and neural crest derivatives expressed 2	Mus musculus	137-140
31284671-7	2019	(3) Linearity in the detector response for NAC in human urine was observed in the range of 5-200 nmol mL-1, and NAC and GSH in the brain tissue homogenates were observed in the range of 0.5-5 nmol mL-1 and 0.5-15 nmol mL-1, respectively.	Acetylcysteine	43-46	L1 cell adhesion molecule	Mus musculus	102-106
21408176-8	2011	Furthermore, chemical variants of chloranil induced a similar effect on ss-dystroglycan and this was prevented by the antioxidant N-acetylcysteine.	Acetylcysteine	130-146	dystroglycan 1	Rattus norvegicus	75-87
24489592-7	2013	Andrographolide significantly induced reactive oxygen species (ROS) formation, p53 activation, Bax, and active caspase-3 expression, and these phenomena were suppressed by pretreating the cells with N-acetyl-L-cysteine, a ROS scavenger, or diphenylene iodonium, a nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (Nox) inhibitor.	Acetylcysteine	199-218	Wistar clone pR53P1 p53 pseudogene	Rattus norvegicus	79-82
24489592-7	2013	Andrographolide significantly induced reactive oxygen species (ROS) formation, p53 activation, Bax, and active caspase-3 expression, and these phenomena were suppressed by pretreating the cells with N-acetyl-L-cysteine, a ROS scavenger, or diphenylene iodonium, a nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (Nox) inhibitor.	Acetylcysteine	199-218	BCL2 associated X, apoptosis regulator	Rattus norvegicus	95-98
23108103-6	2013	Occludin glycation and ZO-1 disruption were prevented by N-acetylcysteine (NAC).	Acetylcysteine	57-73	tight junction protein 1	Rattus norvegicus	23-27
23108103-6	2013	Occludin glycation and ZO-1 disruption were prevented by N-acetylcysteine (NAC).	Acetylcysteine	75-78	tight junction protein 1	Rattus norvegicus	23-27
23853776-7	2013	NAC normalized tissue and plasma levels of 15-F2t-isoprostane, significantly increased cardiac Brg1, HO-1 and p-STAT3 protein expression levels and reduced TNF-alpha and IL-6, resulting in improved cardiac function.	Acetylcysteine	0-3	signal transducer and activator of transcription 3	Rattus norvegicus	112-117
23682786-4	2013	Further, treatment of TOCO and NAC either alone or in combination to AO/TPA- or SANG/TPA-induced mice significantly decreased lipid peroxidation, along with significant revival in glutathione (GSH) content and activities of tyrosinase, histidase, catalase, SOD, GSH peroxidase, and GSH reductase in skin.	Acetylcysteine	31-34	tyrosinase	Mus musculus	224-234
23560513-12	2013	RESULTS: NAC and NAC + OT significantly decreased MDA and TNF-alpha levels and increased IL-10 levels and GPx activities.	Acetylcysteine	9-12	interleukin 10	Rattus norvegicus	89-94
23560513-12	2013	RESULTS: NAC and NAC + OT significantly decreased MDA and TNF-alpha levels and increased IL-10 levels and GPx activities.	Acetylcysteine	17-20	interleukin 10	Rattus norvegicus	89-94
20448054-6	2011	These increases are nSMase2 dependent, and are abrogated by treatment with N-acetyl cysteine or anti-nSMase2 small interfering RNA (siRNA).	Acetylcysteine	75-92	sphingomyelin phosphodiesterase 3	Homo sapiens	20-27
31284671-8	2019	Human plasma linearity ranges covered 0.25-5.00 nmol mL-1 and 0.5-15 nmol mL-1 for NAC and GSH, respectively.	Acetylcysteine	83-86	L1 cell adhesion molecule	Mus musculus	74-78
22096601-6	2011	Although NAC treatment in TgI278T Cbs(-/-) mice caused significant increase in serum tCys and liver GSH, there was no increase in body fat content or in liver Scd-1 levels.	Acetylcysteine	9-12	cystathionine beta-synthase	Mus musculus	34-37
31284671-9	2019	The LODs for NAC and GSH were 0.01 and 0.02 nmol mL-1 while the LOQs were 0.02 and 0.05 nmol mL-1, respectively.	Acetylcysteine	13-16	L1 cell adhesion molecule	Mus musculus	49-53
22926926-7	2012	An antioxidant, N-acetyl cysteine, reduced apicidin-induced cell death, CHOP expression, and mitochondrial dysfunction.	Acetylcysteine	16-33	DNA-damage inducible transcript 3	Mus musculus	72-76
30954547-8	2019	Moreover, the antioxidant N-acetyl-l-cysteine increased cell viability, GLP-1 expressions and the mTOR signaling pathway-related proteins, and inhibited the ROS production.	Acetylcysteine	26-45	mechanistic target of rapamycin kinase	Mus musculus	98-102
30421167-6	2019	Indeed, NAC administration improved the cognitive performance, ROS production, neuroinflammation, and caspase activation induced by GA. NAC did not prevent neuronal death, however protected against alterations induced by GA on Iba-1 and GFAP immunoreactivities and AChE activity.	Acetylcysteine	8-11	allograft inflammatory factor 1	Rattus norvegicus	227-232
22939972-7	2012	Addition of glutathione monoethyl ester, which is cleaved intracellularly to GSH, prevented attenuation of LIF-induced JAK1 and STAT3 activation, as did the reductant N-acetyl-cysteine.	Acetylcysteine	167-184	LIF interleukin 6 family cytokine	Homo sapiens	107-110
23271287-12	2012	The elevated ROS was strongly associated with the activation of JNK and ERK1/2 signal pathways after MPP(+) exposure, since the pretreatment of NAC significantly reduced the upregulation of p-JNK and p-ERK1/2.	Acetylcysteine	144-147	mitogen-activated protein kinase 8	Rattus norvegicus	64-67
23271287-12	2012	The elevated ROS was strongly associated with the activation of JNK and ERK1/2 signal pathways after MPP(+) exposure, since the pretreatment of NAC significantly reduced the upregulation of p-JNK and p-ERK1/2.	Acetylcysteine	144-147	mitogen-activated protein kinase 8	Rattus norvegicus	192-195
20446774-8	2010	Pretreatment with N-acetylcysteine prevented the glucose deprivation-induced ROS accumulation and also the HO-1 expression.	Acetylcysteine	18-34	heme oxygenase 1	Homo sapiens	107-111
21103380-5	2010	This report evaluates the effects of gender hormones on the activity and expression of GSNO-R and its relationship to N-acetyl cysteine (NAC)-induced pulmonary hypertension (PH).	Acetylcysteine	118-135	alcohol dehydrogenase 5 (class III), chi polypeptide	Mus musculus	87-93
22990675-0	2012	Pharmacological enhancement of alpha-glucosidase by the allosteric chaperone N-acetylcysteine.	Acetylcysteine	77-93	sucrase-isomaltase	Homo sapiens	31-48
30421167-6	2019	Indeed, NAC administration improved the cognitive performance, ROS production, neuroinflammation, and caspase activation induced by GA. NAC did not prevent neuronal death, however protected against alterations induced by GA on Iba-1 and GFAP immunoreactivities and AChE activity.	Acetylcysteine	8-11	acetylcholinesterase	Rattus norvegicus	265-269
22618532-0	2012	N-acetylcysteine protects against hypoxia mimetic-induced autophagy by targeting the HIF-1alpha pathway in retinal ganglion cells.	Acetylcysteine	0-16	hypoxia inducible factor 1, alpha subunit	Mus musculus	85-95
21103380-5	2010	This report evaluates the effects of gender hormones on the activity and expression of GSNO-R and its relationship to N-acetyl cysteine (NAC)-induced pulmonary hypertension (PH).	Acetylcysteine	137-140	alcohol dehydrogenase 5 (class III), chi polypeptide	Mus musculus	87-93
22618532-7	2012	NAC-mediated neuroprotection was attributed to the direct scavenging of reactive oxygen species and was mediated by targeting the hypoxia-inducible factor-1alpha pathway via the BNIP3 and PI3K/Akt/mTOR pathways.	Acetylcysteine	0-3	hypoxia inducible factor 1, alpha subunit	Mus musculus	130-161
20826812-8	2010	Moreover, chemical antioxidants, such as N-acetylcysteine and butylated hydroxyanisole, and the NADPH oxidase inhibitor diphenyleneiodonium inhibited Srx induction as well as generation of reactive oxygen species, both of which were also suppressed in Nox2 (NADPH oxidase 2)-deficient bone marrow-derived macrophages.	Acetylcysteine	41-57	sulfiredoxin 1 homolog (S. cerevisiae)	Mus musculus	150-153
30421167-6	2019	Indeed, NAC administration improved the cognitive performance, ROS production, neuroinflammation, and caspase activation induced by GA. NAC did not prevent neuronal death, however protected against alterations induced by GA on Iba-1 and GFAP immunoreactivities and AChE activity.	Acetylcysteine	136-139	allograft inflammatory factor 1	Rattus norvegicus	227-232
22618532-7	2012	NAC-mediated neuroprotection was attributed to the direct scavenging of reactive oxygen species and was mediated by targeting the hypoxia-inducible factor-1alpha pathway via the BNIP3 and PI3K/Akt/mTOR pathways.	Acetylcysteine	0-3	mechanistic target of rapamycin kinase	Mus musculus	197-201
30421167-6	2019	Indeed, NAC administration improved the cognitive performance, ROS production, neuroinflammation, and caspase activation induced by GA. NAC did not prevent neuronal death, however protected against alterations induced by GA on Iba-1 and GFAP immunoreactivities and AChE activity.	Acetylcysteine	136-139	acetylcholinesterase	Rattus norvegicus	265-269
31084929-7	2019	Furthermore, we found that superoxide anion levels were significantly increased in AngII-treated endothelial cells compared with controls and that the ROS scavenger N-acetyl-l-cysteine (NAC) significantly abolished CSE ubiquitination.	Acetylcysteine	165-184	choreoathetosis/spasticity, episodic (paroxysmal choreoathetosis/spasticity)	Homo sapiens	215-218
20720180-5	2010	Indoxyl sulfate evoked reactive oxygen species (ROS), and the antioxidant N-acetylcysteine inhibited indoxyl sulfate-induced p53 expression and phosphorylation, as well as indoxyl sulfate-induced alpha-SMA expression.	Acetylcysteine	74-90	Wistar clone pR53P1 p53 pseudogene	Rattus norvegicus	125-128
31084929-7	2019	Furthermore, we found that superoxide anion levels were significantly increased in AngII-treated endothelial cells compared with controls and that the ROS scavenger N-acetyl-l-cysteine (NAC) significantly abolished CSE ubiquitination.	Acetylcysteine	186-189	choreoathetosis/spasticity, episodic (paroxysmal choreoathetosis/spasticity)	Homo sapiens	215-218
20720180-5	2010	Indoxyl sulfate evoked reactive oxygen species (ROS), and the antioxidant N-acetylcysteine inhibited indoxyl sulfate-induced p53 expression and phosphorylation, as well as indoxyl sulfate-induced alpha-SMA expression.	Acetylcysteine	74-90	actin gamma 2, smooth muscle	Rattus norvegicus	196-205
22964484-3	2012	Moreover, the reactive oxygen species (ROS) scavenger, N-acetylcysteine, blocked MCT2 knockdown-induced growth arrest and cellular senescence, indicating a pivotal role of ROS in this pathway.	Acetylcysteine	55-71	solute carrier family 16 member 7	Homo sapiens	81-85
31046239-9	2019	Sulfotransferase (SULT) inhibitor pentachlorophenol (PCP) suppressed the production of the observed AE-GSH/NAC conjugates in vivo, which suggested that SULTs participated in the process of the metabolic activation of AE.	Acetylcysteine	107-110	carbohydrate sulfotransferase 10	Rattus norvegicus	0-16
20709753-6	2010	Pretreatment of the hMLH1-complemented HCT 116 cells with the antioxidant N-acetylcysteine or 2,2,6,6-tetramethylpiperidine-1-oxyl or the ATM kinase inhibitor KU55933 suppresses hMLH1-dependent DNA damage response to selenium exposure.	Acetylcysteine	74-90	mutL homolog 1	Homo sapiens	20-25
20525644-6	2010	Caspase 3, p38, and p53 inhibitors had no effect on FCCP-induced CASQ2 downregulation; however, it was attenuated by the ROS scavenger N-acetylcysteine (NAC).	Acetylcysteine	135-151	Wistar clone pR53P1 p53 pseudogene	Rattus norvegicus	20-23
31046239-9	2019	Sulfotransferase (SULT) inhibitor pentachlorophenol (PCP) suppressed the production of the observed AE-GSH/NAC conjugates in vivo, which suggested that SULTs participated in the process of the metabolic activation of AE.	Acetylcysteine	107-110	carbohydrate sulfotransferase 10	Rattus norvegicus	18-22
31070451-8	2019	Scavenging reactive oxygen species by N-acetyl cysteine attenuated hypoxia-mediated upregulation of HIF-1alpha, RUNX2, and OCN protein expressions and inhibited extracellular matrix calcification, which effect was mimicked by a specific hydrogen peroxide scavenger sodium pyruvate and a mitochondrial reactive oxygen species inhibitor rotenone.	Acetylcysteine	38-55	hypoxia inducible factor 1, alpha subunit	Mus musculus	100-110
20493918-6	2010	We also found that antioxidants such as N-acetylcysteine and glutathione blocked TG- and BFA-induced cell death and the expression of CHOP and GRP78.	Acetylcysteine	40-56	DNA-damage inducible transcript 3	Mus musculus	134-138
20808797-9	2010	Overall, these results indicate that oral NAC supplementation decreases SNCA levels in brain and partially protects against loss of dopaminergic terminals associated with overexpression of alpha-synuclein in this model.	Acetylcysteine	42-45	synuclein, alpha	Mus musculus	72-76
20808797-9	2010	Overall, these results indicate that oral NAC supplementation decreases SNCA levels in brain and partially protects against loss of dopaminergic terminals associated with overexpression of alpha-synuclein in this model.	Acetylcysteine	42-45	synuclein, alpha	Mus musculus	189-204
31070451-8	2019	Scavenging reactive oxygen species by N-acetyl cysteine attenuated hypoxia-mediated upregulation of HIF-1alpha, RUNX2, and OCN protein expressions and inhibited extracellular matrix calcification, which effect was mimicked by a specific hydrogen peroxide scavenger sodium pyruvate and a mitochondrial reactive oxygen species inhibitor rotenone.	Acetylcysteine	38-55	runt related transcription factor 2	Mus musculus	112-117
20144638-5	2010	BAPTA-AM or NAC abrogated CMS-9-elicited p38 MAPK and JNK activation, and rescued viability of CMS-9-treated K562 cells.	Acetylcysteine	12-15	muscle associated receptor tyrosine kinase	Homo sapiens	26-31
20144638-5	2010	BAPTA-AM or NAC abrogated CMS-9-elicited p38 MAPK and JNK activation, and rescued viability of CMS-9-treated K562 cells.	Acetylcysteine	12-15	muscle associated receptor tyrosine kinase	Homo sapiens	95-100
31070451-8	2019	Scavenging reactive oxygen species by N-acetyl cysteine attenuated hypoxia-mediated upregulation of HIF-1alpha, RUNX2, and OCN protein expressions and inhibited extracellular matrix calcification, which effect was mimicked by a specific hydrogen peroxide scavenger sodium pyruvate and a mitochondrial reactive oxygen species inhibitor rotenone.	Acetylcysteine	38-55	bone gamma-carboxyglutamate protein 2	Mus musculus	123-126
20185348-12	2010	Further, NAC restored these changes induced by IGF-I on both serine and tyrosine phosphorylation of IRS-1.	Acetylcysteine	9-12	insulin receptor substrate 1	Homo sapiens	100-105
31148586-8	2019	NAC inhibited the induction and nuclear localization of phospho-Smad2 protein in bladder tissues and the upregulation of genes related to fibrosis, such as Tgfb2, Tgfb3, Smad2, Smad3, Cxcl10, and Card10.	Acetylcysteine	0-3	SMAD family member 2	Rattus norvegicus	64-69
20214734-8	2010	Six-month treatment with the anti-oxidant N-acetyl cysteine dramatically reduced hepatic steatosis in transgenic mice fed the excess-iron diet through decreased expression of unspliced and spliced XBP-1, p-eIF2alpha, and CHOP.	Acetylcysteine	42-59	DNA-damage inducible transcript 3	Mus musculus	221-225
31148586-8	2019	NAC inhibited the induction and nuclear localization of phospho-Smad2 protein in bladder tissues and the upregulation of genes related to fibrosis, such as Tgfb2, Tgfb3, Smad2, Smad3, Cxcl10, and Card10.	Acetylcysteine	0-3	transforming growth factor, beta 2	Rattus norvegicus	156-161
31148586-8	2019	NAC inhibited the induction and nuclear localization of phospho-Smad2 protein in bladder tissues and the upregulation of genes related to fibrosis, such as Tgfb2, Tgfb3, Smad2, Smad3, Cxcl10, and Card10.	Acetylcysteine	0-3	SMAD family member 2	Rattus norvegicus	170-175
31178664-7	2019	Notably, NAC, a ROS scavenger, could attenuate high glucose-induced ROS formation and IL-18 and IL-1beta mRNA and protein expression and block inflammasome activation.	Acetylcysteine	9-12	interleukin 1 alpha	Homo sapiens	96-104
19944114-7	2010	Similarly, although the potassium chloride co-transporter (KCC) inhibitor (dihydro-indenyl)oxyalkanoic acid (DIOA), and the anti-oxidant, N-acetyl cysteine (NAC) both reversed MCLR cytotoxicity, both were also found to be unexpected OATP1B1 transport inhibitors.	Acetylcysteine	138-155	solute carrier organic anion transporter family member 1B1	Homo sapiens	233-240
19944114-8	2010	Therefore, the mechanism of MCLR-induced cytotoxicity is obscured by the inhibition of OATP1B1 uptake activity by MAP kinase inhibitors, DIOA, and NAC.	Acetylcysteine	147-150	solute carrier organic anion transporter family member 1B1	Homo sapiens	87-94
20112989-7	2010	Scavenging of nickel-induced ROS by NAC or catalase attenuated Akt, ASK1, and p38 MAPK activation and apoptosis, which implies involvement of ROS in the Akt/ASK1/p38 pathway.	Acetylcysteine	36-39	mitogen-activated protein kinase kinase kinase 5	Homo sapiens	68-72
20112989-7	2010	Scavenging of nickel-induced ROS by NAC or catalase attenuated Akt, ASK1, and p38 MAPK activation and apoptosis, which implies involvement of ROS in the Akt/ASK1/p38 pathway.	Acetylcysteine	36-39	mitogen-activated protein kinase kinase kinase 5	Homo sapiens	157-161
30684884-2	2019	The system was established a FRET assembly by positively charged carbon dots (CDs) and negatively charged N-acetyl-l-cysteine capped gold nanoparticles (NAC-AuNPs).	Acetylcysteine	106-125	synuclein alpha	Homo sapiens	153-156
30648648-6	2019	Co-treating MA-10 cells with MEHP and the ROS scavenger N-acetyl cysteine (NAC) blocked the activation of HSL, blunted MEHP-induced STAR, and reduced basal progesterone formation.	Acetylcysteine	56-73	steroidogenic acute regulatory protein	Mus musculus	132-136
20071472-1	2010	BACKGROUND: Intravenous N-acetylcysteine (IV-NAC) is widely recognized as the antidote of choice for acetaminophen overdose.	Acetylcysteine	24-40	synuclein alpha	Homo sapiens	45-48
20206069-9	2010	In the NAC group, mean blood beta-2 microglobulin significantly decreased from 2.38 + or - 0.58 to 1.71 + or - 0.38 mg/dl (p&lt;0.01), and in the aminophylline group, mean urinary beta-2 microglobulin concentration significantly decreased from 337 + or - 31.0 to 239 + or - 34 microg/ml (p&lt;0.01).	Acetylcysteine	7-10	beta-2-microglobulin	Homo sapiens	29-49
30648648-6	2019	Co-treating MA-10 cells with MEHP and the ROS scavenger N-acetyl cysteine (NAC) blocked the activation of HSL, blunted MEHP-induced STAR, and reduced basal progesterone formation.	Acetylcysteine	75-78	steroidogenic acute regulatory protein	Mus musculus	132-136
20012373-3	2010	Similarly, IDPc was induced in murine renal proximal tubular OK cells by high hyperglycemia, while it was abrogated by co-treatment with the antioxidant N-Acetyl-Cysteine (NAC).	Acetylcysteine	153-170	isocitrate dehydrogenase 1 (NADP+), soluble	Mus musculus	11-15
20012373-3	2010	Similarly, IDPc was induced in murine renal proximal tubular OK cells by high hyperglycemia, while it was abrogated by co-treatment with the antioxidant N-Acetyl-Cysteine (NAC).	Acetylcysteine	172-175	isocitrate dehydrogenase 1 (NADP+), soluble	Mus musculus	11-15
30496017-9	2019	Expressions of Brca2, Xpc, Mlh3, Rad51, Xrcc2, Hus1, Rad9a, Cdkn1a, Gadd45a which are the DNA-repair genes were found to be significantly higher in NAC + ALC + IR group than those in individual treatment of ALC or NAC.	Acetylcysteine	148-151	HUS1 checkpoint clamp component	Homo sapiens	47-51
20117097-13	2010	Pre-treatment with NAC suppressed both MUC5AC production and p38 activation.	Acetylcysteine	19-22	mucin 5AC, oligomeric mucus/gel-forming	Homo sapiens	39-45
29923087-8	2019	Studies on the Taldo1 -/- mouse model demonstrate acetaminophen-induced liver failure can be prevented by administration of the antioxidant N-acetylcysteine.	Acetylcysteine	140-156	transaldolase 1	Mus musculus	15-21
19725096-7	2010	NAC prevented NO-induced apoptosis, ROS overproduction, p53 up-regulation, and caspase-3 activation.	Acetylcysteine	0-3	Wistar clone pR53P1 p53 pseudogene	Rattus norvegicus	56-59
30971653-8	2019	Strikingly, NAC canceled these taxodione-caused inhibition of BCR-ABL, STAT5 and Akt.	Acetylcysteine	12-15	signal transducer and activator of transcription 5A	Homo sapiens	71-76
20931090-9	2010	The antioxidant-containing drug N-acetylcysteine increased activity of salivary ALDH presumably by preventing its inactivation in the oral cavity.	Acetylcysteine	32-48	aldehyde dehydrogenase	Nicotiana tabacum	80-84
30655875-7	2019	Furthermore, pretreatment with N-acetyl-L-cysteine, a scavenger of ROS, was able to reverse the effects on cell number and cell cycle arrest induced by ginsenoside Rg3 in PC3 cells.	Acetylcysteine	31-50	chromobox 8	Homo sapiens	171-174
19717140-6	2010	We also examined the affect of ceftriaxone (previously shown to increase GLT-1) and N-acetylcysteine treatment on the expression of GLT-1 and xCT.	Acetylcysteine	84-100	solute carrier family 7 member 11	Homo sapiens	142-145
30107137-9	2018	NAC supplementation also downregulated the expression of inflammatory markers (TNF-alpha, IL-1beta, IL-6) and upregulated the expression of marker genes associated with aging (sirtuin-1) and neurodegeneration (neuron-specific enolase, neuroglobin, synapsin-I, myelin basic protein 2) in old rats.	Acetylcysteine	0-3	enolase 2	Rattus norvegicus	210-233
19493264-6	2010	Gly-I activity was dependent on NAC and closely associated with cell viability.	Acetylcysteine	32-35	glyoxalase I	Homo sapiens	0-5
19493264-7	2010	A approximately 65% loss in Gly-I activity by mercuric chloride/glycerol led to &gt;90% cell death, while restoring a basal activity of Gly-I with NAC was accompanied by complete cell viability.	Acetylcysteine	147-150	glyoxalase I	Homo sapiens	136-141
30559650-5	2018	The astroglial response was also explored by co-immunostaining for GFAP and S100b together with p-JNK and it was found to be particularly exacerbated in the MPTP+NAC+HA-1077 group.	Acetylcysteine	162-165	glial fibrillary acidic protein	Mus musculus	67-71
20054154-7	2010	Co-administration of N-Acetylcysteine (NAC) exerted a strong protective effect against CdCl(2) induced barrier damage and stress related genes, while other antioxidants only attenuated CdCl(2) induced HSP70 and HMOX-1 and showed no protective effect on the barrier collapse.	Acetylcysteine	21-37	heme oxygenase 1	Homo sapiens	211-217
19722195-6	2010	Furthermore, the PERK-ATF4 pathway, which also induces the expression of CHOP, was activated in NAC-treated cells.	Acetylcysteine	96-99	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	17-21
30559650-5	2018	The astroglial response was also explored by co-immunostaining for GFAP and S100b together with p-JNK and it was found to be particularly exacerbated in the MPTP+NAC+HA-1077 group.	Acetylcysteine	162-165	S100 protein, beta polypeptide, neural	Mus musculus	76-81
20358476-3	2010	Exogenous GSH and its precursor N-acetyl-cysteine, but not ascorbic acid (AA) or ebselen, decreased curcumin accumulation in PC3 cells and also prevented curcumin-induced DNA fragmentation.	Acetylcysteine	32-49	chromobox 8	Homo sapiens	125-128
30194941-14	2018	NAC prevented the increases in LC3 II protein, LC3 scores, Beclin1, Atg12 and ERK activity in AAC rats.	Acetylcysteine	0-3	autophagy related 12	Rattus norvegicus	68-73
30017935-10	2018	The free radical scavenger N-acetyl-L-cysteine attenuated TRAF6 expression in HAECs cultured in high glucose medium, and TRAF6 knockdown inhibited high glucose-induced IkappaB-alpha degradation and JNK phosphorylation.	Acetylcysteine	27-46	TNF receptor associated factor 6	Homo sapiens	58-63
20157581-0	2009	Antioxidant N-acetyl-L-cysteine ameliorates symptoms of premature aging associated with the deficiency of the circadian protein BMAL1.	Acetylcysteine	12-31	aryl hydrocarbon receptor nuclear translocator-like	Mus musculus	128-133
19766627-8	2009	These mIg-mediated events were also partially abrogated by ROS scavenger N-acetyl-L-cysteine (NAC).	Acetylcysteine	73-92	chemokine (C-X-C motif) ligand 9	Mus musculus	6-9
19766627-8	2009	These mIg-mediated events were also partially abrogated by ROS scavenger N-acetyl-L-cysteine (NAC).	Acetylcysteine	94-97	chemokine (C-X-C motif) ligand 9	Mus musculus	6-9
29334756-9	2018	We further demonstrated that the general reactive oxygen species inhibitor, Nacetylcysteine (NAC), maintained the regulation of ADAM17 dependent of Trx-1 reductase activity levels; whereas the electron transport chain modulator, rotenone, abolished Trx-1 effect on ADAM17 activity.	Acetylcysteine	76-91	thioredoxin	Homo sapiens	148-153
19830705-5	2009	We also found that a reducing agent dithiothreitol (DTT) and an anti-oxidant N-acetyl cysteine (NAC) inhibited BMTS-mediated caspase-9 and -3 activation, ROS production and induction of Annexin V/propidium iodide double positive cells, suggesting the involvement of ROS in the apoptosis process.	Acetylcysteine	77-94	caspase 9	Homo sapiens	125-141
22864061-6	2012	Furthermore, the induction of HO-1 by sildenafil was accompanied by an increase in reactive oxygen species (ROS) and blocked by N-acetyl-L-cysteine and rotenone.	Acetylcysteine	128-147	heme oxygenase 1	Homo sapiens	30-34
22700867-8	2012	Moreover, the antioxidant, N-acetyl-L-cysteine (NAC), significantly reduced HIF-1alpha, ERK-1,2 phosphorylation, and CCL2 protein levels that were synergistically increased by the combination of PDGF and NiNPs.	Acetylcysteine	27-46	C-C motif chemokine ligand 2	Rattus norvegicus	117-121
22700867-8	2012	Moreover, the antioxidant, N-acetyl-L-cysteine (NAC), significantly reduced HIF-1alpha, ERK-1,2 phosphorylation, and CCL2 protein levels that were synergistically increased by the combination of PDGF and NiNPs.	Acetylcysteine	48-51	C-C motif chemokine ligand 2	Rattus norvegicus	117-121
19830705-5	2009	We also found that a reducing agent dithiothreitol (DTT) and an anti-oxidant N-acetyl cysteine (NAC) inhibited BMTS-mediated caspase-9 and -3 activation, ROS production and induction of Annexin V/propidium iodide double positive cells, suggesting the involvement of ROS in the apoptosis process.	Acetylcysteine	77-94	annexin A5	Homo sapiens	186-195
29334756-9	2018	We further demonstrated that the general reactive oxygen species inhibitor, Nacetylcysteine (NAC), maintained the regulation of ADAM17 dependent of Trx-1 reductase activity levels; whereas the electron transport chain modulator, rotenone, abolished Trx-1 effect on ADAM17 activity.	Acetylcysteine	76-91	thioredoxin	Homo sapiens	249-254
19830705-5	2009	We also found that a reducing agent dithiothreitol (DTT) and an anti-oxidant N-acetyl cysteine (NAC) inhibited BMTS-mediated caspase-9 and -3 activation, ROS production and induction of Annexin V/propidium iodide double positive cells, suggesting the involvement of ROS in the apoptosis process.	Acetylcysteine	96-99	caspase 9	Homo sapiens	125-141
19830705-5	2009	We also found that a reducing agent dithiothreitol (DTT) and an anti-oxidant N-acetyl cysteine (NAC) inhibited BMTS-mediated caspase-9 and -3 activation, ROS production and induction of Annexin V/propidium iodide double positive cells, suggesting the involvement of ROS in the apoptosis process.	Acetylcysteine	96-99	annexin A5	Homo sapiens	186-195
20088405-13	2009	SAC and NAC markedly suppressed the PS-induced increase in alpha-SMA expressions.	Acetylcysteine	8-11	actin gamma 2, smooth muscle	Rattus norvegicus	59-68
22849820-9	2012	Although NAC lowers the level of oxidized proteins in the brains of Twi mice, and dramatically improves immunohistochemical markers of disease, neither treatment results in any clinical improvements in the Twi mouse.	Acetylcysteine	9-12	galactosylceramidase	Mus musculus	68-71
22564156-8	2012	Additionally, N-acetylcysteine and Tiron inhibited zinc-induced HO-1 upregulation and also nuclear translocation of nuclear factor erythroid 2-related factor 2 (Nrf2).	Acetylcysteine	14-30	heme oxygenase 1	Homo sapiens	64-68
22683510-6	2012	In addition, N-acetyl cysteine (NAC), an ROS scavenger, blocked cell cycle G2/M arrest and phosphorylation of ERK1/2 and Cdc25cSer(216) in U87 cells.	Acetylcysteine	13-30	cell division cycle 25C	Homo sapiens	121-126
29334756-9	2018	We further demonstrated that the general reactive oxygen species inhibitor, Nacetylcysteine (NAC), maintained the regulation of ADAM17 dependent of Trx-1 reductase activity levels; whereas the electron transport chain modulator, rotenone, abolished Trx-1 effect on ADAM17 activity.	Acetylcysteine	93-96	thioredoxin	Homo sapiens	148-153
22683510-6	2012	In addition, N-acetyl cysteine (NAC), an ROS scavenger, blocked cell cycle G2/M arrest and phosphorylation of ERK1/2 and Cdc25cSer(216) in U87 cells.	Acetylcysteine	32-35	cell division cycle 25C	Homo sapiens	121-126
19700642-0	2009	Could N-acetylcysteine slow progression of idiopathic pulmonary fibrosis by inhibiting EMT?	Acetylcysteine	6-22	IL2 inducible T cell kinase	Homo sapiens	87-90
22336129-10	2012	The administration of NAC increased GSH, attenuated ROS, cytokines, MPO, JNK, pAKT and caspase-3 and lung permeability associated with decreased activation of nuclear factor-kappaB.	Acetylcysteine	22-25	myeloperoxidase	Rattus norvegicus	68-71
29334756-9	2018	We further demonstrated that the general reactive oxygen species inhibitor, Nacetylcysteine (NAC), maintained the regulation of ADAM17 dependent of Trx-1 reductase activity levels; whereas the electron transport chain modulator, rotenone, abolished Trx-1 effect on ADAM17 activity.	Acetylcysteine	93-96	thioredoxin	Homo sapiens	249-254
22336129-10	2012	The administration of NAC increased GSH, attenuated ROS, cytokines, MPO, JNK, pAKT and caspase-3 and lung permeability associated with decreased activation of nuclear factor-kappaB.	Acetylcysteine	22-25	mitogen-activated protein kinase 8	Rattus norvegicus	73-76
30271093-11	2018	In addition, the ROS scavenger N-acetyl-L-cysteine markedly inhibited increased phosphorylation levels of P38 and HSP27 under H/R.	Acetylcysteine	31-50	heat shock protein family B (small) member 1	Homo sapiens	114-119
19734319-11	2009	Inhibiting HO-1 upregulation with NAC has only a small effect on the antifibrotic properties of 15d-PGJ2 and CDDO in vitro.	Acetylcysteine	34-37	heme oxygenase 1	Homo sapiens	11-15
19808019-4	2009	The increased insulin sensitivity in Gpx1(-/-) mice was attributed to insulin-induced phosphatidylinositol-3-kinase/Akt signaling and glucose uptake in muscle and could be reversed by the antioxidant N-acetylcysteine.	Acetylcysteine	200-216	glutathione peroxidase 1	Mus musculus	37-41
22784044-7	2012	Furthermore, PD-induced ASK1 and ER stress responses were inhibited by the antioxidant N-acetyl-l-cysteine.	Acetylcysteine	87-106	mitogen-activated protein kinase kinase kinase 5	Homo sapiens	24-28
30021379-8	2018	Further experiments indicated that NLRP3-ASC pathway was activated by reactive oxygen species (ROS), since ROS scavenger of N-acetyl-cysteine (NAC) prevented, which was further reduced by PepE addition.	Acetylcysteine	124-141	NLR family, pyrin domain containing 3	Mus musculus	35-40
22552773-8	2012	Antioxidants (N-acetyl-cysteine and vitamin C), which blocked oxidative stress induced by chronic ethanol in WT mice and acute ethanol in Cyp2e1  (-/-)   KI mice, also blunted the induction of CYP2A5 and Nrf2 by ethanol but not the induction of CYP2E1 by ethanol.	Acetylcysteine	14-31	cytochrome P450, family 2, subfamily e, polypeptide 1	Mus musculus	138-144
22552773-8	2012	Antioxidants (N-acetyl-cysteine and vitamin C), which blocked oxidative stress induced by chronic ethanol in WT mice and acute ethanol in Cyp2e1  (-/-)   KI mice, also blunted the induction of CYP2A5 and Nrf2 by ethanol but not the induction of CYP2E1 by ethanol.	Acetylcysteine	14-31	cytochrome P450, family 2, subfamily e, polypeptide 1	Mus musculus	245-251
30021379-8	2018	Further experiments indicated that NLRP3-ASC pathway was activated by reactive oxygen species (ROS), since ROS scavenger of N-acetyl-cysteine (NAC) prevented, which was further reduced by PepE addition.	Acetylcysteine	143-146	NLR family, pyrin domain containing 3	Mus musculus	35-40
19730430-9	2009	Correspondingly, the LGH00031-induced decrease in cell viability and cell cycle arrest, cyclin B1 protein level, and phosphorylation of CDK1 tyrosine 15 were also rescued by NAC that decreased ROS production.	Acetylcysteine	174-177	cyclin B1	Homo sapiens	88-97
19730430-9	2009	Correspondingly, the LGH00031-induced decrease in cell viability and cell cycle arrest, cyclin B1 protein level, and phosphorylation of CDK1 tyrosine 15 were also rescued by NAC that decreased ROS production.	Acetylcysteine	174-177	cyclin dependent kinase 1	Homo sapiens	136-140
29929000-7	2018	Furthermore, using chloroquine and siATG5 significantly enhances ROS production and application of the ROS scavenger N-acetyl-cysteine (NAC) rescues the cells undergoing apoptosis by abrogating the expression of DR5 and finally the caspase cascade.	Acetylcysteine	117-134	TNF receptor superfamily member 10b	Homo sapiens	212-215
22555846-4	2012	The IS-induced expression of p53 and p21 was suppressed by N-acetylcysteine, an antioxidant.	Acetylcysteine	59-75	Wistar clone pR53P1 p53 pseudogene	Rattus norvegicus	29-32
29929000-7	2018	Furthermore, using chloroquine and siATG5 significantly enhances ROS production and application of the ROS scavenger N-acetyl-cysteine (NAC) rescues the cells undergoing apoptosis by abrogating the expression of DR5 and finally the caspase cascade.	Acetylcysteine	136-139	TNF receptor superfamily member 10b	Homo sapiens	212-215
19930842-6	2009	Reduction of HSP27 expression increased the in vitro chemosensitivity of HO8910 cells to paclitaxel and increased paclitaxel-induced apoptosis and ROS production, although the ROS scavenger, N-acetyl-L-cysteine, partly offset the effects of HSP27 siRNA.	Acetylcysteine	191-210	heat shock protein family B (small) member 1	Homo sapiens	13-18
29945211-8	2018	Furthermore, we found that beta-CYP and 3-PBA exposure led to elevated levels of cellular reactive oxygen species (ROS), and that pretreatment with N-acetylcysteine (NAC) blocked the toxic effects caused by beta-CYP and 3-PBA.	Acetylcysteine	148-164	peptidylprolyl isomerase G	Homo sapiens	32-35
19389043-14	2009	Chronic administration of N-acetyl cysteine significantly improved memory retention in tasks, attenuated oxidative damage and acetylcholinesterase activity in aluminium-treated rats.	Acetylcysteine	26-43	acetylcholinesterase	Rattus norvegicus	126-146
23101021-12	2012	The activity of MPO in NAC treatment group was significantly lower than that of LPS group (6.4+-1.8 unit/g vs. 11.2+-6.3 unit/g, tissue) (p&lt;0.048).	Acetylcysteine	23-26	myeloperoxidase	Rattus norvegicus	16-19
22470108-8	2012	NAC treatment for 2 weeks also significantly reduced the MCP-1 mRNA and protein levels by 52 and 60%, respectively (n=4-8, both P&lt;0.01), but had no effect on blood pressure.	Acetylcysteine	0-3	C-C motif chemokine ligand 2	Rattus norvegicus	57-62
22470108-10	2012	NAC administration attenuated JNK activation, but had no effect on ERK.	Acetylcysteine	0-3	mitogen-activated protein kinase 8	Rattus norvegicus	30-33
19398917-12	2009	Western blots revealed a four-fold increase in TGF-beta in the group receiving CCl4, NAC cotreatment abolished TGF-beta signal (P&lt;0.05).	Acetylcysteine	85-88	C-C motif chemokine ligand 4	Homo sapiens	79-83
29945211-8	2018	Furthermore, we found that beta-CYP and 3-PBA exposure led to elevated levels of cellular reactive oxygen species (ROS), and that pretreatment with N-acetylcysteine (NAC) blocked the toxic effects caused by beta-CYP and 3-PBA.	Acetylcysteine	148-164	peptidylprolyl isomerase G	Homo sapiens	212-215
19097988-10	2009	Although both N-acetyl cysteine (NAC) and ascorbic acid (AA) decreased Ni-induced increases in ROS, only NAC prevented Ni-induced increases in MT2A mRNA, suggesting a special role for interactions of Ni, thiols, and Zn release.	Acetylcysteine	105-108	metallothionein 2A	Homo sapiens	143-147
22129233-5	2012	Different signal transduction inhibitors, atorvastatin and N-acetylcysteine (NAC) were used to identify the pathways that inhibited myocardin expression and ROS.	Acetylcysteine	59-75	myocardin	Rattus norvegicus	132-141
22129233-5	2012	Different signal transduction inhibitors, atorvastatin and N-acetylcysteine (NAC) were used to identify the pathways that inhibited myocardin expression and ROS.	Acetylcysteine	77-80	myocardin	Rattus norvegicus	132-141
29945211-8	2018	Furthermore, we found that beta-CYP and 3-PBA exposure led to elevated levels of cellular reactive oxygen species (ROS), and that pretreatment with N-acetylcysteine (NAC) blocked the toxic effects caused by beta-CYP and 3-PBA.	Acetylcysteine	166-169	peptidylprolyl isomerase G	Homo sapiens	32-35
22227002-3	2012	Here we show that N-acetylcysteine (NAC), an anti-oxidant, is capable of preventing social isolation-induced accelerated impairment of contextual fear memory and rundown of hippocampal LTP in 3-month old APP/PS1 mice.	Acetylcysteine	18-34	presenilin 1	Mus musculus	208-211
18791914-5	2009	The DEP-induced increases in peribronchial eosinophils and mucous goblet cells in the lung tissues, and of IL-5 and IL-13 in the BAL fluid, were significantly attenuated by the antioxidant N-acetylcysteine.	Acetylcysteine	189-205	interleukin 5	Mus musculus	107-111
22227002-3	2012	Here we show that N-acetylcysteine (NAC), an anti-oxidant, is capable of preventing social isolation-induced accelerated impairment of contextual fear memory and rundown of hippocampal LTP in 3-month old APP/PS1 mice.	Acetylcysteine	36-39	presenilin 1	Mus musculus	208-211
19234337-12	2009	Studies using human ECs demonstrated that TNF-alpha-induced CCL2 production was also inhibited by the NAD(P)H oxidase inhibitor DPI, the antioxidant N-acetyl-L-cysteine, or the superoxide scavenger Tiron, further indicating that inhibition occurs through the NAD(P)H/ROS pathway.	Acetylcysteine	149-168	C-C motif chemokine ligand 2	Homo sapiens	60-64
29945211-8	2018	Furthermore, we found that beta-CYP and 3-PBA exposure led to elevated levels of cellular reactive oxygen species (ROS), and that pretreatment with N-acetylcysteine (NAC) blocked the toxic effects caused by beta-CYP and 3-PBA.	Acetylcysteine	166-169	peptidylprolyl isomerase G	Homo sapiens	212-215
22227002-4	2012	Increased hippocampal levels of gamma-secretase activity, Abeta-40 and Abeta-42 seen in the isolated APP/PS1 mice were reduced by chronic treatment of NAC.	Acetylcysteine	151-154	presenilin 1	Mus musculus	105-108
22227002-6	2012	NAC pretreatment also reversed isolation-induced decrease in GluR1 Ser831 phosphorylation, surface expression of AMPARs and p35-GluR1-CaMKII interactions.	Acetylcysteine	0-3	calcium/calmodulin-dependent protein kinase II gamma	Mus musculus	134-140
29219630-1	2018	OBJECTIVE: Acetylcysteine (NAC), an effective antidote for paracetamol poisoning, is commonly associated with adverse reactions.	Acetylcysteine	11-25	synuclein alpha	Homo sapiens	27-30
22227002-7	2012	These results suggest that NAC decreases gamma-secretase activity resulting in the attenuation of Abeta production, calpain activity and conversion of p35 to p25 which stabilized p35-GluR1-CaMKII interactions and restored GluR1 and GluR2 surface expression.	Acetylcysteine	27-30	amyloid beta (A4) precursor protein	Mus musculus	98-103
22227002-7	2012	These results suggest that NAC decreases gamma-secretase activity resulting in the attenuation of Abeta production, calpain activity and conversion of p35 to p25 which stabilized p35-GluR1-CaMKII interactions and restored GluR1 and GluR2 surface expression.	Acetylcysteine	27-30	calcium/calmodulin-dependent protein kinase II gamma	Mus musculus	189-195
19436114-8	2009	Remarkably, lifelong administration of the potent antioxidant N-acetylcysteine (NAC) prevented acetaminophen-induced liver failure, restored Fas-dependent hepatocyte apoptosis, and blocked hepatocarcinogenesis in Taldo1-/- mice.	Acetylcysteine	62-78	transaldolase 1	Mus musculus	213-219
29322434-6	2018	RESULTS: The peak CK-MB level was comparable between the two groups (P = 0.327), but patients receiving high-dose NAC demonstrated a significantly larger reduction in hs-TnT (P = 0.02).	Acetylcysteine	114-117	troponin T1, slow skeletal type	Homo sapiens	170-173
19368367-4	2009	N-Acetyl-L-cysteine (10 mM) was incubated with an equimolar concentration of ONE in 0.1 M phosphate buffer (pH 7.4) at 37 degrees C. Within 1 h of incubation, the reaction of N-acetyl-L-cysteine with ONE resulted in the formation of two (C-2 and C-3) Michael addition products possessing a carbonyl functionality.	Acetylcysteine	0-19	complement C2	Homo sapiens	238-249
19093139-9	2009	NAC and MPA completely suppressed OA-induced fibronectin secretion and decreased the levels of TGF-beta and cellular ROS.	Acetylcysteine	0-3	fibronectin 1	Mus musculus	45-56
22261521-7	2012	The antioxidant N-acetylcysteine prevented nicotine-activated production of reactive oxygen species (ROS) and uPAR expression.	Acetylcysteine	16-32	plasminogen activator, urokinase receptor	Homo sapiens	110-114
22096246-5	2012	Thrombus formation was then initiated by the binding of platelet GPIbalpha to endothelial VWF in our model, and this effect was inhibited by the ROS scavenger N-acetylcysteine.	Acetylcysteine	159-175	Von Willebrand factor	Mus musculus	90-93
22085843-9	2012	Furthermore, Cu(2+)/PDTC complex was capable of increasing the phosphorylations of ERK1/2 and JNK, and its upstream kinase MEK1/2 and MKK4, which could be reversed by NAC.	Acetylcysteine	167-170	mitogen-activated protein kinase 8	Rattus norvegicus	94-97
22019695-7	2012	Activation of the Nrf2/HO-1 system after sulforaphane treatment was suppressed by pretreatment with NAC or Ly294002, a PI3K inhibitor.	Acetylcysteine	100-103	heme oxygenase 1	Homo sapiens	23-27
21856376-6	2012	Taken together, the above findings indicate that the specificity of NAC action was not restricted to regulating marker proteins in the extrinsic and JNK pathways as seen in vitro but extended to include intrinsic pathway of metazoan apoptosis as well.	Acetylcysteine	68-71	mitogen-activated protein kinase 8	Rattus norvegicus	149-152
29322434-9	2018	CONCLUSIONS: In this study, NAC improved myocardial reperfusion markers and coronary blood flow, as revealed by differences in peak hs-TnT and TIMI flow grade 3 levels, respectively.	Acetylcysteine	28-31	troponin T1, slow skeletal type	Homo sapiens	135-138
19341424-9	2009	As confirmed by western blotting, the levels of VEGF in BAL fluid were higher in the NAC-treated group than in the COPD group.	Acetylcysteine	85-88	vascular endothelial growth factor A	Rattus norvegicus	48-52
19341424-10	2009	VEGFR2 protein expression was higher in the NAC-treated group than in the COPD group.	Acetylcysteine	44-47	kinase insert domain receptor	Rattus norvegicus	0-6
19341424-13	2009	CONCLUSIONS: NAC attenuates lung damage, pulmonary emphysema and alveolar septal cell apoptosis by partly reversing the decrease in VEGF secretion and VEGFR2 protein expression in smoking-induced COPD in rats.	Acetylcysteine	13-16	vascular endothelial growth factor A	Rattus norvegicus	132-136
19341424-13	2009	CONCLUSIONS: NAC attenuates lung damage, pulmonary emphysema and alveolar septal cell apoptosis by partly reversing the decrease in VEGF secretion and VEGFR2 protein expression in smoking-induced COPD in rats.	Acetylcysteine	13-16	kinase insert domain receptor	Rattus norvegicus	151-157
22526333-6	2012	N-acetyl cysteine, an antioxidant, is able to protect MSCs from  FasL-induced ROS production and subsequent ROS-dependent apoptosis, though the MSCs eventually succumb to ROS-independent death signaling.	Acetylcysteine	0-17	Fas ligand	Homo sapiens	65-69
21806545-13	2012	The gel shift and promoter activity assay showed that Ang II increased AP-1 (activator protein-1)-binding activity and leptin promoter activity, while SP600125, NAC and atorvastatin inhibited the AP-1-binding activity and leptin promoter activity induced by Ang II.	Acetylcysteine	161-164	leptin	Homo sapiens	222-228
29410271-8	2018	In addition, a ROS scavenger N-acetyl-l-cysteine (NAC) down-regulated the protein level of p-p38, p-JNK and Prdx1, and H9c2 cell apoptosis.	Acetylcysteine	29-48	mitogen-activated protein kinase 8	Rattus norvegicus	100-103
21806545-15	2012	Ang II significantly increased secretion of leptin from human VSMCs, and addition of SP600125, atorvastatin and NAC before Ang II stimulation almost completely inhibited the leptin secretion induced by Ang II.	Acetylcysteine	112-115	leptin	Homo sapiens	174-180
29410271-8	2018	In addition, a ROS scavenger N-acetyl-l-cysteine (NAC) down-regulated the protein level of p-p38, p-JNK and Prdx1, and H9c2 cell apoptosis.	Acetylcysteine	29-48	peroxiredoxin 1	Rattus norvegicus	108-113
19263279-1	2009	The D- and L-forms of N-acetylcysteine (NADC, NAC) were tested in antagonizing the toxicity mediated by hydrogen peroxide (H(2)O(2)) or tertiary butyl hydroperoxide (tBHP) in two lung cell lines to assess the effectivity of glutathione synthesis against peroxides.	Acetylcysteine	22-38	synuclein alpha	Homo sapiens	46-49
29410271-8	2018	In addition, a ROS scavenger N-acetyl-l-cysteine (NAC) down-regulated the protein level of p-p38, p-JNK and Prdx1, and H9c2 cell apoptosis.	Acetylcysteine	50-53	mitogen-activated protein kinase 8	Rattus norvegicus	100-103
29410271-8	2018	In addition, a ROS scavenger N-acetyl-l-cysteine (NAC) down-regulated the protein level of p-p38, p-JNK and Prdx1, and H9c2 cell apoptosis.	Acetylcysteine	50-53	peroxiredoxin 1	Rattus norvegicus	108-113
21627650-8	2012	The phosphorylated JNK protein was induced by hypoxia and was abolished by pretreatment with SP600125, losartan (an angiotensin II receptor antagonist) or N-acetylcysteine.	Acetylcysteine	155-171	mitogen-activated protein kinase 8	Rattus norvegicus	19-22
29731195-8	2018	Cellular ROS production was increased by PM treatment, and antioxidant N-acetyl cysteine pretreatment prevented induction of inflammatory cytokines IL-8 and MMP-1.	Acetylcysteine	71-88	matrix metallopeptidase 1	Homo sapiens	157-162
18993042-0	2009	The role of glutathione-S-transferase polymorphisms on clinical outcome of ALI/ARDS patient treated with N-acetylcysteine.	Acetylcysteine	105-121	glutathione S-transferase kappa 1	Homo sapiens	12-37
18993042-3	2009	In the present study we have investigated the effects of NAC treatment (IV NAC in 150mg/kg at the first day followed by 50mg/kg/day for three days) on 27 ICU patients with ALI/ARDS considering the glutathione-S-transferase genetic variations, as an important enzyme contributing in oxidative stress pathways.	Acetylcysteine	57-60	glutathione S-transferase kappa 1	Homo sapiens	197-222
22511847-8	2012	Blocking with GZ, NAC, and JNK significantly suppressed AGE-induced VEGF-A production.	Acetylcysteine	18-21	vascular endothelial growth factor A	Rattus norvegicus	68-74
28961512-18	2018	NAC, given after the establishment of diabetes, may offer protection against the risk for stroke by altering both systemic and vascular prothrombotic responses via enhancing platelet GSH, and GSH-dependent MG elimination, as well as correcting levels of antioxidants such as SOD1 and GPx-1.	Acetylcysteine	0-3	glutathione peroxidase 1	Mus musculus	284-289
23251571-9	2012	ROS accumulation followed E2F1 induction and treatment with the antioxidant N-acetylcysteine, inhibited E2F1-induced Bax translocation to mitochondria and subsequent apoptosis.	Acetylcysteine	76-92	E2F transcription factor 1	Homo sapiens	26-30
18973548-5	2009	After administration of N-acetylcysteine, an antioxidant, to KK-A(y) mice, alveolar bone loss and the expression of endothelial nitric oxide synthase protein in gingival keratinocytes and of hydrogen peroxide concentrations in plasma, were analyzed.	Acetylcysteine	24-40	nitric oxide synthase 3, endothelial cell	Mus musculus	116-149
18973548-8	2009	Administration of N-acetylcysteine to the mice restored endothelial nitric oxide synthase expression in the gingival keratinocytes, suppressed the alveolar bone loss and decreased the hydrogen peroxide concentrations in plasma without the improvement of obesity or diabetes.	Acetylcysteine	18-34	nitric oxide synthase 3, endothelial cell	Mus musculus	56-89
18973548-9	2009	In vitro, stimulation with hydrogen peroxide decreased the expression level of endothelial nitric oxide synthase in cultured keratinocytes, which was restored by the addition of N-acetylcysteine.	Acetylcysteine	178-194	nitric oxide synthase 3, endothelial cell	Mus musculus	79-112
23251571-9	2012	ROS accumulation followed E2F1 induction and treatment with the antioxidant N-acetylcysteine, inhibited E2F1-induced Bax translocation to mitochondria and subsequent apoptosis.	Acetylcysteine	76-92	E2F transcription factor 1	Homo sapiens	104-108
29599711-8	2018	Prenatal NAC administration also resulted in greater glucose tolerance and insulin sensitivity while increasing adiponectin levels, as well as increasing exploratory behavior, an effect accompanied by reduced plasma corticosterone levels in response to restraint stress.	Acetylcysteine	9-12	adiponectin, C1Q and collagen domain containing	Mus musculus	112-123
23226323-4	2012	Nuclear accumulation of annexin A2 is blocked by the antioxidant agent N-acetyl cysteine (NAC) and stimulated by hydrogen peroxide (H2O2), suggesting that this is a reactive oxygen species dependent event.	Acetylcysteine	71-88	annexin A2	Homo sapiens	24-34
19007345-1	2009	OBJECTIVES: The objective was to evaluate the effectiveness of intravenous N-acetylcysteine (IV NAC; 300 mg/kg over 21 hours) in early acute acetaminophen (APAP) overdose patients.	Acetylcysteine	75-91	synuclein alpha	Homo sapiens	96-99
19373608-6	2009	NAC also delayed the induction of apoptosis in dominant negative FADD-expressing malignant cell lines.	Acetylcysteine	0-3	Fas associated via death domain	Homo sapiens	65-69
23226323-4	2012	Nuclear accumulation of annexin A2 is blocked by the antioxidant agent N-acetyl cysteine (NAC) and stimulated by hydrogen peroxide (H2O2), suggesting that this is a reactive oxygen species dependent event.	Acetylcysteine	90-93	annexin A2	Homo sapiens	24-34
29593571-7	2018	As compared to non-treatment, both NAC and PQQ treatment (1) reversed the increase in the ROS level in two muscle samples; (2) attenuated the reduction in the cross-sectional area (CSA) of denervated mouse muscle or in the diameter of fasted C2C12 myotube; (3) increased the myosin heavy chain (MHC) level and decreased the muscle atrophy F-box (MAFbx) and muscle-specific RING finger-1 (MuRF-1) levels in two muscle samples.	Acetylcysteine	35-38	F-box protein 32	Mus musculus	346-351
23077524-7	2012	Here we have tested this hypothesis by treating Nkx3.1 mutant mice with the antioxidant N-acetylcysteine (NAC) for 13 weeks post-weaning.	Acetylcysteine	88-104	NK3 homeobox 1	Mus musculus	48-54
18976633-6	2008	The radical scavenger N-acetyl-l-cysteine profoundly inhibited pkr induction via the reduction of IFN-gamma expression.	Acetylcysteine	22-41	eukaryotic translation initiation factor 2 alpha kinase 2	Homo sapiens	63-66
18840609-8	2008	The increased apoptosis by forced expression of BTG2/TIS21/PC3 could be inhibited by N-acetyl-L-cysteine and polyethylene glycol-catalase.	Acetylcysteine	85-104	BTG anti-proliferation factor 2	Homo sapiens	48-52
18840609-8	2008	The increased apoptosis by forced expression of BTG2/TIS21/PC3 could be inhibited by N-acetyl-L-cysteine and polyethylene glycol-catalase.	Acetylcysteine	85-104	BTG anti-proliferation factor 2	Homo sapiens	53-58
18840609-8	2008	The increased apoptosis by forced expression of BTG2/TIS21/PC3 could be inhibited by N-acetyl-L-cysteine and polyethylene glycol-catalase.	Acetylcysteine	85-104	BTG anti-proliferation factor 2	Homo sapiens	59-62
23077524-7	2012	Here we have tested this hypothesis by treating Nkx3.1 mutant mice with the antioxidant N-acetylcysteine (NAC) for 13 weeks post-weaning.	Acetylcysteine	106-109	NK3 homeobox 1	Mus musculus	48-54
23077524-8	2012	Surprisingly, while NAC treatment decreased ROS levels in Nkx3.1 mutant mouse prostates, it failed to reduce prostatic epithelial hyperplasia/dysplasia.	Acetylcysteine	20-23	NK3 homeobox 1	Mus musculus	58-64
29328400-6	2018	Nacetylcysteine, a Nox4 inhibitor, was demonstrated to inhibit ROS generation, suppress VCAM-1 and ICAM-1 protein expression, and decrease oxidative stress and inflammation in HK-2 cells following overexpression of miR-146a.	Acetylcysteine	0-15	microRNA 146a	Homo sapiens	215-223
29474366-6	2018	Moreover, CRIF1 deficiency-induced vascular adhesion molecule-1 (VCAM-1) expression was consistently attenuated by the antioxidant N-acetyl-cysteine and NF-kappaB inhibitor (BAY11).	Acetylcysteine	131-148	vascular cell adhesion molecule 1	Mus musculus	35-63
20974155-4	2011	Some samples were from MCS-exposed mice treated either with N-acetyl-l-cysteine during pregnancy or with phenethyl isothiocyanate after weaning.	Acetylcysteine	60-79	sperm mitochondria-associated cysteine-rich protein	Mus musculus	23-26
18928619-9	2008	The effect of N-acetylcysteine (a free radical scavenger) on GM-CSF production following exposure to ADM was examined.	Acetylcysteine	14-30	colony stimulating factor 2	Homo sapiens	61-67
18928619-12	2008	N-acetylcysteine significantly decreased the concentration of GM-CSF produced by HFCL/EG treated with ADM.	Acetylcysteine	0-16	colony stimulating factor 2	Homo sapiens	62-68
29474366-6	2018	Moreover, CRIF1 deficiency-induced vascular adhesion molecule-1 (VCAM-1) expression was consistently attenuated by the antioxidant N-acetyl-cysteine and NF-kappaB inhibitor (BAY11).	Acetylcysteine	131-148	vascular cell adhesion molecule 1	Mus musculus	65-71
29294308-11	2018	Both TLR9 deficiency and the antioxidant N-acetyl-L-cysteine treatment improved altered intra- and extracellular TSP-1 levels under high glucose condition.	Acetylcysteine	41-60	tumor suppressor region 1	Mus musculus	113-118
18586083-6	2008	N-Acetyl-L-cysteine blocked gallium-induced MT2A and HO-1 expression and increased gallium"s cytotoxicity.	Acetylcysteine	0-19	metallothionein 2A	Homo sapiens	44-48
22185818-7	2011	ANXA2 depleted cancer cells showed enhanced cellular protein oxidation concomitant with decreased tumor growth compared to control cancer cells and both the protein oxidation and tumor growth deficit were reversed by the antioxidant N-acetyl cysteine, indicating that ANXA2 redox regulatory function plays a major role in tumorigenesis.	Acetylcysteine	233-250	annexin A2	Mus musculus	0-5
22185818-7	2011	ANXA2 depleted cancer cells showed enhanced cellular protein oxidation concomitant with decreased tumor growth compared to control cancer cells and both the protein oxidation and tumor growth deficit were reversed by the antioxidant N-acetyl cysteine, indicating that ANXA2 redox regulatory function plays a major role in tumorigenesis.	Acetylcysteine	233-250	annexin A2	Mus musculus	268-273
29291542-3	2018	Protocatechuic acid, Akt inhibitor, Bay 11-7085 and N-acetylcysteine reduced the lipopolysaccharide-caused production of cytokines and chemokines, expression of cyclooxygenase, increase in the levels and activities of Toll-like receptor-4, p-Akt and mTOR, activation of NF-kappaB, phosphorylation of the JNK and p38-MAPK, and production of reactive oxygen species in keratinocytes.	Acetylcysteine	52-68	toll like receptor 4	Homo sapiens	218-238
21740309-5	2011	VEGF increases IQGAP1-Cys-OH formation, which is prevented by N-acetyl cysteine or dimedone, which inhibits VEGF-induced EC migration and capillary network formation.	Acetylcysteine	62-79	IQ motif containing GTPase activating protein 1	Mus musculus	15-21
18562625-5	2008	In contrast, the antioxidant N-acetyl cysteine and the antidiabetic drug rosiglitazone increased adipose GPx3 expression in obese and diabetic db/db mice.	Acetylcysteine	29-46	glutathione peroxidase 3	Mus musculus	105-109
18353867-7	2008	Among several antioxidants tried, only N-acetylcysteine effectively inhibits TGFbeta-mediated activation of TGase2.	Acetylcysteine	39-55	transglutaminase 2, C polypeptide	Mus musculus	108-114
29375377-7	2017	We also showed that cisplatin and pemetrexed induce the phosphorylation of AXL and Akt, which was also blocked by BGB324 as well as by N-acetylcysteine antioxidant.	Acetylcysteine	135-151	AXL receptor tyrosine kinase	Homo sapiens	75-78
18628592-6	2008	Treatment with N-acetyl-L-cysteine also inhibited expression of apoptotic proteins such as Bax and Smac and abrogated caspase-8 activation.	Acetylcysteine	15-34	diablo IAP-binding mitochondrial protein	Homo sapiens	99-103
21494874-12	2011	Pretreatment of cells with ROS scavenger N-acetylcysteine completely blocked insulin-induced UCP-2 expression (p &lt; 0.01, one-way ANOVA) and significantly suppressed VEGF expression (p &lt; 0.01, one-way ANOVA).	Acetylcysteine	41-57	insulin	Bos taurus	77-84
29115506-6	2018	The results of the present study ndicated that Ang II upregulated MCP-1 expression in osteoblasts, which was mitigated by agonists of the AT1R, including olmesartan, a ROS scavenger N-acetylcysteine (NAC), ammonium pyrrolidinethiocarbamate (PDTC) and nuclear factor (NF)-kappaB, but not by the Ang II type 2 receptor antagonist, PD123319.	Acetylcysteine	182-198	C-C motif chemokine ligand 2	Homo sapiens	66-71
21494874-12	2011	Pretreatment of cells with ROS scavenger N-acetylcysteine completely blocked insulin-induced UCP-2 expression (p &lt; 0.01, one-way ANOVA) and significantly suppressed VEGF expression (p &lt; 0.01, one-way ANOVA).	Acetylcysteine	41-57	uncoupling protein 2	Bos taurus	93-98
18205746-8	2008	Treatment with antioxidants (bilirubin, N-acetylcysteine) protected cells against nicotine-induced cytotoxicity and blocked the upregulation of HO-1, the effects of which were more pronounced in IHOK cells than in HN12 cells.	Acetylcysteine	40-56	heme oxygenase 1	Homo sapiens	144-148
29115506-6	2018	The results of the present study ndicated that Ang II upregulated MCP-1 expression in osteoblasts, which was mitigated by agonists of the AT1R, including olmesartan, a ROS scavenger N-acetylcysteine (NAC), ammonium pyrrolidinethiocarbamate (PDTC) and nuclear factor (NF)-kappaB, but not by the Ang II type 2 receptor antagonist, PD123319.	Acetylcysteine	200-203	C-C motif chemokine ligand 2	Homo sapiens	66-71
29058042-0	2018	Chronic N-acetylcysteine treatment alleviates acute lipopolysaccharide-induced working memory deficit through upregulating caveolin-1 and synaptophysin in mice.	Acetylcysteine	8-24	caveolin 1, caveolae protein	Mus musculus	123-133
18022818-6	2008	Among the relevant pathways, p38MAPK activation sustained the levels of p21 and p27 induced by 3MC, which was eliminated by AhR antagonists and N-acetylcysteine (NAC), an antioxidant.	Acetylcysteine	144-160	H3 histone pseudogene 16	Homo sapiens	72-75
18022818-6	2008	Among the relevant pathways, p38MAPK activation sustained the levels of p21 and p27 induced by 3MC, which was eliminated by AhR antagonists and N-acetylcysteine (NAC), an antioxidant.	Acetylcysteine	144-160	interferon alpha inducible protein 27	Homo sapiens	80-83
18022818-6	2008	Among the relevant pathways, p38MAPK activation sustained the levels of p21 and p27 induced by 3MC, which was eliminated by AhR antagonists and N-acetylcysteine (NAC), an antioxidant.	Acetylcysteine	162-165	H3 histone pseudogene 16	Homo sapiens	72-75
18022818-6	2008	Among the relevant pathways, p38MAPK activation sustained the levels of p21 and p27 induced by 3MC, which was eliminated by AhR antagonists and N-acetylcysteine (NAC), an antioxidant.	Acetylcysteine	162-165	interferon alpha inducible protein 27	Homo sapiens	80-83
18022818-8	2008	A deletion of the DRE (-285/-270) in p21 (-2,300/+8) only partially alleviated the 3MC-induced luciferase activity unless NAC was added, suggesting that there may be a DRE-independent mechanism associated with oxidative stress.	Acetylcysteine	122-125	H3 histone pseudogene 16	Homo sapiens	37-40
21604367-6	2011	Reduced ALP activity and OPN mRNA expression by TEGDMA were partially recovered via cotreatment with NAC.	Acetylcysteine	101-104	secreted phosphoprotein 1	Homo sapiens	25-28
23554696-7	2011	Interestingly, EGF could induce a significant production of ROS, and N-acetyl-L-cysteine, a scavenger of ROS which abolished the EGF-induced ROS generation, cell migration, as well as activation of PI3K/Akt and PAK, but not Rac1.	Acetylcysteine	69-88	epidermal growth factor	Homo sapiens	15-18
23554696-7	2011	Interestingly, EGF could induce a significant production of ROS, and N-acetyl-L-cysteine, a scavenger of ROS which abolished the EGF-induced ROS generation, cell migration, as well as activation of PI3K/Akt and PAK, but not Rac1.	Acetylcysteine	69-88	epidermal growth factor	Homo sapiens	129-132
29058042-0	2018	Chronic N-acetylcysteine treatment alleviates acute lipopolysaccharide-induced working memory deficit through upregulating caveolin-1 and synaptophysin in mice.	Acetylcysteine	8-24	synaptophysin	Mus musculus	138-151
29058042-8	2018	More important, 2-week N-acetylcysteine (NAC) treatment dose-dependently inhibited LPS-induced working memory deficit by improving the ability to use Lose-shift but not Win-shift strategy and significantly inhibited LPS-induced downregulation of Cav-1 and SYP in mPFC.	Acetylcysteine	23-39	caveolin 1, caveolae protein	Mus musculus	246-251
21640077-6	2011	The increases in Pin1 expression and in AP-1 reporter activity in response to UVA were abolished by N-acetylcysteine (NAC) treatment.	Acetylcysteine	100-116	peptidylprolyl cis/trans isomerase, NIMA-interacting 1	Homo sapiens	17-21
18239850-4	2008	The decrease of filamentous actin was transient and was recovered through the activation of p38/Hsp27 MAPK pathway, as well as after treatment with N-acetyl-L-cysteine.	Acetylcysteine	148-167	heat shock protein family B (small) member 1	Homo sapiens	96-101
21640077-6	2011	The increases in Pin1 expression and in AP-1 reporter activity in response to UVA were abolished by N-acetylcysteine (NAC) treatment.	Acetylcysteine	118-121	peptidylprolyl cis/trans isomerase, NIMA-interacting 1	Homo sapiens	17-21
29058042-8	2018	More important, 2-week N-acetylcysteine (NAC) treatment dose-dependently inhibited LPS-induced working memory deficit by improving the ability to use Lose-shift but not Win-shift strategy and significantly inhibited LPS-induced downregulation of Cav-1 and SYP in mPFC.	Acetylcysteine	23-39	synaptophysin	Mus musculus	256-259
18630691-1	2008	OBJECTIVE: To investigate the effects of N-acetylcysteine (NAC)on the expression of IL-8 and the activity of NF-kappaB, which are induced by lipopolysaccharide (LPS) in human uterine smooth cell.	Acetylcysteine	41-57	synuclein alpha	Homo sapiens	59-62
29058042-8	2018	More important, 2-week N-acetylcysteine (NAC) treatment dose-dependently inhibited LPS-induced working memory deficit by improving the ability to use Lose-shift but not Win-shift strategy and significantly inhibited LPS-induced downregulation of Cav-1 and SYP in mPFC.	Acetylcysteine	41-44	caveolin 1, caveolae protein	Mus musculus	246-251
29058042-8	2018	More important, 2-week N-acetylcysteine (NAC) treatment dose-dependently inhibited LPS-induced working memory deficit by improving the ability to use Lose-shift but not Win-shift strategy and significantly inhibited LPS-induced downregulation of Cav-1 and SYP in mPFC.	Acetylcysteine	41-44	synaptophysin	Mus musculus	256-259
29058042-9	2018	CONCLUSIONS: Taken together, our findings demonstrate that chronic NAC treatment alleviates acute LPS-induced working memory deficit through upregulating Cav-1 and SYP in mice.	Acetylcysteine	67-70	caveolin 1, caveolae protein	Mus musculus	154-159
21586653-2	2011	The labeled dosing regimen for Acetadote, the only intravenous N-acetylcysteine (IV-NAC) product approved by the Food and Drug Administration (FDA) for treatment of acetaminophen toxicity, is a complex 3-step process that produces frequent medication errors.	Acetylcysteine	31-40	synuclein alpha	Homo sapiens	84-87
29058042-9	2018	CONCLUSIONS: Taken together, our findings demonstrate that chronic NAC treatment alleviates acute LPS-induced working memory deficit through upregulating Cav-1 and SYP in mice.	Acetylcysteine	67-70	synaptophysin	Mus musculus	164-167
21586653-2	2011	The labeled dosing regimen for Acetadote, the only intravenous N-acetylcysteine (IV-NAC) product approved by the Food and Drug Administration (FDA) for treatment of acetaminophen toxicity, is a complex 3-step process that produces frequent medication errors.	Acetylcysteine	63-79	synuclein alpha	Homo sapiens	84-87
17418620-13	2008	The addition of NAC markedly inhibited the arecoline-induced MT-1 expression (p&lt;0.05).	Acetylcysteine	16-19	metallothionein 1I, pseudogene	Homo sapiens	61-65
29202574-5	2017	Only NAC plus Aa treatment enhance the expression of other genes related to tissue growth and elasticity like FBN1, ITGA1 and ITGB1.	Acetylcysteine	5-8	fibrillin 1	Homo sapiens	110-114
17950393-7	2008	In addition, CBD treatment significantly stimulated the activation of caspase-8, which was abrogated in the presence of NAC or GSH.	Acetylcysteine	120-123	caspase 8	Mus musculus	70-79
18023956-9	2008	Pretreatment of cells with N-acetylcysteine (NAC) resulted in partial protection of Trx1 from oxidation by acrolein.	Acetylcysteine	27-43	thioredoxin	Homo sapiens	84-88
18023956-9	2008	Pretreatment of cells with N-acetylcysteine (NAC) resulted in partial protection of Trx1 from oxidation by acrolein.	Acetylcysteine	45-48	thioredoxin	Homo sapiens	84-88
18220832-6	2008	Focusing on one of these genes, the leukocyte adhesion protein E-selectin, we show that E-selectin is down-modulated with time in culture and upon treatment with NAC at mRNA and protein levels.	Acetylcysteine	162-165	selectin E	Homo sapiens	63-73
18220832-6	2008	Focusing on one of these genes, the leukocyte adhesion protein E-selectin, we show that E-selectin is down-modulated with time in culture and upon treatment with NAC at mRNA and protein levels.	Acetylcysteine	162-165	selectin E	Homo sapiens	88-98
17906114-10	2007	Incubation with H(2)O(2) reduced AdipoR1 expression in cultured cardiomyocytes that were attenuated by N-acetyl-l-cysteine or pravastatin.	Acetylcysteine	103-122	adiponectin receptor 1	Mus musculus	33-40
17979524-6	2007	Prior exposure of cells to N-acetyl-L -cysteine blocked not only the ROS production but also the nuclear translocation of Nrf2 and its ARE binding, as well as HO-1 induction by capsaicin.	Acetylcysteine	27-47	heme oxygenase 1	Homo sapiens	159-163
17936186-6	2007	NAC inhibits HEMA-mediated toxicity through induction of differentiation in DPSCs, because the genes for dentin sialoprotein, osteopontin (OPN), osteocalcin, and alkaline phosphatase, which are induced during differentiation, are also induced by NAC.	Acetylcysteine	0-3	secreted phosphoprotein 1	Homo sapiens	126-137
17936186-6	2007	NAC inhibits HEMA-mediated toxicity through induction of differentiation in DPSCs, because the genes for dentin sialoprotein, osteopontin (OPN), osteocalcin, and alkaline phosphatase, which are induced during differentiation, are also induced by NAC.	Acetylcysteine	0-3	secreted phosphoprotein 1	Homo sapiens	139-142
17942915-9	2007	N-acetyl-L-cysteine blocked the EGFR activation and reduced the N-nitrosodiethylamine-initiated hepatocarcinogenesis to the levels of Cre-Ctrl mice.	Acetylcysteine	0-19	epidermal growth factor receptor	Mus musculus	32-36
17479230-7	2007	Blocking ROS generation with N-acetylcysteine pretreatment, restored cell survival, limited the upregulation of PTEN in response to UCB, and prevented the inhibition of cell proliferation.	Acetylcysteine	29-45	phosphatase and tensin homolog	Homo sapiens	112-116
17504974-8	2007	5-HT-activated PDGFRbeta phosphorylation is blocked by the antioxidant N-acetyl-L-cysteine and the NADPH oxidase inhibitor, DPI.	Acetylcysteine	71-90	platelet derived growth factor receptor, beta polypeptide	Mus musculus	15-24
17917164-1	2007	In this study, we evaluated the effect of lipoic acid (LA) and N-acetyl cysteine (NAC) on oxidative [4-hydroxy-2-nonenal, N(epsilon)-(carboxymethyl)lysine and heme oxygenase-1] and apoptotic (caspase 9 and Bax) markers in fibroblasts from patients with Alzheimer disease (AD) and age-matched and young controls.	Acetylcysteine	82-85	heme oxygenase 1	Homo sapiens	159-175
17917164-1	2007	In this study, we evaluated the effect of lipoic acid (LA) and N-acetyl cysteine (NAC) on oxidative [4-hydroxy-2-nonenal, N(epsilon)-(carboxymethyl)lysine and heme oxygenase-1] and apoptotic (caspase 9 and Bax) markers in fibroblasts from patients with Alzheimer disease (AD) and age-matched and young controls.	Acetylcysteine	82-85	caspase 9	Homo sapiens	192-201
17699792-7	2007	Pretreatment with antioxidants, either N-acetylcysteine or catalase, completely blocked EABE-induced apoptosis, H2O2 accumulation, and up-regulation of DR5 levels.	Acetylcysteine	39-55	TNF receptor superfamily member 10b	Homo sapiens	152-155
17522181-3	2007	This mechanism was redox-sensitive; N-acetylcysteine totally abrogated the down-regulation of SphK1 activity and strongly inhibited Abeta-induced cell death.	Acetylcysteine	36-52	sphingosine kinase 1	Homo sapiens	94-99
17529908-3	2007	The antioxidants dimethyl sulfoxide (DMSO), N-acetyl cysteine, and dimethyl thiourea significantly inhibited lipopolysaccharide (LPS)-induced MCP-1 production in either whole blood or isolated blood cells.	Acetylcysteine	44-61	C-C motif chemokine ligand 2	Homo sapiens	142-147
17526490-6	2007	Pretreatment with the antioxidant N-acetylcysteine (NAC) and expression of MT1 in the Ikkbeta(-)(/)(-) cells prevented JNK activation; moreover, NAC pretreatment, MT1 expression, MKK4 ablation, and JNK inhibition all protected cells from death induced by arsenic.	Acetylcysteine	34-50	mitogen-activated protein kinase kinase 4	Mus musculus	179-183
17526490-6	2007	Pretreatment with the antioxidant N-acetylcysteine (NAC) and expression of MT1 in the Ikkbeta(-)(/)(-) cells prevented JNK activation; moreover, NAC pretreatment, MT1 expression, MKK4 ablation, and JNK inhibition all protected cells from death induced by arsenic.	Acetylcysteine	145-148	mitogen-activated protein kinase kinase 4	Mus musculus	179-183
17631703-5	2007	The level of TNF-alpha in portal vein and plasma ALT increased continually in I/R group at 1 hour and 3 hours after reperfusion compared with SH group, however, they were significantly lowered in the group pretreated by NAC (P&lt;0.05 or P&lt;0.01).	Acetylcysteine	220-223	glutamic pyruvic transaminase, soluble	Mus musculus	49-52
17477906-2	2007	In this report, we showed that p21(Cip1) was degraded at an early phase after low dose H(2)O(2) treatment of a variety of cell types and that preincubation of cells with the antioxidant, N-acetylcysteine, prolonged p21(Cip1) half-life.	Acetylcysteine	187-203	H3 histone pseudogene 16	Homo sapiens	31-34
17331470-5	2007	ATO-induced accumulation of reactive oxygen species (ROS), while the ASK1 activation was suppressed by cotreatment with an antioxidant, N-acetyl-l-cysteine.	Acetylcysteine	136-155	mitogen-activated protein kinase kinase kinase 5	Homo sapiens	69-73
17394166-10	2007	Furthermore, in vitro experiments demonstrated that TF-dependent PCA of hepatocytes is inhibited by N-acetyl-L-cysteine.	Acetylcysteine	100-119	coagulation factor III, tissue factor	Homo sapiens	52-54
17270171-6	2007	N-acetylcysteine treatment attenuated the increased oxidative stress, plasma and renal lipids, urine protein excretion rate, mesangial matrix expansion index, and protein expression of renal CTGF, but did not affect plasma adiponectin levels, renal protein expression of adiponectin receptor 1, phosphorylation of AMPK-alpha (Thr172) and renal protein expression of phospho-ACC (Ser79) in diabetic rats.	Acetylcysteine	0-16	cellular communication network factor 2	Rattus norvegicus	191-195
16924499-11	2007	NAC attenuated HO-1 upregulation, confirming the time course analysis.	Acetylcysteine	0-3	heme oxygenase 1	Homo sapiens	15-19
17260165-4	2007	A key step in the mercapturic acid pathway, efflux of the glutathione-electrophile conjugate has recently been shown to be catalyzed largely by the stress-responsive protein RLIP76, a splice variant peptide endowed by the human gene RALBP1.	Acetylcysteine	18-34	ralA binding protein 1	Homo sapiens	174-180
17260165-4	2007	A key step in the mercapturic acid pathway, efflux of the glutathione-electrophile conjugate has recently been shown to be catalyzed largely by the stress-responsive protein RLIP76, a splice variant peptide endowed by the human gene RALBP1.	Acetylcysteine	18-34	ralA binding protein 1	Homo sapiens	233-239
17266944-1	2007	OBJECTIVES: The aim of this study was to investigate the effect of the antioxidants pyrrolidine dithiocarbamate (PDTC) and N-acetylcysteine (NAC) on the ionizing radiation (IR)- and tumor necrosis factor-alpha (TNF-alpha) induced tissue factor (TF) expression and its release from human umbilical vein endothelial cells (HUVECs).	Acetylcysteine	123-139	coagulation factor III, tissue factor	Homo sapiens	230-243
17266944-1	2007	OBJECTIVES: The aim of this study was to investigate the effect of the antioxidants pyrrolidine dithiocarbamate (PDTC) and N-acetylcysteine (NAC) on the ionizing radiation (IR)- and tumor necrosis factor-alpha (TNF-alpha) induced tissue factor (TF) expression and its release from human umbilical vein endothelial cells (HUVECs).	Acetylcysteine	123-139	coagulation factor III, tissue factor	Homo sapiens	245-247
17266944-1	2007	OBJECTIVES: The aim of this study was to investigate the effect of the antioxidants pyrrolidine dithiocarbamate (PDTC) and N-acetylcysteine (NAC) on the ionizing radiation (IR)- and tumor necrosis factor-alpha (TNF-alpha) induced tissue factor (TF) expression and its release from human umbilical vein endothelial cells (HUVECs).	Acetylcysteine	141-144	coagulation factor III, tissue factor	Homo sapiens	230-243
17266944-1	2007	OBJECTIVES: The aim of this study was to investigate the effect of the antioxidants pyrrolidine dithiocarbamate (PDTC) and N-acetylcysteine (NAC) on the ionizing radiation (IR)- and tumor necrosis factor-alpha (TNF-alpha) induced tissue factor (TF) expression and its release from human umbilical vein endothelial cells (HUVECs).	Acetylcysteine	141-144	coagulation factor III, tissue factor	Homo sapiens	245-247
17250813-3	2007	We hypothesized that chronic treatment with the antioxidant N-acetylcysteine (NAC) would normalize oxidative stress-mediated overexpression of myocardial PKCbeta(2) and CTGF and attenuate the development of myocardial hypertrophy.	Acetylcysteine	60-76	cellular communication network factor 2	Rattus norvegicus	169-173
17250813-3	2007	We hypothesized that chronic treatment with the antioxidant N-acetylcysteine (NAC) would normalize oxidative stress-mediated overexpression of myocardial PKCbeta(2) and CTGF and attenuate the development of myocardial hypertrophy.	Acetylcysteine	78-81	cellular communication network factor 2	Rattus norvegicus	169-173
20020979-10	2007	Interestingly, both TPH and NAC recovered diazinon-induced AChE inhibition.	Acetylcysteine	28-31	acetylcholinesterase	Rattus norvegicus	59-63
17349145-15	2007	Compared with the LPS group, the levels of ALT, NO and iNOS mRNA of NAC group were lower at the time points 6 h and 12 h (P &lt; 0.01).	Acetylcysteine	68-71	glutamic pyruvic transaminase, soluble	Mus musculus	43-46
16952378-0	2006	N-acetylcysteine attenuates TNF-alpha induced changes in secretion of interleukin-6, plasminogen activator inhibitor-1 and adiponectin from 3T3-L1 adipocytes.	Acetylcysteine	0-16	serine (or cysteine) peptidase inhibitor, clade E, member 1	Mus musculus	85-118
16952378-0	2006	N-acetylcysteine attenuates TNF-alpha induced changes in secretion of interleukin-6, plasminogen activator inhibitor-1 and adiponectin from 3T3-L1 adipocytes.	Acetylcysteine	0-16	adiponectin, C1Q and collagen domain containing	Mus musculus	123-134
16952378-9	2006	The present study revealed that NAC inhibited the TNF-alpha-mediated activation of NF-kappaB and improved the adverse changes in the levels of IL-6, PAI-1 and adiponectin in 3T3-L1 adipocytes.	Acetylcysteine	32-35	serine (or cysteine) peptidase inhibitor, clade E, member 1	Mus musculus	149-154
16952378-9	2006	The present study revealed that NAC inhibited the TNF-alpha-mediated activation of NF-kappaB and improved the adverse changes in the levels of IL-6, PAI-1 and adiponectin in 3T3-L1 adipocytes.	Acetylcysteine	32-35	adiponectin, C1Q and collagen domain containing	Mus musculus	159-170
17041759-11	2006	Antioxidants such as vitamin C and N-acetyl cysteine inhibited NE-induced ROS production, JNK phosphorylation, caspase activation and apoptosis.	Acetylcysteine	35-52	mitogen-activated protein kinase 8	Rattus norvegicus	90-93
17023264-8	2006	Similar to NAC, the MEK1/2 inhibitor U0126, the p38 inhibitor SB203580, and the protein kinase inhibitor H-89 selectively inhibited ET-1 upregulation without affecting nuclear p65 translocation, suggesting that NAC inhibits ET-1 upregulation via inhibition of mitogen- and stress-activated protein kinase (MSK).	Acetylcysteine	211-214	mitogen-activated protein kinase kinase 1	Homo sapiens	20-26
16860347-11	2006	Post-treatment with NAC diminished the decrease in MAP, increased the HR, and decreased the markers of organ injury (BUN, Cre, LDH, CPK, GOT, GPT) and inflammatory biomarkers (TNF-alpha, IL-6, IL-10) after LPS.	Acetylcysteine	20-23	interleukin 10	Rattus norvegicus	193-198
21558814-7	2011	We also show that the expression of MCT4 in cancer-associated fibroblasts is due to oxidative stress, and can be prevented by pre-treatment with the anti-oxidant N-acetyl-cysteine.	Acetylcysteine	162-179	solute carrier family 16 member 3	Homo sapiens	36-40
20584210-1	2011	Intravenous N-acetylcysteine (IV-NAC) is usually regarded as a safe antidote to acetaminophen overdose.	Acetylcysteine	12-28	synuclein alpha	Homo sapiens	33-36
21569548-13	2011	NAC completely inhibited celastrol-induced decrease of HSP90 client proteins, catalase and thioredoxin.	Acetylcysteine	0-3	heat shock protein 90 alpha family class A member 1	Homo sapiens	55-60
21569548-13	2011	NAC completely inhibited celastrol-induced decrease of HSP90 client proteins, catalase and thioredoxin.	Acetylcysteine	0-3	thioredoxin	Homo sapiens	91-102
21721350-0	2011	Immunohistochemical expression of apoptosis and VEGF expression on random skin flaps in rats treated with hyperbaric oxygen and N-acetylcysteine.	Acetylcysteine	128-144	vascular endothelial growth factor A	Rattus norvegicus	48-52
21212405-10	2011	N-acetyl-l-cysteine or NADPH oxidase inhibitor treatment reversed CYR61 induction by S1P, indicating that reactive oxygen species are responsible for this process.	Acetylcysteine	0-19	cellular communication network factor 1	Homo sapiens	66-71
21204616-4	2011	RESULTS: Blocking ATM expression in U87MG cells increased intracellular ROS levels and sensitivity to the cytotoxic effects of IR and oxygen stress; effects that could be partly counteracted by the antioxidant N-acetylcysteine (NAC).	Acetylcysteine	210-226	ATM serine/threonine kinase	Homo sapiens	18-21
21204616-4	2011	RESULTS: Blocking ATM expression in U87MG cells increased intracellular ROS levels and sensitivity to the cytotoxic effects of IR and oxygen stress; effects that could be partly counteracted by the antioxidant N-acetylcysteine (NAC).	Acetylcysteine	228-231	ATM serine/threonine kinase	Homo sapiens	18-21
21204616-5	2011	Knock down of ATM rendered cells unable to repair sub-lethal or potentially lethal damage and DNA double strand breaks (DSB) after IR exposure; something that NAC could not counteract.	Acetylcysteine	159-162	ATM serine/threonine kinase	Homo sapiens	14-17
22778864-8	2011	All N-acetyl-l-cysteine fatty acyl thioester derivatives were hydrolyzed by BuChE but not by the related enzyme acetylcholinesterase.	Acetylcysteine	4-23	butyrylcholinesterase	Homo sapiens	76-81
20938987-5	2011	The use of the antioxidant N-acetyl cysteine prevented the induction of HO-1 by curcumin.	Acetylcysteine	27-44	heme oxygenase 1	Homo sapiens	72-76
20959117-1	2011	We have previously reported that pretreatment of human lymphoblastoid cells with the hydroxyl radical scavenger, N-acetyl cysteine, attenuates doxorubicin-induced DNA damage signalling through the ATM protein kinase.	Acetylcysteine	113-130	ATM serine/threonine kinase	Homo sapiens	197-200
21325821-10	2011	The effects of Bay 11-7082 and parthenolide on annexin V binding could be fully reversed by the antioxidant N-acetylcysteine.	Acetylcysteine	108-124	annexin A5	Homo sapiens	47-56
21187656-8	2011	In rats with 1mg NAC, the suppression of myocarditis was not obvious, but APD prolongation and Kv4.2 reduction was attenuated (P&lt;0.05).	Acetylcysteine	17-20	potassium voltage-gated channel subfamily D member 2	Rattus norvegicus	95-100
21873804-11	2011	Moreover, we found that NAC down-regulated the expression of VCAM-1, MMP2 and MMP9, accompanied by inhibition of NF-kappaB activation and reduced expression of RAGE.	Acetylcysteine	24-27	vascular cell adhesion molecule 1	Mus musculus	61-67
21655192-4	2011	Here we show that orally supplementing aged mice with N-acetylcysteine, a precursor for the formation of glutathione, reverses the L-type calcium channel-dependent LTP seen in aged animals to NMDAR-dependent LTP.	Acetylcysteine	54-70	glutamate receptor, ionotropic, NMDA1 (zeta 1)	Mus musculus	192-197
20959717-7	2010	Knock-down of CHOP expression by siRNA transfection and specific inhibitors of p38 (SB203580), JNK (SP600125), and ERK (PD98059) as well as anti-oxidant (N-acetylcysteine) reduced TG- or BFA-induced cell death.	Acetylcysteine	154-170	DNA-damage inducible transcript 3	Mus musculus	14-18
21172010-8	2010	The antioxidants, N-acetylcysteine and glutathione, but not vitamin C or tiron, inhibited perifosine-induced elevation of p-c-Jun, DR4 and DR5.	Acetylcysteine	18-34	TNF receptor superfamily member 10b	Homo sapiens	139-142
20804741-11	2010	TNF-alpha-induced expression of uPA and activation of beta-catenin signaling appear to be mediated by ROS in MCF-10A cells, as both events were blocked by the antioxidant N-acetylcysteine.	Acetylcysteine	171-187	catenin beta 1	Homo sapiens	54-66
22416658-17	2010	Renal antioxidant defense system was re-enforced by NAC, leading to increase in the activities of SOD, CAT, GST and decreases in GSH depletion and MDA level.	Acetylcysteine	52-55	hematopoietic prostaglandin D synthase	Rattus norvegicus	108-111
20816907-0	2010	Up-regulation of caveolin-1 and blood-brain barrier breakdown are attenuated by N-acetylcysteine in thiamine deficiency.	Acetylcysteine	80-96	caveolin 1, caveolae protein	Mus musculus	17-27
20816907-7	2010	Reduction of oxidative stress by NAC, as shown by normalization of reduced glutathione levels and attenuation of endothelial heme oxygenase-1 and nitric oxide synthase expression, resulted in prevention of the up-regulation of caveolin-1 in TD.	Acetylcysteine	33-36	caveolin 1, caveolae protein	Mus musculus	227-237
20816907-8	2010	Normalization of caveolin-1 levels by NAC was accompanied by a reduction in BBB breakdown, indicated by decreased IgG extravasation, normalization of occludin levels and prevention of matrix metalloproteinase-9 up-regulation.	Acetylcysteine	38-41	caveolin 1, caveolae protein	Mus musculus	17-27
21103380-9	2010	Gender differences in GSNO-R activity appear to explain the difference in the ability of NAC to induce PH: female and castrated male animals are protected from NAC-induced PH.	Acetylcysteine	89-92	alcohol dehydrogenase 5 (class III), chi polypeptide	Mus musculus	22-28
21103380-9	2010	Gender differences in GSNO-R activity appear to explain the difference in the ability of NAC to induce PH: female and castrated male animals are protected from NAC-induced PH.	Acetylcysteine	160-163	alcohol dehydrogenase 5 (class III), chi polypeptide	Mus musculus	22-28
20824644-0	2010	N-acetylcysteine counteracts oxidative stress and prevents hCG-induced apoptosis in rat Leydig cells through down regulation of caspase-8 and JNK.	Acetylcysteine	0-16	mitogen-activated protein kinase 8	Rattus norvegicus	142-145
20824644-7	2010	NAC treatment induced down-regulation of upstream JNK/pJNK and down-stream caspase-3 in the target cells.	Acetylcysteine	0-3	mitogen-activated protein kinase 8	Rattus norvegicus	50-53
20824644-8	2010	Taken together, the above findings indicate that NAC counteracted the oxidative stress in Leydig cells induced as a result of repeated hCG stimulation, and inhibited apoptosis by mainly regulating the extrinsic and JNK pathways of metazoan apoptosis.	Acetylcysteine	49-52	mitogen-activated protein kinase 8	Rattus norvegicus	215-218
20648652-8	2010	Administration of N-acetyl-L-cysteine (NAC), a glutathione precursor, to APP/PS-1 mice via drinking water suppressed increased protein oxidation and nitration and also significantly augmented levels and activity of GPx in brain from both age groups.	Acetylcysteine	18-37	presenilin 1	Mus musculus	77-81
20648652-8	2010	Administration of N-acetyl-L-cysteine (NAC), a glutathione precursor, to APP/PS-1 mice via drinking water suppressed increased protein oxidation and nitration and also significantly augmented levels and activity of GPx in brain from both age groups.	Acetylcysteine	39-42	presenilin 1	Mus musculus	77-81
20648652-9	2010	Oral administration of NAC also increased the diminished activity of GR and protected against lipid peroxidation in brains of 9-month-old APP/PS-1 mice only.	Acetylcysteine	23-26	presenilin 1	Mus musculus	142-146
19538479-7	2010	Block of CD83 expression could be reversed by MG scavenger N-acetyl cysteine.	Acetylcysteine	59-76	CD83 molecule	Homo sapiens	9-13
20363232-9	2010	In addition, NAC blunted the Sp1 reduction and hTERT downregulation by curcumin.	Acetylcysteine	13-16	telomerase reverse transcriptase	Homo sapiens	47-52
20862209-5	2010	Release of IL-1beta from macrophages was suppressed by the reactive oxygen species (ROS) scavenger N-acetyl cysteine (NAC) and high extracellular K(+), which are two agents known to inhibit NALP3/cryopyrin/CIAS1 inflammasome formation.	Acetylcysteine	99-116	NLR family, pyrin domain containing 3	Mus musculus	190-195
20862209-5	2010	Release of IL-1beta from macrophages was suppressed by the reactive oxygen species (ROS) scavenger N-acetyl cysteine (NAC) and high extracellular K(+), which are two agents known to inhibit NALP3/cryopyrin/CIAS1 inflammasome formation.	Acetylcysteine	99-116	NLR family, pyrin domain containing 3	Mus musculus	196-205
20862209-5	2010	Release of IL-1beta from macrophages was suppressed by the reactive oxygen species (ROS) scavenger N-acetyl cysteine (NAC) and high extracellular K(+), which are two agents known to inhibit NALP3/cryopyrin/CIAS1 inflammasome formation.	Acetylcysteine	118-121	NLR family, pyrin domain containing 3	Mus musculus	190-195
20862209-5	2010	Release of IL-1beta from macrophages was suppressed by the reactive oxygen species (ROS) scavenger N-acetyl cysteine (NAC) and high extracellular K(+), which are two agents known to inhibit NALP3/cryopyrin/CIAS1 inflammasome formation.	Acetylcysteine	118-121	NLR family, pyrin domain containing 3	Mus musculus	196-205
20005956-9	2010	Further, angiotensin II was found to up-regulate NPC1L1 mRNA and protein levels in Caco-2 cells, which were completely blocked by an angiotensin II type 1 receptor blocker or an anti-oxidant, N-acetylcysteine.	Acetylcysteine	192-208	NPC1 like intracellular cholesterol transporter 1	Homo sapiens	49-55
20157118-6	2010	Pretreatment of the MRC-5 non-cancerous cells with the antioxidant N-acetylcysteine or 2,2,6,6-tetramethylpiperidine-1-oxyl suppresses the selenium-induced ATM activation and senescence.	Acetylcysteine	67-83	ATM serine/threonine kinase	Homo sapiens	156-159
20089932-4	2010	Hypoxia-induced phosphorylation of p38 mitogen-activated protein kinase (MAPK) and stress-activated protein kinase/c-Jun NH(2)-terminal kinase (SAPK/JNK) were inhibited by the antioxidant (N-acetylcysteine, NAC, 10(-6) M) and (taurine, 4x10(-6) M).	Acetylcysteine	189-205	synuclein alpha	Homo sapiens	207-210
20080177-6	2010	In resting cells, NAC decreased mRNA and protein contents of GLUT4, mRNA content and activity of PFK, and lactate production.	Acetylcysteine	18-21	solute carrier family 2 member 4	Rattus norvegicus	61-66
19782051-7	2010	Pretreatment with NAC blocked annexin V-binding, cleavage of PARP-1 and procaspases-3, -8, -9, loss of mitochondrial membrane potential and release of cytochrome c by CDDO-Me.	Acetylcysteine	18-21	annexin A5	Homo sapiens	30-39
20389059-7	2010	Inhibitors of NF-kappaB (ammonium pyrrolidinedithiocarbamate and isohelenin) and an antioxidant (N-acetyl-L-cysteine) suppressed the indoxyl sulfate-induced expression of ICAM-1 and MCP-1 in HUVEC.	Acetylcysteine	97-116	C-C motif chemokine ligand 2	Homo sapiens	182-187
19951696-8	2010	The phosphorylation of P70S6K, downstream of mTOR signaling, and AKT were further reduced by pretreatment with N-acetyl-l-cysteine (NAC), an ROS scavenger, whereas the phosphorylation of ERK1/2 and the conversion of LC3 I to LC3 II were further enhanced.	Acetylcysteine	111-130	ribosomal protein S6 kinase B1	Homo sapiens	23-29
19951696-8	2010	The phosphorylation of P70S6K, downstream of mTOR signaling, and AKT were further reduced by pretreatment with N-acetyl-l-cysteine (NAC), an ROS scavenger, whereas the phosphorylation of ERK1/2 and the conversion of LC3 I to LC3 II were further enhanced.	Acetylcysteine	132-135	ribosomal protein S6 kinase B1	Homo sapiens	23-29
19717140-10	2010	N-acetylcysteine also restored GLT-1 and xCT levels.	Acetylcysteine	0-16	solute carrier family 7 member 11	Homo sapiens	41-44
20054154-7	2010	Co-administration of N-Acetylcysteine (NAC) exerted a strong protective effect against CdCl(2) induced barrier damage and stress related genes, while other antioxidants only attenuated CdCl(2) induced HSP70 and HMOX-1 and showed no protective effect on the barrier collapse.	Acetylcysteine	39-42	heme oxygenase 1	Homo sapiens	211-217
20054154-9	2010	The protective effect of NAC against CdCl(2) induced MT1X, HSP70 and HMOX-1 genes, demonstrates an anti-oxidant effect of NAC in addition to Cd chelation.	Acetylcysteine	25-28	heme oxygenase 1	Homo sapiens	69-75
20054154-9	2010	The protective effect of NAC against CdCl(2) induced MT1X, HSP70 and HMOX-1 genes, demonstrates an anti-oxidant effect of NAC in addition to Cd chelation.	Acetylcysteine	122-125	heme oxygenase 1	Homo sapiens	69-75
19949083-8	2010	SFN formed adducts with cysteine residues in the extracellular domain of TLR4 as confirmed by liquid chromatography-tandem mass spectrometry analysis and the inhibitory effects of SFN on oligomerization and NF-kappaB activation were reversed by thiol donors (DTT and N-acetyl-L-cysteine).	Acetylcysteine	267-286	toll like receptor 4	Homo sapiens	73-77
19703551-5	2009	At 24 h, NAC prevented cytotoxicity and Hsp90 complex disruption.	Acetylcysteine	9-12	heat shock protein 90 alpha family class A member 1	Homo sapiens	40-45
19734319-6	2009	Upregulation of HO-1 coincides with decreased intracellular glutathione (GSH) levels and can be inhibited by N-acetyl cysteine (NAC), a thiol antioxidant and GSH precursor.	Acetylcysteine	109-126	heme oxygenase 1	Homo sapiens	16-20
19734319-6	2009	Upregulation of HO-1 coincides with decreased intracellular glutathione (GSH) levels and can be inhibited by N-acetyl cysteine (NAC), a thiol antioxidant and GSH precursor.	Acetylcysteine	128-131	heme oxygenase 1	Homo sapiens	16-20
19559059-7	2009	N-Acetylcysteine (NAC) intervention promotes neuroprotection of cutaneous sensory neurons through considerable upregulation of Bcl-2 and downregulation of both Bax and caspase-3 mRNA.	Acetylcysteine	0-16	BCL2 associated X, apoptosis regulator	Rattus norvegicus	160-163
19559059-7	2009	N-Acetylcysteine (NAC) intervention promotes neuroprotection of cutaneous sensory neurons through considerable upregulation of Bcl-2 and downregulation of both Bax and caspase-3 mRNA.	Acetylcysteine	18-21	BCL2 associated X, apoptosis regulator	Rattus norvegicus	160-163
19553346-5	2009	NO donors S-nitroso-N-acetylpenicillamine (SNAP)/sodium nitroprusside (SNP) and antioxidants N-acetylcysteine (NAC)/taurine treatments significantly attenuated AGE-inhibited NO production, cGMP synthesis, and inducible NO synthase/cGMP-dependent protein kinase (PKG) activation.	Acetylcysteine	111-114	protein kinase cGMP-dependent 1	Homo sapiens	262-265
19427898-9	2009	We also found that N-acetylcysteine increases intracellular GSH and prevents premature senescence in Gclm(-/-) cells.	Acetylcysteine	19-35	glutamate-cysteine ligase, modifier subunit	Mus musculus	101-105
18830972-9	2009	Expression changes of HO-1 and iNOS were markedly blocked when Jurkat cells were preincubated with NAC, suggesting that ROS resulted in HO-1 and iNOS dysfunction in Jurkat cells.	Acetylcysteine	99-102	heme oxygenase 1	Homo sapiens	22-26
18830972-9	2009	Expression changes of HO-1 and iNOS were markedly blocked when Jurkat cells were preincubated with NAC, suggesting that ROS resulted in HO-1 and iNOS dysfunction in Jurkat cells.	Acetylcysteine	99-102	heme oxygenase 1	Homo sapiens	136-140
19428345-13	2009	Furthermore, pretreatment with N-acetylcysteine (NAC) reduced these enhanced effects.	Acetylcysteine	31-47	synuclein alpha	Homo sapiens	49-52
19370474-3	2009	Cellular GGT is a prerequisite for metabolism of GSH conjugates that detoxify xenobiotics to mercapturic acid.	Acetylcysteine	93-109	gamma-glutamyltransferase light chain family member 3	Homo sapiens	9-12
19436114-8	2009	Remarkably, lifelong administration of the potent antioxidant N-acetylcysteine (NAC) prevented acetaminophen-induced liver failure, restored Fas-dependent hepatocyte apoptosis, and blocked hepatocarcinogenesis in Taldo1-/- mice.	Acetylcysteine	80-83	transaldolase 1	Mus musculus	213-219
19436114-9	2009	These data reveal a protective role for the TAL-mediated branch of the PPP against hepatocarcinogenesis and identify NAC as a promising treatment for liver disease in TAL deficiency.	Acetylcysteine	117-120	transaldolase 1	Mus musculus	44-47
19103434-8	2009	CONCLUSIONS: These results indicate that the cystine-glutamate exchanger and the glial glutamate transporter are downregulated after nicotine self-administration, and augmenting exchanger activity with N-acetylcysteine reduced the number of cigarettes smoked in nicotine-dependent individuals.	Acetylcysteine	202-218	solute carrier family 1 member 3	Rattus norvegicus	81-108
19159629-9	2009	NAC was also able to normalize DeltaPsim, inhibit cytochrome c release, increase Bcl-2 and decrease Bax expression and procaspase-9 activation.	Acetylcysteine	0-3	BCL2 associated X, apoptosis regulator	Rattus norvegicus	100-103
29202574-5	2017	Only NAC plus Aa treatment enhance the expression of other genes related to tissue growth and elasticity like FBN1, ITGA1 and ITGB1.	Acetylcysteine	5-8	integrin subunit alpha 1	Homo sapiens	116-121
28946937-6	2017	The ROS scavenger N-acetylcysteine inhibited CLB2.0-induced IL-6 secretion, thereby decreasing the CLB2.0-induced MUC5AC expression, whereas CLB2.0-induced MUC1 expression increased.	Acetylcysteine	18-34	mucin 5AC, oligomeric mucus/gel-forming	Homo sapiens	114-120
19126599-7	2009	This phenomenon was reversed by the reactive oxygen species (ROS) scavenger N-acetylcysteine (NAC), demonstrated that ROS might activate GSK-3beta.	Acetylcysteine	76-92	glycogen synthase kinase 3 beta	Mus musculus	137-146
19126599-7	2009	This phenomenon was reversed by the reactive oxygen species (ROS) scavenger N-acetylcysteine (NAC), demonstrated that ROS might activate GSK-3beta.	Acetylcysteine	94-97	glycogen synthase kinase 3 beta	Mus musculus	137-146
19033395-9	2009	Furthermore, we found that arsenic-induced AhR activation and -enhanced CYP1A1 expression can be further increased by a prooxidant, buthionine-(S,R)-sulfoximine, and suppressed by antioxidants, such as N-acetylcysteine and catalase.	Acetylcysteine	202-218	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	72-78
29046125-8	2017	NAC suppressed GFAP overexpression in 6- and 12-week-old offspring mice following maternal CB-NP exposure.	Acetylcysteine	0-3	glial fibrillary acidic protein	Mus musculus	15-19
19050604-10	2009	Dx, administered before or after AP, and NAC reduced the leukocytosis induced by AP and blocked the ability of circulating monocytes to produce tumor necrosis factor-alpha and monocyte chemoattractant protein-1; however none of them significantly reduced the overexpression of intercellular cell adhesion molecule-1 found in monocytes 6 hrs after inducing AP.	Acetylcysteine	41-44	C-C motif chemokine ligand 2	Rattus norvegicus	176-210
19009558-4	2009	N-Acetylcysteine (ROS scavenger) and BAPTA-AM (Ca(2+) chelator) abrogated p38 MAPK activation and upregulation of Fas and FasL expression, but restored phosphorylation of ERK.	Acetylcysteine	0-16	Fas ligand	Homo sapiens	122-126
18829152-4	2009	When N-acetyl-L-cysteine or glutathione-monoethyl ester, a potent antioxidant, was added to cell culture, hmox-1 upregulation was attenuated, suggesting that oxidative stress caused by sonication is involved in this process.	Acetylcysteine	5-24	heme oxygenase 1	Homo sapiens	106-112
28782507-3	2017	Exposing YD8 cells to Cd reduced the expression levels of catalase and superoxide dismutase 1/2 and induced the expression of HO-1 as well as autophagy and apoptosis, which were reversed by N-acetyl-l-cysteine (NAC).	Acetylcysteine	190-209	heme oxygenase 1	Homo sapiens	126-130
29018354-10	2017	NAC improved insulin sensitivity, reduced urine TBARS, adipose macrophage number and Itgam and Mrc mRNA and increased Slc2a4 and Ppara.	Acetylcysteine	0-3	solute carrier family 2 member 4	Rattus norvegicus	118-124
18599524-8	2008	The antioxidant N-acetylcysteine significantly inhibited ROS generation, Akt/protein kinase B, and tuberin phosphorylation and resulted in deceased 8-oxodG accumulation and upregulation of OGG1 protein expression.	Acetylcysteine	16-32	TSC complex subunit 2	Rattus norvegicus	99-106
18599524-8	2008	The antioxidant N-acetylcysteine significantly inhibited ROS generation, Akt/protein kinase B, and tuberin phosphorylation and resulted in deceased 8-oxodG accumulation and upregulation of OGG1 protein expression.	Acetylcysteine	16-32	8-oxoguanine DNA glycosylase	Rattus norvegicus	189-193
18586083-6	2008	N-Acetyl-L-cysteine blocked gallium-induced MT2A and HO-1 expression and increased gallium"s cytotoxicity.	Acetylcysteine	0-19	heme oxygenase 1	Homo sapiens	53-57
17015178-9	2006	Cell invasion assays revealed that NAC enhanced endostatin"s ability to inhibit human cancer cell invasion.	Acetylcysteine	35-38	collagen type XVIII alpha 1 chain	Homo sapiens	48-58
29018354-10	2017	NAC improved insulin sensitivity, reduced urine TBARS, adipose macrophage number and Itgam and Mrc mRNA and increased Slc2a4 and Ppara.	Acetylcysteine	0-3	peroxisome proliferator activated receptor alpha	Rattus norvegicus	129-134
18512759-0	2008	N-acetylcysteine prevents beta-amyloid toxicity by a stimulatory effect on p35/cyclin-dependent kinase 5 activity in cultured cortical neurons.	Acetylcysteine	0-16	cyclin dependent kinase 5	Homo sapiens	79-104
18512759-4	2008	NAC increased cyclin-dependent kinase 5 (Cdk5) phosphorylation, an effect that was blocked by Cdk5 inhibitor.	Acetylcysteine	0-3	cyclin dependent kinase 5	Homo sapiens	14-39
28715154-7	2017	It is revealed that 3 h after the introduction of LPS, levels of reactive oxygen species in the kidney were significantly increased, and the injection of the antioxidant N-acetylcysteine afforded protection from AKI, evaluated by urine KIM-1 and NGAL levels.	Acetylcysteine	170-186	hepatitis A virus cellular receptor 1	Rattus norvegicus	236-241
18512759-4	2008	NAC increased cyclin-dependent kinase 5 (Cdk5) phosphorylation, an effect that was blocked by Cdk5 inhibitor.	Acetylcysteine	0-3	cyclin dependent kinase 5	Homo sapiens	41-45
18512759-4	2008	NAC increased cyclin-dependent kinase 5 (Cdk5) phosphorylation, an effect that was blocked by Cdk5 inhibitor.	Acetylcysteine	0-3	cyclin dependent kinase 5	Homo sapiens	94-98
18512759-5	2008	The neuroprotective effect of NAC was significantly attenuated by Cdk5 inhibitors or in neurons transfected with Cdk5 or p35 small interfering RNA (siRNA).	Acetylcysteine	30-33	cyclin dependent kinase 5	Homo sapiens	66-70
18512759-5	2008	The neuroprotective effect of NAC was significantly attenuated by Cdk5 inhibitors or in neurons transfected with Cdk5 or p35 small interfering RNA (siRNA).	Acetylcysteine	30-33	cyclin dependent kinase 5	Homo sapiens	113-117
18512759-8	2008	This effect of NAC was blocked by the Cdk5 inhibitors roscovitine and butyrolactone.	Acetylcysteine	15-18	cyclin dependent kinase 5	Homo sapiens	38-42
17003133-7	2006	Stimulation of de novo GSH synthesis by oral N-acetyl-cysteine normalized the low fertility rate of TAL(+/-) males without affecting the sterility of TAL(-/-) males.	Acetylcysteine	45-62	transaldolase 1	Mus musculus	100-103
17283870-8	2006	Mox-LDL at 5 microg/ml showed the maximal mitogenic effect (211%), which was inhibited by free radical scavenger (catalase), intracellular and extracellular antioxidants (N-acetylcysteine and probucol), nicotinamide adenine dinucleotide phosphate oxidase inhibitor (diphenylene iodonium), or c-Jun N-terminal kinase (JNK) inhibitor (SP600125).	Acetylcysteine	171-187	monooxygenase DBH like 1	Homo sapiens	0-3
18512759-9	2008	In addition, NAC increased Cdk5/p35 kinase activity but reduced Cdk5 kinase activity.	Acetylcysteine	13-16	cyclin dependent kinase 5	Homo sapiens	27-31
28386633-4	2017	We analyzed the findings on mercapturic acid pathway (MAP) transporter RLIP76, which has broad and critical effects on multiple pathways as essential for carcinogenesis, oxidative stress and drug-resistance, is over-expressed in NB.	Acetylcysteine	28-44	ralA binding protein 1	Homo sapiens	71-77
18512759-9	2008	In addition, NAC increased Cdk5/p35 kinase activity but reduced Cdk5 kinase activity.	Acetylcysteine	13-16	cyclin dependent kinase 5	Homo sapiens	64-68
18512759-11	2008	The effect of NAC was completely blocked by Cdk5 inhibitors.	Acetylcysteine	14-17	cyclin dependent kinase 5	Homo sapiens	44-48
18512759-12	2008	NAC reversed the A beta(25-35)-induced decrease in the expression of Bcl-2, which could be blocked by the MAPK kinase (MEK) inhibitor or Cdk5 inhibitors.	Acetylcysteine	0-3	cyclin dependent kinase 5	Homo sapiens	137-141
18512759-13	2008	These results suggest that NAC-mediated neuroprotection against A beta toxicity is likely mediated by the p35/Cdk5-ERKs-Bcl-2 signal pathway.	Acetylcysteine	27-30	cyclin dependent kinase 5	Homo sapiens	110-114
16987003-7	2006	To assess the potential role of reactive oxygen species in MAPK activation, cells were stretched in the presence of N-acetylcysteine, which had no effect on p38(MAPK) activation, but significantly inhibited ERK1/2(MAPK) activation and MCP-1 expression.	Acetylcysteine	116-132	C-C motif chemokine ligand 2	Rattus norvegicus	235-240
16750528-0	2006	A novel antioxidant N-acetylcysteine amide prevents gp120- and Tat-induced oxidative stress in brain endothelial cells.	Acetylcysteine	20-36	inter-alpha-trypsin inhibitor heavy chain 4	Homo sapiens	52-57
28686657-12	2017	CONCLUSIONS: Treatment resulted in detectable concentrations of NAC and probenecid in CSF and was not associated with undesirable effects after TBI in children.	Acetylcysteine	64-67	colony stimulating factor 2	Homo sapiens	86-89
16787924-4	2006	We show that ATP, acting on metabotropic P2Y1 receptors, increased the frequency of GABA(A)-mediated spontaneous postsynaptic currents (SPSCs) in CA3 principal cells, an effect that was prevented by the antioxidant N-acetyl-cysteine or by catalase, an enzyme that breaks down H2O2.	Acetylcysteine	215-232	purinergic receptor P2Y1	Homo sapiens	41-45
16760673-0	2006	Activation of ATM and histone H2AX phosphorylation induced by mitoxantrone but not by topotecan is prevented by the antioxidant N-acetyl-L-cysteine.	Acetylcysteine	128-147	ATM serine/threonine kinase	Homo sapiens	14-17
16760673-6	2006	The induction of both ATM activation and H2AX phosphorylation by MXT was prevented to a large extent by N-acetyl-L-cysteine (NAC), a scavenger of reactive oxygen species (ROS).	Acetylcysteine	104-123	ATM serine/threonine kinase	Homo sapiens	22-25
18535259-5	2008	The induction of GCLM and NQO1 was attenuated by reduction of electrophilic groups with sodium borohydrate, as well as treatment with thiol antioxidant N-acetylcysteine, suggesting that the thiol reactivity of oxPAPC is largely mediating its effect on Nrf2-responsive genes.	Acetylcysteine	152-168	glutamate-cysteine ligase, modifier subunit	Mus musculus	17-21
18419763-6	2008	Inhibition of reactive oxygen species (ROS) by N-acetyl-cysteine or diphenylene iodonium significantly suppressed the expression of MMP-3, MMP-9, NO and TNF-alpha in LPS-stimulated microglia, suggesting that ROS is an early signaling inducer in LPS-stimulated microglial cells.	Acetylcysteine	47-64	matrix metallopeptidase 3	Mus musculus	132-137
28560439-12	2017	Pretreatment with NAC abrogated the inhibitory effect of ISL on activation of STAT3 and blocked the cleavage of caspase-9, -7 and -3, and that of PARP in Caki cells.	Acetylcysteine	18-21	caspase 9	Homo sapiens	112-132
18442981-7	2008	N-Acetylcysteine, a thiol antioxidant, prevented all of the TA-induced effects, including oxidation of heat shock proteins, degradation of Hsp90 client proteins, and apoptosis.	Acetylcysteine	0-16	heat shock protein 90 alpha family class A member 1	Homo sapiens	139-144
16672643-9	2006	We were surprised to find that NAC blocked SU9516-mediated inhibition of RNA Pol II CTD phosphorylation on serine 2, reductions in Mcl-1 mRNA levels, and Mcl-1 down-regulation.	Acetylcysteine	31-34	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	131-136
16672643-9	2006	We were surprised to find that NAC blocked SU9516-mediated inhibition of RNA Pol II CTD phosphorylation on serine 2, reductions in Mcl-1 mRNA levels, and Mcl-1 down-regulation.	Acetylcysteine	31-34	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	154-159
28744353-7	2017	Hydrogen peroxide-induced Lipin1 or SREBP-2 expression was significantly reduced by N-acetyl-l-cysteine treatment, indicating that reactive oxygen species (ROS) were implicated in Lipin1 expression.	Acetylcysteine	84-103	lipin 1	Homo sapiens	26-32
28744353-7	2017	Hydrogen peroxide-induced Lipin1 or SREBP-2 expression was significantly reduced by N-acetyl-l-cysteine treatment, indicating that reactive oxygen species (ROS) were implicated in Lipin1 expression.	Acetylcysteine	84-103	lipin 1	Homo sapiens	180-186
16804527-8	2006	Pyrrolidinedithiocarbamate and NAC antagonised p53-dependent but potentiated p53-independent apoptotic activity.	Acetylcysteine	31-34	transformation related protein 53, pseudogene	Mus musculus	47-50
28393248-7	2017	c-JUN N-terminal kinase (JNK)/insulin receptor substrate 1 (IRS1)/AKT/GSK signaling was explored using western blot analysis in HepG2 cells treated with high glucose and/or EGCG or N-acetyl-cysteine.	Acetylcysteine	181-198	insulin receptor substrate 1	Homo sapiens	30-58
16804527-8	2006	Pyrrolidinedithiocarbamate and NAC antagonised p53-dependent but potentiated p53-independent apoptotic activity.	Acetylcysteine	31-34	transformation related protein 53, pseudogene	Mus musculus	77-80
28393248-7	2017	c-JUN N-terminal kinase (JNK)/insulin receptor substrate 1 (IRS1)/AKT/GSK signaling was explored using western blot analysis in HepG2 cells treated with high glucose and/or EGCG or N-acetyl-cysteine.	Acetylcysteine	181-198	insulin receptor substrate 1	Homo sapiens	60-64
28189848-11	2017	Accordingly, this massive cleavage of caspase-7 at early time points was inhibitable by the radical scavenger N-acetylcysteine (NAC).	Acetylcysteine	110-126	caspase 7	Homo sapiens	38-47
16530877-6	2006	Addition of increasing concentrations of N-acetylcysteine (NAC) led to down-regulation of HO-1 in cells expressing HCV proteins.	Acetylcysteine	41-57	heme oxygenase 1	Homo sapiens	90-94
16530877-6	2006	Addition of increasing concentrations of N-acetylcysteine (NAC) led to down-regulation of HO-1 in cells expressing HCV proteins.	Acetylcysteine	59-62	heme oxygenase 1	Homo sapiens	90-94
16632470-9	2006	In contrast, treatment of HEL cells with the antioxidant N-acetylcysteine decreased cell growth or expression of cyclin D2 and increased expression of p27(Kip).	Acetylcysteine	57-73	interferon alpha inducible protein 27	Homo sapiens	151-154
16249273-8	2006	NAC and DPI also inhibited phosphorylation of 4E-BP1 on Thr46 and association of eIF4E with eIF4G, steps that are important in the initiation phase of mRNA translation.	Acetylcysteine	0-3	eukaryotic translation initiation factor 4E binding protein 1	Homo sapiens	46-52
16249273-9	2006	NAC and DPI also blocked Akt activation which is required for 4E-BP1 phosphorylation.	Acetylcysteine	0-3	eukaryotic translation initiation factor 4E binding protein 1	Homo sapiens	62-68
28189848-11	2017	Accordingly, this massive cleavage of caspase-7 at early time points was inhibitable by the radical scavenger N-acetylcysteine (NAC).	Acetylcysteine	128-131	caspase 7	Homo sapiens	38-47
28432944-7	2017	We also found that the phototoxic action of Pc9-T1107 was partially reversed in the presence of antioxidants, such as TROLOX and N-acetyl-cysteine.	Acetylcysteine	129-146	proprotein convertase subtilisin/kexin type 9	Mus musculus	44-47
16307259-5	2006	NAC, on the other hand, was found to partially restore the activity of acetylcholinesterase in carbofuran treated animals.	Acetylcysteine	0-3	acetylcholinesterase	Rattus norvegicus	71-91
27706903-6	2017	Standard of care, N-acetylcysteine and, to a lesser extent, tauroursodeoxycholic treatment were associated with significantly lower transaminase levels, hepatocyte death, unfolded protein response activation, oxidative stress markers, caspase 1 expression and NLRP3 levels.	Acetylcysteine	18-34	NLR family, pyrin domain containing 3	Mus musculus	260-265
27706903-7	2017	Importantly, the combination of N-acetylcysteine and tauroursodeoxycholic acid improved serum transaminase levels, reduced histopathological liver damage, UPR-activated CHOP, oxidative stress, caspase 1 expression, NLRP3 levels, IL-1beta levels and the expression of pro-inflammatory cytokines and this to a greater extend than N-acetylcysteine alone.	Acetylcysteine	32-48	DNA-damage inducible transcript 3	Mus musculus	169-173
27706903-7	2017	Importantly, the combination of N-acetylcysteine and tauroursodeoxycholic acid improved serum transaminase levels, reduced histopathological liver damage, UPR-activated CHOP, oxidative stress, caspase 1 expression, NLRP3 levels, IL-1beta levels and the expression of pro-inflammatory cytokines and this to a greater extend than N-acetylcysteine alone.	Acetylcysteine	32-48	NLR family, pyrin domain containing 3	Mus musculus	215-220
16761701-0	2006	Efficacy of the antioxidant N-acetylcysteine (NAC) in protecting ears exposed to loud music.	Acetylcysteine	28-44	synuclein alpha	Homo sapiens	46-49
28465675-5	2017	Recent work has shown supplementation with a cysteine donor (N-acetylcysteine; NAC) improves antioxidant capacity by augmenting glutathione levels and reducing markers of oxidative stress, as well as ergogenic potential through association with delayed fatigue in numerous experimental models.	Acetylcysteine	61-77	synuclein alpha	Homo sapiens	79-82
16515547-7	2006	Furthermore, suppression of the 6-OHDA-generated reactive oxygen species (ROS) by pre-incubation of cells with N-acetyl-L-cysteine effectively inhibited the 6-OHDA-induced activation of ASK1, p38 and JNK, and protected the cells from apoptosis.	Acetylcysteine	111-130	mitogen-activated protein kinase kinase kinase 5	Homo sapiens	186-190
16377052-10	2006	Erdosteine, NAC, and vitamin E significantly reduced the increases in TNF-alpha staining and lung MPO activity.	Acetylcysteine	12-15	myeloperoxidase	Rattus norvegicus	98-101
28496415-8	2017	The extracellular ROS responses to both CSE types were totally inhibited by N-acetyl-cysteine (NAC; a ROS scavenger).	Acetylcysteine	76-93	choreoathetosis/spasticity, episodic (paroxysmal choreoathetosis/spasticity)	Homo sapiens	40-43
28496415-8	2017	The extracellular ROS responses to both CSE types were totally inhibited by N-acetyl-cysteine (NAC; a ROS scavenger).	Acetylcysteine	95-98	choreoathetosis/spasticity, episodic (paroxysmal choreoathetosis/spasticity)	Homo sapiens	40-43
27539140-8	2017	Furthermore, treatment of cells with specific inhibitors of ERK and JNK or NAC significantly promoted the DHM-induced activation of caspase-9/-7/-3 and PARP cleavage and also sensitized the antitumorigenic effect of DHM on NSCLC cells.	Acetylcysteine	75-78	caspase 9	Homo sapiens	132-141
19771260-10	2006	Pretreating the HT-29 cells with N-acetyl-L-cysteine, which is a thiol-containing antioxidant, inhibited the As(2)O(3)-induced apoptosis and caspase activation.	Acetylcysteine	33-52	caspase 9	Homo sapiens	141-148
16389042-6	2006	Pretreatment and/or posttreatment with NAC attenuated IL-6 in the maternal serum and amniotic fluid and IL-10 in the amniotic fluid.	Acetylcysteine	39-42	interleukin 10	Rattus norvegicus	104-109
28127704-6	2017	Supplementation of N-acetyl-L-cysteine (NAC) obviously reduced the ratio of development arrest (39.01 +- 2.74 vs. 71.18 +- 5.34%, p &lt; 0.05), which was accompanied by an increase in ROS level, and H2O2 treatment sharply increased messenger RNA (mRNA) expression and protein levels of p53 and p53-ser15.	Acetylcysteine	19-38	transformation related protein 53, pseudogene	Mus musculus	286-289
16369183-8	2006	NAC administration increased the ReGSH (P = 0.036) and decreased the MDA, MPO, and NN (P = 0.008, P = 0.01, P = 0.032, respectively), compared with the CLP group.	Acetylcysteine	0-3	myeloperoxidase	Rattus norvegicus	74-77
16489261-3	2005	Both NAC and LCAR pretreatment markedly decreased MPO and Cu/Zn-SOD activity compared to colitis group.	Acetylcysteine	5-8	myeloperoxidase	Rattus norvegicus	50-53
16263306-12	2005	The protective effect of NAC treatment against oxidative cell damage reduced the pancreatic injury and maintained and enhanced the ability of acinar cells to produce IL-10 at early AP stages.	Acetylcysteine	25-28	interleukin 10	Rattus norvegicus	166-171
28127704-6	2017	Supplementation of N-acetyl-L-cysteine (NAC) obviously reduced the ratio of development arrest (39.01 +- 2.74 vs. 71.18 +- 5.34%, p &lt; 0.05), which was accompanied by an increase in ROS level, and H2O2 treatment sharply increased messenger RNA (mRNA) expression and protein levels of p53 and p53-ser15.	Acetylcysteine	19-38	transformation related protein 53, pseudogene	Mus musculus	294-297
28127704-6	2017	Supplementation of N-acetyl-L-cysteine (NAC) obviously reduced the ratio of development arrest (39.01 +- 2.74 vs. 71.18 +- 5.34%, p &lt; 0.05), which was accompanied by an increase in ROS level, and H2O2 treatment sharply increased messenger RNA (mRNA) expression and protein levels of p53 and p53-ser15.	Acetylcysteine	40-43	transformation related protein 53, pseudogene	Mus musculus	286-289
28127704-6	2017	Supplementation of N-acetyl-L-cysteine (NAC) obviously reduced the ratio of development arrest (39.01 +- 2.74 vs. 71.18 +- 5.34%, p &lt; 0.05), which was accompanied by an increase in ROS level, and H2O2 treatment sharply increased messenger RNA (mRNA) expression and protein levels of p53 and p53-ser15.	Acetylcysteine	40-43	transformation related protein 53, pseudogene	Mus musculus	294-297
27278858-0	2017	Probenecid, an organic anion transporter 1 and 3 inhibitor, increases plasma and brain exposure of N-acetylcysteine.	Acetylcysteine	99-115	solute carrier family 22 member 6	Homo sapiens	15-48
16172181-7	2005	Monocyte chemoattractant protein 1 values were higher in patients with greater delays in N-acetylcysteine treatment and in patients with higher values of prothrombin time.	Acetylcysteine	89-105	C-C motif chemokine ligand 2	Homo sapiens	0-34
16192891-11	2005	Exogenous H2O2 enhanced IL-8 secretion and N-acetyl cysteine (NAC) prevented IL-1alpha-induced ROS production and IL-8 secretion.	Acetylcysteine	62-65	interleukin 1 alpha	Homo sapiens	77-86
15940258-5	2005	The DATS-mediated decrease in protein level and Ser(216) phosphorylation of Cdc 25 C as well as G(2)-M phase cell cycle arrest were significantly attenuated in the presence of N-acetylcysteine implicating reactive oxygen species (ROS) in cell cycle arrest caused by DATS.	Acetylcysteine	176-192	cell division cycle 25C	Homo sapiens	76-84
27278858-11	2017	Time- and concentration-dependent NAC uptake that was inhibitable by probenecid was observed with OAT1 and OAT3.	Acetylcysteine	34-37	solute carrier family 22 member 6	Homo sapiens	98-102
27278858-11	2017	Time- and concentration-dependent NAC uptake that was inhibitable by probenecid was observed with OAT1 and OAT3.	Acetylcysteine	34-37	solute carrier family 22 member 8	Homo sapiens	107-111
27278858-14	2017	Our results indicate for the first time that NAC is substrate for OAT1 and OAT3 and that probenecid increases NAC plasma and brain exposure in vivo.	Acetylcysteine	45-48	solute carrier family 22 member 6	Homo sapiens	66-70
27278858-14	2017	Our results indicate for the first time that NAC is substrate for OAT1 and OAT3 and that probenecid increases NAC plasma and brain exposure in vivo.	Acetylcysteine	45-48	solute carrier family 22 member 8	Homo sapiens	75-79
28161410-10	2017	MSA and SS increased the levels of oxidative proteins in PEL cells, and the anti-oxidant agent (N-acetyl-l-cysteine) restored cell viability and suppressed caspase-7 activation in PEL cells treated with MSA or SS.	Acetylcysteine	96-115	caspase 7	Homo sapiens	156-165
15890751-6	2005	N-acetylcysteine inactivated strain-induced ROS and inhibited p42/44 MAP kinase phosphorylation and strain-induced proliferation.	Acetylcysteine	0-16	cyclin dependent kinase 20	Homo sapiens	62-65
15908511-0	2005	Transport of N-acetylcysteine s-conjugates of methylmercury in Madin-Darby canine kidney cells stably transfected with human isoform of organic anion transporter 1.	Acetylcysteine	13-29	solute carrier family 22 member 6	Homo sapiens	136-163
15908511-3	2005	The present investigation was designed to study the transport of N-acetyl cysteine (NAC) S-conjugates of both methylmercury (CH(3)Hg-NAC) and inorganic mercury (NAC-Hg-NAC) in renal epithelial cells [Madin-Darby canine kidney (MDCK) cells] stably transfected with the human isoform of OAT1 (hOAT1).	Acetylcysteine	65-82	solute carrier family 22 member 6	Homo sapiens	285-289
15908511-3	2005	The present investigation was designed to study the transport of N-acetyl cysteine (NAC) S-conjugates of both methylmercury (CH(3)Hg-NAC) and inorganic mercury (NAC-Hg-NAC) in renal epithelial cells [Madin-Darby canine kidney (MDCK) cells] stably transfected with the human isoform of OAT1 (hOAT1).	Acetylcysteine	65-82	solute carrier family 22 member 6	Homo sapiens	291-296
15908511-3	2005	The present investigation was designed to study the transport of N-acetyl cysteine (NAC) S-conjugates of both methylmercury (CH(3)Hg-NAC) and inorganic mercury (NAC-Hg-NAC) in renal epithelial cells [Madin-Darby canine kidney (MDCK) cells] stably transfected with the human isoform of OAT1 (hOAT1).	Acetylcysteine	84-87	solute carrier family 22 member 6	Homo sapiens	285-289
15908511-3	2005	The present investigation was designed to study the transport of N-acetyl cysteine (NAC) S-conjugates of both methylmercury (CH(3)Hg-NAC) and inorganic mercury (NAC-Hg-NAC) in renal epithelial cells [Madin-Darby canine kidney (MDCK) cells] stably transfected with the human isoform of OAT1 (hOAT1).	Acetylcysteine	84-87	solute carrier family 22 member 6	Homo sapiens	291-296
15908511-5	2005	Data on saturation kinetics, time dependence, substrate specificity, and temperature dependence for the transport of CH(3)Hg-NAC and NAC-Hg-NAC indicate that both of these two mercuric species are indeed transportable substrates of hOAT1.	Acetylcysteine	125-128	solute carrier family 22 member 6	Homo sapiens	232-237
15908511-5	2005	Data on saturation kinetics, time dependence, substrate specificity, and temperature dependence for the transport of CH(3)Hg-NAC and NAC-Hg-NAC indicate that both of these two mercuric species are indeed transportable substrates of hOAT1.	Acetylcysteine	133-136	solute carrier family 22 member 6	Homo sapiens	232-237
15908511-5	2005	Data on saturation kinetics, time dependence, substrate specificity, and temperature dependence for the transport of CH(3)Hg-NAC and NAC-Hg-NAC indicate that both of these two mercuric species are indeed transportable substrates of hOAT1.	Acetylcysteine	133-136	solute carrier family 22 member 6	Homo sapiens	232-237
15908511-8	2005	Furthermore, the rates of survival of the hOAT1-transfected MDCK cells were significantly lower than those of corresponding control MDCK cells when they were exposed to cytotoxic concentrations of CH(3)Hg-NAC or NAC-Hg-NAC.	Acetylcysteine	205-208	solute carrier family 22 member 6	Homo sapiens	42-47
15908511-8	2005	Furthermore, the rates of survival of the hOAT1-transfected MDCK cells were significantly lower than those of corresponding control MDCK cells when they were exposed to cytotoxic concentrations of CH(3)Hg-NAC or NAC-Hg-NAC.	Acetylcysteine	212-215	solute carrier family 22 member 6	Homo sapiens	42-47
15908511-8	2005	Furthermore, the rates of survival of the hOAT1-transfected MDCK cells were significantly lower than those of corresponding control MDCK cells when they were exposed to cytotoxic concentrations of CH(3)Hg-NAC or NAC-Hg-NAC.	Acetylcysteine	212-215	solute carrier family 22 member 6	Homo sapiens	42-47
15908511-9	2005	Collectively, the present data support the hypothesis that CH(3)Hg-NAC and NAC-Hg-NAC are transportable substrates of OAT1 and thus potentially transportable mercuric species taken up in vivo at the basolateral membrane of proximal tubular epithelial cells.	Acetylcysteine	67-70	solute carrier family 22 member 6	Homo sapiens	118-122
15908511-9	2005	Collectively, the present data support the hypothesis that CH(3)Hg-NAC and NAC-Hg-NAC are transportable substrates of OAT1 and thus potentially transportable mercuric species taken up in vivo at the basolateral membrane of proximal tubular epithelial cells.	Acetylcysteine	75-78	solute carrier family 22 member 6	Homo sapiens	118-122
15908511-9	2005	Collectively, the present data support the hypothesis that CH(3)Hg-NAC and NAC-Hg-NAC are transportable substrates of OAT1 and thus potentially transportable mercuric species taken up in vivo at the basolateral membrane of proximal tubular epithelial cells.	Acetylcysteine	75-78	solute carrier family 22 member 6	Homo sapiens	118-122
16103692-11	2005	The antioxidants pyrrolidine dithiocarbamate and N-acetylcysteine, the flavin protein inhibitor diphenylene iodonium, and the NADP(H) oxidase inhibitor apocynin blocked MMP-1 release, suggesting a redox-sensitive mechanism involving NADP(H) oxidase.	Acetylcysteine	49-65	matrix metallopeptidase 1	Homo sapiens	169-174
15917250-8	2005	Only Yes and JNK activation were sensitive to N-acetylcysteine, inhibitors of NADPH oxidase, PKCzeta, or sphingomyelinase, indicating that the CD95L-induced ROS response is upstream of Yes and JNK but not of Fyn and c-Src activation.	Acetylcysteine	46-62	mitogen-activated protein kinase 8	Rattus norvegicus	13-16
15956119-6	2005	This correlated with inhibition of hyperglycemia-induced PAI-1 expression by GF109203X, NAC, and GSH.	Acetylcysteine	88-91	serpin family E member 1	Homo sapiens	57-62
15634943-6	2005	Moreover, inhibition of gamma-GT with acivicin increases the concentration of GSH and N-acetylcysteine conjugates of N-methyl-alpha-MeDA in brain dialysate, and there is a direct correlation between the concentrations of metabolites in dialysate and the extent of neurotoxicity, measured by decreases in serotonin (5-HT) and 5-hydroxyindole acetic (5-HIAA) levels.	Acetylcysteine	86-102	gamma-glutamyltransferase 1	Rattus norvegicus	24-32
15854525-17	2005	The expression of IkappaBalpha protein was increased by ACEI (P &lt; 0.05), irbesartan and NAC (both P &lt; 0.01).	Acetylcysteine	91-94	NFKB inhibitor alpha	Rattus norvegicus	18-30
15854525-23	2005	the IkappaBalpha protein expression was significantly decreased in the NAC and NAC+ Aldo intervention groups (both P &lt; 0.05).	Acetylcysteine	71-74	NFKB inhibitor alpha	Rattus norvegicus	4-16
15854525-23	2005	the IkappaBalpha protein expression was significantly decreased in the NAC and NAC+ Aldo intervention groups (both P &lt; 0.05).	Acetylcysteine	79-82	NFKB inhibitor alpha	Rattus norvegicus	4-16
15585325-5	2005	In addition, the effect of IL-18 was blocked by the antioxidant, N-acetyl-L-cysteine (NAC), indicating that IL-18 regulates ROI production, which is involved in SCF production.	Acetylcysteine	65-84	kit ligand	Mus musculus	161-164
15585325-5	2005	In addition, the effect of IL-18 was blocked by the antioxidant, N-acetyl-L-cysteine (NAC), indicating that IL-18 regulates ROI production, which is involved in SCF production.	Acetylcysteine	86-89	kit ligand	Mus musculus	161-164
17999162-5	2008	The numbers of cells undergoing apoptosis/necrosis, as well as of those displaying the activation of apoptosis-inducing enzymes of caspase family, were respectively increased or reduced by THF/nC60/70 or C60/70(OH)n. The antioxidant N-acetylcysteine and mitochondrial permeability transition inhibitor cyclosporin A each partly blocked the cytotoxic action of TNF, indicating the involvement of oxidative stress and mitochondrial dysfunction in the TNF cytotoxicity.	Acetylcysteine	233-249	thin fur	Mus musculus	189-192
18715889-12	2008	Compared with AAP group, the levels of ALT were lower after AAP ingestion in AAP-NAC, AAP-Se, and AAP-Se-NAC groups at the 8th hour.	Acetylcysteine	81-84	glutamic pyruvic transaminase, soluble	Mus musculus	39-42
18715889-12	2008	Compared with AAP group, the levels of ALT were lower after AAP ingestion in AAP-NAC, AAP-Se, and AAP-Se-NAC groups at the 8th hour.	Acetylcysteine	105-108	glutamic pyruvic transaminase, soluble	Mus musculus	39-42
18064629-5	2008	Antioxidant N-acetyl-L-cysteine or NAC blocks UV-induced MEK/ERK activation and down-regulation of AQP3.	Acetylcysteine	12-31	aquaporin 3 (Gill blood group)	Homo sapiens	99-103
18250162-4	2008	Oxidative modification of PRX induced by 6-OHDA was blocked in the presence of N-acetylcysteine, suggesting that reactive oxygen species (ROS) generated by 6-OHDA induce oxidation of PRX.	Acetylcysteine	79-95	periaxin	Mus musculus	26-29
18250162-4	2008	Oxidative modification of PRX induced by 6-OHDA was blocked in the presence of N-acetylcysteine, suggesting that reactive oxygen species (ROS) generated by 6-OHDA induce oxidation of PRX.	Acetylcysteine	79-95	periaxin	Mus musculus	183-186
18278066-8	2008	Moreover, NAC significantly improved the ifosfamide-induced glutathione depletion and the decrease of glutathione S-transferase activity, lowered the elevation of lipid peroxides and prevented typical morphological damages in renal tubules and glomeruli.	Acetylcysteine	10-13	hematopoietic prostaglandin D synthase	Rattus norvegicus	102-127
18258657-8	2008	Finally, we show that NAC treatment reduced caveolin-3 protein levels and increased the sarcolemmal expression of beta-dystroglycan and the dystrophin homologue, utrophin.	Acetylcysteine	22-25	caveolin 3	Mus musculus	44-54
18187174-8	2008	In addition, the downstream targets of p27, including CDK4, cyclin D1 and phosphorylated-Rb proteins, increased in 1 microM tt-DDE-treated cells and these changes were prevented by NAC co-treatment.	Acetylcysteine	181-184	interferon alpha inducible protein 27	Homo sapiens	39-42
18031542-7	2008	The UVB-induced HSP27 phosphorylation was inhibited when melanocytes were treated with the antioxidant N-acetyl cysteine or inhibitor of p38 MAP kinase prior to UVB exposure, suggesting that UVB induced HSP27 phosphorylation through reactive oxygen species/p38 MAP kinase pathway.	Acetylcysteine	103-120	heat shock protein family B (small) member 1	Homo sapiens	16-21
18031542-7	2008	The UVB-induced HSP27 phosphorylation was inhibited when melanocytes were treated with the antioxidant N-acetyl cysteine or inhibitor of p38 MAP kinase prior to UVB exposure, suggesting that UVB induced HSP27 phosphorylation through reactive oxygen species/p38 MAP kinase pathway.	Acetylcysteine	103-120	heat shock protein family B (small) member 1	Homo sapiens	203-208
19099954-9	2008	beta-galactosidase activity was not affected by NAC in the 1-day + NAC group but was significantly higher in 5-day + NAC and 10-day + NAC groups compared with the 5-day, 10-day groups (all P &lt; 0.05).	Acetylcysteine	67-70	galactosidase, beta 1	Rattus norvegicus	0-18
19099954-9	2008	beta-galactosidase activity was not affected by NAC in the 1-day + NAC group but was significantly higher in 5-day + NAC and 10-day + NAC groups compared with the 5-day, 10-day groups (all P &lt; 0.05).	Acetylcysteine	67-70	galactosidase, beta 1	Rattus norvegicus	0-18
19099954-9	2008	beta-galactosidase activity was not affected by NAC in the 1-day + NAC group but was significantly higher in 5-day + NAC and 10-day + NAC groups compared with the 5-day, 10-day groups (all P &lt; 0.05).	Acetylcysteine	67-70	galactosidase, beta 1	Rattus norvegicus	0-18
18026714-2	2008	The aim of the present study was to examine the effects of two orally administered antioxidants, N-acetylcysteine (NAC) and taurine (TAU), on lipotoxicity in humans.	Acetylcysteine	97-113	synuclein alpha	Homo sapiens	115-118
18062818-7	2007	Pre-treatment of cells with NAC (0.5-5 mM), dose-dependently antagonised astroglial apoptotic cell death induced by gp 120, an effect accompanied by significant attenuation of MDA accumulation.	Acetylcysteine	28-31	inter-alpha-trypsin inhibitor heavy chain 4	Homo sapiens	116-122
18062818-10	2007	All the effects of gp120 on astroglial cells were counteracted by NAC thus suggesting a novel and potentially useful approach in the treatment of glutammatergic disorders found in HAD patients.	Acetylcysteine	66-69	inter-alpha-trypsin inhibitor heavy chain 4	Homo sapiens	19-24
18077580-5	2007	Furthermore, NAC inhibited arsenite-induced elevation in the expression of stress proteins, such as heat shock protein 70 and heme oxygenase 1, as well as arsenite-induced phosphorylation of p38 mitogen-activated protein kinase.	Acetylcysteine	13-16	heme oxygenase 1	Homo sapiens	126-142
17693623-7	2007	Vice versa, increased GSH content in hepatocytes from aged animals by treatment with N-acetylcysteine inhibits NSMase activity and restores normal IL-1beta response.	Acetylcysteine	85-101	sphingomyelin phosphodiesterase 2	Rattus norvegicus	111-117
15489221-10	2004	In contrast, preincubation of cells with the hydroxyl radical scavenger, N-acetylcysteine, significantly attenuated the doxorubicin-mediated phosphorylation and accumulation of p53, p53-DNA binding, and the phosphorylation of H2AX, Nbs1, SMC1, Chk1, and Chk2, suggesting that hydroxyl radicals contribute to the doxorubicin-induced activation of ATM-dependent pathways.	Acetylcysteine	73-89	nibrin	Homo sapiens	232-236
15489221-10	2004	In contrast, preincubation of cells with the hydroxyl radical scavenger, N-acetylcysteine, significantly attenuated the doxorubicin-mediated phosphorylation and accumulation of p53, p53-DNA binding, and the phosphorylation of H2AX, Nbs1, SMC1, Chk1, and Chk2, suggesting that hydroxyl radicals contribute to the doxorubicin-induced activation of ATM-dependent pathways.	Acetylcysteine	73-89	structural maintenance of chromosomes 1A	Homo sapiens	238-242
15489221-10	2004	In contrast, preincubation of cells with the hydroxyl radical scavenger, N-acetylcysteine, significantly attenuated the doxorubicin-mediated phosphorylation and accumulation of p53, p53-DNA binding, and the phosphorylation of H2AX, Nbs1, SMC1, Chk1, and Chk2, suggesting that hydroxyl radicals contribute to the doxorubicin-induced activation of ATM-dependent pathways.	Acetylcysteine	73-89	ATM serine/threonine kinase	Homo sapiens	346-349
15520183-5	2004	Epidermal growth factor receptor activity by asbestos is blocked by N-acetyl-l-cysteine, suggesting that it is an initial redox-activated event leading to downstream AP-1 proto-oncogene up-regulation.	Acetylcysteine	68-87	epidermal growth factor receptor	Mus musculus	0-32
15569474-17	2004	After treatment with N-acetylcysteine, IFN-gamma increased and the IL-4/IFN-gamma ratio decreased.	Acetylcysteine	21-37	interferon gamma	Rattus norvegicus	39-48
15569474-17	2004	After treatment with N-acetylcysteine, IFN-gamma increased and the IL-4/IFN-gamma ratio decreased.	Acetylcysteine	21-37	interferon gamma	Rattus norvegicus	72-81
15569474-26	2004	N-acetylcysteine has no effect on IL-4, but increases IFN-gamma levels and brings the IL-4/IFN-gamma ratio back to normal.	Acetylcysteine	0-16	interferon gamma	Rattus norvegicus	54-63
15569474-26	2004	N-acetylcysteine has no effect on IL-4, but increases IFN-gamma levels and brings the IL-4/IFN-gamma ratio back to normal.	Acetylcysteine	0-16	interferon gamma	Rattus norvegicus	91-100
17549512-7	2007	Rephosphorylation of FAK after ATP repletion was enhanced by N-acetylcysteine, a reactive oxygen species scavenger.	Acetylcysteine	61-77	protein tyrosine kinase 2	Rattus norvegicus	21-24
18067231-12	2007	In contrast, the expressions of IRS-1, IRS-2, Glut-2 in NAC group increased by 40.2%, 30.2% and 19.1%, respectively than those in HF group.	Acetylcysteine	56-59	solute carrier family 2 member 2	Rattus norvegicus	46-52
28039148-10	2017	Furthermore, GPx1 knockdown-mediated reductive and oxidative stress could be antagonized by a thiol-oxidizing agent diamide and a thiol-containing compound N-acetylcysteine (NAC), respectively.	Acetylcysteine	156-172	glutathione peroxidase 1	Mus musculus	13-17
17646573-8	2007	Treatment with antioxidants, N-acetylcysteine (10 mmol/L), or ebselen (40 micromol/L) also attenuated aldosterone-induced insulin receptor substrate-1 degradation (n=4).	Acetylcysteine	29-45	insulin receptor substrate 1	Homo sapiens	122-150
17707397-0	2007	Neutral sphingomyelinase inhibition participates to the benefits of N-acetylcysteine treatment in post-myocardial infarction failing heart rats.	Acetylcysteine	68-84	sphingomyelin phosphodiesterase 2	Rattus norvegicus	0-24
17707397-5	2007	Biochemical studies at two time-points of NAC treatment, 3 days and 1 month, showed that inhibition of the neutral sphingomyelinase (N-SMase), Bcl-2 depletion and caspase-3 activation, were key, early and lasting events associated with glutathione repletion.	Acetylcysteine	42-45	sphingomyelin phosphodiesterase 2	Rattus norvegicus	107-131
17707397-7	2007	These data indicate that, besides glutathione deficiency, N-SMase activation is associated with post-MI CHF progression, and that blockade of N-SMase activation participates to post-infarction failing heart recovery achieved by NAC treatment.	Acetylcysteine	228-231	sphingomyelin phosphodiesterase 2	Rattus norvegicus	142-149
17707397-8	2007	NAC treatment in post-MI rats is a way to disrupt the vicious sTNF-alpha/TNF-R1/N-SMase cycle.	Acetylcysteine	0-3	sphingomyelin phosphodiesterase 2	Rattus norvegicus	80-87
15600251-7	2004	We observed that the animals treated with N-acetylcysteine showed an improvement in the antioxidant activity given by an increase in the total antioxidant status and glutathione reductase levels in serum.	Acetylcysteine	42-58	glutathione-disulfide reductase	Rattus norvegicus	166-187
15473893-13	2004	Glutathione S-transferase activity was decreased by NAC.	Acetylcysteine	52-55	glutathione S-transferase kappa 1	Homo sapiens	0-25
28039148-10	2017	Furthermore, GPx1 knockdown-mediated reductive and oxidative stress could be antagonized by a thiol-oxidizing agent diamide and a thiol-containing compound N-acetylcysteine (NAC), respectively.	Acetylcysteine	174-177	glutathione peroxidase 1	Mus musculus	13-17
15460446-7	2004	Pretreatment of H-ras MCF10A cells with an antioxidant N-acetylcysteine (NAC) significantly reversed capsaicin-induced growth inhibition, suggesting that ROS may mediate the apoptosis of H-ras-transformed cells induced by capsaicin.	Acetylcysteine	55-71	HRas proto-oncogene, GTPase	Homo sapiens	16-21
15460446-7	2004	Pretreatment of H-ras MCF10A cells with an antioxidant N-acetylcysteine (NAC) significantly reversed capsaicin-induced growth inhibition, suggesting that ROS may mediate the apoptosis of H-ras-transformed cells induced by capsaicin.	Acetylcysteine	55-71	HRas proto-oncogene, GTPase	Homo sapiens	187-192
17548252-7	2007	The levels of portal vein TNF-alpha and plasma ALT increased continuously in the I/R group at 1 and 3 hours of reperfusion compared with the SH group; however, they declined significantly in the group pretreated with NAC (P&lt;0.05).	Acetylcysteine	217-220	glutamic pyruvic transaminase, soluble	Mus musculus	47-50
28039148-11	2017	Moreover, NAC attenuated GPx1 knockdown-induced cell apoptosis, while diamide prevented GPx1 knockdown-suppressed chondrocyte proliferation.	Acetylcysteine	10-13	glutathione peroxidase 1	Mus musculus	25-29
15460446-7	2004	Pretreatment of H-ras MCF10A cells with an antioxidant N-acetylcysteine (NAC) significantly reversed capsaicin-induced growth inhibition, suggesting that ROS may mediate the apoptosis of H-ras-transformed cells induced by capsaicin.	Acetylcysteine	73-76	HRas proto-oncogene, GTPase	Homo sapiens	16-21
15460446-7	2004	Pretreatment of H-ras MCF10A cells with an antioxidant N-acetylcysteine (NAC) significantly reversed capsaicin-induced growth inhibition, suggesting that ROS may mediate the apoptosis of H-ras-transformed cells induced by capsaicin.	Acetylcysteine	73-76	HRas proto-oncogene, GTPase	Homo sapiens	187-192
28054986-7	2017	Moreover, blockage of ROS production by using the ROS inhibitor N-acetyl-l-cysteine totally reversed SFN-mediated down-regulation of JAK2/Src-STAT3 signaling activation and the subsequent effects on apoptosis by blocking the induction of apoptosis-related genes in GBM cells.	Acetylcysteine	64-83	RNA exonuclease 2	Homo sapiens	101-104
15355665-20	2004	NAC had no effect on IL-4, but increased IFNgamma, and the IL-4/IFNgamma ratio returned to normal.	Acetylcysteine	0-3	interferon gamma	Rattus norvegicus	41-49
17309078-7	2007	Inhibition of ROS production by N-acetyl-L-cysteine and catalase prevented necrosis and switched the cell death mode to apoptosis that depends on mitochondrial death pathway involving caspase-9 and caspase-3 activation, indicating a critical role of ROS in determination of GD-induced cell death mode.	Acetylcysteine	32-51	caspase 9	Homo sapiens	184-193
17440103-8	2007	Finally, N-acetylcysteine, an inhibitor of ROS, inhibits sanguinarine-induced generation of ROS, up-regulation of DR5, Bax conformational changes, activation of caspase-3, and down-regulation of IAPs.	Acetylcysteine	9-25	TNF receptor superfamily member 10b	Homo sapiens	114-117
26278389-7	2017	The antioxidants N-acetyl cysteine and vitamin C lowered the alcohol elevation of ROS and blunted the alcohol induction of CYP2A5, but not CYP2E1, suggesting ROS play a novel role in the crosstalk between CYP2E1 and CYP2A5.	Acetylcysteine	17-34	cytochrome P450, family 2, subfamily e, polypeptide 1	Mus musculus	205-211
27717985-8	2017	TQ or NAC pretreatment significantly decreased elevated serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), and myeloperoxidase (MPO) activities, malondialdehyde (MDA) level, and NO production.	Acetylcysteine	6-9	myeloperoxidase	Rattus norvegicus	132-147
15024026-6	2004	Inhibition of intracellular ROS production by N-acetylcysteine, TEMPO, Me(2)SO, 1,10-phenanthroline, or allopurinol resulted in a decreased 15dPGJ(2)-dependent HO-1 expression in the cells.	Acetylcysteine	46-62	heme oxygenase 1	Homo sapiens	160-164
27717985-8	2017	TQ or NAC pretreatment significantly decreased elevated serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), and myeloperoxidase (MPO) activities, malondialdehyde (MDA) level, and NO production.	Acetylcysteine	6-9	myeloperoxidase	Rattus norvegicus	149-152
15209356-9	2004	Here, we suggest that the degradations of IkappaB alpha and IkappaB beta and the following activation of NF-kappaB are the targets of NAC and that NF-kappaB transcription factor is a pivotal clue to regulation of differentiation in TNFalpha-exposed osteoblasts.	Acetylcysteine	134-137	NFKB inhibitor alpha	Rattus norvegicus	42-55
17204747-10	2007	NAC also inhibited procaspase-9 processing, activation of enzymatic activity of caspase-9, -7, and -8, and poly(ADP-ribose) polymerase cleavage induced by acrolein.	Acetylcysteine	0-3	caspase 9	Homo sapiens	22-31
27434868-7	2016	Pretreatment with 5mM N-acetyl-l-cysteine (an inhibitor of ROS formation) or 10muM U0126 (an inhibitor of ERK1/2) significantly prevented the induction of periostin in CSE-treated PASMCs.	Acetylcysteine	22-41	periostin	Homo sapiens	155-164
17612979-8	2007	Administration of a second dose of 1,200 mg/kg NAC 4 hours after the first decreased skin GST activity a further 20% whereas kidney GST activity remained elevated at levels similar to those obtained after 1 dose of NAC.	Acetylcysteine	47-50	hematopoietic prostaglandin D synthase	Rattus norvegicus	90-93
17612979-9	2007	Administration of a third dose of NAC 4 hours after the second dose increased liver GST activity significantly as compared to background but did not affect skin, kidney, or lung GST activity.	Acetylcysteine	34-37	hematopoietic prostaglandin D synthase	Rattus norvegicus	84-87
14746574-11	2004	Exposure of BRECs to gliclazide or antioxidants such as vitamin E or N-acetyl-l-cysteine resulted in a significant decrease in AGE-induced activation of PKC-, MAPK- and NF-kappaB-signalling pathways.	Acetylcysteine	69-88	protein kinase C beta	Bos taurus	153-156
17143561-6	2007	This was reinforced by the finding that pretreatment with the antioxidants N-acetylcysteine, vitamin E and catalase prevented HO-1 induction by curcumin.	Acetylcysteine	75-91	heme oxygenase 1	Homo sapiens	126-130
27572503-13	2016	In addition, the H2O2-induced elevation of p-ERK and p-NF-kappaB in BxPC-3 and Panc-1 cells were reduced by curcumin, NAC and PD 98059 (an ERK inhibitor).	Acetylcysteine	118-121	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	43-48
15065005-14	2004	NAC treatment decreased plasma amylase and lipase levels significantly (P &lt; 0.05).	Acetylcysteine	0-3	lipase G, endothelial type	Rattus norvegicus	43-49
27474283-1	2016	A facile yet sensitive and selective method was proposed for Hg(2+) detection based on N-acetyl-L-cysteine(NAC)-induced colorimetric response of AuNPs.	Acetylcysteine	87-106	synuclein alpha	Homo sapiens	107-110
16211988-7	2004	A significant difference in SCC change at 48 hours after the angiography was found (-0.07 mg/dl NAC, 0.09 mg/dl placebo, P = 0.04).	Acetylcysteine	96-99	serpin family B member 3	Homo sapiens	28-31
16990448-3	2006	Recent studies suggested that N-acetylcysteine enhances the extracellular degradation of PDGF-beta receptor by cathepsin B, thus suggesting that the absence of PDGF-beta receptors in quiescent cells is due to an active process of elimination and not to a lack of expression.	Acetylcysteine	30-46	platelet derived growth factor, B polypeptide	Mus musculus	89-98
17108135-7	2006	Conversely, treatment of Hsp27 siRNA-transfected cells with N-acetylcysteine, an antioxidant and GSH precursor, reversed their sensitivity to 17-AAG.	Acetylcysteine	60-76	heat shock protein family B (small) member 1	Homo sapiens	25-30
16211988-10	2004	CONCLUSIONS: In patients with mild renal impairment patients undergoing angiographic procedures, HPOD of NAC were more effective than placebo in preventing SCC change 48 hours.	Acetylcysteine	105-108	serpin family B member 3	Homo sapiens	156-159
17023264-0	2006	Evidence that N-acetylcysteine inhibits TNF-alpha-induced cerebrovascular endothelin-1 upregulation via inhibition of mitogen- and stress-activated protein kinase.	Acetylcysteine	14-30	salt inducible kinase 1	Homo sapiens	118-162
27363620-0	2016	N-Acetyl-l-cysteine exacerbates generation of IL-10 in cells stimulated with endotoxin in vitro and produces antipyresis via IL-10 dependent pathway in vivo.	Acetylcysteine	0-19	interleukin 10	Rattus norvegicus	46-51
16737972-11	2006	Interestingly, the antioxidants vitamin E and N-acetylcysteine abolished both the alcohol-mediated down-regulation of C/EBPalpha binding activity and hepcidin expression in the liver and the up-regulation of duodenal divalent metal transporter 1.	Acetylcysteine	46-62	hepcidin antimicrobial peptide	Homo sapiens	150-158
16543607-6	2006	H(2)O(2) mimicked the synergistic effects of CSE, while antioxidant N-acetyl-L-cysteine prevented synergistic induction of MUC5AC mucin by CSE.	Acetylcysteine	68-87	mucin 5AC, oligomeric mucus/gel-forming	Homo sapiens	123-129
16338951-4	2006	Insulin-like growth factor I (IGF-I) and inducible nitric oxide synthase (iNOS) mRNA expressions were found downregulated in the liver by NAC.	Acetylcysteine	138-141	insulin-like growth factor 1	Rattus norvegicus	0-28
14657342-7	2003	NAC pretreatment augmented integrin alpha-4-dependent fibronectin adhesion and aggregation of Jurkat cells without changing its expression by fluorescence-activated cell sorter, suggesting that reduction of surface disulfides can affect proteins function.	Acetylcysteine	0-3	integrin subunit alpha 4	Homo sapiens	27-43
27363620-0	2016	N-Acetyl-l-cysteine exacerbates generation of IL-10 in cells stimulated with endotoxin in vitro and produces antipyresis via IL-10 dependent pathway in vivo.	Acetylcysteine	0-19	interleukin 10	Rattus norvegicus	125-130
16338951-4	2006	Insulin-like growth factor I (IGF-I) and inducible nitric oxide synthase (iNOS) mRNA expressions were found downregulated in the liver by NAC.	Acetylcysteine	138-141	insulin-like growth factor 1	Rattus norvegicus	30-35
16338951-5	2006	The studies indicate that NAC can serve as a chemopreventive agent for rat hepatocarcinogenesis induced by MeIQx by reducing cell proliferation, which may involve IGF-I and iNOS downregulation.	Acetylcysteine	26-29	insulin-like growth factor 1	Rattus norvegicus	163-168
27363620-9	2016	Furthermore, in these cells we observed a significant increase in IL-10 level (142.1+-2.62pg/mL in NAC+LPS stimulated cells vs. 54.4+-0.6pg/mL in LPS stimulated cells, p&lt;0.001).	Acetylcysteine	99-102	interleukin 10	Rattus norvegicus	66-71
27363620-10	2016	The injection of anti-IL-10 antibody into the rats abolished antipyretic properties of NAC.	Acetylcysteine	87-90	interleukin 10	Rattus norvegicus	22-27
14680076-6	2003	The bleomycin-induced increases in lung tumour necrosis factor-alpha and myeloperoxidase activity were reduced by NAC treatment.	Acetylcysteine	114-117	myeloperoxidase	Rattus norvegicus	73-88
27149563-0	2016	A histological and immunohistochemical study of the effects of N-acetyl cysteine on retinopathy of prematurity by modifying insulin-like growth factor-1.	Acetylcysteine	63-80	insulin-like growth factor 1	Rattus norvegicus	124-152
14627497-4	2003	Furthermore, PDTC and NAC prevented the decrease (from 0.50+/-0.10 to 0.80+/-0.20 or 1.20+/-0.24, respectively) and phosphorylation (from 2.00+/-0.15 to 0.46+/-0.10 or 0.41+/-0.10, respectively) of IkappaBalpha protein in the cytoplasm.	Acetylcysteine	22-25	NFKB inhibitor alpha	Rattus norvegicus	198-210
16455066-5	2006	Glc-HSA-induced E-selectin expression was completely suppressed by the NADPH oxidase inhibitor diphenylene iodonium chloride and the reactive oxygen species (ROS) scavenger N-acetyl-L-cysteine.	Acetylcysteine	173-192	selectin E	Homo sapiens	16-26
27149563-12	2016	NAC appeared to be an effective vascular-protective agent for ROP by decreasing IGF-1 expression.	Acetylcysteine	0-3	insulin-like growth factor 1	Rattus norvegicus	80-85
27356027-4	2016	Extracellular release of annexin A2 was also enhanced after H2O2 and nicotine treatments, which was suppressed by pretreatment with the antioxidant, N-acetyl cysteine.	Acetylcysteine	149-166	annexin A2	Homo sapiens	25-35
16598818-5	2006	IL-10 deprivation or the addition of N-acetylcysteine, which replenishes intracellular glutathione level during priming, cancelled the effect of EDC on the promotion of Th2 polarization.	Acetylcysteine	37-53	heart and neural crest derivatives expressed 2	Mus musculus	169-172
14521937-6	2003	7-Ketocholesterol, an oxidized lipid in oxLDL particles, induced the production of fibronectin and the activation of SP-1, those which were suppressed by N-acetylcysteine.	Acetylcysteine	154-170	fibronectin 1	Rattus norvegicus	83-94
14516795-4	2003	Elimination of H(2)O(2) by catalase or N-acetyl-L-cysteine inhibited the arsenite-induced activation of p70(s6k) and ERK1/2, indicating the possible role of H(2)O(2) in the arsenite activation of the p70(s6k) and the ERK1/2 signaling pathways.	Acetylcysteine	39-58	ribosomal protein S6 kinase B1	Homo sapiens	104-111
12883092-4	2003	The animals were sacrificed at 12 h. NAC treatment before APAP resulted in serum AST, serum nitrate plus nitrite as a measure of nitric oxide (NO) production, and hepatic cytokine levels that were similar to the controls.	Acetylcysteine	37-40	solute carrier family 17 (anion/sugar transporter), member 5	Mus musculus	81-84
16516148-6	2006	Finally, we show that N-acetyl cysteine (NAC), a potent antioxidant, reverted the curcumin-induced mutant huntingtin aggregation and proteasomal malfunction in the mutant huntingtin expressing cells.	Acetylcysteine	22-39	huntingtin	Mus musculus	106-116
16516148-6	2006	Finally, we show that N-acetyl cysteine (NAC), a potent antioxidant, reverted the curcumin-induced mutant huntingtin aggregation and proteasomal malfunction in the mutant huntingtin expressing cells.	Acetylcysteine	22-39	huntingtin	Mus musculus	171-181
16516148-6	2006	Finally, we show that N-acetyl cysteine (NAC), a potent antioxidant, reverted the curcumin-induced mutant huntingtin aggregation and proteasomal malfunction in the mutant huntingtin expressing cells.	Acetylcysteine	41-44	huntingtin	Mus musculus	106-116
16516148-6	2006	Finally, we show that N-acetyl cysteine (NAC), a potent antioxidant, reverted the curcumin-induced mutant huntingtin aggregation and proteasomal malfunction in the mutant huntingtin expressing cells.	Acetylcysteine	41-44	huntingtin	Mus musculus	171-181
12883092-6	2003	In mice treated with NAC at 1 h, cytokines and serum AST were normal at 12 h, but APAP protein adducts were present in the hepatic centrilobular areas.	Acetylcysteine	21-24	solute carrier family 17 (anion/sugar transporter), member 5	Mus musculus	53-56
12883092-8	2003	In mice treated with NAC at 2 h and sacrificed at 12 h, serum AST was reduced by 80%.	Acetylcysteine	21-24	solute carrier family 17 (anion/sugar transporter), member 5	Mus musculus	62-65
16631521-7	2006	ALA significantly increased ROS, and this effect was blocked by N-acetyl-cysteine, which also inhibited ALA-induced activation of p44/42 mitogen-activated protein kinase (MAPK) and AP-1, HO-1 expression, and HO activity.	Acetylcysteine	64-81	heme oxygenase 1	Homo sapiens	187-191
27106530-5	2016	NAC and Ac-DEVD-CHO partially reversed CuE-induced cleavage of caspase-3, caspase-7, and PARP.	Acetylcysteine	0-3	caspase 7	Homo sapiens	74-83
16081117-9	2006	NAC also abrogated APAP-induced increases in TNFalpha, KC/gro, and IL-10, but augmented expression of the anti-inflammatory cytokines interleukin-4 (IL-4) and transforming growth factor-beta (TGFbeta).	Acetylcysteine	0-3	interleukin 4	Mus musculus	134-147
13679868-4	2003	Treatment of MM cells with an antioxidant N-acetyl-L-cysteine blocks 2ME2, but not Dex-induced apoptosis as well as release of mitochondrial proteins cytochrome c (cyto c) and Smac.	Acetylcysteine	42-61	diablo IAP-binding mitochondrial protein	Homo sapiens	176-180
27102435-0	2016	N-acetylcysteine negatively regulates Notch3 and its malignant signaling.	Acetylcysteine	0-16	notch receptor 3	Homo sapiens	38-44
16081117-9	2006	NAC also abrogated APAP-induced increases in TNFalpha, KC/gro, and IL-10, but augmented expression of the anti-inflammatory cytokines interleukin-4 (IL-4) and transforming growth factor-beta (TGFbeta).	Acetylcysteine	0-3	interleukin 4	Mus musculus	149-153
27102435-3	2016	In this study, we demonstrated a negative regulation of Notch3 by NAC in cancer cells.	Acetylcysteine	66-69	notch receptor 3	Homo sapiens	56-62
12824159-4	2003	Surprisingly, when GSH is increased in the c-Myc low expressing cells by treatment with N-acetyl-L-cysteine, cells escape crisis.	Acetylcysteine	88-107	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	43-48
27102435-4	2016	HeLa cells treated with NAC exhibited a time- and concentration-dependent decrease in Notch3 levels and its downstream effectors Hes1 and HRT1 in a manner independent of f-secretase or glutathione.	Acetylcysteine	24-27	notch receptor 3	Homo sapiens	86-92
16452234-6	2006	Pretreatment with N-acetyl-l-cysteine and overexpression of catalase inhibited sulforaphane-induced up-regulation of DR5 and almost completely blocked the cotreatment-induced apoptosis.	Acetylcysteine	18-37	TNF receptor superfamily member 10b	Homo sapiens	117-120
27102435-7	2016	While the mRNA expression of Notch3 was not altered by NAC, functional inhibition of lysosome, but not proteasome, blocked the NAC-dependent reduction of Notch3 levels.	Acetylcysteine	127-130	notch receptor 3	Homo sapiens	154-160
27102435-8	2016	Furthermore, results from Notch3 silencing and N3ICD overexpression demonstrated that NAC prevented malignant phenotypes through down-regulation of Notch3 protein in multiple cancer cells.	Acetylcysteine	86-89	notch receptor 3	Homo sapiens	26-32
15982852-4	2006	The antioxidant N-acetyl-L-cysteine (NAC) inhibited IL-3-induced tyrosine phosphorylation of Jak2, IL-3 receptor betac subunit (IL-3Rbetac), and STAT5 as well as activation-specific phosphorylation of Akt, MEK, and ERK, while treatment of cells with H2O2 activated these signaling events.	Acetylcysteine	16-35	Janus kinase 2	Mus musculus	93-97
15982852-4	2006	The antioxidant N-acetyl-L-cysteine (NAC) inhibited IL-3-induced tyrosine phosphorylation of Jak2, IL-3 receptor betac subunit (IL-3Rbetac), and STAT5 as well as activation-specific phosphorylation of Akt, MEK, and ERK, while treatment of cells with H2O2 activated these signaling events.	Acetylcysteine	16-35	signal transducer and activator of transcription 5A	Mus musculus	145-150
12823615-6	2003	BUN and serum creatinine, ALT and AST levels which were increased significantly following AA treatment decreased significantly after pretreatment with either vitamin E, melatonin or NAC; however, they were not reduced to control levels.	Acetylcysteine	182-185	solute carrier family 17 (anion/sugar transporter), member 5	Mus musculus	34-37
15982852-4	2006	The antioxidant N-acetyl-L-cysteine (NAC) inhibited IL-3-induced tyrosine phosphorylation of Jak2, IL-3 receptor betac subunit (IL-3Rbetac), and STAT5 as well as activation-specific phosphorylation of Akt, MEK, and ERK, while treatment of cells with H2O2 activated these signaling events.	Acetylcysteine	37-40	Janus kinase 2	Mus musculus	93-97
27102435-8	2016	Furthermore, results from Notch3 silencing and N3ICD overexpression demonstrated that NAC prevented malignant phenotypes through down-regulation of Notch3 protein in multiple cancer cells.	Acetylcysteine	86-89	notch receptor 3	Homo sapiens	148-154
15982852-4	2006	The antioxidant N-acetyl-L-cysteine (NAC) inhibited IL-3-induced tyrosine phosphorylation of Jak2, IL-3 receptor betac subunit (IL-3Rbetac), and STAT5 as well as activation-specific phosphorylation of Akt, MEK, and ERK, while treatment of cells with H2O2 activated these signaling events.	Acetylcysteine	37-40	signal transducer and activator of transcription 5A	Mus musculus	145-150
27102435-9	2016	In summary, NAC reduces Notch3 levels through lysosome-dependent protein degradation, thereby negatively regulates Notch3 malignant signaling in cancer cells.	Acetylcysteine	12-15	notch receptor 3	Homo sapiens	24-30
15982852-5	2006	NAC also inhibited the EpoR-induced transphosphorylation of IL-3Rbetac.	Acetylcysteine	0-3	erythropoietin receptor	Mus musculus	23-27
16449798-6	2006	This mechanism is supported by the ability of N-acetyl cysteine (NAC) to prevent dissociation of Trx-ASK1 and activation of the p38 MAPK pathway.	Acetylcysteine	65-68	mitogen-activated protein kinase kinase kinase 5	Mus musculus	101-105
12821233-2	2003	BACKGROUND: Oral acetylcysteine (NAC) may provide better prophylaxis against RCIN than intravenous (i.v.)	Acetylcysteine	17-31	synuclein alpha	Homo sapiens	33-36
27102435-9	2016	In summary, NAC reduces Notch3 levels through lysosome-dependent protein degradation, thereby negatively regulates Notch3 malignant signaling in cancer cells.	Acetylcysteine	12-15	notch receptor 3	Homo sapiens	115-121
27102435-10	2016	These results implicate a novel NAC treatment in sensitizing Notch3-expressing tumors.	Acetylcysteine	32-35	notch receptor 3	Homo sapiens	61-67
26809688-4	2016	The DNA damage foci contained gammaH2AFX and TP53BP1, indicative of double-strand breaks (DSBs) and could be reversed by antioxidant treatments such as N-Acetylcysteine (NAC) or reduced glutathione ethyl ester (GSHee).	Acetylcysteine	152-168	tumor protein p53 binding protein 1	Homo sapiens	45-52
12676768-4	2003	V(2)O(5)-induced HB-EGF mRNA expression was abolished by N-acetyl-l-cysteine, suggesting an oxidant-mediated effect.	Acetylcysteine	57-76	heparin binding EGF like growth factor	Homo sapiens	17-23
12556226-9	2003	Furthermore, when cells were supplemented with N -acetyl-L-cysteine together with copper, there was a clear negative effect on cell survival, which was exacerbated by TPx overexpression.	Acetylcysteine	47-67	thioredoxin peroxidase 1	Drosophila melanogaster	167-170
16243536-8	2006	Piceatannol-mediated HO-1 induction was abrogated in the presence of N-acetylcysteine and glutathione, but not by other antioxidants.	Acetylcysteine	69-85	heme oxygenase 1	Homo sapiens	21-25
16107508-8	2006	Furthermore, EGF rapidly increased formation of H2O2, and pretreatment with antioxidant (N-acetyl-L-cysteine) inhibited EGF-induced increase of [Ca2+]i.	Acetylcysteine	89-108	epidermal growth factor	Mus musculus	120-123
27107686-13	2016	NAC also prevented chondrogenic differentiation of TrxR2 deficiency cells by suppression of ECM gene expression, GAGs accumulation and mineralization, as well as attenuation of Akt signaling.	Acetylcysteine	0-3	multimerin 1	Homo sapiens	92-95
16456238-8	2006	Ang II also increased both the NADPH oxidase subunits gp91 phox and p22phox mRNA expression, which was abolished with apocynin and NAC.	Acetylcysteine	131-134	cytochrome b-245 alpha chain	Homo sapiens	68-75
16456238-11	2006	That both NAC and apocynin reduced ROS activities and abolished Ang II-mediated increase in p22phox and gp91phox activity further suggest that such redox cycling occurs via both NADPH oxidase-dependent and -independent pathways.	Acetylcysteine	10-13	cytochrome b-245 alpha chain	Homo sapiens	92-99
12711260-8	2003	An anti-oxidant, N-acetylcysteine, or PEDF completely prevented the leptin-induced upregulation of vascular endothelial growth factor (VEGF) mRNA levels as well as any increase in DNA synthesis in microvascular EC.	Acetylcysteine	17-33	leptin	Homo sapiens	68-74
12609744-6	2003	Shear stress at 15 dyn/cm(2) for 30 min induced a significant increase in the intracellular peroxide concentration, and the down-regulation of ECE-1 and ET-1 mRNA expression by shear stress was attenuated almost completely on treatment with N-acetyl cysteine (NAC), an antioxidant (20 mM).	Acetylcysteine	241-258	endothelin converting enzyme 1	Homo sapiens	143-148
27059143-7	2016	Treatment with N-acetylcysteine as an ROS scavenger reduced augmented HO-1 levels in MsrB3-depleted cells.	Acetylcysteine	15-31	heme oxygenase 1	Homo sapiens	70-74
12609744-6	2003	Shear stress at 15 dyn/cm(2) for 30 min induced a significant increase in the intracellular peroxide concentration, and the down-regulation of ECE-1 and ET-1 mRNA expression by shear stress was attenuated almost completely on treatment with N-acetyl cysteine (NAC), an antioxidant (20 mM).	Acetylcysteine	260-263	endothelin converting enzyme 1	Homo sapiens	143-148
12514114-6	2003	This postulation is supported by the following findings: Ferrocene generates H2O2 by autooxidation; N-acetylcysteine, a free-radical scavenger, reduces its antitumor effect; and it stimulates GTPase activity catalyzed by pure recombinant p21ras and activates ERK 1/2 in wild Jurkat T cells but fails to do so in the Jurkat T cells expressing p21ras in which cysteine 118 was replaced by serine.	Acetylcysteine	100-116	HRas proto-oncogene, GTPase	Homo sapiens	238-244
12514114-6	2003	This postulation is supported by the following findings: Ferrocene generates H2O2 by autooxidation; N-acetylcysteine, a free-radical scavenger, reduces its antitumor effect; and it stimulates GTPase activity catalyzed by pure recombinant p21ras and activates ERK 1/2 in wild Jurkat T cells but fails to do so in the Jurkat T cells expressing p21ras in which cysteine 118 was replaced by serine.	Acetylcysteine	100-116	HRas proto-oncogene, GTPase	Homo sapiens	342-348
12524169-4	2003	Concomitantly, the late activation of apoptosis signal-regulating kinase 1 (ASK1) and c-Jun N-terminal protein kinase (JNK) was also prevented by Naspm or NAC.	Acetylcysteine	155-158	mitogen-activated protein kinase 8	Rattus norvegicus	86-117
12524169-4	2003	Concomitantly, the late activation of apoptosis signal-regulating kinase 1 (ASK1) and c-Jun N-terminal protein kinase (JNK) was also prevented by Naspm or NAC.	Acetylcysteine	155-158	mitogen-activated protein kinase 8	Rattus norvegicus	119-122
16336626-8	2006	Consistent with a potential role of reactive oxygen species (ROS), Phe-induced phosphorylation of EGF-R was attenuated by the antioxidant, N-acetylcysteine.	Acetylcysteine	139-155	epidermal growth factor receptor	Mus musculus	98-103
26846682-11	2016	N-acetylcysteine restored Brg1, Nrf2 and p-STAT3, and IsoPostC-induced protection in H9C2 cells exposed to HG and HR.	Acetylcysteine	0-16	signal transducer and activator of transcription 3	Rattus norvegicus	43-48
16274885-7	2005	In parallel, pretreatment with the antioxidant N-acetylcysteine (NAC) did not alter Cyp1a1 mRNA expression but completely abrogated the inhibition of Cyp1a1 activity induction by all three metals.	Acetylcysteine	47-63	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	150-156
16274885-7	2005	In parallel, pretreatment with the antioxidant N-acetylcysteine (NAC) did not alter Cyp1a1 mRNA expression but completely abrogated the inhibition of Cyp1a1 activity induction by all three metals.	Acetylcysteine	65-68	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	150-156
12490582-11	2003	Alterations in mitochondrial function preceded significant increases in ALT activity, which was first manifested at 2 h. Pretreatment with NAC (1200 mg/kg) abrogated DCE-induced GSH depletion and inhibited disturbances in mitochondrial respiration.	Acetylcysteine	139-142	glutamic pyruvic transaminase, soluble	Mus musculus	72-75
12490582-12	2003	Moreover, NAC protected against increased ALT activity, suggesting that the protective effect of NAC is due to increased GSH for conjugation reactions and/or its antioxidant property.	Acetylcysteine	10-13	glutamic pyruvic transaminase, soluble	Mus musculus	42-45
12490582-12	2003	Moreover, NAC protected against increased ALT activity, suggesting that the protective effect of NAC is due to increased GSH for conjugation reactions and/or its antioxidant property.	Acetylcysteine	97-100	glutamic pyruvic transaminase, soluble	Mus musculus	42-45
16286925-4	2005	Downregulation of p53 results in excessive oxidation of DNA, increased mutation rate and karyotype instability, which are prevented by incubation with the antioxidant N-acetylcysteine (NAC).	Acetylcysteine	167-183	transformation related protein 53	Mus musculus	18-21
16286925-4	2005	Downregulation of p53 results in excessive oxidation of DNA, increased mutation rate and karyotype instability, which are prevented by incubation with the antioxidant N-acetylcysteine (NAC).	Acetylcysteine	185-188	transformation related protein 53	Mus musculus	18-21
26935987-8	2016	Cotreatment with N-acetyl-L-cysteine inhibited sulforaphane-inhibited invasion and upregulation of E-cadherin and almost completely abolished the sulforaphane-induced expression of Vimentin.	Acetylcysteine	17-36	vimentin	Homo sapiens	181-189
16286925-5	2005	Dietary supplementation with NAC prevented frequent lymphomas characteristic of Trp53-knockout mice, and slowed the growth of lung cancer xenografts deficient in p53.	Acetylcysteine	29-32	transformation related protein 53	Mus musculus	80-85
16286925-5	2005	Dietary supplementation with NAC prevented frequent lymphomas characteristic of Trp53-knockout mice, and slowed the growth of lung cancer xenografts deficient in p53.	Acetylcysteine	29-32	transformation related protein 53	Mus musculus	82-85
12519694-9	2003	Studies on the susceptibility of CYP1A1 to SeCys conjugates implicated a thiol-reactive intermediate, as evidenced by reduced inhibition levels in the presence of glutathione and N-acetyl cysteine.	Acetylcysteine	179-196	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	33-39
26643864-7	2016	Treatment of the rats with N-acetylcysteine produced significant (P &lt; 0.001) down-regulation of STAT3 mRNA expression and protein phosphorylation.	Acetylcysteine	27-43	signal transducer and activator of transcription 3	Rattus norvegicus	99-104
16223606-6	2005	This up-regulation of PHGPx was inhibited by treatment with the anti-oxidants, pyrrolidine dithiocarbamate, and N-acetyl-L-cysteine, and by inhibitors of NFkappaB and Src kinases.	Acetylcysteine	112-131	glutathione peroxidase 4	Homo sapiens	22-27
26567248-8	2016	In the kidney, the damaged renal structure recovered with OA or NAC administration, through an increase in nephrin and endothelial selective adhesion molecules and a decrease in transforming growth factor-beta/p-smad2/3 and ER stress.	Acetylcysteine	64-67	NPHS1 adhesion molecule, nephrin	Rattus norvegicus	107-114
16243047-13	2005	There was significant decrease at serum and lung MPO and MDA levels after the NAC application in groups D and E, when compared with group C (P = 0.0001, for each comparison).	Acetylcysteine	78-81	myeloperoxidase	Rattus norvegicus	49-52
12480817-8	2002	Sponge implant assays demonstrate that VEGF-, but not S1P-, induced angiogenesis is significantly reduced in wild-type mice treated with NAC and in gp91(phox-/-) mice, suggesting that ROS derived from gp91(phox)-containing NAD(P)H oxidase play an important role in angiogenesis in vivo.	Acetylcysteine	137-140	paired Ig-like receptor B	Mus musculus	201-205
12444151-7	2002	To determine whether ROS induced by M-CSF played a role in Erk activation, we found that N-acetylcysteine and diphenyleneiodonium both suppressed Erk activation in M-CSF-treated monocytes.	Acetylcysteine	89-105	colony stimulating factor 1	Homo sapiens	36-41
12444151-7	2002	To determine whether ROS induced by M-CSF played a role in Erk activation, we found that N-acetylcysteine and diphenyleneiodonium both suppressed Erk activation in M-CSF-treated monocytes.	Acetylcysteine	89-105	colony stimulating factor 1	Homo sapiens	164-169
15860507-7	2005	N-Acetyl-L-cysteine, superoxide (O2-) dismutase and catalase attenuated the EGCG-induced pro-MMP-7 production, suggesting an involvement of oxidative stress in these events.	Acetylcysteine	0-19	matrix metallopeptidase 7	Homo sapiens	93-98
26804764-10	2016	Moreover, The activation of AMPK/mTOR/p70s6k/4EBP1 and JNK signalling pathways induced by NP could be efficiently reversed by pretreatment of N-acetylcysteine or 3-MA.	Acetylcysteine	142-158	ribosomal protein S6 kinase B1	Rattus norvegicus	38-50
15869713-1	2005	We report that N-acetyl-L-cysteine (NAC) treatment blocked induction of TNF-alpha, IL-1beta, IFN-gamma and iNOS in the CNS and attenuated clinical disease in the myelin basic protein induced model of experimental allergic encephalomyelitis (EAE) in Lewis rats.	Acetylcysteine	15-34	interferon gamma	Rattus norvegicus	93-102
15869713-1	2005	We report that N-acetyl-L-cysteine (NAC) treatment blocked induction of TNF-alpha, IL-1beta, IFN-gamma and iNOS in the CNS and attenuated clinical disease in the myelin basic protein induced model of experimental allergic encephalomyelitis (EAE) in Lewis rats.	Acetylcysteine	36-39	interferon gamma	Rattus norvegicus	93-102
15869713-5	2005	Splenocytes from NAC-treated EAE animals showed reduced IFN-gamma production, a Th1 cytokine and increased IL-10 production, an anti-inflammatory cytokine.	Acetylcysteine	17-20	interferon gamma	Rattus norvegicus	56-65
15869713-5	2005	Splenocytes from NAC-treated EAE animals showed reduced IFN-gamma production, a Th1 cytokine and increased IL-10 production, an anti-inflammatory cytokine.	Acetylcysteine	17-20	interleukin 10	Rattus norvegicus	107-112
15845704-4	2005	We investigated the effect of NAC on the expression of CD11b and CD62L in endotoxin-stimulated human whole blood.	Acetylcysteine	30-33	selectin L	Homo sapiens	65-70
12366393-9	2002	A short-term (5 week) ingestion of TP + NAC by female Swiss and BALB/c mice improved leucocyte function, increasing chemotaxis, the proliferative response to Con A, IL-2 release and NK activity and decreasing the adherence of lymphocytes.	Acetylcysteine	40-43	interleukin 2	Mus musculus	165-169
26804764-10	2016	Moreover, The activation of AMPK/mTOR/p70s6k/4EBP1 and JNK signalling pathways induced by NP could be efficiently reversed by pretreatment of N-acetylcysteine or 3-MA.	Acetylcysteine	142-158	mitogen-activated protein kinase 8	Rattus norvegicus	55-58
15698597-12	2005	Conversely, L-cystathionine and N-acetyl-L-cysteine inhibited the translocation to membrane of p47(phox) and p67(phox) in a concentration-dependent manner.	Acetylcysteine	32-51	pleckstrin	Homo sapiens	95-104
15698597-12	2005	Conversely, L-cystathionine and N-acetyl-L-cysteine inhibited the translocation to membrane of p47(phox) and p67(phox) in a concentration-dependent manner.	Acetylcysteine	32-51	pleckstrin	Homo sapiens	99-103
12052825-5	2002	A scavenger of reactive oxygenated species (ROS), N-acetylcysteine (NAC) at 20 mm, completely suppresses the activation of MAP kinases and ASK1, suggesting a role for oxidative stress in the activation mechanism.	Acetylcysteine	50-66	mitogen-activated protein kinase kinase kinase 5	Homo sapiens	139-143
26807660-9	2016	ROS scavenger N-acetyl-l-cysteine reversed inhibition of AKT pathway and expression of Foxp3 from 18.6% to 26.6% in T cells.	Acetylcysteine	14-33	forkhead box P3	Mus musculus	87-92
12052825-5	2002	A scavenger of reactive oxygenated species (ROS), N-acetylcysteine (NAC) at 20 mm, completely suppresses the activation of MAP kinases and ASK1, suggesting a role for oxidative stress in the activation mechanism.	Acetylcysteine	68-71	mitogen-activated protein kinase kinase kinase 5	Homo sapiens	139-143
12023963-6	2002	In addition, a fusion between p47(phox) and the TRAF4 C terminus constitutively activated JNK, and this activation was decreased by the antioxidant N-acetyl cysteine.	Acetylcysteine	148-165	pleckstrin	Homo sapiens	30-33
12023963-6	2002	In addition, a fusion between p47(phox) and the TRAF4 C terminus constitutively activated JNK, and this activation was decreased by the antioxidant N-acetyl cysteine.	Acetylcysteine	148-165	pleckstrin	Homo sapiens	34-38
12165081-0	2002	N-acetylcysteine inhibits the induction of an antigen-specific antibody response down-regulating CD40 and CD27 co-stimulatory molecules.	Acetylcysteine	0-16	CD27 molecule	Homo sapiens	106-110
15698597-16	2005	L-cystathionine and N-acetyl-L-cysteine suppressed fMLP- and PMA-induced superoxide generation by the inhibition of translocation to membrane of p47(phox) and p67(phox).	Acetylcysteine	20-39	pleckstrin	Homo sapiens	145-154
15698597-16	2005	L-cystathionine and N-acetyl-L-cysteine suppressed fMLP- and PMA-induced superoxide generation by the inhibition of translocation to membrane of p47(phox) and p67(phox).	Acetylcysteine	20-39	pleckstrin	Homo sapiens	149-153
12165081-4	2002	The NAC-induced inhibitory effect might be a functional consequence of: (i) a down-regulation of the expression on the B cell surface of CD40 and CD27 co-stimulatory molecules and (ii) a down-regulation of interleukin (IL-4) production.	Acetylcysteine	4-7	CD27 molecule	Homo sapiens	146-150
26891662-5	2016	In the amygdala, JNK was increased in diabetics treated with saline or NAC.	Acetylcysteine	71-74	mitogen-activated protein kinase 8	Rattus norvegicus	17-20
15790131-5	2005	Treatment with 100 mg/kg NAC for 7 days significantly decreased tissue myeloperoxidase, glutathione and nitric oxide concentrations.	Acetylcysteine	25-28	myeloperoxidase	Rattus norvegicus	71-86
15802865-5	2005	The post-irradiation treatment of the cells with N-acetyl-L-cysteine (NAC) abolished the up-regulation of the expression of Fas and DR5 on the plasma membrane.	Acetylcysteine	49-68	TNF receptor superfamily member 10b	Homo sapiens	132-135
12093470-11	2002	N-Acetylcysteine afforded modest protection to TU toxicity by shifting 50% cytotoxicity for TU from 5x10(-5) to 1x10(-3) M. TU mutagenicity was assayed by the development of ouabain resistance in parental and FMO 3 C3H/10T1/2 cells.	Acetylcysteine	0-16	flavin containing monooxygenase 3	Mus musculus	209-214
12027535-12	2002	Finally, the expression of TGF-betaRI was slightly increased in the presence of combined LPS and L-NMMA or NAC whereas that of TGFbeta-RII was reduced in the same conditions.	Acetylcysteine	107-110	transforming growth factor beta receptor 1	Homo sapiens	27-37
26466512-1	2016	This study assessed whether NAC could prevent cyclophosphamide (CY)-induced damage, by measuring the anti-Mullerian hormone (AMH) levels.	Acetylcysteine	28-31	anti-Mullerian hormone	Rattus norvegicus	125-128
11864783-7	2002	The treatment of tumor cells with the antioxidant N-acetylcysteine was able to prevent Zn(2+)-induced apoptosis, as well as the increase of p53 and Fas ligand protein induced by zinc.	Acetylcysteine	50-66	transformation related protein 53, pseudogene	Mus musculus	140-143
15542064-10	2004	N-Acetyl-cysteine blocked this increase of ROS production as well as DAS-induced ERK activation, Nrf2 protein expression and nuclear translocation, and ho-1 gene activation.	Acetylcysteine	0-17	heme oxygenase 1	Homo sapiens	152-156
15555789-11	2004	Treatment of rats with NAC significantly elevated the reduced GSH levels while decreasing MDA levels and MPO activity.	Acetylcysteine	23-26	myeloperoxidase	Rattus norvegicus	105-108
11751160-7	2002	Pretreatment with NF-kappaB inhibitors N-acetylcysteine (NAC) and N-tosylphenyalanine chloromethyl ketone (TPCK) blocked cerulein-induced NF-kappaB activation and abolished cerulein"s effect on MCP-1 synthesis.	Acetylcysteine	39-55	C-C motif chemokine ligand 2	Rattus norvegicus	194-199
26466512-6	2016	AMH concentrations of the CY + NAC group at 72 hours were also significantly lower than those of the NAC group (p = 0.002) and the control group (p = 0.002).	Acetylcysteine	31-34	anti-Mullerian hormone	Rattus norvegicus	0-3
11751160-7	2002	Pretreatment with NF-kappaB inhibitors N-acetylcysteine (NAC) and N-tosylphenyalanine chloromethyl ketone (TPCK) blocked cerulein-induced NF-kappaB activation and abolished cerulein"s effect on MCP-1 synthesis.	Acetylcysteine	57-60	C-C motif chemokine ligand 2	Rattus norvegicus	194-199
26466512-6	2016	AMH concentrations of the CY + NAC group at 72 hours were also significantly lower than those of the NAC group (p = 0.002) and the control group (p = 0.002).	Acetylcysteine	101-104	anti-Mullerian hormone	Rattus norvegicus	0-3
15648272-1	2004	PURPOSE: The effects and mechanisms of different antioxidants, methionine, glutathione, acetylcysteine, and ascorbic acid (AscH2), on the oxidation of methionine residues in granulocyte colony-stimulating factor (G-CSF) and human parathyroid hormone fragment 13-34 (hPTH 13-34) by hydrogen peroxide (H2O2) were quantified and analyzed.	Acetylcysteine	88-102	colony stimulating factor 3	Homo sapiens	174-211
26466512-7	2016	The AMH levels of CY and CY + NAC groups at 72 hours were significantly lower than those at 24 hours.	Acetylcysteine	30-33	anti-Mullerian hormone	Rattus norvegicus	4-7
15621696-7	2004	The AHR-ligand-mediated decrease in cyp1a1 activity was reversed by the antioxidant N-acetylcysteine.	Acetylcysteine	84-100	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	36-42
26466512-8	2016	The 24-h and 72-h AMH levels in the NAC and control groups were similar.	Acetylcysteine	36-39	anti-Mullerian hormone	Rattus norvegicus	18-21
26235215-3	2015	In this work, we investigated the reaction between platinated adducts of a methionine-rich motif of yeast CTR1 (Mets7) and N-acetyl-cysteine (AcCys) or N-acetyl-histidine (AcHis), mimicking metal-binding residues downstream the CTR1 channel.	Acetylcysteine	123-140	high-affinity Cu transporter CTR1	Saccharomyces cerevisiae S288C	106-110
15472968-2	2004	D-Asp was derivatized using o-phthaldialdehyde/N-acetyl-L-cysteine (OPA/NAC).	Acetylcysteine	47-66	synuclein alpha	Homo sapiens	72-75
15203192-9	2004	N-Acetylcysteine, a ROS scavenger, exhibited a response similar to that of DPI and inhibited ET-1-stimulated ERK1/2, PKB, and Pyk2 phosphorylation.	Acetylcysteine	0-16	protein tyrosine kinase 2 beta	Homo sapiens	117-120
12031258-8	2001	Most importantly, preexposure of HMEC-1 to antioxidants, such as pyrrolidine dithiocarbamate (PDTC) or N-acetylcysteine (NAC), attenuated linoleic acid-induced MCP-1 mRNA expression.	Acetylcysteine	103-119	C-C motif chemokine ligand 2	Homo sapiens	160-165
12031258-8	2001	Most importantly, preexposure of HMEC-1 to antioxidants, such as pyrrolidine dithiocarbamate (PDTC) or N-acetylcysteine (NAC), attenuated linoleic acid-induced MCP-1 mRNA expression.	Acetylcysteine	121-124	C-C motif chemokine ligand 2	Homo sapiens	160-165
26235215-3	2015	In this work, we investigated the reaction between platinated adducts of a methionine-rich motif of yeast CTR1 (Mets7) and N-acetyl-cysteine (AcCys) or N-acetyl-histidine (AcHis), mimicking metal-binding residues downstream the CTR1 channel.	Acetylcysteine	123-140	high-affinity Cu transporter CTR1	Saccharomyces cerevisiae S288C	228-232
26622184-9	2015	Finally, MCL-induced Drp1-mediated cell death could be reversed by N-acetyl-L-cysteine (the ROS scavenger) in breast cancer cells.	Acetylcysteine	67-86	dynamin 1 like	Homo sapiens	21-25
11514101-6	2001	The antioxidant, N-acetyl-cysteine, blocked the suppression of FasL expression in response to arsenite.	Acetylcysteine	17-34	Fas ligand	Homo sapiens	63-67
15371168-9	2004	When measured on study day 30, total GST activity for kidney and skin from NAC-treated animals were increased 39% to 131% as compared to controls.	Acetylcysteine	75-78	hematopoietic prostaglandin D synthase	Rattus norvegicus	37-40
25772235-6	2015	Addition of the ROS scavenger N-acetyl cysteine prevented p62 accumulation in PFKFB4-depleted cells, suggesting that the upregulation of p62 and autophagy was a response to oxidative stress caused by PFKFB4 elimination.	Acetylcysteine	30-47	6-phosphofructo-2-kinase/fructose-2,6-biphosphatase 4	Homo sapiens	78-84
15185295-9	2004	Administration of N-acetyl L-cysteine or a chimeric superoxide dismutase (SOD)-SOD2/3, a genetically engineered SOD-abrogated ALT release in H/R-perfused PP zones, implicating a role for superoxide (O(2) (-)).	Acetylcysteine	18-37	glutamic pyruvic transaminase, soluble	Mus musculus	126-129
14731112-7	2004	Antioxidant N -acetylcysteine and SB203580, an antioxidant and inhibitor of p38 MAPK (mitogen-activated protein kinase), abolished MG132-inducible HO-1 expression.	Acetylcysteine	12-29	heme oxygenase 1	Homo sapiens	147-151
11350215-5	2001	NAC reduced Delta Psi(m) dissipation, caspase 9 activation, and apoptosis, indicating a role for PFOA-induced ROS.	Acetylcysteine	0-3	caspase 9	Homo sapiens	38-47
11346471-4	2001	In contrast, irradiated cells with mt p53 showed 89% inhibition of cell death with Ac-DMQD-CHO and 98% inhibition with the antioxidant N-acetyl-L-cysteine (NAC).	Acetylcysteine	135-154	Wistar clone pR53P1 p53 pseudogene	Rattus norvegicus	38-41
25772235-6	2015	Addition of the ROS scavenger N-acetyl cysteine prevented p62 accumulation in PFKFB4-depleted cells, suggesting that the upregulation of p62 and autophagy was a response to oxidative stress caused by PFKFB4 elimination.	Acetylcysteine	30-47	6-phosphofructo-2-kinase/fructose-2,6-biphosphatase 4	Homo sapiens	200-206
11346471-4	2001	In contrast, irradiated cells with mt p53 showed 89% inhibition of cell death with Ac-DMQD-CHO and 98% inhibition with the antioxidant N-acetyl-L-cysteine (NAC).	Acetylcysteine	156-159	Wistar clone pR53P1 p53 pseudogene	Rattus norvegicus	38-41
26289753-7	2015	Preincubation with the antioxidant N-acetyl-l-cysteine (NAC) resulted in increased DMT1 at the apical membrane before and after addition of iron.	Acetylcysteine	35-54	solute carrier family 11 member 2	Homo sapiens	83-87
11154755-2	2000	Here we report the novel use of a chemically defined medium, which we refer to as NBN since it contains N-2 supplement, B-27 supplement, and N-acetyl-L-cysteine, for maintaining O4+/O1- immunopanned pro-oligodendroglia.	Acetylcysteine	141-160	nibrin	Homo sapiens	82-85
15198077-11	2004	Arsenic-induced alteration of glucose 6-phosphatase activity in both liver and kidney was also counteracted by NAC.	Acetylcysteine	111-114	glucose-6-phosphatase catalytic subunit 1	Rattus norvegicus	30-51
14963003-9	2004	Likewise, nuclear export of TERT protein, loss in the overall TERT activity, and the onset of replicative senescence were delayed by incubation with N-acetylcysteine.	Acetylcysteine	149-165	telomerase reverse transcriptase	Homo sapiens	28-32
14963003-9	2004	Likewise, nuclear export of TERT protein, loss in the overall TERT activity, and the onset of replicative senescence were delayed by incubation with N-acetylcysteine.	Acetylcysteine	149-165	telomerase reverse transcriptase	Homo sapiens	62-66
15078196-5	2004	More importantly, orally ingested ITCs are efficiently absorbed, rapidly and almost exclusively excreted and concentrated in the urine as N-acetylcysteine conjugates (NAC-ITC).	Acetylcysteine	138-154	synuclein alpha	Homo sapiens	167-170
11035069-7	2000	CD49d integrin expression was dependent on cell maturation, as its induction was abrogated by N:-acetylcysteine, which inhibits NF-kappaB activation and the functional and phenotypic maturation of MDDC.	Acetylcysteine	94-111	integrin subunit alpha 4	Homo sapiens	0-5
14588144-3	2003	The increases of DNA fragmentation, Bax/Bcl-2 ratio, and caspase activities were abrogated by BAPTA-AM (an intracellular Ca(2+) chelator) and N-acetyl-L-cysteine (an antioxidant), and augmented by wortmannin [a phosphatidylinositol 3-kinase (PI3K) inhibitor].	Acetylcysteine	142-161	BCL2 associated X, apoptosis regulator	Bos taurus	36-39
26449648-6	2015	The increase of ATP5b and CTGF protein expression in AGEs-treated renal tubular cells was reversed by antioxidant N-acetylcysteine.	Acetylcysteine	114-130	ATP synthase, H+ transporting mitochondrial F1 complex, beta subunit	Mus musculus	16-21
14588144-3	2003	The increases of DNA fragmentation, Bax/Bcl-2 ratio, and caspase activities were abrogated by BAPTA-AM (an intracellular Ca(2+) chelator) and N-acetyl-L-cysteine (an antioxidant), and augmented by wortmannin [a phosphatidylinositol 3-kinase (PI3K) inhibitor].	Acetylcysteine	142-161	BCL2 apoptosis regulator	Bos taurus	40-45
26043815-5	2015	LA and NAC prevented these effects by the modulation of ERK and HO1 pathways.	Acetylcysteine	7-10	heme oxygenase 1	Homo sapiens	64-67
14678967-4	2003	Antioxidants (N-acetyl-L-cysteine and Tiron) and inhibitors of mitochondrial permeability transition (cyclosporine A and bongkrekic acid) inhibit Ad.mda-7-induced mitochondrial dysfunction and apoptosis.	Acetylcysteine	14-33	interleukin 24	Homo sapiens	149-154
14607909-7	2003	We found that NAC increased splenocyte IL-4 production via an effect on APCs.	Acetylcysteine	14-17	amyloid P component, serum	Homo sapiens	72-76
10993916-5	2000	Experiments with a thiol antioxidant (N-acetylcysteine) in vivo and nitric oxide (NO) donors in vitro confirmed that reactive oxygen species were required for p53 activation.	Acetylcysteine	38-54	transformation related protein 53, pseudogene	Mus musculus	159-162
10936175-6	2000	Cisplatin-induced p53 accumulation was suppressed by NAC treatment, whereas p53 accumulation was retarded by Trolox treatment.	Acetylcysteine	53-56	transformation related protein 53, pseudogene	Mus musculus	18-21
26057332-6	2015	Second, the regulation of G-CSF and its receptor was measured following eccentric exercise-induced muscle damage and the expression levels we investigated for redox sensitivity by administering the antioxidant N-acetylcysteine (NAC).	Acetylcysteine	210-226	colony stimulating factor 3	Homo sapiens	26-31
10775566-4	2000	Preincubation of VSMCs with either N-acetyl-L-cysteine and/or alpha-lipoic acid significantly decreased bradykinin-induced cytosolic and nuclear phosphorylation of p42(mapk) and p44(mapk).	Acetylcysteine	35-54	cyclin dependent kinase 20	Homo sapiens	164-167
10657671-6	2000	The membrane anchorage of LAT, and consequently the phosphorylation of LAT and the cellular activation of the synovial fluid T lymphocytes upon TCR engagement, is restored in synovial fluid T lymphocytes after supplementation of the intracellular glutathione levels with N-acetyl-l -cysteine.	Acetylcysteine	271-291	T cell receptor beta variable 20/OR9-2 (non-functional)	Homo sapiens	144-147
12829440-11	2003	Diphenylene iodonium and N-acetylcysteine inhibited rhRANTES-induced ERK activation and HSC proliferation, indicating that NADPH oxidase-dependent production of reactive oxygen species was required.	Acetylcysteine	25-41	EPH receptor B2	Homo sapiens	69-72
12942544-4	2003	Both GSE and NAC resulted in significant exacerbation of the LPS-stimulated increase in COX-2 gene and protein expression and prostaglandin release, and suppressed the LPS-induced decrease in COX-1.	Acetylcysteine	13-16	cytochrome c oxidase subunit I	Bos taurus	192-197
26109726-5	2015	A Nox inhibitor, diphenylene iodonium, and antioxidants such as N-acetyl cysteine blocked proliferation of MT1 and MT2 cells.	Acetylcysteine	64-81	metallothionein 1I, pseudogene	Homo sapiens	107-110
12878207-7	2003	Pretreatment with N-acetylcysteine, PD 98059, and SB 203580 decreased HO-1 upregulation in spermine NONOate-treated cells.	Acetylcysteine	18-34	heme oxygenase 1	Homo sapiens	70-74
11319275-0	2000	N-acetyl-L-cysteine simultaneously increases mitogenesis and suppresses apoptosis in mitogen-stimulated B-lymphocytes from p53 haploinsufficient Tg.AC (v-Ha-ras) mice.	Acetylcysteine	0-19	transformation related protein 53, pseudogene	Mus musculus	123-126
11319275-2	2000	We examined the effect of N-acetyl-l-cysteine (NAC) on mitogenesis and apoptosis in splenocytes from p53 haploinsufficient Tg.AC (v-Ha-ras) mice.	Acetylcysteine	47-50	transformation related protein 53, pseudogene	Mus musculus	101-104
11319275-9	2000	Furthermore, NAC increased the number of CD45R+ B cells, but decreased CD3+ T cells showing enhanced survival of B cells under these conditions.	Acetylcysteine	13-16	protein tyrosine phosphatase, receptor type, C	Mus musculus	41-46
26109726-5	2015	A Nox inhibitor, diphenylene iodonium, and antioxidants such as N-acetyl cysteine blocked proliferation of MT1 and MT2 cells.	Acetylcysteine	64-81	metallothionein 2A	Homo sapiens	115-118
12850239-8	2003	Moreover, lectin-II-induced activation of caspase-9 and 3-like protease and cleavage of poly(ADP-ribose) polymerase (PARP) were inhibited by pretreatment of cells with thiol antioxidants, GSH and NAC.	Acetylcysteine	196-199	caspase 9	Homo sapiens	42-51
26006043-0	2015	Suppression of methylmercury-induced IL-6 and MCP-1 expressions by N-acetylcysteine in U-87MG human astrocytoma cells.	Acetylcysteine	67-83	C-C motif chemokine ligand 2	Homo sapiens	46-51
10567914-1	2000	The adult T cell leukemia-derived factor (ADF), or human thioredoxin (hTRX), has a radical scavenging effect similar to that of N-acetyl cysteine (NAC).	Acetylcysteine	128-145	thioredoxin	Homo sapiens	42-45
10567914-1	2000	The adult T cell leukemia-derived factor (ADF), or human thioredoxin (hTRX), has a radical scavenging effect similar to that of N-acetyl cysteine (NAC).	Acetylcysteine	128-145	thioredoxin	Homo sapiens	57-68
10567914-1	2000	The adult T cell leukemia-derived factor (ADF), or human thioredoxin (hTRX), has a radical scavenging effect similar to that of N-acetyl cysteine (NAC).	Acetylcysteine	147-150	thioredoxin	Homo sapiens	42-45
26006043-7	2015	MeHg-induced expression of MCP-1 and IL-6 mRNA was reduced by 10-20% in the presence of 5mM NAC (co-treatment experiment) compared to cells treated with MeHg only.	Acetylcysteine	92-95	C-C motif chemokine ligand 2	Homo sapiens	27-32
10567914-1	2000	The adult T cell leukemia-derived factor (ADF), or human thioredoxin (hTRX), has a radical scavenging effect similar to that of N-acetyl cysteine (NAC).	Acetylcysteine	147-150	thioredoxin	Homo sapiens	57-68
10567914-1	2000	The adult T cell leukemia-derived factor (ADF), or human thioredoxin (hTRX), has a radical scavenging effect similar to that of N-acetyl cysteine (NAC).	Acetylcysteine	147-150	thioredoxin	Homo sapiens	70-74
12801522-6	2003	Treatment of cells with N-acetyl-cysteine for 2h after 8h of pretreatment with GSNO caused an increase in glutathione and nullified ASK1 activation.	Acetylcysteine	24-41	mitogen-activated protein kinase kinase kinase 5	Homo sapiens	132-136
12882449-2	2003	Therefore the current study investigated whether N-acetylcysteine (NAC), an antioxidative agent, inhibits the interleukin (IL)-1beta-induced expression and production of eotaxin and monocyte chemotactic protein (MCP)-1 in human airway smooth muscle cells (HASMC).	Acetylcysteine	49-65	C-C motif chemokine ligand 2	Homo sapiens	182-218
12882449-2	2003	Therefore the current study investigated whether N-acetylcysteine (NAC), an antioxidative agent, inhibits the interleukin (IL)-1beta-induced expression and production of eotaxin and monocyte chemotactic protein (MCP)-1 in human airway smooth muscle cells (HASMC).	Acetylcysteine	67-70	C-C motif chemokine ligand 2	Homo sapiens	182-218
12882449-3	2003	NAC (10 mM) decreased the expression of eotaxin and MCP-1, by 46 +/- 11% (n=7) and 87 +/- 4% (n=6), respectively; the eotaxin release was inhibited by 75 +/- 5% (n=7), whereas the MCP-1 release was decreased by 69 +/- 41% (n=10).	Acetylcysteine	0-3	C-C motif chemokine ligand 2	Homo sapiens	52-57
26006043-8	2015	Pre-treatment of cells with 0.5 or 5mM NAC at 0.5 or 1h and its subsequent washout before MeHg addition suppressed MCP-1 and IL-6 cytokine expressions.	Acetylcysteine	39-42	C-C motif chemokine ligand 2	Homo sapiens	115-120
12882449-3	2003	NAC (10 mM) decreased the expression of eotaxin and MCP-1, by 46 +/- 11% (n=7) and 87 +/- 4% (n=6), respectively; the eotaxin release was inhibited by 75 +/- 5% (n=7), whereas the MCP-1 release was decreased by 69 +/- 41% (n=10).	Acetylcysteine	0-3	C-C motif chemokine ligand 2	Homo sapiens	180-185
12882449-6	2003	The present study demonstrated that N-acetylcysteine inhibits the interleukin-1beta-induced eotaxin and monocyte chemotactic protein 1 expression and production due to a decreased activation of p38 mitogen-activated protein kinase.	Acetylcysteine	36-52	C-C motif chemokine ligand 2	Homo sapiens	104-134
10558905-6	1999	N-Acetylcysteine and diphenyleneiodonium, both of which inhibit the accumulation of intracellular ROS, each blocked silica-induced degradation of IkappaB-alpha but had no effect on that of the Prx enzymes, suggesting that ROS do not contribute to Prx proteolysis.	Acetylcysteine	0-16	NFKB inhibitor alpha	Rattus norvegicus	146-159
25896131-5	2015	Treatment with NF-kappaB inhibitor N-acetylcysteine significantly inhibited the increase of SCF.	Acetylcysteine	35-51	KIT ligand	Rattus norvegicus	92-95
25826445-6	2015	N-acetyl cysteine, a ROS scavenger, blocked irisin-induced AMPK phosphorylation.	Acetylcysteine	0-17	fibronectin type III domain containing 5	Homo sapiens	44-50
10527705-6	1999	Infusion of NAc twice daily for 4 days following transplantation further altered chemokine mRNA expression (increased MCP-1 and RANTES; decreased CINC); led to more enhanced type 2 cytokine production relative to control animals; and further increased xenograft survival.	Acetylcysteine	12-15	C-C motif chemokine ligand 2	Homo sapiens	118-123
12585963-4	2003	Either N-acetylcysteine, an antioxidant, or deferoxamine, an iron chelator, resulted in a dose-dependent inhibition of HO-1 mRNA and protein induction during glucose deprivation, suggesting a redox- and iron-dependent mechanism.	Acetylcysteine	7-23	heme oxygenase 1	Homo sapiens	119-123
10336562-0	1999	Induction of stromelysin gene expression by tumor necrosis factor alpha is inhibited by dexamethasone, salicylate, and N-acetylcysteine in synovial fibroblasts.	Acetylcysteine	119-135	tumor necrosis factor	Bos taurus	44-71
25999707-0	2015	Effect of N-acetylcysteine in COPD patients with different microsomal epoxide hydrolase genotypes.	Acetylcysteine	10-26	epoxide hydrolase 1	Homo sapiens	59-87
10336562-8	1999	Free radical scavenger antioxidant, N-acetylcysteine (but not other antioxidants) also suppressed the TNF-alpha induction (36-100%) of stromelysin suggesting involvement of reactive oxygen species in the induction process.	Acetylcysteine	36-52	tumor necrosis factor	Bos taurus	102-111
10381639-3	1999	Preincubation of chemosensitive cells with antioxidants such as N-acetyl-cysteine (NAC) or glutathione (GSH), significantly reduced doxorubicin-induced apoptosis, hyperexpression of ROS, loss of mitochondrial membrane potential (DeltaPsim) and upregulation of CD95-L expression.	Acetylcysteine	64-81	Fas ligand	Homo sapiens	260-266
12684259-4	2003	Rats receiving N-acetylcysteine (300 mg kg(-1) day(-1), intraperitoneal) had less augmented lung wet weight, and lower levels of proteins, lactate dehydrogenase, neutrophil and macrophage counts in bronchoalveolar lavage fluid and lung myeloperoxidase activity with a betterment of histological score at 3 days postbleomycin.	Acetylcysteine	15-31	myeloperoxidase	Rattus norvegicus	236-251
12521669-7	2003	For the cocaine alone and cocaine and LPS groups, NAC pretreatment significantly decreased serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities with absence of necrotic hepatic lesions, indicating a reduction of liver injury.	Acetylcysteine	50-53	glutamic pyruvic transaminase, soluble	Mus musculus	97-121
12521669-7	2003	For the cocaine alone and cocaine and LPS groups, NAC pretreatment significantly decreased serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities with absence of necrotic hepatic lesions, indicating a reduction of liver injury.	Acetylcysteine	50-53	glutamic pyruvic transaminase, soluble	Mus musculus	123-126
12521669-7	2003	For the cocaine alone and cocaine and LPS groups, NAC pretreatment significantly decreased serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities with absence of necrotic hepatic lesions, indicating a reduction of liver injury.	Acetylcysteine	50-53	solute carrier family 17 (anion/sugar transporter), member 5	Mus musculus	132-158
12521669-7	2003	For the cocaine alone and cocaine and LPS groups, NAC pretreatment significantly decreased serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities with absence of necrotic hepatic lesions, indicating a reduction of liver injury.	Acetylcysteine	50-53	solute carrier family 17 (anion/sugar transporter), member 5	Mus musculus	160-163
10381639-3	1999	Preincubation of chemosensitive cells with antioxidants such as N-acetyl-cysteine (NAC) or glutathione (GSH), significantly reduced doxorubicin-induced apoptosis, hyperexpression of ROS, loss of mitochondrial membrane potential (DeltaPsim) and upregulation of CD95-L expression.	Acetylcysteine	83-86	Fas ligand	Homo sapiens	260-266
10203355-10	1999	Pyrrolidine dithiocarbamate (PDTC), N-acetyl-L-cysteine, dexamethasone (Dex), HerA, and AG490 partially inhibited LPS/ IFN-gamma- or TNF-alpha/IFN-gamma-induced nitrite production.	Acetylcysteine	36-55	interferon gamma	Rattus norvegicus	119-128
25999707-3	2015	The purpose of this study was to evaluate whether different EPHX1 enzyme activity is related to differential therapeutic effects of treatment with NAC in COPD.	Acetylcysteine	147-150	epoxide hydrolase 1	Homo sapiens	60-65
10203355-10	1999	Pyrrolidine dithiocarbamate (PDTC), N-acetyl-L-cysteine, dexamethasone (Dex), HerA, and AG490 partially inhibited LPS/ IFN-gamma- or TNF-alpha/IFN-gamma-induced nitrite production.	Acetylcysteine	36-55	interferon gamma	Rattus norvegicus	143-152
25999707-10	2015	CONCLUSION: NAC treatment in COPD patients with extremely slow/slow EPHX1 enzyme activity improves FEV1 and the SGRQ symptom score, especially in those with mild-to-moderate COPD, and polymorphism in the EPHX1 gene may have a significant role in differential responses to treatment with NAC in patients with COPD.	Acetylcysteine	12-15	epoxide hydrolase 1	Homo sapiens	68-73
12471614-6	2003	Moreover, beta(2)m significantly enhanced the production of reactive oxygen species (ROS) during 12-48 hr treatment, and beta(2)m-induced apoptosis was almost totally inhibited in cells pre-treated with the antioxidant N-acetylcysteine (NAC), providing evidence that beta(2)m-induced apoptosis in CCRF-HSB-2 cells is ROS-dependent.	Acetylcysteine	219-235	beta-2-microglobulin	Homo sapiens	10-18
12471614-6	2003	Moreover, beta(2)m significantly enhanced the production of reactive oxygen species (ROS) during 12-48 hr treatment, and beta(2)m-induced apoptosis was almost totally inhibited in cells pre-treated with the antioxidant N-acetylcysteine (NAC), providing evidence that beta(2)m-induced apoptosis in CCRF-HSB-2 cells is ROS-dependent.	Acetylcysteine	219-235	beta-2-microglobulin	Homo sapiens	121-129
12471614-6	2003	Moreover, beta(2)m significantly enhanced the production of reactive oxygen species (ROS) during 12-48 hr treatment, and beta(2)m-induced apoptosis was almost totally inhibited in cells pre-treated with the antioxidant N-acetylcysteine (NAC), providing evidence that beta(2)m-induced apoptosis in CCRF-HSB-2 cells is ROS-dependent.	Acetylcysteine	219-235	beta-2-microglobulin	Homo sapiens	121-129
12471614-6	2003	Moreover, beta(2)m significantly enhanced the production of reactive oxygen species (ROS) during 12-48 hr treatment, and beta(2)m-induced apoptosis was almost totally inhibited in cells pre-treated with the antioxidant N-acetylcysteine (NAC), providing evidence that beta(2)m-induced apoptosis in CCRF-HSB-2 cells is ROS-dependent.	Acetylcysteine	237-240	beta-2-microglobulin	Homo sapiens	10-18
12471614-6	2003	Moreover, beta(2)m significantly enhanced the production of reactive oxygen species (ROS) during 12-48 hr treatment, and beta(2)m-induced apoptosis was almost totally inhibited in cells pre-treated with the antioxidant N-acetylcysteine (NAC), providing evidence that beta(2)m-induced apoptosis in CCRF-HSB-2 cells is ROS-dependent.	Acetylcysteine	237-240	beta-2-microglobulin	Homo sapiens	121-129
12471614-6	2003	Moreover, beta(2)m significantly enhanced the production of reactive oxygen species (ROS) during 12-48 hr treatment, and beta(2)m-induced apoptosis was almost totally inhibited in cells pre-treated with the antioxidant N-acetylcysteine (NAC), providing evidence that beta(2)m-induced apoptosis in CCRF-HSB-2 cells is ROS-dependent.	Acetylcysteine	237-240	beta-2-microglobulin	Homo sapiens	121-129
9973469-6	1999	Addition of thiol-reducing compounds, such as L-cystine, 2-ME, or N-acetyl cysteine, restored FasL expression.	Acetylcysteine	66-83	Fas ligand	Homo sapiens	94-98
25999707-10	2015	CONCLUSION: NAC treatment in COPD patients with extremely slow/slow EPHX1 enzyme activity improves FEV1 and the SGRQ symptom score, especially in those with mild-to-moderate COPD, and polymorphism in the EPHX1 gene may have a significant role in differential responses to treatment with NAC in patients with COPD.	Acetylcysteine	12-15	epoxide hydrolase 1	Homo sapiens	204-209
12388243-3	2003	Antioxidants, such as pyrrolidine dithiocarbamate (PDTC) and N-acetylcysteine (NAC), significantly inhibited IL-4-induced MCP-1 mRNA expression.	Acetylcysteine	61-77	C-C motif chemokine ligand 2	Homo sapiens	122-127
25999707-10	2015	CONCLUSION: NAC treatment in COPD patients with extremely slow/slow EPHX1 enzyme activity improves FEV1 and the SGRQ symptom score, especially in those with mild-to-moderate COPD, and polymorphism in the EPHX1 gene may have a significant role in differential responses to treatment with NAC in patients with COPD.	Acetylcysteine	287-290	epoxide hydrolase 1	Homo sapiens	204-209
12388243-3	2003	Antioxidants, such as pyrrolidine dithiocarbamate (PDTC) and N-acetylcysteine (NAC), significantly inhibited IL-4-induced MCP-1 mRNA expression.	Acetylcysteine	79-82	C-C motif chemokine ligand 2	Homo sapiens	122-127
9853298-3	1998	The treatment with NAC or AA induced a significant inhibition of viral replication and apoptosis in Fel-039 cells and tumor necrosis factor alpha (TNF-alpha)-treated CRFK cells infected with FIV.	Acetylcysteine	19-22	tumor necrosis factor	Felis catus	118-145
25935150-6	2015	Furthermore, Abeta stimulated the production of reactive oxygen species in endothelial cells and concomitant treatments of the cells with the antioxidant N-acetyl-cysteine (NAC) prevented Abeta effects in promoting HSP90/eNOS interaction and rescued agonist-mediated Akt and eNOS phosphorylation.	Acetylcysteine	154-171	heat shock protein 90 alpha family class A member 1	Homo sapiens	215-220
9853298-3	1998	The treatment with NAC or AA induced a significant inhibition of viral replication and apoptosis in Fel-039 cells and tumor necrosis factor alpha (TNF-alpha)-treated CRFK cells infected with FIV.	Acetylcysteine	19-22	tumor necrosis factor	Felis catus	147-156
25935150-6	2015	Furthermore, Abeta stimulated the production of reactive oxygen species in endothelial cells and concomitant treatments of the cells with the antioxidant N-acetyl-cysteine (NAC) prevented Abeta effects in promoting HSP90/eNOS interaction and rescued agonist-mediated Akt and eNOS phosphorylation.	Acetylcysteine	173-176	heat shock protein 90 alpha family class A member 1	Homo sapiens	215-220
9853298-4	1998	Both cell lines in the presence of noncytotoxic concentrations of NAC or AA showed in increase of intracellular glutathione (GSH) level, which might protect the cells against oxidative stresses exerted by FIV infection and TNF-alpha treatment.	Acetylcysteine	66-69	tumor necrosis factor	Felis catus	223-232
14518593-5	2003	Telmisartan, a newly developed Ang II type 1 receptor antagonist, or an antioxidant N-acetylcysteine significantly inhibited PDGF-B gene induction in Ang II-exposed pericytes.	Acetylcysteine	84-100	platelet derived growth factor subunit B	Bos taurus	125-131
24961937-6	2015	In vivo studies revealed that acute co-incubation of N-acetylcysteine or hydrogen-rich saline with VEGF effectively suppressed VEGF-induced angiogenesis and migration of HUVEC accompanied by decreasing of oxidative stress and inflammatory cytokines.	Acetylcysteine	53-69	vascular endothelial growth factor A	Rattus norvegicus	99-103
24961937-6	2015	In vivo studies revealed that acute co-incubation of N-acetylcysteine or hydrogen-rich saline with VEGF effectively suppressed VEGF-induced angiogenesis and migration of HUVEC accompanied by decreasing of oxidative stress and inflammatory cytokines.	Acetylcysteine	53-69	vascular endothelial growth factor A	Rattus norvegicus	127-131
12226097-6	2002	The addition of N-acetyl-l-cysteine or glutathione ethyl ester inhibited the apoptotic process, thus confirming the key role of glutathione in programmed cell death induced by c-Myc.	Acetylcysteine	16-35	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	176-181
9544582-7	1998	Furthermore, NAC-mediated inhibition occurs after degradation of IkappaB-alpha and nuclear translocation of NF-kappaB.	Acetylcysteine	13-16	NFKB inhibitor alpha	Rattus norvegicus	65-78
25833396-9	2015	The onset of p53 activation was concurrent with higher levels of reactive oxygen species (ROS) that resulted in ROS-dependent apoptotic cell death, a fate that could be rescued by treating with the ROS scavenger N-acetylcysteine.	Acetylcysteine	212-228	transformation related protein 53, pseudogene	Mus musculus	13-16
11819251-5	1998	Co-administration of DADS and NAC completely protected mice.GSH level in this group lowered by about 35% and 30% at 2 and 4 hours, and ALT was 126 plus minus 18 and 157.5 plus minus 36.6 Sigma units at 2 and 4 hours.	Acetylcysteine	30-33	glutamic pyruvic transaminase, soluble	Mus musculus	135-138
9521863-4	1998	Removal of NAC from the culture medium stimulates SMCs to synchronously reenter the cell cycle as judged by induction of cyclin D1 and B-myb gene expression during mid and late G1 phase, respectively, and induction of histone gene expression and [3H]thymidine incorporation during S phase.	Acetylcysteine	11-14	MYB proto-oncogene like 2	Homo sapiens	135-140
12171932-10	2002	The inhibition of PDGF-BB-induced Akt phosphorylation by NEM was completely reversed by PP2A inhibitors fostriecin and okadaic acid, ceramide synthase inhibitor fumonisin B1, and ROS scavenger N-acetylcysteine (NAC).	Acetylcysteine	193-209	protein phosphatase 2 phosphatase activator	Homo sapiens	88-92
12171932-10	2002	The inhibition of PDGF-BB-induced Akt phosphorylation by NEM was completely reversed by PP2A inhibitors fostriecin and okadaic acid, ceramide synthase inhibitor fumonisin B1, and ROS scavenger N-acetylcysteine (NAC).	Acetylcysteine	211-214	protein phosphatase 2 phosphatase activator	Homo sapiens	88-92
12237339-10	2002	These results indicate that the MeHg antidotes NAC and DMPS and their mercaptide complexes are transported by Oat1 but are comparatively poor substrates for Oat3.	Acetylcysteine	47-50	solute carrier family 22 member 8	Rattus norvegicus	157-161
9470017-1	1998	We compared the clinical course of pediatric patients (n = 25) with acetaminophen poisoning treated with an investigational intravenous preparation of N-acetylcysteine (IV-NAC) with that of historical control subjects (n = 29) treated with conventional oral NAC (O-NAC) therapy.	Acetylcysteine	151-167	synuclein alpha	Homo sapiens	172-175
25680460-8	2015	Abeta oligomer-induced IL-1beta production was inhibited not only by the cathepsin B inhibitor CA-074-Me but also by the reactive oxygen species (ROS) inhibitor N-acetylcysteine.	Acetylcysteine	161-177	amyloid beta (A4) precursor protein	Mus musculus	0-5
9201021-8	1997	Strain- or oxidant-induced MCP-1 mRNA levels could be inhibited by treating ECs with catalase or antioxidant N-acetyl-cysteine (NAC).	Acetylcysteine	109-126	C-C motif chemokine ligand 2	Homo sapiens	27-32
9201021-8	1997	Strain- or oxidant-induced MCP-1 mRNA levels could be inhibited by treating ECs with catalase or antioxidant N-acetyl-cysteine (NAC).	Acetylcysteine	128-131	C-C motif chemokine ligand 2	Homo sapiens	27-32
12066227-19	2002	We conclude that the combination of s.c. rIL-2 with oral MPA and anti-oxidant agents ALA and NAC in an intermittent schedule, repeated for a long-term period, is feasible, has a very low toxicity and results in the improvement of biological markers which are predictive for patient outcome.	Acetylcysteine	93-96	interleukin 2	Rattus norvegicus	41-46
11940570-7	2002	LPS stimulated pro-IL-1 message/protein between 3 and 10 h; however, there was a 40% reduction of pro-IL-1 in preincubation of the antioxidant, N-acetylcysteine (NAC).	Acetylcysteine	144-160	interleukin 1 alpha	Homo sapiens	102-106
11940570-7	2002	LPS stimulated pro-IL-1 message/protein between 3 and 10 h; however, there was a 40% reduction of pro-IL-1 in preincubation of the antioxidant, N-acetylcysteine (NAC).	Acetylcysteine	162-165	interleukin 1 alpha	Homo sapiens	102-106
11940570-8	2002	Moreover, NAC moderated LPS-induced IL-1 secretion partially via interleukin 1-converting enzyme.	Acetylcysteine	10-13	interleukin 1 alpha	Homo sapiens	36-40
11940570-10	2002	In contrast, NAC reduced ERK activity to 60% and decreased p38 activity to the basal level, but JNK activity was induced 2-fold.	Acetylcysteine	13-16	EPH receptor B2	Homo sapiens	25-28
25455449-7	2015	In plasma, cysteine- or N-acetylcysteine-conjugated DPH was detected, and these thiol conjugates levels were correlated with the plasma alanine aminotransferase (ALT) levels.	Acetylcysteine	24-40	glutamic pyruvic transaminase, soluble	Mus musculus	136-160
11940570-12	2002	On the other hand, NAC and diphenyleneiodonium chloride partially inhibited LPS-induced Rac activity and protein-tyrosine kinase (PTK), indicating that LPS-mediated ROS and NADPH oxidase correspond to Rac activation and IL-1 expression.	Acetylcysteine	19-22	interleukin 1 alpha	Homo sapiens	220-224
11884408-7	2002	We found that ROS production by V12-H-Ras expression was mediated by the Ras/phosphatidylinositol 3-kinase (PI3K)/Rac1/NADPH oxidase-dependent pathway and that pretreatment of V12-H-Ras-transformed cells with an antioxidant (N-acetylcysteine) and an NADPH oxidase inhibitor (diphenyleneiodonium) decreased DNA repair capacity.	Acetylcysteine	225-241	phosphoinositide-3-kinase regulatory subunit 1	Mus musculus	73-106
9202959-8	1997	NAC treatment decreased gamma-GT activity by -42% in the air-exposed cells.	Acetylcysteine	0-3	gamma-glutamyltransferase 1	Rattus norvegicus	24-32
25455449-7	2015	In plasma, cysteine- or N-acetylcysteine-conjugated DPH was detected, and these thiol conjugates levels were correlated with the plasma alanine aminotransferase (ALT) levels.	Acetylcysteine	24-40	glutamic pyruvic transaminase, soluble	Mus musculus	162-165
9483174-3	1997	Scavengers of reactive oxygen intermediates such as N-acetyl cysteine or pyrrolidine dithiocarbamate were able to block TF induction.	Acetylcysteine	52-69	coagulation factor III, tissue factor	Homo sapiens	120-122
25047070-13	2015	Effects of QD232 on Src/FAK and STAT3 phosphorylation were blocked by N-acetylcysteine or glutathione.	Acetylcysteine	70-86	Rous sarcoma oncogene	Mus musculus	20-23
8950199-6	1996	The AO, N-acetylcysteine (NAC), decreased the extent of cartilage PG depletion caused by TNF-alpha and IL-1 alpha and by the ROS, hydrogen peroxide and superoxide anion, confirming that the cytokines operate through ROS and that ROS can initiate cartilage PG depletion.	Acetylcysteine	8-24	interleukin 1 alpha	Homo sapiens	103-113
8950199-6	1996	The AO, N-acetylcysteine (NAC), decreased the extent of cartilage PG depletion caused by TNF-alpha and IL-1 alpha and by the ROS, hydrogen peroxide and superoxide anion, confirming that the cytokines operate through ROS and that ROS can initiate cartilage PG depletion.	Acetylcysteine	26-29	interleukin 1 alpha	Homo sapiens	103-113
12460510-4	2002	RESULTS: Postinjury WBC in BALF, MPO activity in pulmonary tissue and H(2)O(2) content decreased obviously after NAC treatment.	Acetylcysteine	113-116	myeloperoxidase	Rattus norvegicus	33-36
25047070-13	2015	Effects of QD232 on Src/FAK and STAT3 phosphorylation were blocked by N-acetylcysteine or glutathione.	Acetylcysteine	70-86	PTK2 protein tyrosine kinase 2	Mus musculus	24-27
25970706-7	2015	Treating cells with antioxidant N-acetyl-cysteine (NAC) partially rescues the proliferation defect of the breast CAFs caused by ATM deficiency.	Acetylcysteine	32-49	ATM serine/threonine kinase	Homo sapiens	128-131
11888918-1	2002	Thiol antioxidants, typified by N-acetyl cysteine, are known to induce p53-dependent apoptosis in transformed mouse embryo fibroblasts but not in normal mouse embryo fibroblasts.	Acetylcysteine	32-49	transformation related protein 53, pseudogene	Mus musculus	71-74
12047048-10	2002	Synergistic interactions of mox-LDL with 5-HT, Ang-II, ET-1, or U-II were significantly inhibited by NAC (400 micromol/l).	Acetylcysteine	101-104	monooxygenase DBH like 1	Homo sapiens	28-31
12047048-10	2002	Synergistic interactions of mox-LDL with 5-HT, Ang-II, ET-1, or U-II were significantly inhibited by NAC (400 micromol/l).	Acetylcysteine	101-104	urotensin 2	Homo sapiens	64-68
8805638-4	1996	The thiol antioxidants N-acetyl cysteine and glutathione blocked Fas-induced death triggered via cross-linking either by IgM anti-Fas or cell-bound FasL, while the other inhibitors of activation-induced death did not block this late lethal step.	Acetylcysteine	23-40	Fas ligand	Homo sapiens	148-152
8769100-8	1996	ECs pretreated with antioxidant, N-acetyl-cysteine, abolished the strain-induced ROS generation as well as strained-induced PAI-1 release.	Acetylcysteine	33-50	serpin family E member 1	Homo sapiens	124-129
25970706-7	2015	Treating cells with antioxidant N-acetyl-cysteine (NAC) partially rescues the proliferation defect of the breast CAFs caused by ATM deficiency.	Acetylcysteine	51-54	ATM serine/threonine kinase	Homo sapiens	128-131
8774698-7	1996	The extent of transcriptional activation of the fos, jun and HO genes in M1 cells treated with LPS was strongly reduced by a scavenger of oxygen radicals (N-acetyl-L-cysteine), but a specific inhibitor of protein kinase C only reduced transcriptional activation by 10-20%.	Acetylcysteine	155-174	FBJ osteosarcoma oncogene	Mus musculus	48-51
11862125-10	2002	The mitogenic effect of mox-LDL, ox-LDL, or LPC and their interaction with ET-1 were inhibited by defatted albumin (10 microg/ml), antioxidant N-acetylcysteine (400 microM), the reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxidase inhibitor diphenylene iodonium (1 microM).	Acetylcysteine	144-159	monooxygenase DBH like 1	Homo sapiens	24-27
11862125-12	2002	The synergistic interaction of mox-LDL, ox-LDL, or LPC with ET-1 was completely reversed by the combined use of N-acetylcysteine and TAK044.	Acetylcysteine	112-128	monooxygenase DBH like 1	Homo sapiens	31-34
26646579-8	2015	The effect of oxaliplatin on annexin-V-binding and forward scatter was rather augmented by removal of extracellular Ca2+, but was significantly blunted in the presence of the antioxidant N-acetyl-cysteine (1 mM).	Acetylcysteine	187-204	annexin A5	Homo sapiens	29-38
11782348-0	2002	Inhibition of benzo(a)pyrene-induced lung tumorigenesis in A/J mice by dietary N-acetylcysteine conjugates of benzyl and phenethyl isothiocyanates during the postinitiation phase is associated with activation of mitogen-activated protein kinases and p53 activity and induction of apoptosis.	Acetylcysteine	79-95	transformation related protein 53, pseudogene	Mus musculus	250-253
11782348-13	2002	Phosphorylation of p53 was also higher than the constitutive levels in both ITC-NAC-treated groups, but no induction of p53 expression was detected.	Acetylcysteine	80-83	transformation related protein 53, pseudogene	Mus musculus	19-22
11782348-14	2002	This study demonstrates the chemopreventive efficacy of the NAC conjugates of PEITC and BITC administered in the diet after a single dose of B(a)P for lung tumorigenesis and provides the first in vivo evidence that activation of MAP kinases, AP-1 transcription factors, p53 phosphorylation, and the induction of apoptosis may be involved in the chemopreventive activity of these compounds.	Acetylcysteine	60-63	transformation related protein 53, pseudogene	Mus musculus	270-273
12502184-2	2002	We found that the inhibitory properties of IL-1 on STAT signalling cascade in human hepatoma HepG2 cells are considerably decreased not only in the presence of MAP kinase inhibitors SB203580 and PD98059 but also by some antioxidants (N-acetyl cysteine and pyrrolidine dithiocarbamate) and by anti-inflammatory cytokine IL-4.	Acetylcysteine	234-251	interleukin 1 alpha	Homo sapiens	43-47
11799073-9	2002	Incubation of VSMCs with the antioxidant N-acetylcysteine suppressed GSA-elicited mRNA induction of MCP-1 and IL-6.	Acetylcysteine	41-57	C-C motif chemokine ligand 2	Homo sapiens	100-105
8647183-5	1996	The possible implications for negative selection of NAC-mediated inhibition of TCR-signaled thymocyte cell death was examined in thymic organ culture.	Acetylcysteine	52-55	T cell receptor beta variable 20/OR9-2 (non-functional)	Homo sapiens	79-82
8669050-11	1996	CONCLUSION: N-acetylcysteine is capable to co-stimulate radioprotective cytokines like IL-1 alpha and IL-1 beta and to enhance IL-2 in vitro, whereas higher doses result in a suppression.	Acetylcysteine	12-28	interleukin 1 alpha	Homo sapiens	87-97
8546677-15	1996	Interestingly, NAC is also an inducer for GSTP1.	Acetylcysteine	15-18	glutathione S-transferase pi 1	Homo sapiens	42-47
27405831-5	1995	In contrast, NAC pretreated rats given paraquat had the same lung lavage CINC levels and lung tissue MPO activity as saline-pretreated rats given paraquat.	Acetylcysteine	13-16	myeloperoxidase	Rattus norvegicus	101-104
25821351-3	2015	The expression of IL-2, IL-6, TNF-alpha, and IFN-gamma was significantly reduced in the NAC-treated groups.	Acetylcysteine	88-91	interleukin 2	Mus musculus	18-22
12467136-0	2002	Timing of supplementation with the antioxidant N-acetyl-L-cysteine reduces tumor multiplicity in novel, cancer-prone p53 haploinsufficient Tg.AC (v-Ha-ras) transgenic mice but has no impact on malignant progression.	Acetylcysteine	47-66	transformation related protein 53, pseudogene	Mus musculus	117-120
25821351-5	2015	Additionally, NAC reduced autophagosome formation, as assessed by detecting the expression of LC3 and Beclin 1.	Acetylcysteine	14-17	microtubule-associated protein 1 light chain 3 alpha	Mus musculus	94-97
11532857-0	2001	Dietary N-acetyl-L-cysteine modulates benzo[a]pyrene-induced skin tumors in cancer-prone p53 haploinsufficient Tg.AC (v-Ha-ras) mice.	Acetylcysteine	8-27	transformation related protein 53, pseudogene	Mus musculus	89-92
25821351-5	2015	Additionally, NAC reduced autophagosome formation, as assessed by detecting the expression of LC3 and Beclin 1.	Acetylcysteine	14-17	beclin 1, autophagy related	Mus musculus	102-110
11500052-9	2001	Treatment of animals with an antioxidant N-acetylcysteine administered ip greatly diminished the levels of shortened Bcl-2 and Bax proteins.	Acetylcysteine	41-57	BCL2 associated X, apoptosis regulator	Rattus norvegicus	127-130
7769841-12	1995	NAC protection against ara-C killing was seen for OCI/AML-1 and 2 cells, but not for OCI/AML-5 cells.	Acetylcysteine	0-3	RUNX family transcription factor 1	Homo sapiens	50-59
26257840-7	2015	Moreover, CPF treatment significantly enhances the expression of BZLF-1, and the increased BZLF-1 expression was ameliorated by N-acetylcysteine (NAC) incubation.	Acetylcysteine	128-144	protein Zta	Human gammaherpesvirus 4	91-97
7849291-6	1995	Immunofluorescence studies of human monocytes using polyclonal anti-TF antibody showed that N-acetyl-cysteine treatment prevented the characteristic plasmalemmal localization of TF antigen that occurs in response to LPS.	Acetylcysteine	92-109	coagulation factor III, tissue factor	Homo sapiens	68-70
11506852-8	2001	Therapeutic concentrations of vitamin C, vitamin E, and acetylcysteine (all at 25 microg/mL) inhibited DNA fragmentation and attenuated cleavage of plasminogen activator inhibitor type 2 and cytokeratin-18 neoepitope formation.	Acetylcysteine	56-70	keratin 18	Homo sapiens	191-205
11337489-4	2001	We also have shown that TNF induces tyrosine phosphorylation and internalization of the overexpressed EGFR in NIH3T3 cells and the endogenously expressed EGFR in A431 cells and that the transactivation by TNF is suppressed by N-acetyl-l-cysteine or overexpression of an endogenous reducing molecule, thioredoxin, but not by phosphatidylinositol 3-kinase inhibitors and protein kinase C inhibitor.	Acetylcysteine	226-245	epidermal growth factor receptor	Mus musculus	102-106
11337489-4	2001	We also have shown that TNF induces tyrosine phosphorylation and internalization of the overexpressed EGFR in NIH3T3 cells and the endogenously expressed EGFR in A431 cells and that the transactivation by TNF is suppressed by N-acetyl-l-cysteine or overexpression of an endogenous reducing molecule, thioredoxin, but not by phosphatidylinositol 3-kinase inhibitors and protein kinase C inhibitor.	Acetylcysteine	226-245	epidermal growth factor receptor	Mus musculus	154-158
7849291-6	1995	Immunofluorescence studies of human monocytes using polyclonal anti-TF antibody showed that N-acetyl-cysteine treatment prevented the characteristic plasmalemmal localization of TF antigen that occurs in response to LPS.	Acetylcysteine	92-109	coagulation factor III, tissue factor	Homo sapiens	178-180
26257840-7	2015	Moreover, CPF treatment significantly enhances the expression of BZLF-1, and the increased BZLF-1 expression was ameliorated by N-acetylcysteine (NAC) incubation.	Acetylcysteine	146-149	protein Zta	Human gammaherpesvirus 4	91-97
7851416-4	1995	Induction of HSP27 kinase activity by TNF or H2O2 was completely inhibited by first treating the cells with the antioxidant N-acetyl-L-cysteine, suggesting that generation of reactive oxygen metabolites was the key triggering element of this induction.	Acetylcysteine	124-143	heat shock protein family B (small) member 1	Homo sapiens	13-18
11408612-7	2001	The use of the antioxidant N-acetyl cysteine and caspase inhibitors prevents CDDP-induced apoptosis in c-Myc low-expressing clones, demonstrating that ROS, caspase-1, and caspase-3 are required for apoptotic cell death.	Acetylcysteine	27-44	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	103-108
25308201-9	2015	Both azithromycin and n-acetyl cysteine suppressed CD4 T-cell granzyme B production, but only azithromycin was effective at reducing CD8+ T-cell granzyme B production in vitro.	Acetylcysteine	22-39	granzyme B	Homo sapiens	62-72
11158190-10	2001	However, when N-acetylcysteine or selenium was added with EGF for 1 month, levels of intracellular peroxide and 8-hydroxyguanosine in DNA were comparable to those in control cells (r =.795).	Acetylcysteine	14-30	epidermal growth factor	Homo sapiens	58-61
8313381-2	1994	When the glutathione conjugate of EA was incubated with a 5-fold molar excess of N-acetyl-L-cysteine or GST P1-1, a time-dependent transfer of EA to N-acetyl-L-cysteine or GST P1-1 was observed.	Acetylcysteine	81-100	glutathione S-transferase pi 1	Homo sapiens	172-180
8313381-2	1994	When the glutathione conjugate of EA was incubated with a 5-fold molar excess of N-acetyl-L-cysteine or GST P1-1, a time-dependent transfer of EA to N-acetyl-L-cysteine or GST P1-1 was observed.	Acetylcysteine	149-168	glutathione S-transferase pi 1	Homo sapiens	104-112
21573453-6	1993	Proliferin induction by a recently identified promoter of transformation, tri-n-butyltin chloride, was stimulated by catalase, superoxide dismutase and retinoic acid, but inhibited at higher concentrations of N-acetyl cysteine.	Acetylcysteine	209-226	prolactin family 2, subfamily c, member 2	Mus musculus	0-10
25536346-4	2014	Conversely, antioxidant N-acetyl-L-cysteine significantly reduced CCN1 expression and prevented ROS-induced loss of type I collagen in both human dermal fibroblasts and human skin in vivo.	Acetylcysteine	24-43	cellular communication network factor 1	Homo sapiens	66-70
1581851-4	1992	Reducing the dose of NAC or cysteamine by 50% greatly reduced their hepatoprotective effect while the co-administration of the reduced doses of NAC (250 mg/kg) and cysteamine (50 mg/kg) following acetaminophen overdose prevented elevation of serum ALT activity (39.2 +/- 1.17 and 32.5 +/- 5.63 U/mL at 12 and 24 h post-injection, p less than 0.001) and preserved normal mouse hepatic histology.	Acetylcysteine	21-24	glutamic pyruvic transaminase, soluble	Mus musculus	248-251
11346894-9	2000	Plasma ALT concentrations were significantly lower (p &lt; 0.01) in mice treated with 2.5 mmol/kg of S-adenosyl-L-methionine than in those given N-acetylcysteine.	Acetylcysteine	145-161	glutamic pyruvic transaminase, soluble	Mus musculus	7-10
11197525-4	2000	The involvement of ROS is suggested by experiments where the stimulation of fibroblasts with TNF-alpha or IL-1alpha are performed in the presence of N-acetylcysteine which increases the intracellular antioxidant potential.	Acetylcysteine	149-165	interleukin 1 alpha	Homo sapiens	106-115
11031216-10	2000	Incubation of ECs with N:-acetyl cysteine inhibited production of IL-8 and MCP-1 induced by LDL(-) and oxLDL by &gt;50%.	Acetylcysteine	23-41	C-C motif chemokine ligand 2	Homo sapiens	75-80
11029607-9	2000	T cell GSH, adjusted for CD4 T cell count and beta2-microglobulin levels, also increased in the NAC-treated subjects (P = 0.04).	Acetylcysteine	96-99	beta-2-microglobulin	Homo sapiens	46-65
10963726-4	2000	NAC also attenuated the ileum injury (histology) as well as the increase in the tissue levels of myeloperoxidase (MPO) and malondialdehyde (MDA) caused by SAO shock in the ileum.	Acetylcysteine	0-3	myeloperoxidase	Rattus norvegicus	97-112
25041185-5	2014	ROS scavenger N-acetylcysteine reduced expression of HSP70 and HSP32 (haeme oxygenase-1, HO-1).	Acetylcysteine	14-30	heat shock protein family A (Hsp70) member 1B	Rattus norvegicus	53-58
10963726-4	2000	NAC also attenuated the ileum injury (histology) as well as the increase in the tissue levels of myeloperoxidase (MPO) and malondialdehyde (MDA) caused by SAO shock in the ileum.	Acetylcysteine	0-3	myeloperoxidase	Rattus norvegicus	114-117
11707313-2	2000	(2) Depending on the dose used, NAC administered intracolonically was found to reduce the extent of colonic damage, along with a decrease in myeloperoxidase (MPO) activity, colonic wet weight and wet/dry weight ratio.	Acetylcysteine	32-35	myeloperoxidase	Rattus norvegicus	141-156
11707313-2	2000	(2) Depending on the dose used, NAC administered intracolonically was found to reduce the extent of colonic damage, along with a decrease in myeloperoxidase (MPO) activity, colonic wet weight and wet/dry weight ratio.	Acetylcysteine	32-35	myeloperoxidase	Rattus norvegicus	158-161
2262910-13	1990	Poly I-C pretreatment produced respective 3-fold and 1.3-fold increases in the production of cysteine and mercapturic acid conjugates (P less than 0.05), which correlated with peak ALT concentrations (cysteine, r = 0.92, P less than 0.001; mercapturic acid, r = 0.75, P = 0.006).	Acetylcysteine	106-122	glutamic pyruvic transaminase, soluble	Mus musculus	181-184
24717091-9	2014	The annexin-V binding after salinomycin treatment was significantly blunted but not abrogated in the nominal absence of extracellular Ca(2+) or in the presence of antioxidant n-acetyl cysteine (1 mM).	Acetylcysteine	175-192	annexin A5	Homo sapiens	4-13
2200749-9	1990	Cath-G induced detachment was profoundly inhibited by SBTI, GSH and NAC.	Acetylcysteine	68-71	cathepsin G	Homo sapiens	0-6
33819738-7	2021	Following N-acetylcysteine treatment, apoptotic rates of the cancer cell lines decreased from 38.9% to 7.3%, and the expression of Cl-PARP, Cl-Caspase-3 and Cl-Caspase-9 also decreased, confirming that compound 6g induced apoptosis through ROS induction.	Acetylcysteine	10-26	caspase 9	Homo sapiens	160-169
21055460-0	2011	Suppression of human prostate cancer PC-3 cell growth by N-acetylcysteine involves over-expression of Cyr61.	Acetylcysteine	57-73	cellular communication network factor 1	Homo sapiens	102-107
10861855-6	2000	Depletion of glutathione in these cells with buthionine-sulfoximine (BSO) correlated with a significant stimulation of NO-mediated apoptosis whereas the exposure of NO-sensitive APO-S cells to the glutathione precursor N-acetylcysteine (NAC) resulted in a substantial suppression of this effect.	Acetylcysteine	219-235	aminopeptidase O (putative)	Homo sapiens	178-181
10771256-6	2000	Five patients, four with EPM 1 (Unverricht-Lundborg disease) and one patient with EPM2 (Lafora body disease) were treated with 6 g/day of NAC.	Acetylcysteine	138-141	EPM2A glucan phosphatase, laforin	Homo sapiens	82-86
10771256-9	2000	NAC improved markedly and stabilized the neurological symptoms in patients with EPM 1 but had a doubtful effect in the patient with EPM 2.	Acetylcysteine	0-3	EPM2A glucan phosphatase, laforin	Homo sapiens	132-137
21055460-5	2011	Moreover, NAC treatment suppressed the activation of NF-kappaB induced by IKK-beta as detected by the NF-kappaB reporter gene assay.	Acetylcysteine	10-13	inhibitor of nuclear factor kappa B kinase subunit beta	Homo sapiens	74-82
21055460-7	2011	In addition to these effects, NAC treatment elicited a dose- and time-dependent increase in the Cyr61 expression that was accompanied by an increase in its mRNA and blocked by cycloheximide pretreatment.	Acetylcysteine	30-33	cellular communication network factor 1	Homo sapiens	96-101
25305669-0	2014	N-acetylcysteine prevents endoplasmic reticulum stress elicited in macrophages by serum albumin drawn from chronic kidney disease rats and selectively affects lipid transporters, ABCA-1 and ABCG-1.	Acetylcysteine	0-16	ATP binding cassette subfamily G member 1	Rattus norvegicus	190-196
21055460-9	2011	The NAC-induced increase in Cyr61 protein levels was suppressed by the PI3K inhibitor (Ly294002) and, to a lesser extent, MEK/Erk1/2 inhibitor (PD98059).	Acetylcysteine	4-7	cellular communication network factor 1	Homo sapiens	28-33
10807739-6	2000	JNK and ERK were activated by ET-1 binding to a single receptor (ET-1A) but differed in their downstream mechanisms: only JNK activation was sensitive to the radical scavenger N-acetylcysteine and diphenylene iodonium, an inhibitor of NADPH oxidase, indicating a role for ROS.	Acetylcysteine	176-192	mitogen-activated protein kinase 8	Rattus norvegicus	0-3
10807739-6	2000	JNK and ERK were activated by ET-1 binding to a single receptor (ET-1A) but differed in their downstream mechanisms: only JNK activation was sensitive to the radical scavenger N-acetylcysteine and diphenylene iodonium, an inhibitor of NADPH oxidase, indicating a role for ROS.	Acetylcysteine	176-192	mitogen-activated protein kinase 8	Rattus norvegicus	122-125
10625299-4	2000	Using cultured rat neonatal cardiac myocytes, we found that the antioxidant N-acetylcysteine blocked the DOX-induced decrease in SERCA2 mRNA levels, as well as the DOX-induced increase in H(2)O(2) concentration; thus, H(2)O(2) is an intracellular mediator of DOX activity.	Acetylcysteine	76-92	ATPase sarcoplasmic/endoplasmic reticulum Ca2+ transporting 2	Rattus norvegicus	129-135
34915176-9	2022	Further results showed that the trimethyl-histone H3-K4 (H3K4me3) level of MCT4 was reduced by Dex, and the ROS scavenger N-Acetyl-l-cysteine (NAC) and alpha-ketoglutarate (alpha-KG) alleviated the Dex-induced chondrocyte matrix synthesis obstruction and high level of ROS by up-regulating the H3K4me3 level of MCT4 and its expression.	Acetylcysteine	122-141	solute carrier family 16 member 3	Homo sapiens	311-315
25305669-18	2014	ABCA-1 expression was lower (87% and 70%, p &lt; 0.001) in macrophage treated with Sham + NAC and CKD albumin respectively in comparison to Sham albumin; ABCG-1 was higher (4 and 7 times, p &lt; 0.001) in macrophages treated with Sham + NAC and CKD + NAC albumin, respectively in comparison to Sham and CKD albumin.	Acetylcysteine	90-93	ATP binding cassette subfamily G member 1	Rattus norvegicus	154-160
34915176-9	2022	Further results showed that the trimethyl-histone H3-K4 (H3K4me3) level of MCT4 was reduced by Dex, and the ROS scavenger N-Acetyl-l-cysteine (NAC) and alpha-ketoglutarate (alpha-KG) alleviated the Dex-induced chondrocyte matrix synthesis obstruction and high level of ROS by up-regulating the H3K4me3 level of MCT4 and its expression.	Acetylcysteine	143-146	solute carrier family 16 member 3	Homo sapiens	311-315
25305669-19	2014	Apo A-I mediated cholesterol efflux was lower (59% and 70%, p &lt; 0.0001) in macrophage treated with Sham + NAC and CKD albumin respectively in comparison to Sham albumin, however, the HDL2 mediated cholesterol efflux was higher (54% and 25%, p &lt; 0.0001) in macrophage treated with Sham + NAC albumin, in comparison to Sham and CKD + NAC albumin, respectively.	Acetylcysteine	109-112	apolipoprotein A1	Rattus norvegicus	0-7
25305669-19	2014	Apo A-I mediated cholesterol efflux was lower (59% and 70%, p &lt; 0.0001) in macrophage treated with Sham + NAC and CKD albumin respectively in comparison to Sham albumin, however, the HDL2 mediated cholesterol efflux was higher (54% and 25%, p &lt; 0.0001) in macrophage treated with Sham + NAC albumin, in comparison to Sham and CKD + NAC albumin, respectively.	Acetylcysteine	293-296	apolipoprotein A1	Rattus norvegicus	0-7
10547276-8	1999	The mean MCP-1 level for LPS-treated monocytes was 4903+/-1540 pg/ml 20 h for normal subjects and was significantly elevated in AH patients to 11589+/-3266 pg/ml/20 h. AH patient monocyte MCP-1 production was decreased in vitro when monocytes were treated with N-acetylcysteine (5 mM) and also decreased over the 6-month study as the patients improved clinically.	Acetylcysteine	261-277	C-C motif chemokine ligand 2	Homo sapiens	9-14
25305669-19	2014	Apo A-I mediated cholesterol efflux was lower (59% and 70%, p &lt; 0.0001) in macrophage treated with Sham + NAC and CKD albumin respectively in comparison to Sham albumin, however, the HDL2 mediated cholesterol efflux was higher (54% and 25%, p &lt; 0.0001) in macrophage treated with Sham + NAC albumin, in comparison to Sham and CKD + NAC albumin, respectively.	Acetylcysteine	293-296	apolipoprotein A1	Rattus norvegicus	0-7
34957591-1	2021	Paracetamol poisoning continues to be a worldwide problem and despite the availability of an effective antidote, acetylcysteine (NAC), the optimal way to use this antidote, particularly following very large doses of paracetamol, has not been established.	Acetylcysteine	113-127	synuclein alpha	Homo sapiens	129-132
25305669-22	2014	Despite diminishing ABCA-1, NAC increases ABCG-1 that counteracts the reduction in apo A-I-mediated cholesterol efflux.	Acetylcysteine	28-31	ATP binding cassette subfamily G member 1	Rattus norvegicus	42-48
34926192-10	2021	However, the addition of NAC reduced the concentrations of TNF-alpha (153.67+-2.31 pg/mL) and cleaved PARP (5.55+-0.31 fold) and the number of apoptotic cells.	Acetylcysteine	25-28	poly (ADP-ribose) polymerase 1	Rattus norvegicus	102-106
25461556-7	2014	The involvement of ROS in DR5 upregulation confirmed that pretreatment with antioxidants, including N-acetyl-L-cysteine and glutathione, significantly inhibits CPT-TRAIL-induced cell death by suppressing DR5 expression.	Acetylcysteine	100-119	TNF receptor superfamily member 10b	Homo sapiens	26-29
34912495-8	2021	The implicated therapeutic mechanisms of NAC extend from enhancing hepatic GSH levels to reducing biomarkers of paracetamol toxicity such as keratin-18 and circulating caspase-cleaved cytokeratin-18.	Acetylcysteine	41-44	keratin 18	Homo sapiens	141-151
10521241-8	1999	With ischemia, flow-adapted cells exhibited increases of 1.7-fold in nuclear NF-kappaB and 1.5-fold in nuclear AP-1; these changes were abolished by pretreatment with N-acetylcysteine or DPI.	Acetylcysteine	167-183	Jun proto-oncogene, AP-1 transcription factor subunit	Bos taurus	111-115
34912495-8	2021	The implicated therapeutic mechanisms of NAC extend from enhancing hepatic GSH levels to reducing biomarkers of paracetamol toxicity such as keratin-18 and circulating caspase-cleaved cytokeratin-18.	Acetylcysteine	41-44	keratin 18	Homo sapiens	184-198
25461556-7	2014	The involvement of ROS in DR5 upregulation confirmed that pretreatment with antioxidants, including N-acetyl-L-cysteine and glutathione, significantly inhibits CPT-TRAIL-induced cell death by suppressing DR5 expression.	Acetylcysteine	100-119	TNF receptor superfamily member 10b	Homo sapiens	204-207
10498608-9	1999	Moreover, GSH and NAC significantly reduced eosinophil apoptosis mediated by a monoclonal antibody directed to Fas antigen.	Acetylcysteine	18-21	Fas cell surface death receptor	Homo sapiens	111-122
25289048-4	2014	Pretreatment with N-acetylcysteine, an antioxidant chemical compound, inhibited the activation of ASK1, JNK and Bim, as well as the apoptosis induced by casticin.	Acetylcysteine	18-34	mitogen-activated protein kinase kinase kinase 5	Homo sapiens	98-102
10523329-8	1999	N-Acetyl-L-cysteine upregulated nitrite production and inducible nitric oxide synthase expression induced by combination treatment with interleukin-1beta and either interferon-gamma or tumor necrosis factor-alpha.	Acetylcysteine	0-19	interferon gamma	Rattus norvegicus	165-212
34553295-8	2021	MR dramatically sensitized TNBC cells to TXNRD1 silencing and the TXNRD inhibitor auranofin, as determined by crystal violet staining and caspase activity; these effects were suppressed by the antioxidant N-acetylcysteine.	Acetylcysteine	205-221	peroxiredoxin 5	Homo sapiens	66-71
25289048-4	2014	Pretreatment with N-acetylcysteine, an antioxidant chemical compound, inhibited the activation of ASK1, JNK and Bim, as well as the apoptosis induced by casticin.	Acetylcysteine	18-34	BCL2 like 11	Homo sapiens	112-115
10487485-8	1999	Results also demonstrated that under the condition; in which N-acetylcysteine inhibited the copper-induced apoptosis, this antioxidant also abolished the gene expression of egr-1.	Acetylcysteine	61-77	early growth response 1	Mus musculus	173-178
25016575-9	2014	Furthermore, two kinases involved in STAT3 activation, known as JAK2 and JAK3, appeared down-regulated in presence of NAC.	Acetylcysteine	118-121	Janus kinase 3	Homo sapiens	73-77
34530696-7	2021	By performing qRT-PCR using aortic samples from these mice, we identified that SIRT-1, SIRT-3, FOXO-1 could be somehow responsible for aging-related fibrosis.Conclusions: NAC ameliorates aortic fibrosis in aging wild type mice partly by promoting M2 macrophage polarization.	Acetylcysteine	171-174	sirtuin 1	Mus musculus	79-85
34530696-7	2021	By performing qRT-PCR using aortic samples from these mice, we identified that SIRT-1, SIRT-3, FOXO-1 could be somehow responsible for aging-related fibrosis.Conclusions: NAC ameliorates aortic fibrosis in aging wild type mice partly by promoting M2 macrophage polarization.	Acetylcysteine	171-174	sirtuin 3	Mus musculus	87-93
34530696-7	2021	By performing qRT-PCR using aortic samples from these mice, we identified that SIRT-1, SIRT-3, FOXO-1 could be somehow responsible for aging-related fibrosis.Conclusions: NAC ameliorates aortic fibrosis in aging wild type mice partly by promoting M2 macrophage polarization.	Acetylcysteine	171-174	forkhead box O1	Mus musculus	95-101
24810251-3	2014	Principal component analysis, based on untargeted mass spectra, indicated that treatment of CSC-exposed HBECs with O-methyl-L-tyrosinyl-gamma-L-glutamyl-L-cysteinylglycine (UPF1) acted faster than did N-acetylcysteine to revert the effect of CSC.	Acetylcysteine	201-217	UPF1 RNA helicase and ATPase	Homo sapiens	173-177
34606154-6	2021	Antioxidants (N-acetylcysteine, idebenone, resveratrol, edaravone) improved alpha-glucosidase activity in rhGAA-treated cells, enhanced enzyme processing, and improved mannose-6-phosphate receptor localization.	Acetylcysteine	14-30	sucrase-isomaltase	Homo sapiens	76-93
34156614-6	2021	NAC also significantly increased the expression and distribution of zonula occludens 1 (ZO-1), decreased the relative mRNA and protein expression levels of Bax, Bid, caspase-3, and caspase-9, and increased Bcl-2 expression level and inhibited the decrease of mitochondrial membrane potential.	Acetylcysteine	0-3	caspase 9	Homo sapiens	181-190
10513606-12	1999	ECs treated with N-acetyl-cysteine abolished HO-1 gene induction.	Acetylcysteine	17-34	heme oxygenase 1	Homo sapiens	45-49
10378453-5	1999	In acetaminophen-treated mice serum alanine aminotransferase (ALT) was 779 +/- 271 at 2 h, 7421 +/- 552 IU/l at 4 h, 5732 +/- 523 IU/l at 8 h, and 5984 +/- 497 IU/l at 24 h. In acetaminophen plus deferoxamine-treated mice, serum ALT was 80 +/- 10 at 2 h, 472 +/- 74 IU/l at 4 h, 2149 +/- 597 IU/l at 8 h, and 5766 +/- 388 at 24 h. Deferoxamine at 1 h after acetaminophen did not decrease serum ALT at 12 h; however, deferoxamine at 1 and 4 h, or deferoxamine at 1 h plus N-acetylcysteine at 4 h to replete hepatic glutathione, decreased the toxicity from 5625 +/- 310 IU/l to 3436 +/- 546 IU/l and 3003 +/- 282 IU/l, respectively.	Acetylcysteine	471-487	glutamic pyruvic transaminase, soluble	Mus musculus	36-60
10378453-5	1999	In acetaminophen-treated mice serum alanine aminotransferase (ALT) was 779 +/- 271 at 2 h, 7421 +/- 552 IU/l at 4 h, 5732 +/- 523 IU/l at 8 h, and 5984 +/- 497 IU/l at 24 h. In acetaminophen plus deferoxamine-treated mice, serum ALT was 80 +/- 10 at 2 h, 472 +/- 74 IU/l at 4 h, 2149 +/- 597 IU/l at 8 h, and 5766 +/- 388 at 24 h. Deferoxamine at 1 h after acetaminophen did not decrease serum ALT at 12 h; however, deferoxamine at 1 and 4 h, or deferoxamine at 1 h plus N-acetylcysteine at 4 h to replete hepatic glutathione, decreased the toxicity from 5625 +/- 310 IU/l to 3436 +/- 546 IU/l and 3003 +/- 282 IU/l, respectively.	Acetylcysteine	471-487	glutamic pyruvic transaminase, soluble	Mus musculus	62-65
34755672-5	2021	The effects of chrysin, LPS, and their combination on the mRNA expressions of iNOS and COX-2 were detected using RT-PCR; Western blotting was performed to examine the changes in cellular expressions of p-AKT, p-PRAS40, p-mTOR, mTOR, p-P70S6k, p-S6RP and S6RP following the treatments with LPS, N-Acetyl-L-cysteine, and chrysin, alone or in combinations.	Acetylcysteine	294-313	mechanistic target of rapamycin kinase	Mus musculus	221-225
25218171-6	2014	DSCR1 transfection-induced changes were increased by treatment with IL-1beta, which was suppressed by NAC and BAPTA.	Acetylcysteine	102-105	regulator of calcineurin 1	Homo sapiens	0-5
34755672-5	2021	The effects of chrysin, LPS, and their combination on the mRNA expressions of iNOS and COX-2 were detected using RT-PCR; Western blotting was performed to examine the changes in cellular expressions of p-AKT, p-PRAS40, p-mTOR, mTOR, p-P70S6k, p-S6RP and S6RP following the treatments with LPS, N-Acetyl-L-cysteine, and chrysin, alone or in combinations.	Acetylcysteine	294-313	mechanistic target of rapamycin kinase	Mus musculus	227-231
34755672-9	2021	Chrysin treatment significantly reduced the generation of endogenous ROS, and treatment with N-Acetyl-L-cysteine to eliminate intracellular ROS obviously reduced the expressions of iNOS and COX-2 (P < 0.05) and blocked the AKT/mTOR pathway (P < 0.05).	Acetylcysteine	93-112	mechanistic target of rapamycin kinase	Mus musculus	227-231
34482039-12	2021	CONCLUSIONS: Reversible alteration of mRNA levels by removing morphine from culture medium, and effect of NAC in co-treatment of morphine plus NAC, emphasize the role of reactive oxygen species in down-regulation of the expression of hTERT and TERF2 by morphine.	Acetylcysteine	106-109	telomerase reverse transcriptase	Homo sapiens	234-239
10205148-14	1999	Consequently, this Egr-1 gene induction was abolished after ECs were treated with N-acetylcysteine or catalase.	Acetylcysteine	82-98	early growth response 1	Homo sapiens	19-24
10203358-8	1999	The induction of hillocks by NAC was correlated with downregulation of alpha-SMA as well as attenuated activity of the CArG box element (the cis-element relevant to the expression of the alpha-SMA gene and growth-associated genes).	Acetylcysteine	29-32	actin gamma 2, smooth muscle	Rattus norvegicus	71-80
10203358-8	1999	The induction of hillocks by NAC was correlated with downregulation of alpha-SMA as well as attenuated activity of the CArG box element (the cis-element relevant to the expression of the alpha-SMA gene and growth-associated genes).	Acetylcysteine	29-32	actin gamma 2, smooth muscle	Rattus norvegicus	187-196
9747510-9	1998	In contrast to OP, N-acetylcysteine (NAC), an antioxidant and membrane-permeable reducing reagent, enhanced the HO-1 mRNA elevation induced by hyperoxia, although NAC inhibited the mRNA elevation induced by NaAsO2, CdCl2 and H2O2.	Acetylcysteine	19-35	heme oxygenase 1	Homo sapiens	112-116
9747510-9	1998	In contrast to OP, N-acetylcysteine (NAC), an antioxidant and membrane-permeable reducing reagent, enhanced the HO-1 mRNA elevation induced by hyperoxia, although NAC inhibited the mRNA elevation induced by NaAsO2, CdCl2 and H2O2.	Acetylcysteine	37-40	heme oxygenase 1	Homo sapiens	112-116
34482039-12	2021	CONCLUSIONS: Reversible alteration of mRNA levels by removing morphine from culture medium, and effect of NAC in co-treatment of morphine plus NAC, emphasize the role of reactive oxygen species in down-regulation of the expression of hTERT and TERF2 by morphine.	Acetylcysteine	143-146	telomerase reverse transcriptase	Homo sapiens	234-239
24299490-0	2014	N-acetyl-L-cysteine protects against cadmium-induced neuronal apoptosis by inhibiting ROS-dependent activation of Akt/mTOR pathway in mouse brain.	Acetylcysteine	0-19	mechanistic target of rapamycin kinase	Mus musculus	118-122
34098069-5	2021	Elevated ROS and NLRP3, caspase-1, IL-1beta and IL-18 were detected, which was attenuated by N-acetylcysteine.	Acetylcysteine	93-109	interleukin 1 alpha	Homo sapiens	35-43
9726445-7	1998	Both IL-8 and MIP-2 secretion were inhibited, although to varying degrees, by such antioxidants as TMTU, DMSO, catalase, and N-acetylcysteine.	Acetylcysteine	125-141	C-X-C motif chemokine ligand 2	Homo sapiens	14-19
24299490-9	2014	Furthermore, Cd-induced activation of Akt/mTOR pathway in the brain was also inhibited by NAC.	Acetylcysteine	90-93	mechanistic target of rapamycin kinase	Mus musculus	42-46
34478580-9	2021	Scavenging of ROS by N-acetylcysteine treatment could restore the decreased lipid accumulation of CELSR2 knockdown cells.	Acetylcysteine	21-37	cadherin, EGF LAG seven-pass G-type receptor 2	Mus musculus	98-104
34684414-8	2021	Moreover, NAC and ALA augmented the expression of GLUT4 and the phosphorylation state of Akt (Ser473) and GSK3beta (Ser9), which improved the intracellular insulin transduction pathway.	Acetylcysteine	10-13	solute carrier family 2 member 4	Rattus norvegicus	50-55
34531444-8	2021	The effect was rescued by antioxidant, N-acetyl cysteine, thereby implying a ROS-specific effect and in the trophoblast cells, OS triggers UPR pathway through IRE1alpha-XBP1 axis.	Acetylcysteine	39-56	X-box binding protein 1	Homo sapiens	169-173
9766835-4	1998	NAC treatment raised nerve glutathione levels compared to untreated nerves, as indicated using hemeoxygenase-1 (hsp32) immunoreactivity as a marker of glutathione depletion.	Acetylcysteine	0-3	heme oxygenase 1	Homo sapiens	112-117
24299490-11	2014	CONCLUSIONS: NAC protects against Cd-induced neuronal apoptosis in mouse brain partially by inhibiting ROS-dependent activation of Akt/mTOR pathway.	Acetylcysteine	13-16	mechanistic target of rapamycin kinase	Mus musculus	135-139
9564042-5	1998	Treatment of cells with N-acetyl-L-cysteine also inhibited serum withdrawal-, TNF-alpha- and hydrogen peroxide-induced activation of ASK1 as well as apoptosis.	Acetylcysteine	24-43	mitogen-activated protein kinase kinase kinase 5	Homo sapiens	133-137
34588976-10	2021	NAC also activated Sirt1 and preserved its protein level and subsequently promoted mitochondria biogenesis via deacetylating PGC1a.	Acetylcysteine	0-3	sirtuin 1	Mus musculus	19-24
34479474-9	2021	NAC could inhibit cell migration and invasion, elevate E-cadherin expression, the ratio of CD3+, CD4+, CD8+ and CD4+/CD8+T lymphocytes, and levels of IgG, IgA, and IgM, and reduce N-cadherin expression and levels of IL-6 and TNF-alpha in CSE cells and serum of COPD rats.	Acetylcysteine	0-3	cadherin 1	Rattus norvegicus	55-65
25052713-7	2014	NAC or ALC also dramatically lessened PINK1 level and mitochondrial accumulation of Parkin, indicating that ROS were related to PINK1/Parkin pathway.	Acetylcysteine	0-3	PTEN induced putative kinase 1	Mus musculus	38-43
34479474-9	2021	NAC could inhibit cell migration and invasion, elevate E-cadherin expression, the ratio of CD3+, CD4+, CD8+ and CD4+/CD8+T lymphocytes, and levels of IgG, IgA, and IgM, and reduce N-cadherin expression and levels of IL-6 and TNF-alpha in CSE cells and serum of COPD rats.	Acetylcysteine	0-3	cadherin 2	Rattus norvegicus	180-190
9518655-3	1998	Addition of N-acetyl-l-cysteine to the culture medium reduced the increment of MT-I/II in trisomy 16 cortical cells.	Acetylcysteine	12-31	metallothionein 3	Mus musculus	79-86
9692114-0	1998	N-acetylcysteine inhibits IL-1 alpha-induced IL-8 secretion by bronchial epithelial cells.	Acetylcysteine	0-16	interleukin 1 alpha	Homo sapiens	26-36
34575651-7	2021	NAC induces necrosis but suppresses annexin V-detected apoptosis in oral cancer cells.	Acetylcysteine	0-3	annexin A5	Homo sapiens	36-45
25052713-7	2014	NAC or ALC also dramatically lessened PINK1 level and mitochondrial accumulation of Parkin, indicating that ROS were related to PINK1/Parkin pathway.	Acetylcysteine	0-3	PTEN induced putative kinase 1	Mus musculus	128-133
24970110-6	2014	N-Acetylcysteine also resulted in an elevation of superoxide dismutase, glutathione peroxidase, glutathione reductase activities, as well as non-protein thiols, and total reactive antioxidant potential levels, which were decreased after aspartame exposure.	Acetylcysteine	0-16	glutathione-disulfide reductase	Rattus norvegicus	96-117
17657622-4	1998	NAC alone caused a marked reduction in the mortality rate of PCM-treated mice and a sharp drop in their plasma AST and ALT activities to near normal values.	Acetylcysteine	0-3	solute carrier family 17 (anion/sugar transporter), member 5	Mus musculus	111-114
17657622-4	1998	NAC alone caused a marked reduction in the mortality rate of PCM-treated mice and a sharp drop in their plasma AST and ALT activities to near normal values.	Acetylcysteine	0-3	glutamic pyruvic transaminase, soluble	Mus musculus	119-122
34440609-11	2021	Scavenging ROS via N-acetylcysteine (NAC) reversed CB-2-induced autophagy inhibition and its inhibitory effect against A549 cells.	Acetylcysteine	19-35	cannabinoid receptor 2	Homo sapiens	51-55
24970110-8	2014	Furthermore, catalase and glutathione S-transferase, whose activities were reduced due to aspartame treatment, remained decreased even after N-acetylcysteine exposure.	Acetylcysteine	141-157	hematopoietic prostaglandin D synthase	Rattus norvegicus	26-51
34440609-11	2021	Scavenging ROS via N-acetylcysteine (NAC) reversed CB-2-induced autophagy inhibition and its inhibitory effect against A549 cells.	Acetylcysteine	37-40	cannabinoid receptor 2	Homo sapiens	51-55
25177911-8	2014	Furthermore, compared with the IH group, antioxidant (NAC) pretreatment significantly decreased IH-mediated beta-cell apoptosis and reversed the ratio of Bcl-2/Bax expression (P&lt;0.05).	Acetylcysteine	54-57	BCL2 associated X, apoptosis regulator	Rattus norvegicus	160-163
34753839-9	2021	NAC incorporated at a concentration of 2.5 mM showed higher mineralization and considerably increased gene expression levels of runt-related transcription factor 2 (RUNX2), COL1A1, DSPP, and DMP-1.	Acetylcysteine	0-3	dentin matrix acidic phosphoprotein 1	Homo sapiens	191-196
25438539-10	2014	NAC was also found to suppress the levels of GRP78, PERK and CHOP expression in NaF-treated cells (p&lt;0.01).	Acetylcysteine	0-3	DNA-damage inducible transcript 3	Rattus norvegicus	61-65
34254625-5	2021	Using human hepatocellular carcinoma (HepG2) cells, we confirmed that the interaction between dynamin-related protein 1 (DRP1)-dependent mitochondrial fission and oxidative stress promoted mitochondrial damage and mitochondria-dependent apoptosis induced by AgNPs, as determined by the elimination of DRP1 or addition of N-acetylcysteine (NAC).	Acetylcysteine	321-337	dynamin 1 like	Homo sapiens	94-119
34475984-5	2021	The inhibition of ROS generation by N-acetyl-l-cysteine not only recovered cell migration and viability, but also reduced beta-catenin accumulation and JNK and ERK activation.	Acetylcysteine	36-55	catenin beta 1	Homo sapiens	122-134
25086357-9	2014	In addition, we observed reactive oxygen species (ROS) scavenger N-acetyl-l-cysteine reversed the down-regulation of CBS and H2S generation caused by rotenone in microglia.	Acetylcysteine	65-84	cystathionine beta-synthase	Mus musculus	117-120
34307672-8	2021	Besides, NAC (N-acetylcysteine), a potent ROS scavenger, significantly inhibited the PICK1-silencing-induced apoptosis.	Acetylcysteine	9-12	protein interacting with PRKCA 1	Homo sapiens	85-90
34307672-8	2021	Besides, NAC (N-acetylcysteine), a potent ROS scavenger, significantly inhibited the PICK1-silencing-induced apoptosis.	Acetylcysteine	14-30	protein interacting with PRKCA 1	Homo sapiens	85-90
34120018-4	2021	This study explores how the cystine/glutamate transporter xCT may mediate N-acetylcysteine uptake and how N-acetylcysteine alters placental redox status.	Acetylcysteine	74-90	solute carrier family 7 member 11	Homo sapiens	58-61
34120018-5	2021	METHODS: The involvement of xCT in NAC uptake by the human placenta was studied in perfused placenta and Xenopus oocytes.	Acetylcysteine	35-38	solute carrier family 7 member 11	Homo sapiens	28-31
34120018-8	2021	RESULTS: Maternoplacental N-acetylcysteine administration stimulated intracellular glutamate efflux suggesting a role of the exchange transporter xCT, which was localised to the microvillous membrane of the placental syncytiotrophoblast.	Acetylcysteine	26-42	solute carrier family 7 member 11	Homo sapiens	146-149
34120018-11	2021	DISCUSSION: This study suggests that xCT mediates N-acetylcysteine uptake into the placenta and that N-acetylcysteine treatment of placental tissue alters the placental proteome while regulating the redox sensitive Maxi-chloride channel.	Acetylcysteine	50-66	solute carrier family 7 member 11	Homo sapiens	37-40
34213003-10	2021	Histopathological injury score, plasma MPO, AST, ALT, tissue MPO and tissue MDA values were statistically significantly lower in the treatment groups, prominently in the levosimendan and NAS combination group concerning liver histopathological damage.	Acetylcysteine	187-190	myeloperoxidase	Rattus norvegicus	39-42
34213003-10	2021	Histopathological injury score, plasma MPO, AST, ALT, tissue MPO and tissue MDA values were statistically significantly lower in the treatment groups, prominently in the levosimendan and NAS combination group concerning liver histopathological damage.	Acetylcysteine	187-190	myeloperoxidase	Rattus norvegicus	61-64
34202008-2	2021	As sulforaphane N-acetylcysteine (SFN-NAC), a major sulforaphane metabolite, has presented similar pharmacological activities to those of SFN, it is crucial to simultaneously analyze the pharmacokinetics and activities of SFN and SFN-NAC, to comprehensively elucidate the efficacy of SFN-containing products.	Acetylcysteine	16-32	synuclein alpha	Homo sapiens	38-41
34172808-5	2021	MCT4 expression in the cell lines is suppressed by N-acetyl-L-cysteine.	Acetylcysteine	51-70	solute carrier family 16 member 3	Homo sapiens	0-4
34103686-7	2021	CDCA2 depletion contributes to the suppression of cell proliferation and induction of apoptosis due to reactive oxygen species (ROS)-mediated stress, which can be reversed by antioxidants N-acetyl cysteine (NAC) and glutathione (GSH).	Acetylcysteine	188-205	cell division cycle associated 2	Homo sapiens	0-5
34103686-7	2021	CDCA2 depletion contributes to the suppression of cell proliferation and induction of apoptosis due to reactive oxygen species (ROS)-mediated stress, which can be reversed by antioxidants N-acetyl cysteine (NAC) and glutathione (GSH).	Acetylcysteine	207-210	cell division cycle associated 2	Homo sapiens	0-5
34064109-4	2021	Inhibition of apigenin-induced reactive oxygen species (ROS) generation by a ROS scavenger N-acetyl-L-cysteine blocked the lipid raft membrane localization and activation of ASM and formation of ceramide-enriched lipid raft membranes, returned PI3K-Akt-GTP-Rac1-modulated CDK1-cyclin B1 activity, and subsequently restored the BCL-2/BCL-xL-regulated ER-mitochondrial bioenergetic activity.	Acetylcysteine	91-110	cyclin dependent kinase 1	Homo sapiens	272-276
34064109-4	2021	Inhibition of apigenin-induced reactive oxygen species (ROS) generation by a ROS scavenger N-acetyl-L-cysteine blocked the lipid raft membrane localization and activation of ASM and formation of ceramide-enriched lipid raft membranes, returned PI3K-Akt-GTP-Rac1-modulated CDK1-cyclin B1 activity, and subsequently restored the BCL-2/BCL-xL-regulated ER-mitochondrial bioenergetic activity.	Acetylcysteine	91-110	cyclin B1	Homo sapiens	277-286
35446108-8	2022	Cells that were treated with ROS scavengers, N-acetyl-L-cysteine or MitoQ, significantly reduced the amount of ROS and Tau dimerization, indicating the involvement of oxidative stress in Tau aggregation.	Acetylcysteine	45-64	microtubule associated protein tau	Homo sapiens	119-122
35446108-8	2022	Cells that were treated with ROS scavengers, N-acetyl-L-cysteine or MitoQ, significantly reduced the amount of ROS and Tau dimerization, indicating the involvement of oxidative stress in Tau aggregation.	Acetylcysteine	45-64	microtubule associated protein tau	Homo sapiens	187-190
35636015-14	2022	Treatment with N-Acetylcysteine (NAC), a ROS scavenger or the autophagy inhibitor 3-Methyladenine (3-MA) abolished the decreased malignant phenotypes in TRIM22 overexpressing OS cells.	Acetylcysteine	15-31	tripartite motif containing 22	Homo sapiens	153-159
35636015-14	2022	Treatment with N-Acetylcysteine (NAC), a ROS scavenger or the autophagy inhibitor 3-Methyladenine (3-MA) abolished the decreased malignant phenotypes in TRIM22 overexpressing OS cells.	Acetylcysteine	33-36	tripartite motif containing 22	Homo sapiens	153-159
35098531-2	2022	The publication of an academic RCT (n=83) reporting oral (N)-acetylcysteine (NAC) to reduce CIN led to >70 clinical trials, 23 systematic reviews, and two large RCTs showing no benefit.	Acetylcysteine	57-75	synuclein alpha	Homo sapiens	77-80
35567930-8	2022	In addition, N-acetylcysteine, a well-known antioxidant, led to decrease in oxidative markers induced by BaP.	Acetylcysteine	13-29	prohibitin 2	Mus musculus	105-108
35629355-8	2022	Pretreatment with N-acetylcysteine (NAC) reduced Apl-1-induced mitochondria-dependent apoptosis and preserved the expression of NOX, HO-1, and HIF-1a.	Acetylcysteine	18-34	acireductone dioxygenase 1	Homo sapiens	49-54
35629355-8	2022	Pretreatment with N-acetylcysteine (NAC) reduced Apl-1-induced mitochondria-dependent apoptosis and preserved the expression of NOX, HO-1, and HIF-1a.	Acetylcysteine	18-34	heme oxygenase 1	Homo sapiens	133-137
35629355-8	2022	Pretreatment with N-acetylcysteine (NAC) reduced Apl-1-induced mitochondria-dependent apoptosis and preserved the expression of NOX, HO-1, and HIF-1a.	Acetylcysteine	36-39	acireductone dioxygenase 1	Homo sapiens	49-54
35629355-8	2022	Pretreatment with N-acetylcysteine (NAC) reduced Apl-1-induced mitochondria-dependent apoptosis and preserved the expression of NOX, HO-1, and HIF-1a.	Acetylcysteine	36-39	heme oxygenase 1	Homo sapiens	133-137
35498131-11	2022	N-Acetyl-L-cysteine (NAC) administration also inhibited oxidative stress and activation of the calpain system and the NLRP3 inflammasome.	Acetylcysteine	0-19	NLR family, pyrin domain containing 3	Mus musculus	118-123
35498131-11	2022	N-Acetyl-L-cysteine (NAC) administration also inhibited oxidative stress and activation of the calpain system and the NLRP3 inflammasome.	Acetylcysteine	21-24	NLR family, pyrin domain containing 3	Mus musculus	118-123
34653248-6	2022	Although Gpr109a-/- T cells did not exhibit immune deficits at steady state, following allo-activation Gpr109a-/- T cells underwent increased apoptosis and had impaired mitochondrial oxidative phosphorylation, which was reversible through antioxidant treatment with N-acetyl cysteine (NAC).	Acetylcysteine	266-283	hydroxycarboxylic acid receptor 2	Mus musculus	103-110
34653248-6	2022	Although Gpr109a-/- T cells did not exhibit immune deficits at steady state, following allo-activation Gpr109a-/- T cells underwent increased apoptosis and had impaired mitochondrial oxidative phosphorylation, which was reversible through antioxidant treatment with N-acetyl cysteine (NAC).	Acetylcysteine	285-288	hydroxycarboxylic acid receptor 2	Mus musculus	103-110
35396503-13	2022	However, the ROS inhibitor N-acetylcysteine (NAC) promoted the protective effect of TUG1 knockdown on H/R-induced cardiomyocyte damage.	Acetylcysteine	27-43	taurine upregulated gene 1	Mus musculus	84-88
35396503-13	2022	However, the ROS inhibitor N-acetylcysteine (NAC) promoted the protective effect of TUG1 knockdown on H/R-induced cardiomyocyte damage.	Acetylcysteine	45-48	taurine upregulated gene 1	Mus musculus	84-88
34982346-9	2022	ET-1 mediated mRNA expression of GAG synthesizing enzymes C4ST-1 and ChSy-1 was also blocked by TGBFR1 antagonists, SB431542, broad spectrum ET receptor antagonist bosentan, DPI and ROS scavenger N-acetyl-L-cysteine.	Acetylcysteine	196-215	carbohydrate sulfotransferase 11	Homo sapiens	58-64
35270009-10	2022	Furthermore, pretreatment of cells with SP600125 (JNK inhibitor; 10 muM) or NAC (1 mM) or transfection with JNK-specific siRNA obviously attenuated the MeHg-induced JNK phosphorylation, CHOP and XBP-1 protein expression, apoptotic events, and insulin secretion dysfunction.	Acetylcysteine	76-79	mitogen-activated protein kinase 8	Rattus norvegicus	165-168
35270009-10	2022	Furthermore, pretreatment of cells with SP600125 (JNK inhibitor; 10 muM) or NAC (1 mM) or transfection with JNK-specific siRNA obviously attenuated the MeHg-induced JNK phosphorylation, CHOP and XBP-1 protein expression, apoptotic events, and insulin secretion dysfunction.	Acetylcysteine	76-79	DNA-damage inducible transcript 3	Rattus norvegicus	186-190
35270009-10	2022	Furthermore, pretreatment of cells with SP600125 (JNK inhibitor; 10 muM) or NAC (1 mM) or transfection with JNK-specific siRNA obviously attenuated the MeHg-induced JNK phosphorylation, CHOP and XBP-1 protein expression, apoptotic events, and insulin secretion dysfunction.	Acetylcysteine	76-79	X-box binding protein 1	Rattus norvegicus	195-200
35270009-11	2022	NAC significantly inhibited MeHg-activated JNK signaling, but SP600125 could not effectively reduce MeHg-induced ROS generation.	Acetylcysteine	0-3	mitogen-activated protein kinase 8	Rattus norvegicus	43-46
35023144-11	2022	In beagle models that received TmLRP, HSP70, NLRP3, Caspase-1, IL-1beta, and IL-18 were highly expressed in the wound tissue or urine, and could also be reduced by NAC pretreatment.	Acetylcysteine	164-167	interleukin 1 alpha	Homo sapiens	63-71
9353266-7	1997	Additional treatment with the antioxidant and GSH precursor N-acetylcysteine resulted in partial restoration of intracellular GSH levels and in reduced induction of CD95 ligand mRNA.	Acetylcysteine	60-76	Fas cell surface death receptor	Homo sapiens	165-169
9353266-8	1997	Induction of CD95 ligand mRNA by bleomycin was further reduced by combined treatment with N-acetylcysteine and deferoxamine.	Acetylcysteine	90-106	Fas cell surface death receptor	Homo sapiens	13-17
9374724-8	1997	The antioxidant N-acetyl-L-cysteine markedly inhibited SNN-induced HO-1 mRNA expression, whereas peroxynitrite did not induce HO-1 expression in aSMC.	Acetylcysteine	16-35	heme oxygenase 1	Homo sapiens	67-71
9351437-10	1997	Pretreatment of cells with 500 mumol/L NAC for 1 hour attenuated approximately 50% of Aug II-induced JNK activation, suggesting that ROIs, at least partially, mediate Ang II-induced JNK activation.	Acetylcysteine	39-42	mitogen-activated protein kinase 8	Rattus norvegicus	101-104
9351437-10	1997	Pretreatment of cells with 500 mumol/L NAC for 1 hour attenuated approximately 50% of Aug II-induced JNK activation, suggesting that ROIs, at least partially, mediate Ang II-induced JNK activation.	Acetylcysteine	39-42	mitogen-activated protein kinase 8	Rattus norvegicus	182-185
9351437-11	1997	Furthermore, 12-HETE-induced JNK activation was reduced by approximately 90% by NAC.	Acetylcysteine	80-83	mitogen-activated protein kinase 8	Rattus norvegicus	29-32
9231700-5	1997	Both NAC and cimetidine caused a partial improvement of survival rate, plasma GOT and GPT activities.	Acetylcysteine	5-8	glutamic pyruvic transaminase, soluble	Mus musculus	86-89
9231700-7	1997	However, concomitant administration of NAC and cimetidine produced a 100% survival rate and a marked reduction in plasma GOT and GPT activities to within the normal range, while significantly raising hepatic GSH concentrations to values close to those measured in saline-treated control animals.	Acetylcysteine	39-42	glutamic pyruvic transaminase, soluble	Mus musculus	129-132
8981050-4	1997	The PQ-enhanced, NAC-inhibited release of arachidonic acid (AA) by alveolar epithelial type II cells did, however, explain our in vivo results, when one assumes that the AM synthesize their 5-lipoxygenase products from alveolar epithelial cell-derived AA, an hypothesis demonstrated already by other researchers.	Acetylcysteine	17-20	arachidonate 5-lipoxygenase	Rattus norvegicus	190-204
9011676-10	1997	Among the ischemia groups, the human thioredoxin group showed significantly higher arterial oxygen tension at 30, 60, and 90 minutes after reperfusion than the control group, although there was no significant difference between the N-acetylcysteine and control groups.	Acetylcysteine	232-248	thioredoxin	Homo sapiens	37-48
34972717-7	2022	Maspin protein expression decreased after treatment with paclitaxel and NAC.	Acetylcysteine	72-75	serpin family B member 5	Homo sapiens	0-6
24976129-6	2014	In addition, the N-acetylcysteine inhibited ROS/RNS generation, elevation of antioxidants level, expression of ERK1/2, Akt, tuberin phosphorylation, resulted in deceased 8-OHdG accumulation and upregulation of OGG1 protein expression suggesting no involvement of Akt and ERK1/2MAPK pathways after CEES and LPS challenge.	Acetylcysteine	17-33	TSC complex subunit 2	Mus musculus	124-131
8806670-2	1996	In response to stimulation with hydrogen peroxide (100-400 microM), gene expression of HB-EGF and AR increased in a dose-dependent manner, peaked at 3 h, and returned to the base line at 7 h. Hydrogen peroxide-induced HB-EGF and AR gene expression was blocked by pretreatment with an antioxidant N-acetyl-cysteine.	Acetylcysteine	296-313	amphiregulin	Rattus norvegicus	98-100
25157234-4	2014	The cytotoxicity of these GSH conjugates depends essentially on GST and gamma-glutamyl transferases (gammaGT), the enzymes which initiate the mercapturic acid synthesis pathway.	Acetylcysteine	142-158	glutathione S-transferase kappa 1	Homo sapiens	64-67
8555406-1	1995	The sulfoxidation of the mercapturic acid N-acetyl-S-(1,2,3,4,4-pentachlorobuta-1,3-dienyl)-L-cysteine (N-Ac-PCBC), a urinary metabolite of the renal toxin hexachlorobutadiene (HCBD), was studied in human liver microsomes and with purified cDNA expressed human liver cytochrome P450 (P450) enzymes.	Acetylcysteine	25-41	EPH receptor B2	Homo sapiens	109-113
7755283-7	1995	Treatment of C2C12 cells with H2O2 induces a dose-dependent increase in c-jun/c-fos heterodimer binding, specifically reverted by the cysteine derivative and glutathione precursor N-acetyl-L-cysteine (NAC).	Acetylcysteine	180-199	FBJ osteosarcoma oncogene	Mus musculus	78-83
24684653-7	2014	Mitochondria appear fragmented and depolarized in GSNOR-KO myofibers and myotubes, conditions that are reverted by N-acetylcysteine treatment.	Acetylcysteine	115-131	alcohol dehydrogenase 5 (class III), chi polypeptide	Mus musculus	50-55
7755283-7	1995	Treatment of C2C12 cells with H2O2 induces a dose-dependent increase in c-jun/c-fos heterodimer binding, specifically reverted by the cysteine derivative and glutathione precursor N-acetyl-L-cysteine (NAC).	Acetylcysteine	201-204	FBJ osteosarcoma oncogene	Mus musculus	78-83
7841193-6	1995	N-Acetylcysteine inhibited IL1-induced interleukin-2 in EL4, however, demonstrating that N-acetylcysteine was biologically active.	Acetylcysteine	0-16	interleukin 2	Mus musculus	39-52
24824652-6	2014	An antioxidant, N-acetyl-L-cysteine (NAC), prevented IH-induced hepatic insulin resistance in parallel with prevention of decreased IkappaBalpha content, increased JNK phosphorylation (markers of IKKbeta and JNK activation, respectively), increased serine phosphorylation of IRS-1 and IRS-2, and impaired insulin signaling in the liver without affecting IH-induced hepatic PKCdelta activation.	Acetylcysteine	16-35	NFKB inhibitor alpha	Rattus norvegicus	132-144
7967675-10	1994	Thus it would appear that human thioredoxin has a protective effect on transplanted lungs, as does N-acetylcysteine, and that its action may be a radical scavenger effect.	Acetylcysteine	99-115	thioredoxin	Homo sapiens	32-43
24824652-6	2014	An antioxidant, N-acetyl-L-cysteine (NAC), prevented IH-induced hepatic insulin resistance in parallel with prevention of decreased IkappaBalpha content, increased JNK phosphorylation (markers of IKKbeta and JNK activation, respectively), increased serine phosphorylation of IRS-1 and IRS-2, and impaired insulin signaling in the liver without affecting IH-induced hepatic PKCdelta activation.	Acetylcysteine	16-35	mitogen-activated protein kinase 8	Rattus norvegicus	164-167
7521369-10	1994	Activated NF-kappa B was apparent from 20 min and remained for up to 24 h. N-acetylcysteine (NAC) and pyrollidinedithiocarbamate (PDTC), which were shown to inhibit activation of NF-kappa B in Jurkat E6.1 lymphoblasts and EL4.NOB-1 thymoma, failed to block IL-1 activation of NF-kappa B in 1321N1 astrocytoma.	Acetylcysteine	75-91	NIN1 (RPN12) binding protein 1 homolog	Homo sapiens	226-231
7521369-10	1994	Activated NF-kappa B was apparent from 20 min and remained for up to 24 h. N-acetylcysteine (NAC) and pyrollidinedithiocarbamate (PDTC), which were shown to inhibit activation of NF-kappa B in Jurkat E6.1 lymphoblasts and EL4.NOB-1 thymoma, failed to block IL-1 activation of NF-kappa B in 1321N1 astrocytoma.	Acetylcysteine	75-91	interleukin 1 alpha	Homo sapiens	257-261
24824652-6	2014	An antioxidant, N-acetyl-L-cysteine (NAC), prevented IH-induced hepatic insulin resistance in parallel with prevention of decreased IkappaBalpha content, increased JNK phosphorylation (markers of IKKbeta and JNK activation, respectively), increased serine phosphorylation of IRS-1 and IRS-2, and impaired insulin signaling in the liver without affecting IH-induced hepatic PKCdelta activation.	Acetylcysteine	16-35	mitogen-activated protein kinase 8	Rattus norvegicus	208-211
7521369-10	1994	Activated NF-kappa B was apparent from 20 min and remained for up to 24 h. N-acetylcysteine (NAC) and pyrollidinedithiocarbamate (PDTC), which were shown to inhibit activation of NF-kappa B in Jurkat E6.1 lymphoblasts and EL4.NOB-1 thymoma, failed to block IL-1 activation of NF-kappa B in 1321N1 astrocytoma.	Acetylcysteine	93-96	NIN1 (RPN12) binding protein 1 homolog	Homo sapiens	226-231
7521369-10	1994	Activated NF-kappa B was apparent from 20 min and remained for up to 24 h. N-acetylcysteine (NAC) and pyrollidinedithiocarbamate (PDTC), which were shown to inhibit activation of NF-kappa B in Jurkat E6.1 lymphoblasts and EL4.NOB-1 thymoma, failed to block IL-1 activation of NF-kappa B in 1321N1 astrocytoma.	Acetylcysteine	93-96	interleukin 1 alpha	Homo sapiens	257-261
24824652-6	2014	An antioxidant, N-acetyl-L-cysteine (NAC), prevented IH-induced hepatic insulin resistance in parallel with prevention of decreased IkappaBalpha content, increased JNK phosphorylation (markers of IKKbeta and JNK activation, respectively), increased serine phosphorylation of IRS-1 and IRS-2, and impaired insulin signaling in the liver without affecting IH-induced hepatic PKCdelta activation.	Acetylcysteine	37-40	NFKB inhibitor alpha	Rattus norvegicus	132-144
24824652-6	2014	An antioxidant, N-acetyl-L-cysteine (NAC), prevented IH-induced hepatic insulin resistance in parallel with prevention of decreased IkappaBalpha content, increased JNK phosphorylation (markers of IKKbeta and JNK activation, respectively), increased serine phosphorylation of IRS-1 and IRS-2, and impaired insulin signaling in the liver without affecting IH-induced hepatic PKCdelta activation.	Acetylcysteine	37-40	mitogen-activated protein kinase 8	Rattus norvegicus	164-167
24824652-6	2014	An antioxidant, N-acetyl-L-cysteine (NAC), prevented IH-induced hepatic insulin resistance in parallel with prevention of decreased IkappaBalpha content, increased JNK phosphorylation (markers of IKKbeta and JNK activation, respectively), increased serine phosphorylation of IRS-1 and IRS-2, and impaired insulin signaling in the liver without affecting IH-induced hepatic PKCdelta activation.	Acetylcysteine	37-40	mitogen-activated protein kinase 8	Rattus norvegicus	208-211
7943258-5	1994	The decrease in NO2- and the increase in lipid peroxides in response to TNF were prevented by pretreatment (15 min prior to and throughout the incubation) with either calphostin C (1 microM; a specific PKC inhibitor) or the antioxidants N-acetylcysteine (1 mM), 4,5-dihydroxy-1,3-benzene disulfonic acid (Tiron) (10 mM), and superoxide dismutase (10 U/ml).	Acetylcysteine	237-253	tumor necrosis factor	Bos taurus	72-75
7943258-7	1994	Pretreatment with calphostin C or N-acetylcysteine prior to TNF (10 U/ml) revealed an increase in NO2- levels above control treatment.	Acetylcysteine	34-50	tumor necrosis factor	Bos taurus	60-63
24726884-8	2014	N-acetylcysteine (NAC), an antioxidant, suppressed the phosphorylation of ATM and p53 and, to a less extent, Chk2, but NAC increased the phosphorylation and nuclear foci formation of H2AX.	Acetylcysteine	0-16	transformation related protein 53, pseudogene	Mus musculus	82-85
24726884-8	2014	N-acetylcysteine (NAC), an antioxidant, suppressed the phosphorylation of ATM and p53 and, to a less extent, Chk2, but NAC increased the phosphorylation and nuclear foci formation of H2AX.	Acetylcysteine	18-21	transformation related protein 53, pseudogene	Mus musculus	82-85
24534112-5	2014	NAC significantly attenuated DOI-induced head twitch response and expression of c-Fos and Egr-2 in the infralimbic and motor cortex and suppressed the increase in the frequency of excitatory field potentials elicited by DOI in the medial prefrontal cortex.	Acetylcysteine	0-3	FBJ osteosarcoma oncogene	Mus musculus	80-85
8203575-8	1994	The peak lactate and the maximal tumor necrosis factor (TNF) levels were lower in the NAC than in the control group (5.2 +/- 0.4 vs. 7.6 +/- 0.4 mM, and 0.14 +/- 0.03 vs. 1.21 +/- 0.58 ng/ml, respectively; both P &lt; 0.01).	Acetylcysteine	86-89	tumor necrosis factor	Canis lupus familiaris	33-54
24534112-5	2014	NAC significantly attenuated DOI-induced head twitch response and expression of c-Fos and Egr-2 in the infralimbic and motor cortex and suppressed the increase in the frequency of excitatory field potentials elicited by DOI in the medial prefrontal cortex.	Acetylcysteine	0-3	early growth response 2	Mus musculus	90-95
8203575-8	1994	The peak lactate and the maximal tumor necrosis factor (TNF) levels were lower in the NAC than in the control group (5.2 +/- 0.4 vs. 7.6 +/- 0.4 mM, and 0.14 +/- 0.03 vs. 1.21 +/- 0.58 ng/ml, respectively; both P &lt; 0.01).	Acetylcysteine	86-89	tumor necrosis factor	Canis lupus familiaris	56-59
24500083-8	2014	Moreover, a regulatory role of ROS for HO-1 regulation in these cells is demonstrated by studies with the antioxidant N-acetylcysteine and exogenous hydrogenperoxide.	Acetylcysteine	118-134	heme oxygenase 1	Homo sapiens	39-43
8307954-9	1994	Insulin-mimicked H2O2 action, reducing the expression of both mRNAs, and N-acetylcysteine, which increases intracellular glutathione levels, completely reversed the insulin effect on both mRNAs and the H2O2 effect on CYP1A1 mRNA, but only partially reversed the H2O2 effect on CYP1A2 mRNA.	Acetylcysteine	73-89	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	217-223
8307954-9	1994	Insulin-mimicked H2O2 action, reducing the expression of both mRNAs, and N-acetylcysteine, which increases intracellular glutathione levels, completely reversed the insulin effect on both mRNAs and the H2O2 effect on CYP1A1 mRNA, but only partially reversed the H2O2 effect on CYP1A2 mRNA.	Acetylcysteine	73-89	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	277-283
24588654-6	2014	Moreover, treatment of NHEKs with Z-Ligustilide increased reactive oxygen species (ROS) and L-N-acetylcysteine (L-NAC, an antioxidant) attenuated Z-ligustilide-induced Nrf2 nuclear translocation and HO-1 expression.	Acetylcysteine	92-110	heme oxygenase 1	Homo sapiens	199-203
24588654-6	2014	Moreover, treatment of NHEKs with Z-Ligustilide increased reactive oxygen species (ROS) and L-N-acetylcysteine (L-NAC, an antioxidant) attenuated Z-ligustilide-induced Nrf2 nuclear translocation and HO-1 expression.	Acetylcysteine	112-117	heme oxygenase 1	Homo sapiens	199-203
24588654-7	2014	L-NAC or knock-down of Nrf2 significantly attenuated the inhibitory effects of Z-Ligustilide on BaP-induced CYP1A1 upregulation in NHEKs.	Acetylcysteine	0-5	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	108-114
24258150-6	2014	In the chemically induced SCC model, treatment of K14-Angptl2 Tg mice with the antioxidant N-acetyl cysteine (NAC) significantly reduced oxidative stress in skin tissue and the frequency of SCC development.	Acetylcysteine	91-108	keratin 14	Mus musculus	50-53
8370158-14	1993	The anti-tumour effect of haemin and IL-2 was enhanced (63% decrease in metastases) by administration of the thiol compound, N-acetylcysteine.	Acetylcysteine	125-141	interleukin 2	Mus musculus	37-41
8339252-14	1993	N-Acetylcysteine and taurine slightly but significantly increased only the GST activity in the liver.	Acetylcysteine	0-16	hematopoietic prostaglandin D synthase	Rattus norvegicus	75-78
8339559-6	1993	Because GST is the first enzyme in the mercapturic acid pathway, which detoxifies xenobiotic substrates including aldehydes, as by-products of membrane lipid peroxidation, an elevated GSH turnover might be necessary to counteract oxidative threats.	Acetylcysteine	39-55	glutathione S-transferase kappa 1	Homo sapiens	8-11
24258150-6	2014	In the chemically induced SCC model, treatment of K14-Angptl2 Tg mice with the antioxidant N-acetyl cysteine (NAC) significantly reduced oxidative stress in skin tissue and the frequency of SCC development.	Acetylcysteine	91-108	angiopoietin-like 2	Mus musculus	54-61
1581851-1	1992	N-Acetylcysteine (NAC) is protective against acetaminophen-induced hepatotoxicity primarily by providing precursor for the glutathione synthetase pathway, while cysteamine has been demonstrated to alter the cytochrome P-450 dependent formation of toxic acetaminophen metabolite.	Acetylcysteine	0-16	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	207-223
1581851-3	1992	Administration of cysteamine (100 mg/kg) or NAC (500 mg/kg) significantly reduced serum ALT activity (p less than 0.001).	Acetylcysteine	44-47	glutamic pyruvic transaminase, soluble	Mus musculus	88-91
24258150-6	2014	In the chemically induced SCC model, treatment of K14-Angptl2 Tg mice with the antioxidant N-acetyl cysteine (NAC) significantly reduced oxidative stress in skin tissue and the frequency of SCC development.	Acetylcysteine	110-113	keratin 14	Mus musculus	50-53
24258150-6	2014	In the chemically induced SCC model, treatment of K14-Angptl2 Tg mice with the antioxidant N-acetyl cysteine (NAC) significantly reduced oxidative stress in skin tissue and the frequency of SCC development.	Acetylcysteine	110-113	angiopoietin-like 2	Mus musculus	54-61
24477002-4	2014	We show that supplementing the diet with the antioxidants N-acetylcysteine (NAC) and vitamin E markedly increases tumor progression and reduces survival in mouse models of B-RAF- and K-RAS-induced lung cancer.	Acetylcysteine	58-74	Braf transforming gene	Mus musculus	172-177
1489511-3	1992	These conjugation reactions are catalyzed by several classes of glutathione-S-transferase isoenzymes and thus result in the urinary or biliary excretion of N-acetyl-L-cysteine-S-conjugates (mercapturic acids).	Acetylcysteine	156-177	glutathione S-transferase kappa 1	Homo sapiens	64-89
1489511-3	1992	These conjugation reactions are catalyzed by several classes of glutathione-S-transferase isoenzymes and thus result in the urinary or biliary excretion of N-acetyl-L-cysteine-S-conjugates (mercapturic acids).	Acetylcysteine	190-207	glutathione S-transferase kappa 1	Homo sapiens	64-89
24477002-4	2014	We show that supplementing the diet with the antioxidants N-acetylcysteine (NAC) and vitamin E markedly increases tumor progression and reduces survival in mouse models of B-RAF- and K-RAS-induced lung cancer.	Acetylcysteine	58-74	Kirsten rat sarcoma viral oncogene homolog	Mus musculus	183-188
24477002-4	2014	We show that supplementing the diet with the antioxidants N-acetylcysteine (NAC) and vitamin E markedly increases tumor progression and reduces survival in mouse models of B-RAF- and K-RAS-induced lung cancer.	Acetylcysteine	76-79	Braf transforming gene	Mus musculus	172-177
1928874-1	1991	STUDY OBJECTIVE: To determine the safety and efficacy of a 48-hour IV N-acetylcysteine (IV NAC) treatment protocol for acute acetaminophen overdose.	Acetylcysteine	70-86	synuclein alpha	Homo sapiens	91-94
24477002-4	2014	We show that supplementing the diet with the antioxidants N-acetylcysteine (NAC) and vitamin E markedly increases tumor progression and reduces survival in mouse models of B-RAF- and K-RAS-induced lung cancer.	Acetylcysteine	76-79	Kirsten rat sarcoma viral oncogene homolog	Mus musculus	183-188
24477002-6	2014	NAC and vitamin E increase tumor cell proliferation by reducing ROS, DNA damage, and p53 expression in mouse and human lung tumor cells.	Acetylcysteine	0-3	transformation related protein 53, pseudogene	Mus musculus	85-88
24239896-6	2014	In addition, the CM-mediated induction of HO-1 and activation of Nrf2 was abolished by acetylcysteine.	Acetylcysteine	87-101	heme oxygenase 1	Homo sapiens	42-46
1651705-4	1991	and optical spectroscopic studies show that the thiol-containing compounds N-(2-mercaptopropionyl) glycine and N-acetylcysteine and the trihydroxamate desferrioxamine attenuate these processes by reducing the ferryl myoglobin species to metmyoglobin, with the formation of thiyl radicals and the desferrioxamine nitroxide radical respectively.	Acetylcysteine	111-127	myoglobin	Homo sapiens	216-225
24157283-9	2014	Additionally, exposure of Neuro-2a cells to iAs triggered endoplasmic reticulum (ER) stress identified through several key molecules (GRP 78, CHOP, XBP-1, and caspase-12), which was prevented by NAC.	Acetylcysteine	195-198	DNA-damage inducible transcript 3	Mus musculus	142-146
25123250-16	2014	Both DHLA and NAC increased MMP-1 activity when SSc cells were stimulated with PDGF.	Acetylcysteine	14-17	matrix metallopeptidase 1	Homo sapiens	28-33
32796956-7	2021	Knockdown of IDH1 in NB4 cells caused the similar phenotype as GCN B treatment, and supplementation of N-acetylcysteine partially rescued the apoptosis caused by IDH1 interference in NB4 cells.	Acetylcysteine	103-119	isocitrate dehydrogenase (NADP(+)) 1	Homo sapiens	162-166
33775218-11	2021	BM-MNCs combination with NAC or ALA exerted significant antioxidant, anti-inflammatory and anti-cytogenetical aberrations effect compared to each of them alone.HighlightsCCl4 elevated ALT, AST, TNF-alpha, IL-6 and MDACCl4 reduced ALB, IL-10, SOD, CAT, GPx and TACCCl4 increased the number of DNA breaks in liverNAC, ALA and BM-MNCs reduced ALT, AST, while, increase albumin, CAT, TAC, GPx, SODNAC, ALA and BM-MNCs decreased in MDA, IL-6 and TNF-alpha and increased IL-10.	Acetylcysteine	25-28	interleukin 10	Rattus norvegicus	235-240
33775218-11	2021	BM-MNCs combination with NAC or ALA exerted significant antioxidant, anti-inflammatory and anti-cytogenetical aberrations effect compared to each of them alone.HighlightsCCl4 elevated ALT, AST, TNF-alpha, IL-6 and MDACCl4 reduced ALB, IL-10, SOD, CAT, GPx and TACCCl4 increased the number of DNA breaks in liverNAC, ALA and BM-MNCs reduced ALT, AST, while, increase albumin, CAT, TAC, GPx, SODNAC, ALA and BM-MNCs decreased in MDA, IL-6 and TNF-alpha and increased IL-10.	Acetylcysteine	25-28	interleukin 10	Rattus norvegicus	465-470
24817286-12	2014	Interestingly, NAC and DMT reduced ROS production and suppressed p53 activation in renal cells exposed to cisplatin.	Acetylcysteine	15-18	Wistar clone pR53P1 p53 pseudogene	Rattus norvegicus	65-68
23758132-6	2013	Treatment of RA PB T cells with the GSH precursor N-acetyl cysteine increased CD45 phosphatase activity and proliferation, while it decreased Lck kinase phosphorylation, which is regulated by CD45.	Acetylcysteine	50-67	LCK proto-oncogene, Src family tyrosine kinase	Homo sapiens	142-145
33763172-7	2021	On the contrary, overexpression of BECN1 or treating cells with the antioxidant N-acetylcysteine (NAC) could restore the survival of hTERT knockdown cells.	Acetylcysteine	80-96	telomerase reverse transcriptase	Homo sapiens	133-138
33763172-7	2021	On the contrary, overexpression of BECN1 or treating cells with the antioxidant N-acetylcysteine (NAC) could restore the survival of hTERT knockdown cells.	Acetylcysteine	98-101	telomerase reverse transcriptase	Homo sapiens	133-138
23948867-9	2013	Moreover N-acetyl cysteine and ascorbic acid mediated inhibition of EGFR and downstream signalling molecules indicate the involvement of reactive oxygen species.	Acetylcysteine	9-26	epidermal growth factor receptor	Mus musculus	68-72
33807834-7	2021	In terms of flow cytometry and Western blotting, PHA induced apoptotic expression (annexin V, and intrinsic and extrinsic apoptotic signaling), which was suppressed by NAC and an apoptosis inhibitor (Z-VAD-FMK), in breast cancer cells.	Acetylcysteine	168-171	annexin A5	Homo sapiens	83-92
24263157-4	2013	Administration of N-acetyl-L-cysteine, an inhibitor of reactive oxygen species, eliminated Ad-mda-7- and GA-mediated cytotoxicity.	Acetylcysteine	18-37	interleukin 24	Homo sapiens	94-99
32796068-7	2020	N-acetylcysteine (NAC), a strong antioxidant and ROS scavenger, abrogated DRP1-dependent mitochondrial fragmentation and neurite degeneration.	Acetylcysteine	0-16	dynamin 1 like	Homo sapiens	74-78
32796068-7	2020	N-acetylcysteine (NAC), a strong antioxidant and ROS scavenger, abrogated DRP1-dependent mitochondrial fragmentation and neurite degeneration.	Acetylcysteine	18-21	dynamin 1 like	Homo sapiens	74-78
24001789-10	2013	Antioxidative N-acetyl-cysteine (NAC) strongly inhibited the level of Egr-1 and phosphorylated ERK expression in ZnO-NPs treated cells.	Acetylcysteine	14-31	early growth response 1	Homo sapiens	70-75
26331632-5	2015	The addition of N-acetylcysteine (NAC), but not specific inhibitors of p38 (SB202190), PI3K (LY294002), and MEK1 (PD098059) attenuated AVA-induced HO-1 expression, demonstrating an important role for reactive oxygen species, but not PI3K or MAPK activation, in activating the HO-1 pathway.	Acetylcysteine	16-32	heme oxygenase 1	Homo sapiens	147-151
26331632-5	2015	The addition of N-acetylcysteine (NAC), but not specific inhibitors of p38 (SB202190), PI3K (LY294002), and MEK1 (PD098059) attenuated AVA-induced HO-1 expression, demonstrating an important role for reactive oxygen species, but not PI3K or MAPK activation, in activating the HO-1 pathway.	Acetylcysteine	16-32	heme oxygenase 1	Homo sapiens	276-280
24001789-10	2013	Antioxidative N-acetyl-cysteine (NAC) strongly inhibited the level of Egr-1 and phosphorylated ERK expression in ZnO-NPs treated cells.	Acetylcysteine	33-36	early growth response 1	Homo sapiens	70-75
23246962-8	2013	Concurrent administration of the ROS inhibitor N-acetylcysteine abrogated beta-catenin/HIF pathway activity and restored adenoma architecture.	Acetylcysteine	47-63	catenin beta 1	Homo sapiens	74-86
25264565-2	2015	The influence of genetic polymorphisms of NAT2, UGT1A1 and GSTP1 on generation of the terminal mercapturic acid derivatives and analgesic effects was evaluated to identify potential genetic risk factors for hepatotoxicity of flupirtine.	Acetylcysteine	95-111	glutathione S-transferase pi 1	Homo sapiens	59-64
21055460-10	2011	Taken together, our data suggest that the antiproliferative effect of NAC is partially mediated by intracellular ROS production, the inhibition of NF-kappaB activity, and the activation of PI3K- and/or MEK/Erk-related intracellular signaling pathways, which lead to up-regulation of Cyr61 expression.	Acetylcysteine	70-73	cellular communication network factor 1	Homo sapiens	283-288
34924003-9	2021	Using transcriptomic analysis to identify potential gene targets, we found that TMBIM1 was significantly upregulated upon NAC and GSH treatment.	Acetylcysteine	122-125	transmembrane BAX inhibitor motif containing 1	Mus musculus	80-86
23700228-8	2013	Emodin-induced induction of DR5 was mediated through the generation of reactive oxygen species (ROS), as N-acetylcysteine blocked the induction of DR5 and the induction of apoptosis.	Acetylcysteine	105-121	TNF receptor superfamily member 10b	Homo sapiens	28-31
34762904-7	2021	3-OH-NBP induced remarkable cell death and oxidative stresses in hepatocytes, which correlated well with the levels of glutathione and N-acetylcysteine adducts (3-GSH-NBP and 3-NAC-NBP) in cell supernatants.	Acetylcysteine	135-151	synuclein alpha	Homo sapiens	177-180
34899969-9	2021	Result: NAC could effectively improve the immune status of COPD patients as well as the COPD mouse model by downregulating proinflammation and inflammation cytokines including IL-1beta, interferon- (IFN-) gamma, tumor necrosis factor- (TNF-) alpha, and IL-18.	Acetylcysteine	8-11	interleukin 1 alpha	Mus musculus	176-184
23700228-8	2013	Emodin-induced induction of DR5 was mediated through the generation of reactive oxygen species (ROS), as N-acetylcysteine blocked the induction of DR5 and the induction of apoptosis.	Acetylcysteine	105-121	TNF receptor superfamily member 10b	Homo sapiens	147-150
23515941-7	2013	Finally, pretreatment with the antioxidant N-acetyl-L-cysteine (NAC) reduced the OTA-induced DNA DSBs, ATM phosphorylation, and G2 arrest.	Acetylcysteine	43-62	ATM serine/threonine kinase	Homo sapiens	103-106
34810128-8	2021	Inhibiting the production of ROS with a ROS scavenger N-acetyl-L-cysteine (NAC) attenuated the activation of NLRP3 inflammasome.	Acetylcysteine	54-73	NLR family, pyrin domain containing 3	Mus musculus	109-114
34810128-8	2021	Inhibiting the production of ROS with a ROS scavenger N-acetyl-L-cysteine (NAC) attenuated the activation of NLRP3 inflammasome.	Acetylcysteine	75-78	NLR family, pyrin domain containing 3	Mus musculus	109-114
25610275-10	2013	Erdosteine and NAC significantly reduced the local induction of bax and caspase 3 and significantly increased the reduced local production of bcl-2.	Acetylcysteine	15-18	BCL2 associated X, apoptosis regulator	Rattus norvegicus	64-67
34601074-8	2021	The transcript for IL-10 gene was significantly upregulated in all treatment regimens compared to SCI group, and was highest in HBO+NAC ones.	Acetylcysteine	132-135	interleukin 10	Rattus norvegicus	19-24
23747931-0	2013	N-Acetylcysteine and allopurinol up-regulated the Jak/STAT3 and PI3K/Akt pathways via adiponectin and attenuated myocardial postischemic injury in diabetes.	Acetylcysteine	0-16	signal transducer and activator of transcription 3	Rattus norvegicus	54-59
23747931-3	2013	We postulated that NAC and ALP attenuated diabetic MI/R injury by up-regulating phosphatidylinositol 3-kinase/Akt (PI3K/Akt) and Janus kinase 2/signal transducer and activator of transcription-3 (JAK2/STAT3) pathways subsequent to adiponectin (APN) activation.	Acetylcysteine	19-22	phosphatidylinositol-4,5-bisphosphate 3-kinase, catalytic subunit gamma	Rattus norvegicus	115-123
23747931-3	2013	We postulated that NAC and ALP attenuated diabetic MI/R injury by up-regulating phosphatidylinositol 3-kinase/Akt (PI3K/Akt) and Janus kinase 2/signal transducer and activator of transcription-3 (JAK2/STAT3) pathways subsequent to adiponectin (APN) activation.	Acetylcysteine	19-22	signal transducer and activator of transcription 3	Rattus norvegicus	201-206
23747931-6	2013	NAC and ALP decreased MI/R injury in D rats, enhanced phosphorylation of Akt and STAT3, and increased NO and APN.	Acetylcysteine	0-3	signal transducer and activator of transcription 3	Rattus norvegicus	81-86
23747931-7	2013	High glucose and hypoxia/reoxygenation exposure induced cell death and Akt and STAT3 inactivation in cultured cardiomyocytes, which were prevented by NAC and ALP.	Acetylcysteine	150-153	signal transducer and activator of transcription 3	Rattus norvegicus	79-84
34749650-10	2021	N-acetyl-L-cysteine (NAC) reversed the DI effect on the LPS + ATP-induced macrophage pyroptosis and upregulated the IL-1beta expression.	Acetylcysteine	0-19	interleukin 1 alpha	Homo sapiens	116-124
23747931-10	2013	Gene silencing with AdipoR2 siRNA or STAT3 siRNA but not AdipoR1 siRNA abolished the protection of NAC and ALP.	Acetylcysteine	99-102	adiponectin receptor 2	Rattus norvegicus	20-27
34749650-10	2021	N-acetyl-L-cysteine (NAC) reversed the DI effect on the LPS + ATP-induced macrophage pyroptosis and upregulated the IL-1beta expression.	Acetylcysteine	21-24	interleukin 1 alpha	Homo sapiens	116-124
23747931-10	2013	Gene silencing with AdipoR2 siRNA or STAT3 siRNA but not AdipoR1 siRNA abolished the protection of NAC and ALP.	Acetylcysteine	99-102	signal transducer and activator of transcription 3	Rattus norvegicus	37-42
23747931-11	2013	In conclusion, NAC and ALP prevented diabetic MI/R injury through PI3K/Akt and Jak2/STAT3 and cardiac APN may serve as a mediator via AdipoR2 in this process.	Acetylcysteine	15-18	signal transducer and activator of transcription 3	Rattus norvegicus	84-89
23747931-11	2013	In conclusion, NAC and ALP prevented diabetic MI/R injury through PI3K/Akt and Jak2/STAT3 and cardiac APN may serve as a mediator via AdipoR2 in this process.	Acetylcysteine	15-18	adiponectin receptor 2	Rattus norvegicus	134-141
22532030-1	2013	This study determined whether N-acetylcysteine (NAC) could affect intestinal redox status, proinflammatory cytokines, epidermal growth factor (EGF), EGF receptor (EGFR), Toll-like receptor-4 (TLR4), and aquaporin-8 in a lipopolysaccharide (LPS)-challenged piglet model.	Acetylcysteine	48-51	epidermal growth factor	Homo sapiens	118-141
34732600-1	2022	OBJECTIVE: To examine N-acetylcysteine"s (NAC"s) renoprotective effect in adult cardiac surgeryMethods: PubMed, Ovid Medline, and Embase were searched for randomized controlled trials published between January 1990 and May 2021 that investigated the effect of NAC in preventing acute kidney injury (AKI) in patients undergoing cardiac surgery.	Acetylcysteine	22-38	synuclein alpha	Homo sapiens	42-45
34732600-1	2022	OBJECTIVE: To examine N-acetylcysteine"s (NAC"s) renoprotective effect in adult cardiac surgeryMethods: PubMed, Ovid Medline, and Embase were searched for randomized controlled trials published between January 1990 and May 2021 that investigated the effect of NAC in preventing acute kidney injury (AKI) in patients undergoing cardiac surgery.	Acetylcysteine	22-38	synuclein alpha	Homo sapiens	260-263
34739934-8	2021	The findings demonstrated that NAC relieved NiCl2-induced autophagy and reversed the activation of Akt/AMPK/mTOR pathway.	Acetylcysteine	31-34	mechanistic target of rapamycin kinase	Mus musculus	108-112
22532030-9	2013	Moreover, NAC prevented LPS-induced increases in abundances of intestinal HSP70 and NF-kappaB p65 proteins and TLR4 mRNA.	Acetylcysteine	10-13	toll like receptor 4	Homo sapiens	111-115
22532030-10	2013	NAC supplementation enhanced plasma EGF concentration and intestinal EGFR mRNA levels.	Acetylcysteine	0-3	epidermal growth factor	Homo sapiens	36-39
24037197-7	2013	NAC treatment of ECwt-infected mice reduced Hsc70 and PDI expression to levels similar to those observed in villi from uninfected control mice.	Acetylcysteine	0-3	protein disulfide isomerase associated 3	Mus musculus	54-57
24001404-16	2013	CONCLUSION: Dietary supplementation with NAC can alleviate AA-induced colitis in a porcine model through regulating anti-oxidative responses, cell apoptosis, and EGF gene expression.	Acetylcysteine	41-44	epidermal growth factor	Homo sapiens	162-165
34815794-2	2021	Although N-acetylcysteine (NAC) showed positive effects in alleviating contrast-induced AKI, the clinical applications are strongly restrained due to the low bioavailability, low renal accumulation, short renal retention time, and high dosage-induced toxicity.	Acetylcysteine	9-25	synuclein alpha	Homo sapiens	27-30
23748041-4	2013	Proteinase 3 induced neuronal cell death as evidenced by MTT analysis as well as propidium iodide staining, which was prevented by pretreatment with an antioxidant, N-acetyl cysteine.	Acetylcysteine	165-182	proteinase 3	Rattus norvegicus	0-12
34171359-5	2021	The antioxidant compound, N-acetyl-cysteine, abrogated nicotine-activated production of reactive oxygen species and inhibited CYP1A1 expression by nicotine.	Acetylcysteine	26-43	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	126-132
23860378-14	2013	NAC also blocked stromal induction of MCT4, indicating that NAC effectively functions as an "MCT4 inhibitor".	Acetylcysteine	60-63	solute carrier family 16 member 3	Homo sapiens	93-97
23623839-2	2013	Although Cyr61 was found by us to be overproduced in androgen-independent PC-3 cells treated with N-acetylcysteine (NAC), its significance is still unclear.	Acetylcysteine	98-114	cellular communication network factor 1	Homo sapiens	9-14
34664816-10	2021	However, non-significant variations in the IL-1beta and IL-17 levels suggest an alternative way of NAC effectiveness without influencing the measured cytokines.	Acetylcysteine	99-102	interleukin 1 alpha	Homo sapiens	43-51
34102208-0	2021	N-acetylcysteine alleviates ocular surface damage in STZ-induced diabetic mice by inhibiting the ROS/NLRP3/Caspase-1/IL-1beta signaling pathway.	Acetylcysteine	0-16	NLR family, pyrin domain containing 3	Mus musculus	101-106
34102208-0	2021	N-acetylcysteine alleviates ocular surface damage in STZ-induced diabetic mice by inhibiting the ROS/NLRP3/Caspase-1/IL-1beta signaling pathway.	Acetylcysteine	0-16	interleukin 1 alpha	Mus musculus	117-125
34102208-10	2021	Moreover, NAC markedly attenuated ROS accumulation and decreased NLRP3, IL-1beta and caspase-1 levels in diabetic cornea and conjunctiva.	Acetylcysteine	10-13	NLR family, pyrin domain containing 3	Mus musculus	65-70
34102208-10	2021	Moreover, NAC markedly attenuated ROS accumulation and decreased NLRP3, IL-1beta and caspase-1 levels in diabetic cornea and conjunctiva.	Acetylcysteine	10-13	interleukin 1 alpha	Mus musculus	72-80
23623839-2	2013	Although Cyr61 was found by us to be overproduced in androgen-independent PC-3 cells treated with N-acetylcysteine (NAC), its significance is still unclear.	Acetylcysteine	116-119	cellular communication network factor 1	Homo sapiens	9-14
34102208-11	2021	These results suggest that NAC improves ocular surface damage in STZ-induced diabetic mice, which may be related to the inhibition of the ROS/NLRP3/Caspase-1/IL-1beta signaling pathway.	Acetylcysteine	27-30	NLR family, pyrin domain containing 3	Mus musculus	142-147
34102208-11	2021	These results suggest that NAC improves ocular surface damage in STZ-induced diabetic mice, which may be related to the inhibition of the ROS/NLRP3/Caspase-1/IL-1beta signaling pathway.	Acetylcysteine	27-30	interleukin 1 alpha	Mus musculus	158-166
23623839-3	2013	We therefore aimed to determine how and why Cyr61 protein is overexpressed in NAC-treated cells.	Acetylcysteine	78-81	cellular communication network factor 1	Homo sapiens	44-49
34167418-0	2021	The effect of N-acetyl cysteine and doxycycline on TNF-alpha-Rel-a inflammatory pathway and downstream angiogenesis factors in the cornea of rats injured by 2-chloroethyl-ethyl sulfide.	Acetylcysteine	14-31	RELA proto-oncogene, NF-kB subunit	Rattus norvegicus	61-66
23623839-4	2013	Here, we found that Cyr61 protein level markedly increased in cells treated with NAC at high cell seeding density.	Acetylcysteine	81-84	cellular communication network factor 1	Homo sapiens	20-25
23552724-7	2013	Moreover, N-acetylcysteine (NAC), a potent antioxidant, blocked acute alcohol effect on inhibition of macrophage MFG-E8 gene expression and efferocytosis.	Acetylcysteine	10-26	milk fat globule EGF and factor V/VIII domain containing	Mus musculus	113-119
34254625-5	2021	Using human hepatocellular carcinoma (HepG2) cells, we confirmed that the interaction between dynamin-related protein 1 (DRP1)-dependent mitochondrial fission and oxidative stress promoted mitochondrial damage and mitochondria-dependent apoptosis induced by AgNPs, as determined by the elimination of DRP1 or addition of N-acetylcysteine (NAC).	Acetylcysteine	321-337	dynamin 1 like	Homo sapiens	121-125
34254625-5	2021	Using human hepatocellular carcinoma (HepG2) cells, we confirmed that the interaction between dynamin-related protein 1 (DRP1)-dependent mitochondrial fission and oxidative stress promoted mitochondrial damage and mitochondria-dependent apoptosis induced by AgNPs, as determined by the elimination of DRP1 or addition of N-acetylcysteine (NAC).	Acetylcysteine	339-342	dynamin 1 like	Homo sapiens	94-119
34254625-5	2021	Using human hepatocellular carcinoma (HepG2) cells, we confirmed that the interaction between dynamin-related protein 1 (DRP1)-dependent mitochondrial fission and oxidative stress promoted mitochondrial damage and mitochondria-dependent apoptosis induced by AgNPs, as determined by the elimination of DRP1 or addition of N-acetylcysteine (NAC).	Acetylcysteine	339-342	dynamin 1 like	Homo sapiens	121-125
23552724-7	2013	Moreover, N-acetylcysteine (NAC), a potent antioxidant, blocked acute alcohol effect on inhibition of macrophage MFG-E8 gene expression and efferocytosis.	Acetylcysteine	28-31	milk fat globule EGF and factor V/VIII domain containing	Mus musculus	113-119
23546866-7	2013	Antioxidant N-acetyl cysteine attenuated ASK1 dephosphorylation and p38 MAPK activation, indicating that shikonin-induced ROS is involved in the activation of Akt/ASK1/p38 pathway.	Acetylcysteine	12-29	mitogen-activated protein kinase kinase kinase 5	Homo sapiens	41-45
34267196-4	2021	We employed C. elegans to demonstrate that chronic administration of GSH or NAC to young or aged animals perturbs global gene expression, inhibits skn-1-mediated transcription, and accelerates aging.	Acetylcysteine	76-79	BZIP domain-containing protein;Protein skinhead-1	Caenorhabditis elegans	147-152
23546866-7	2013	Antioxidant N-acetyl cysteine attenuated ASK1 dephosphorylation and p38 MAPK activation, indicating that shikonin-induced ROS is involved in the activation of Akt/ASK1/p38 pathway.	Acetylcysteine	12-29	mitogen-activated protein kinase kinase kinase 5	Homo sapiens	163-167
34356340-8	2021	The protective effects of NAC were, at least, partly due to a decrease in the production of tumor necrosis factor-alpha (TNF-alpha) by acinar cells, which was concomitant with the inhibition of NF-kappaB(p65) nuclear translocation.	Acetylcysteine	26-29	v-rel reticuloendotheliosis viral oncogene homolog A (avian)	Mus musculus	194-208
34208683-5	2021	As an anti-inflammatory compound, NAC can reduce levels of tumor necrosis factor-alpha (TNF-alpha) and interleukins (IL-6 and IL-1beta) by suppressing the activity of nuclear factor kappa B (NF-kappaB).	Acetylcysteine	34-37	interleukin 1 alpha	Homo sapiens	126-134
23840748-6	2013	Compound 1a-induced generation of intracellular reactive oxygen species through cytochrome P450 1A1 was identified as a major mechanism of its effect for DNA damage, mitochondria dysfunction and apoptosis, which was reversed by antioxidant N-acetylcysteine as well as cytochrome P450 1A1 inhibitor and specific siRNA.	Acetylcysteine	240-256	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	80-99
35417724-0	2022	Inhibitory effects of zinc chloride (ZnCl2), n-acetyl-L-cysteine (NAC), and calcium/calmodulin dependent protein kinase II inhibitor (KN93) on Cd2+-induced abnormal cell morphology and membrane permeability.	Acetylcysteine	45-64	CD2 molecule	Homo sapiens	143-146
35417724-0	2022	Inhibitory effects of zinc chloride (ZnCl2), n-acetyl-L-cysteine (NAC), and calcium/calmodulin dependent protein kinase II inhibitor (KN93) on Cd2+-induced abnormal cell morphology and membrane permeability.	Acetylcysteine	66-69	CD2 molecule	Homo sapiens	143-146
35417724-4	2022	0.5 mmol L-1 NAC and 5 mumol L-1 KN93 could significantly inhibit the effects of Cd2+ on the morphology and membrane permeability of MCF-7 cells (p < 0.01).	Acetylcysteine	13-16	CD2 molecule	Homo sapiens	81-84
35417724-6	2022	The results of cell activity experiment showed that 10 mumol L-1 ZnCl2, 0.5 mmol L-1 NAC and 5 mumol L-1 KN93 could inhibit the effect of Cd2+ on the activity of MCF-7 cells.	Acetylcysteine	85-88	CD2 molecule	Homo sapiens	138-141
35417724-7	2022	By comparing the inhibitory effects of ZnCl2, NAC and KN93 on Cd2+- induced cytotoxicity, 5 mumol L-1 KN93 had the robust effect on the maintenance of MCF-7 cell morphology and cell membrane integrity.	Acetylcysteine	46-49	CD2 molecule	Homo sapiens	62-65
35507947-8	2022	In addition, the expression of Gdf9, Lif, Bax, and Bcl2 genes were increased and Amh was decreased in groups cultured in the presence of NAC compared to groups cultured without NAC.	Acetylcysteine	137-140	growth differentiation factor 9	Mus musculus	31-35
35507947-8	2022	In addition, the expression of Gdf9, Lif, Bax, and Bcl2 genes were increased and Amh was decreased in groups cultured in the presence of NAC compared to groups cultured without NAC.	Acetylcysteine	137-140	leukemia inhibitory factor	Mus musculus	37-40
23840748-6	2013	Compound 1a-induced generation of intracellular reactive oxygen species through cytochrome P450 1A1 was identified as a major mechanism of its effect for DNA damage, mitochondria dysfunction and apoptosis, which was reversed by antioxidant N-acetylcysteine as well as cytochrome P450 1A1 inhibitor and specific siRNA.	Acetylcysteine	240-256	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	268-287
35507947-8	2022	In addition, the expression of Gdf9, Lif, Bax, and Bcl2 genes were increased and Amh was decreased in groups cultured in the presence of NAC compared to groups cultured without NAC.	Acetylcysteine	177-180	growth differentiation factor 9	Mus musculus	31-35
35507947-8	2022	In addition, the expression of Gdf9, Lif, Bax, and Bcl2 genes were increased and Amh was decreased in groups cultured in the presence of NAC compared to groups cultured without NAC.	Acetylcysteine	177-180	leukemia inhibitory factor	Mus musculus	37-40
23421903-14	2013	Knowing there are several important cysteine residues near the ligand-binding site of alpha4 nAChRs, we tested the antioxidant NAC and found that it too blocked the induction of fibronectin expression by EtOH.	Acetylcysteine	127-130	fibronectin 1	Mus musculus	178-189
35428330-13	2022	Additionally, the ROS scavengers N-Acetylcysteine (N-Ace) was also found to inhibit the nuclear translocation of NF-kappaB and the mRNA expression of IL-6 and MCP-1 induced by LPS, which suggested that ROS was essential for the nuclear translocation of NF-kappaB.	Acetylcysteine	33-49	C-C motif chemokine ligand 2	Rattus norvegicus	159-164
35428330-13	2022	Additionally, the ROS scavengers N-Acetylcysteine (N-Ace) was also found to inhibit the nuclear translocation of NF-kappaB and the mRNA expression of IL-6 and MCP-1 induced by LPS, which suggested that ROS was essential for the nuclear translocation of NF-kappaB.	Acetylcysteine	51-56	C-C motif chemokine ligand 2	Rattus norvegicus	159-164
35418176-5	2022	N-Acetyl-L-cysteine (NAC, ROS scavenger) partially blocked HCC cell proliferation and migration induced by OPN.	Acetylcysteine	0-19	secreted phosphoprotein 1	Homo sapiens	107-110
23717422-6	2013	In addition, sanguinarine effectively increased the activation of the c-Jun N-terminal kinase (JNK) and the expression of the early growth response gene-1 (Egr-1), which was recovered by pretreatment with NAC.	Acetylcysteine	205-208	early growth response 1	Homo sapiens	156-161
35418176-5	2022	N-Acetyl-L-cysteine (NAC, ROS scavenger) partially blocked HCC cell proliferation and migration induced by OPN.	Acetylcysteine	21-24	secreted phosphoprotein 1	Homo sapiens	107-110
35453441-11	2022	NAC effectively prevented neuronal death and GPx1 downregulation in CA1 neurons, and restored GPx1 expression to the control level in CA1 astrocytes.	Acetylcysteine	0-3	carbonic anhydrase 1	Rattus norvegicus	68-71
26417226-6	2013	NAC significantly decreased neutrophil and eosinophil count in BALF as well as inflammatory cytokines (IL-13 and IL-5).We concluded that addition of NAC to asthma therapy has beneficial preventive effects in an animal model of steroid resistant acute exacerbation of asthma.	Acetylcysteine	0-3	interleukin 5	Mus musculus	113-117
35453441-11	2022	NAC effectively prevented neuronal death and GPx1 downregulation in CA1 neurons, and restored GPx1 expression to the control level in CA1 astrocytes.	Acetylcysteine	0-3	carbonic anhydrase 1	Rattus norvegicus	134-137
35582415-7	2022	In addition, increased expression of caspase-3, KIM-1 and NGAL suffering from VCM was also reversed by NAC in vivo and in vitro.	Acetylcysteine	103-106	hepatitis A virus cellular receptor 1	Rattus norvegicus	48-53
35582415-8	2022	NAC inhibited ROS production, decreased cell apoptosis by decreasing the Bax/Bcl-2 ratio and caspase-3 expression in HK-2 cells and regulated oxidative stress indicators in the kidney by decreasing GSH, SOD and CAT activity and increasing MDA levels.	Acetylcysteine	0-3	BCL2 associated X, apoptosis regulator	Rattus norvegicus	73-76
35582415-9	2022	Furthermore, NAC could effectively reverse VCM-associated increased P38 MAPK/JNK phosphorylation.	Acetylcysteine	13-16	mitogen-activated protein kinase 8	Rattus norvegicus	77-80
35582415-10	2022	Conclusions: The results demonstrated that NAC had a protective effect against nephrotoxicity from VCM by inhibiting oxidative stress and apoptosis via P38 MAPK/JNK.	Acetylcysteine	43-46	mitogen-activated protein kinase 8	Rattus norvegicus	161-164
26417226-6	2013	NAC significantly decreased neutrophil and eosinophil count in BALF as well as inflammatory cytokines (IL-13 and IL-5).We concluded that addition of NAC to asthma therapy has beneficial preventive effects in an animal model of steroid resistant acute exacerbation of asthma.	Acetylcysteine	149-152	interleukin 5	Mus musculus	113-117
22944050-0	2013	N-acetylcysteine (NAC) inhibits cell growth by mediating the EGFR/Akt/HMG box-containing protein 1 (HBP1) signaling pathway in invasive oral cancer.	Acetylcysteine	0-16	HMG-box transcription factor 1	Homo sapiens	70-98
35235429-5	2022	Treatment of EAE mice with the ROS scavenger N-acetyl cysteine (NAC) blocked the Npnt-FD antibody-induced decrease in Th17 differentiation and increase in Treg differentiation.	Acetylcysteine	45-62	nephronectin	Mus musculus	81-85
22944050-0	2013	N-acetylcysteine (NAC) inhibits cell growth by mediating the EGFR/Akt/HMG box-containing protein 1 (HBP1) signaling pathway in invasive oral cancer.	Acetylcysteine	0-16	HMG-box transcription factor 1	Homo sapiens	100-104
35065161-5	2022	It caused impairment of mitochondrial membrane potential by increasing pro-apoptotic BAX, and BAK1 expressions, and decreasing anti-apoptotic BCL2 expression, along with the induction of caspase-9/3 activation, however, these attributes were compromised in presence of N-acetyl-L-cysteine (NAC), a free radical scavenger.	Acetylcysteine	269-288	caspase 9	Homo sapiens	187-198
22944050-0	2013	N-acetylcysteine (NAC) inhibits cell growth by mediating the EGFR/Akt/HMG box-containing protein 1 (HBP1) signaling pathway in invasive oral cancer.	Acetylcysteine	18-21	HMG-box transcription factor 1	Homo sapiens	70-98
22944050-0	2013	N-acetylcysteine (NAC) inhibits cell growth by mediating the EGFR/Akt/HMG box-containing protein 1 (HBP1) signaling pathway in invasive oral cancer.	Acetylcysteine	18-21	HMG-box transcription factor 1	Homo sapiens	100-104
22944050-5	2013	RESULTS: NAC treatment suppressed cell growth, with concomitantly increased expression of HMG box-containing protein 1 (HBP1), a transcription suppressor, and decreased EGFR/Akt activation, in EGFR-overexpressing HSC-3 oral cancer cells.	Acetylcysteine	9-12	HMG-box transcription factor 1	Homo sapiens	90-118
22944050-5	2013	RESULTS: NAC treatment suppressed cell growth, with concomitantly increased expression of HMG box-containing protein 1 (HBP1), a transcription suppressor, and decreased EGFR/Akt activation, in EGFR-overexpressing HSC-3 oral cancer cells.	Acetylcysteine	9-12	HMG-box transcription factor 1	Homo sapiens	120-124
35401119-8	2022	Furthermore, rescue experiments with antioxidant N-acetylcysteine (NAC) showed that the expression of 4-HNE and the apoptosis in SGNs were significantly decreased, while the number of surviving SGNs was increased in peroxynitrite + NAC group compared the peroxynitrite-only group and in peroxynitrite + gpx1 -/- + NAC group vs. peroxynitrite + gpx1 -/- group.	Acetylcysteine	49-65	glutathione peroxidase 1	Mus musculus	303-307
22944050-6	2013	HBP1 knockdown attenuated the growth arrest and apoptosis induced by NAC.	Acetylcysteine	69-72	HMG-box transcription factor 1	Homo sapiens	0-4
35401119-8	2022	Furthermore, rescue experiments with antioxidant N-acetylcysteine (NAC) showed that the expression of 4-HNE and the apoptosis in SGNs were significantly decreased, while the number of surviving SGNs was increased in peroxynitrite + NAC group compared the peroxynitrite-only group and in peroxynitrite + gpx1 -/- + NAC group vs. peroxynitrite + gpx1 -/- group.	Acetylcysteine	49-65	glutathione peroxidase 1	Mus musculus	344-348
22944050-8	2013	CONCLUSION: Taken together, our data indicate that NAC exerts its growth-inhibitory function through modulating EGFR/Akt signaling and HBP1 expression in EGFR-overexpressing oral cancer.	Acetylcysteine	51-54	HMG-box transcription factor 1	Homo sapiens	135-139
35401119-8	2022	Furthermore, rescue experiments with antioxidant N-acetylcysteine (NAC) showed that the expression of 4-HNE and the apoptosis in SGNs were significantly decreased, while the number of surviving SGNs was increased in peroxynitrite + NAC group compared the peroxynitrite-only group and in peroxynitrite + gpx1 -/- + NAC group vs. peroxynitrite + gpx1 -/- group.	Acetylcysteine	67-70	glutathione peroxidase 1	Mus musculus	303-307
35401119-8	2022	Furthermore, rescue experiments with antioxidant N-acetylcysteine (NAC) showed that the expression of 4-HNE and the apoptosis in SGNs were significantly decreased, while the number of surviving SGNs was increased in peroxynitrite + NAC group compared the peroxynitrite-only group and in peroxynitrite + gpx1 -/- + NAC group vs. peroxynitrite + gpx1 -/- group.	Acetylcysteine	67-70	glutathione peroxidase 1	Mus musculus	344-348
23319318-10	2013	TNF-alpha-induced MCP-1 mRNA expression was inhibited by N-acetylcysteine (NAC), Syk inhibitor, Syk-siRNA and MPA.	Acetylcysteine	75-78	C-C motif chemokine ligand 2	Homo sapiens	18-23
23092328-11	2013	Also cells treated with the anti-oxidants N-acetylcysteine or HO-effector molecule bilirubin showed protection against heme insults, which may explain the increased protection by HO-1 compared to BCRP.	Acetylcysteine	42-58	heme oxygenase 1	Homo sapiens	179-183
35270019-8	2022	Induction of SA-beta-gal activity was prevented by the antioxidant N-acetyl cysteine in endothelial cells from DRG2 KO mice.	Acetylcysteine	67-84	developmentally regulated GTP binding protein 2	Mus musculus	111-115
23128467-0	2013	N-acetylcysteine potentiates doxorubicin-induced ATM and p53 activation             in ovarian cancer cells.	Acetylcysteine	0-16	ATM serine/threonine kinase	Homo sapiens	49-52
23128467-9	2013	Pretreatment of CaOV3 cells with antioxidant N-acetylcysteine (NAC),             but not pyrrolidine dithiocarbamate (PDTC) potentiates doxorubicin-induced phosphorylation             of p53 and ATM.	Acetylcysteine	45-61	ATM serine/threonine kinase	Homo sapiens	195-198
23128467-9	2013	Pretreatment of CaOV3 cells with antioxidant N-acetylcysteine (NAC),             but not pyrrolidine dithiocarbamate (PDTC) potentiates doxorubicin-induced phosphorylation             of p53 and ATM.	Acetylcysteine	63-66	ATM serine/threonine kinase	Homo sapiens	195-198
23782641-10	2013	NAC also attenuated the ratio of sub-G1, the generation of DNA fragmentation and the expression of Bcl-2, Bax, caspase-3, and caspase-9.	Acetylcysteine	0-3	caspase 9	Homo sapiens	126-135
35249163-8	2022	Since acetylcysteine (ACC) has been shown to reduce inflammatory markers in the airways, its potential influence on DMBT1 expression was analyzed.	Acetylcysteine	6-20	deleted in malignant brain tumors 1	Mus musculus	116-121
35249163-8	2022	Since acetylcysteine (ACC) has been shown to reduce inflammatory markers in the airways, its potential influence on DMBT1 expression was analyzed.	Acetylcysteine	22-25	deleted in malignant brain tumors 1	Mus musculus	116-121
24039617-9	2013	Further studies revealed that adriamycin increased ROS and up-regulated P-gp in MCF-7S cells, which could be reversed by N-acetylcysteine treatment.	Acetylcysteine	121-137	phosphoglycolate phosphatase	Homo sapiens	72-76
35236897-9	2022	NRDC may be also involved in ROS-mediated in vivo thermogenesis because the inhibitory effects of N-acetyl cysteine, an ROS scavenger, on beta3 agonist-induced thermogenesis were stronger in Adipo-KO mice.	Acetylcysteine	98-115	nardilysin, N-arginine dibasic convertase, NRD convertase 1	Mus musculus	0-4
35057925-2	2022	In this work, N-acetyl-l-cysteine capped-copper nanoclusters (NAC-CuNCs) were incorporated into 3D mesoporous silica particles (M-SiO2) through electrostatic assembly.	Acetylcysteine	14-33	synuclein alpha	Homo sapiens	62-65
24112955-4	2013	RESULTS: NAC treatment inhibited fat accumulation and reduced the expression of obesity-related proteins, including monoamine oxidase A, heat shock protein 70 (HSP70), aminoacylase -1 (ACY-1), and transketolase.	Acetylcysteine	9-12	monoamine oxidase A	Homo sapiens	116-135
22664745-14	2013	The levels of lung cytoplasmic p-IkappaB-alpha expression was mitigated by NAC, and NF-kappaB p65 DNA binding activity was also significantly decreased in the NAC group.	Acetylcysteine	75-78	NFKB inhibitor alpha	Rattus norvegicus	33-46
35045287-6	2022	Dysfunction of Pnpla2-null SCs is associated with energy insufficiency and oxidative stress that can be partially rescued by antioxidant (N-acetylcysteine) treatment.	Acetylcysteine	138-154	patatin like phospholipase domain containing 2	Homo sapiens	15-21
22664745-14	2013	The levels of lung cytoplasmic p-IkappaB-alpha expression was mitigated by NAC, and NF-kappaB p65 DNA binding activity was also significantly decreased in the NAC group.	Acetylcysteine	159-162	NFKB inhibitor alpha	Rattus norvegicus	33-46
35083343-8	2022	Using ferrostatin, rotenone, and N-acetyl-L-cysteine, we confirmed that metabolic and redox regulation is responsible for FAC-mediated PD-L1 expression.	Acetylcysteine	33-52	CD274 molecule	Homo sapiens	135-140
23072389-1	2012	Programmed cell death can occur through two separate pathways caused by treatment of Saccharomyces cerevisiae with acetic acid (AA-PCD), which differ from one another essentially with respect to their sensitivity to N-acetylcysteine (NAC) and to the role played by cytochrome c and metacaspase YCA1.	Acetylcysteine	234-237	Ca(2+)-dependent cysteine protease MCA1	Saccharomyces cerevisiae S288C	294-298
23072389-5	2012	NAC-insensitive AA-PCD pathway takes place essentially without macroautophagy, even if the shift of extracellular pH to acidic values required for AA-PCD to occur leads itself to increased or decreased macroautophagy in YCA1 or cytochrome c-lacking cells.	Acetylcysteine	0-3	Ca(2+)-dependent cysteine protease MCA1	Saccharomyces cerevisiae S288C	220-224
22562160-9	2012	Co-incubation of NCCIT cells with bleomycin and 10 mM NAC abolished bleomycin-induced increases in caspase-3 and caspase-9 activities, Bax, and Cyt-c levels and bleomycin-induced decrease in Bcl-2 level.	Acetylcysteine	54-57	caspase 9	Homo sapiens	113-122
22922338-7	2012	CHOP induction was also reactive oxygen species (ROS)-dependent, as shown by capsazepine"s ability to induce ROS and by the quenching of ROS by N-acetylcysteine or glutathione, which prevented induction of CHOP and DR5 and consequent sensitization to TRAIL.	Acetylcysteine	144-160	TNF receptor superfamily member 10b	Homo sapiens	215-218
22743636-5	2012	At 3 days after TNFalpha stimulation, 30 muM telmisartan or 20 mM NAC administered before and during TNFalpha stimulation prevented the enhancement of LPC content in LDL and monocyte chemoattractant protein-1 mRNA by LDL incubation with TNFalpha-stimulated HUVEC.	Acetylcysteine	66-69	C-C motif chemokine ligand 2	Homo sapiens	174-208
23026584-11	2012	NAC decreased ALT activity in all groups, even in association with I/R (P &lt; .05), reflecting a modulation of the injury.	Acetylcysteine	0-3	glutamic pyruvic transaminase, soluble	Mus musculus	14-17
22700875-6	2012	N-acetyl cysteine (NAC) rescued Blp-RNAi-treated cells from cell cycle arrest, indicating that increased production of ROS is the primary cause of the proliferation and survival defects in Blp-depleted cells.	Acetylcysteine	0-17	black pearl	Drosophila melanogaster	32-35
22700875-6	2012	N-acetyl cysteine (NAC) rescued Blp-RNAi-treated cells from cell cycle arrest, indicating that increased production of ROS is the primary cause of the proliferation and survival defects in Blp-depleted cells.	Acetylcysteine	0-17	black pearl	Drosophila melanogaster	189-192
22700875-6	2012	N-acetyl cysteine (NAC) rescued Blp-RNAi-treated cells from cell cycle arrest, indicating that increased production of ROS is the primary cause of the proliferation and survival defects in Blp-depleted cells.	Acetylcysteine	19-22	black pearl	Drosophila melanogaster	32-35
22700875-6	2012	N-acetyl cysteine (NAC) rescued Blp-RNAi-treated cells from cell cycle arrest, indicating that increased production of ROS is the primary cause of the proliferation and survival defects in Blp-depleted cells.	Acetylcysteine	19-22	black pearl	Drosophila melanogaster	189-192
22700875-7	2012	blp hypomorph larvae had a 35% decreased number of plasmatocytes with a 45% reduced active mitochondrial staining and their viability was increased 2-fold by administration of NAC, which blocked melanotic lesions.	Acetylcysteine	176-179	black pearl	Drosophila melanogaster	0-3
22664789-11	2012	Furthermore, the use of NAC significantly reduced the expression of NFkB normally observed in RAM exposed to CSE.	Acetylcysteine	24-27	RELA proto-oncogene, NF-kB subunit	Rattus norvegicus	68-72
22683601-8	2012	Consequently, cotreatment with the antioxidant N-acetyl-l-cysteine blocked the translocation of DJ-1 into the nucleus.	Acetylcysteine	47-66	Parkinson disease (autosomal recessive, early onset) 7	Mus musculus	96-100
22046978-7	2012	NAC administered prior to and after LPS significantly reduced fetal brain IL-6 at E18 and E20 and IL-10 at E20.	Acetylcysteine	0-3	interleukin 10	Rattus norvegicus	98-103
22749995-6	2012	In addition, N-Acetyl-L-Cysteine treatment significantly decreased immature erythroblasts and apoptotic cells increased in Prx II(-/-) BMCs.	Acetylcysteine	13-32	periaxin	Mus musculus	123-126
22554771-9	2012	An antioxidant drug, N-acetyl-l-cysteine significantly inhibited TNF-alpha-induced phosphorylation of p38 and JNK.	Acetylcysteine	21-40	mitogen-activated protein kinase 8	Rattus norvegicus	110-113
22517678-5	2012	HKII mitochondrial binding is also important for the hypertrophic effects, as HKII dissociation from the mitochondria resulted in de novo hypertrophy, which was also attenuated by NAC.	Acetylcysteine	180-183	hexokinase 2	Mus musculus	0-4
22517678-5	2012	HKII mitochondrial binding is also important for the hypertrophic effects, as HKII dissociation from the mitochondria resulted in de novo hypertrophy, which was also attenuated by NAC.	Acetylcysteine	180-183	hexokinase 2	Mus musculus	78-82
22453841-8	2012	NAC down-regulated MCP-1, CINC and P-selectin in BPDO- but not in NaTc-induced AP.	Acetylcysteine	0-3	C-C motif chemokine ligand 2	Rattus norvegicus	19-24
22453841-10	2012	NAC reduced lung MPO activity in mild but not in severe AP.	Acetylcysteine	0-3	myeloperoxidase	Rattus norvegicus	17-20
22245600-5	2012	By using rat mesangial cell line and primary mesangial cells, we found that NADPH oxidase inhibitor (apocynin) and ROS inhibitor (N-acetyl cysteine) both inhibited HG-induced mesangial cell proliferation and fibronectin expression.	Acetylcysteine	130-147	fibronectin 1	Rattus norvegicus	208-219
22505981-13	2012	However, N-acetylcysteine, a potent glutathione-based antioxidant, was capable of almost completely preventing the glycerol-mediated adverse outcomes, such as cell death, glyoxalase I inactivation, and heat shock protein 90 degradation.	Acetylcysteine	9-25	glyoxalase I	Homo sapiens	171-183
21952821-9	2012	VEGF and ICAM-1 expressions were significantly up-regulated in retinal blood vessels from diabetic rats, and such up-regulation was attenuated by N-acetylcysteine treatment.	Acetylcysteine	146-162	vascular endothelial growth factor A	Rattus norvegicus	0-4
21952821-11	2012	Long-term N-acetylcysteine treatment exerts protective effects on the diabetic retinas, possibly through its down-regulation of the expression of VEGF and ICAM-1, and reduction of reactive oxygen species content in retinal vascular tissues in diabetic rats.	Acetylcysteine	10-26	vascular endothelial growth factor A	Rattus norvegicus	146-150
22198183-9	2012	Preincubating RLE-6TN cells with N-acetylcysteine, an antioxidant, abolished the radiation-induced phosphorylation of ERK and altered protein levels of Snail, E-cadherin, and alpha-SMA.	Acetylcysteine	33-49	cadherin 1	Rattus norvegicus	159-169
22198183-9	2012	Preincubating RLE-6TN cells with N-acetylcysteine, an antioxidant, abolished the radiation-induced phosphorylation of ERK and altered protein levels of Snail, E-cadherin, and alpha-SMA.	Acetylcysteine	33-49	actin gamma 2, smooth muscle	Rattus norvegicus	175-184
22245127-8	2012	The regulation of the expression of Bcl-2-family proteins, the release of cytochrome c and the activation of caspases 9, 3 and 6 were inhibited in the presence of NAC.	Acetylcysteine	163-166	caspase 6	Homo sapiens	109-117
22241216-11	2012	NAC was effectively significant in preventing TGF-beta and IL-6 expression and further augmented the IL-10 expression.	Acetylcysteine	0-3	interleukin 10	Rattus norvegicus	101-106
22134636-7	2012	The ability of NAC to alter Dox-induced NF-kappaB activity is contingent on the ROS-mediated S-glutathionylation of IKK-beta.	Acetylcysteine	15-18	inhibitor of nuclear factor kappa B kinase subunit beta	Homo sapiens	116-124
21660448-9	2012	Pretreatment with N-acetylcysteine (NAC) inhibited DMF-induced upregulation of DR5, CHOP, GPR78, and ATF4 protein expression and blocked the cotreatment-induced apoptosis.	Acetylcysteine	18-34	TNF receptor superfamily member 10b	Homo sapiens	79-82
21660448-9	2012	Pretreatment with N-acetylcysteine (NAC) inhibited DMF-induced upregulation of DR5, CHOP, GPR78, and ATF4 protein expression and blocked the cotreatment-induced apoptosis.	Acetylcysteine	36-39	TNF receptor superfamily member 10b	Homo sapiens	79-82
22739240-7	2012	The H(2)O(2)-induced gene repression or activation of SP-A, SP-B, SP-D and ABCA3 was blocked by pretreatment with the antioxidants N-acetyl-L-cysteine (NAC) and catalase.	Acetylcysteine	131-150	ATP binding cassette subfamily A member 3	Homo sapiens	75-80
22739240-7	2012	The H(2)O(2)-induced gene repression or activation of SP-A, SP-B, SP-D and ABCA3 was blocked by pretreatment with the antioxidants N-acetyl-L-cysteine (NAC) and catalase.	Acetylcysteine	131-150	synuclein alpha	Homo sapiens	152-155
21806545-9	2012	Atorvastatin, SP600125, JNK siRNA (small interfering RNA) and NAC (N-acetylcysteine) completely attenuated the leptin and phospho-JNK protein expression induced by Ang II.	Acetylcysteine	62-65	leptin	Homo sapiens	111-117
21806545-9	2012	Atorvastatin, SP600125, JNK siRNA (small interfering RNA) and NAC (N-acetylcysteine) completely attenuated the leptin and phospho-JNK protein expression induced by Ang II.	Acetylcysteine	67-83	leptin	Homo sapiens	111-117
21826188-6	2012	The ATO/CMEMM-induced activation of caspase-3 and caspase-9 can be blocked by NAC.	Acetylcysteine	78-81	caspase 9	Homo sapiens	50-59
22946344-6	2012	Likewise, NAC prevented the induction of apoptosis (annexin V-FITC binding and cleavage of PARP-1 and procaspases-3,-8 and -9) and reversed the loss of mitochondrial membrane potential and release of cytochrome c from mitochondria by CDDO-Me.	Acetylcysteine	10-13	annexin A5	Homo sapiens	52-61
22044588-8	2012	Furthermore, the activation of Bnip3 and mitophagy due to p53/TIGAR inhibition were reversed with antioxidant N-acetyl-cysteine, indicating that this adaptive response requires ROS signal.	Acetylcysteine	110-127	transformation related protein 53, pseudogene	Mus musculus	58-61
23006535-8	2012	Consistently, NAC partially attenuated pulmonary fibrosis and inhibited TGF-beta(1) and alpha-SMA expression in this model.	Acetylcysteine	14-17	actin gamma 2, smooth muscle	Rattus norvegicus	88-97
22012146-1	2011	The complex formation between Cd(II) ions and N-acetylcysteine (H(2)NAC) in aqueous solution was investigated using Cd K- and L(3)-edge X-ray absorption and (113)Cd NMR spectroscopic techniques.	Acetylcysteine	46-62	synuclein alpha	Homo sapiens	68-71
22001321-11	2011	Inhibitor of HO-1 activity, tin protoporphyrin IX, further increased HA-mediated reactivation of HIV-1 "mini-virus" in Jurkat clones, and this effect was also inhibited by N-acetyl cysteine.	Acetylcysteine	172-189	heme oxygenase 1	Homo sapiens	13-17
21903093-11	2011	Pretreatment with N-acetyl-L-cysteine and glutathione inhibited GGS-induced ER-stress, and CHOP and DR5 upregulation and almost completely blocked GGS/TRAIL-induced apoptosis.	Acetylcysteine	18-37	TNF receptor superfamily member 10b	Homo sapiens	100-103
21877197-9	2011	Treatment for NuB2 cells with N-acetyl-L: -cysteine, diphenyleneiodonium, or apocynin decreased CK18 protein levels indicating its regulation involving reactive oxygen species and flavoprotein Nox.	Acetylcysteine	30-51	keratin 18	Homo sapiens	96-100
22090786-13	2011	The thiol antioxidants, acetylcysteine (NAC) and GSH restored GSH content and attenuated casticin-induced apoptosis.	Acetylcysteine	24-38	synuclein alpha	Homo sapiens	40-43
21961969-7	2011	Furthermore, N-Acetyl-L-cysteine (NAC) or 1,2-bisethane-N,N,N",N"-tetraacetic acid tetrakis ester (BAPTA-AM) could decrease the apoptosis rate, the release of cyto-c and cleaved caspase-3 in SDT group, SERCA(2) degradation was found in SDT group and could also be prevented by the addition of NAC.	Acetylcysteine	13-32	ATPase sarcoplasmic/endoplasmic reticulum Ca2+ transporting 2	Rattus norvegicus	202-210
21961969-7	2011	Furthermore, N-Acetyl-L-cysteine (NAC) or 1,2-bisethane-N,N,N",N"-tetraacetic acid tetrakis ester (BAPTA-AM) could decrease the apoptosis rate, the release of cyto-c and cleaved caspase-3 in SDT group, SERCA(2) degradation was found in SDT group and could also be prevented by the addition of NAC.	Acetylcysteine	34-37	ATPase sarcoplasmic/endoplasmic reticulum Ca2+ transporting 2	Rattus norvegicus	202-210
22242225-0	2011	[N-acetylcysteine (NAC) inhibited pulmonary fibrosis in acute respiratory distress syndrome (ARDS)].	Acetylcysteine	1-17	synuclein alpha	Homo sapiens	19-22
21620964-7	2011	Pretreatment with anti-oxidants (N-acetylcysteine (NAC) or glutathione) significantly reduced Bay-induced HO-1 mRNA/protein expression, nuclear translocation of Nrf2 and phosphorylation of Akt.	Acetylcysteine	33-49	heme oxygenase 1	Homo sapiens	106-110
21620964-7	2011	Pretreatment with anti-oxidants (N-acetylcysteine (NAC) or glutathione) significantly reduced Bay-induced HO-1 mRNA/protein expression, nuclear translocation of Nrf2 and phosphorylation of Akt.	Acetylcysteine	51-54	heme oxygenase 1	Homo sapiens	106-110
21854604-11	2011	Decrease in CREB mRNA levels in Abeta-treated neurons was reversed by the antioxidant, N-acetyl cysteine.	Acetylcysteine	87-104	cAMP responsive element binding protein 1	Rattus norvegicus	12-16
21635873-5	2011	Interestingly, the glutathione donor N-acetyl-l-cysteine or the NADPH oxidase inhibitor apocynin blocked the induction of HO-1 by compound C. Finally, compound C stimulated EC death and this was potentiated by silencing HO-1 expression and reversed by the administration of CO, biliverdin, or bilirubin.	Acetylcysteine	37-56	heme oxygenase 1	Homo sapiens	122-126
3707618-5	1986	Under physiological conditions, oct-1-en-3-one, prepared chemically, reacted non-enzymically with N-acetylcysteine with a t1/2 of about 6 sec.	Acetylcysteine	98-114	solute carrier family 22 member 1	Rattus norvegicus	32-37
21635873-5	2011	Interestingly, the glutathione donor N-acetyl-l-cysteine or the NADPH oxidase inhibitor apocynin blocked the induction of HO-1 by compound C. Finally, compound C stimulated EC death and this was potentiated by silencing HO-1 expression and reversed by the administration of CO, biliverdin, or bilirubin.	Acetylcysteine	37-56	heme oxygenase 1	Homo sapiens	220-224
21391979-10	2011	Generation of ROS induced phosphorylation of p42/p44 mitogen-activated protein kinase (MAPK), p38 MAPK and JNK1/2, which was attenuated by DPI and APO and the ROS scavenger N-acetylcysteine.	Acetylcysteine	173-189	cyclin dependent kinase 20	Homo sapiens	45-48
21574020-5	2011	Resveratrol (10 nM) or N-acetylcysteine (NAC, 20 mM) diminished the transcriptional activity of hypoxiainducible factor-1 and hypoxia-induced expression of VEGF.	Acetylcysteine	23-39	vascular endothelial growth factor A	Rattus norvegicus	156-160
21574020-5	2011	Resveratrol (10 nM) or N-acetylcysteine (NAC, 20 mM) diminished the transcriptional activity of hypoxiainducible factor-1 and hypoxia-induced expression of VEGF.	Acetylcysteine	41-44	vascular endothelial growth factor A	Rattus norvegicus	156-160
21681839-2	2011	However, their effectiveness is limited by drug resistance, which, in some cancers, has been associated with an overexpression of pi class glutathione S-transferase (GST P1-1), an important enzyme in the mercapturic acid detoxification pathway.	Acetylcysteine	204-220	glutathione S-transferase pi 1	Homo sapiens	166-174
3947396-7	1986	Studies on a purified ligandin (isoenzyme 1-2) from rat liver showed that further metabolism of the glutathione conjugates, to the corresponding cysteines or mercapturic acids, resulted in products with inhibitory properties approximately three orders of magnitude less potent than those of the parent S-substituted glutathiones.	Acetylcysteine	158-175	glutathione S-transferase alpha 2	Rattus norvegicus	22-30
3698928-7	1986	Nac also inhibited the CS-induced increase in the number of secretory cells with AGP, but had little effect on the CS-induced reduction in the number of cells with NGP.	Acetylcysteine	0-3	orosomucoid 1	Rattus norvegicus	81-84
21433060-5	2011	Anti-oxidants such as vitamin C or N-acetyl cysteine (NAC) blocked the strain-mediated increases of Cx 43, Nkx 2.5, and alpha5/beta1 integrins.	Acetylcysteine	35-52	hemoglobin, beta adult major chain	Mus musculus	120-132
6968166-4	1980	It was found that N-acetyl cysteine decreased the elastic modulus, leading to improved mucociliary transport at concentrations such that the mucin did not precipitate.	Acetylcysteine	18-35	mucin	Canis lupus familiaris	141-146
21433060-5	2011	Anti-oxidants such as vitamin C or N-acetyl cysteine (NAC) blocked the strain-mediated increases of Cx 43, Nkx 2.5, and alpha5/beta1 integrins.	Acetylcysteine	54-57	hemoglobin, beta adult major chain	Mus musculus	120-132
33951536-6	2021	N-acetyl cysteine, a thiol repletion agent that supports neuronal glutathione metabolism, suppressed the PFF - induced redox stress and c-Abl activation in the wild-type neurons, and likewise suppressed alpha-synuclein aggregation.	Acetylcysteine	0-17	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	136-141
21395287-3	2011	When 10 mM of N-acetyl-l-cysteine was added to the incubation mixtures, the phenyl acetic acid product was reduced and at 25 mM or higher concentration of NAC, formation of the phenyl acetic acid was abolished.	Acetylcysteine	14-33	synuclein alpha	Homo sapiens	155-158
21131132-9	2011	Expression of CD11a (p &lt; 0.05), CD18 (p &lt; 0.05) and CD97 (p &lt; 0.01) on the granulocytes were significantly lower in the NAC treated group, similarly to lymphocyte CD 49d (p &lt; 0.05) and monocyte CD 49d (p &lt; 0.01) and CD 97 (p &lt; 0.05) expression.	Acetylcysteine	129-132	adhesion G protein-coupled receptor E5	Homo sapiens	58-62
33905761-10	2021	The protein expression of p-JNK was also inhibited and the promotion effects of FB1 were significantly alleviated when NAC was used.	Acetylcysteine	119-122	mitogen-activated protein kinase 8	Sus scrofa	28-31
33825597-8	2021	However, Pifithrin-alpha (p53 inhibitor) and N-Acetylcysteine (NAC) could reduce cell apoptosis, lung structural damage and oxidative stress, accelerate the expression of Bcl-2, while suppressing the expression of Bax, total caspase-3 and cleaved caspase-3.	Acetylcysteine	45-61	BCL2-associated X protein	Mus musculus	214-217
33825597-8	2021	However, Pifithrin-alpha (p53 inhibitor) and N-Acetylcysteine (NAC) could reduce cell apoptosis, lung structural damage and oxidative stress, accelerate the expression of Bcl-2, while suppressing the expression of Bax, total caspase-3 and cleaved caspase-3.	Acetylcysteine	45-61	caspase 3	Mus musculus	225-234
21131132-9	2011	Expression of CD11a (p &lt; 0.05), CD18 (p &lt; 0.05) and CD97 (p &lt; 0.01) on the granulocytes were significantly lower in the NAC treated group, similarly to lymphocyte CD 49d (p &lt; 0.05) and monocyte CD 49d (p &lt; 0.01) and CD 97 (p &lt; 0.05) expression.	Acetylcysteine	129-132	integrin subunit alpha 4	Homo sapiens	172-178
33825597-8	2021	However, Pifithrin-alpha (p53 inhibitor) and N-Acetylcysteine (NAC) could reduce cell apoptosis, lung structural damage and oxidative stress, accelerate the expression of Bcl-2, while suppressing the expression of Bax, total caspase-3 and cleaved caspase-3.	Acetylcysteine	45-61	caspase 3	Mus musculus	247-256
33825597-8	2021	However, Pifithrin-alpha (p53 inhibitor) and N-Acetylcysteine (NAC) could reduce cell apoptosis, lung structural damage and oxidative stress, accelerate the expression of Bcl-2, while suppressing the expression of Bax, total caspase-3 and cleaved caspase-3.	Acetylcysteine	63-66	BCL2-associated X protein	Mus musculus	214-217
21131132-9	2011	Expression of CD11a (p &lt; 0.05), CD18 (p &lt; 0.05) and CD97 (p &lt; 0.01) on the granulocytes were significantly lower in the NAC treated group, similarly to lymphocyte CD 49d (p &lt; 0.05) and monocyte CD 49d (p &lt; 0.01) and CD 97 (p &lt; 0.05) expression.	Acetylcysteine	129-132	integrin subunit alpha 4	Homo sapiens	206-212
33825597-8	2021	However, Pifithrin-alpha (p53 inhibitor) and N-Acetylcysteine (NAC) could reduce cell apoptosis, lung structural damage and oxidative stress, accelerate the expression of Bcl-2, while suppressing the expression of Bax, total caspase-3 and cleaved caspase-3.	Acetylcysteine	63-66	caspase 3	Mus musculus	225-234
21131132-9	2011	Expression of CD11a (p &lt; 0.05), CD18 (p &lt; 0.05) and CD97 (p &lt; 0.01) on the granulocytes were significantly lower in the NAC treated group, similarly to lymphocyte CD 49d (p &lt; 0.05) and monocyte CD 49d (p &lt; 0.01) and CD 97 (p &lt; 0.05) expression.	Acetylcysteine	129-132	adhesion G protein-coupled receptor E5	Homo sapiens	231-236
33825597-8	2021	However, Pifithrin-alpha (p53 inhibitor) and N-Acetylcysteine (NAC) could reduce cell apoptosis, lung structural damage and oxidative stress, accelerate the expression of Bcl-2, while suppressing the expression of Bax, total caspase-3 and cleaved caspase-3.	Acetylcysteine	63-66	caspase 3	Mus musculus	247-256
21087961-7	2011	H(2)O(2) also increased phosphorylation of EGFR(Y845) parallel to that of activated Src, but both were eliminated by NAC and PP1 (Src inhibitor).	Acetylcysteine	117-120	epidermal growth factor receptor	Mus musculus	43-47
33453249-4	2021	Concomitant treatment with the antioxidant N-acetyl-cysteine (NAC) reversed only the increased TXNIP expression.	Acetylcysteine	43-60	thioredoxin interacting protein	Rattus norvegicus	95-100
33453249-4	2021	Concomitant treatment with the antioxidant N-acetyl-cysteine (NAC) reversed only the increased TXNIP expression.	Acetylcysteine	62-65	thioredoxin interacting protein	Rattus norvegicus	95-100
33453249-7	2021	Podocytes treatment with NAC reversed Nox4, Col4a1, Acta2, and Tgfb1 increased expression but did not abrogate the reduced expression of nephrin.	Acetylcysteine	25-28	NADPH oxidase 4	Rattus norvegicus	38-42
21087961-7	2011	H(2)O(2) also increased phosphorylation of EGFR(Y845) parallel to that of activated Src, but both were eliminated by NAC and PP1 (Src inhibitor).	Acetylcysteine	117-120	Rous sarcoma oncogene	Mus musculus	130-133
20848084-13	2011	Pretreatment of A549 cells with NAC significantly ameliorated LPS-caused alterations in caspase-9 activation and DNA damage.	Acetylcysteine	32-35	caspase 9	Homo sapiens	88-97
34026460-6	2021	DGUOK mutant iHep and iHep-Orgs, but not control and corrected one, are more sensitive to iron overload-induced ferroptosis, which can be rescued by N-Acetylcysteine (NAC).	Acetylcysteine	149-165	deoxyguanosine kinase	Homo sapiens	0-5
34026460-6	2021	DGUOK mutant iHep and iHep-Orgs, but not control and corrected one, are more sensitive to iron overload-induced ferroptosis, which can be rescued by N-Acetylcysteine (NAC).	Acetylcysteine	167-170	deoxyguanosine kinase	Homo sapiens	0-5
20978740-9	2011	NAC blocked the WNT pathway activation induced by HNE.	Acetylcysteine	0-3	Wnt family member 2	Rattus norvegicus	16-19
33401054-6	2021	Scavenging of ROS in the presence of N-acetylcysteine (NAC) almost blocks the loss of mitochondrial membrane Deltapsim, activation of JNK, cleavage of caspase-3, -9, and an induction of apoptosis in SHK treated PEL cells.	Acetylcysteine	37-53	mitogen-activated protein kinase 8	Mus musculus	134-137
33401054-6	2021	Scavenging of ROS in the presence of N-acetylcysteine (NAC) almost blocks the loss of mitochondrial membrane Deltapsim, activation of JNK, cleavage of caspase-3, -9, and an induction of apoptosis in SHK treated PEL cells.	Acetylcysteine	37-53	caspase 3	Mus musculus	151-164
20978740-13	2011	NAC treatment reduced HNE and 3-nitrotyrosine levels and attenuated the upregulation of LRP6, beta-catenin and CTGF in diabetic rat retina.	Acetylcysteine	0-3	catenin beta 1	Rattus norvegicus	94-106
33401054-6	2021	Scavenging of ROS in the presence of N-acetylcysteine (NAC) almost blocks the loss of mitochondrial membrane Deltapsim, activation of JNK, cleavage of caspase-3, -9, and an induction of apoptosis in SHK treated PEL cells.	Acetylcysteine	55-58	mitogen-activated protein kinase 8	Mus musculus	134-137
33401054-6	2021	Scavenging of ROS in the presence of N-acetylcysteine (NAC) almost blocks the loss of mitochondrial membrane Deltapsim, activation of JNK, cleavage of caspase-3, -9, and an induction of apoptosis in SHK treated PEL cells.	Acetylcysteine	55-58	caspase 3	Mus musculus	151-164
20978740-13	2011	NAC treatment reduced HNE and 3-nitrotyrosine levels and attenuated the upregulation of LRP6, beta-catenin and CTGF in diabetic rat retina.	Acetylcysteine	0-3	cellular communication network factor 2	Rattus norvegicus	111-115
33443102-5	2021	In particular, we found that PKC activation promotes the redox-dependent cytoplasmic localization of KRIT1, whereas inhibition of PKC or treatment with the antioxidant N-acetylcysteine leads to KRIT1 nuclear accumulation.	Acetylcysteine	168-184	KRIT1 ankyrin repeat containing	Homo sapiens	194-199
21170508-5	2011	Pretreatment with N-acetyl-L-cysteine (NAC) significantly inhibited the cell death induced by the combined treatment with BBR and TRAIL as well as recovered the expression levels of c-FLIP and Mcl-1 downregulated by treatment with BBR.	Acetylcysteine	18-37	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	193-198
21266772-4	2011	show that the drug N-acetylcysteine (NAC) can decrease the size of vWF multimers in vitro and in vivo, resolving thrombi in mice.	Acetylcysteine	19-35	Von Willebrand factor	Mus musculus	67-70
21266772-4	2011	show that the drug N-acetylcysteine (NAC) can decrease the size of vWF multimers in vitro and in vivo, resolving thrombi in mice.	Acetylcysteine	37-40	Von Willebrand factor	Mus musculus	67-70
33359261-11	2021	Remarkably, the apoptosis observed in CD4 T cells with MMP depolarization was prevented by incubation with N-acetyl cysteine (NAC).	Acetylcysteine	107-124	CD4 molecule	Sus scrofa	38-41
21266777-9	2011	Injection of NAC into ADAMTS13-deficient mice led to the rapid resolution of thrombi produced by ionophore treatment of the mesenteric venules and reduced plasma vWF multimers.	Acetylcysteine	13-16	Von Willebrand factor	Mus musculus	162-165
33359261-11	2021	Remarkably, the apoptosis observed in CD4 T cells with MMP depolarization was prevented by incubation with N-acetyl cysteine (NAC).	Acetylcysteine	126-129	CD4 molecule	Sus scrofa	38-41
21254278-0	2011	N-acetyl-L-cysteine counteracts oxidative stress and prevents H2O2 induced germ cell apoptosis through down-regulation of caspase-9 and JNK/c-Jun.	Acetylcysteine	0-19	caspase 9	Homo sapiens	122-131
33507837-0	2021	N-acetyl cysteine can blunt metabolic and cardiovascular effects via down-regulation of cardiotrophin-1 in rat model of fructose-induced metabolic syndrome.	Acetylcysteine	0-17	cardiotrophin 1	Rattus norvegicus	88-103
21127198-12	2011	We observed that DBA-induced induction of DR5 and DR4 was mediated through generation of reactive oxygen species (ROS), as N-acetylcysteine blocked the induction of death receptors and suppression of cell survival proteins by DBA.	Acetylcysteine	123-139	TNF receptor superfamily member 10b	Homo sapiens	42-45
33564320-5	2021	Consequently, the expression of integrin beta1 was significantly inhibited by EGCG and NAC.	Acetylcysteine	87-90	integrin subunit beta 1	Homo sapiens	32-46
20955365-8	2011	Glutamate-induced p53 activation was preceded by accumulation of reactive oxygen species, and co-treatment with N-acetyl-cysteine prevented glutamate-induced p53 activation and GADD45alpha expression.	Acetylcysteine	112-129	transformation related protein 53, pseudogene	Mus musculus	158-161
33381973-6	2021	Glutathione-S-transferase theta 1 (GSTT1) facilitates the conjugation of DEB to glutathione as the first step of its detoxification and subsequent elimination via the mercapturic acid pathway.	Acetylcysteine	167-183	glutathione S-transferase theta 1	Homo sapiens	0-33
33381973-6	2021	Glutathione-S-transferase theta 1 (GSTT1) facilitates the conjugation of DEB to glutathione as the first step of its detoxification and subsequent elimination via the mercapturic acid pathway.	Acetylcysteine	167-183	glutathione S-transferase theta 1	Homo sapiens	35-40
21778718-7	2011	NAC reduced the paclitaxel-induced increase in activated caspase-10 levels, but potentiated that for caspase-3.	Acetylcysteine	0-3	caspase 10	Homo sapiens	57-67
33488104-11	2021	miR-129-3p downregulation produced a significant increase in calcium overload, reactive oxygen species (ROS) generation, MMP-2 expression, cytochrome c release and cell apoptosis, and antioxidant N-acetyl cysteine (NAC) rescued the effects of miR-129-3p downregulation.	Acetylcysteine	196-213	microRNA 1293	Homo sapiens	0-10
33488104-11	2021	miR-129-3p downregulation produced a significant increase in calcium overload, reactive oxygen species (ROS) generation, MMP-2 expression, cytochrome c release and cell apoptosis, and antioxidant N-acetyl cysteine (NAC) rescued the effects of miR-129-3p downregulation.	Acetylcysteine	215-218	microRNA 1293	Homo sapiens	0-10
21311702-0	2011	Getting a Knack for NAC: N-Acetyl-Cysteine.	Acetylcysteine	25-42	synuclein alpha	Homo sapiens	20-23
32862473-3	2021	8-MOP enhanced reactive oxygen species (ROS) production by UVA light, and the effect of 8-MOP on TRPA1 could be abolished by the antioxidant N-acetyl cysteine and by removal of critical cysteine residues from the N-terminus domain of the channel.	Acetylcysteine	141-158	transient receptor potential cation channel, subfamily A, member 1	Mus musculus	97-102
21311702-1	2011	N-acetyl-cysteine, N-acetylcysteine, N-acetyl cysteine, and N-acetyl-L-cysteine are all designations for the same compound, which is abbreviated as NAC.	Acetylcysteine	0-17	synuclein alpha	Homo sapiens	148-151
21311702-1	2011	N-acetyl-cysteine, N-acetylcysteine, N-acetyl cysteine, and N-acetyl-L-cysteine are all designations for the same compound, which is abbreviated as NAC.	Acetylcysteine	19-35	synuclein alpha	Homo sapiens	148-151
21311702-1	2011	N-acetyl-cysteine, N-acetylcysteine, N-acetyl cysteine, and N-acetyl-L-cysteine are all designations for the same compound, which is abbreviated as NAC.	Acetylcysteine	37-54	synuclein alpha	Homo sapiens	148-151
21311702-1	2011	N-acetyl-cysteine, N-acetylcysteine, N-acetyl cysteine, and N-acetyl-L-cysteine are all designations for the same compound, which is abbreviated as NAC.	Acetylcysteine	60-79	synuclein alpha	Homo sapiens	148-151
20845026-8	2011	NAC exhibited no significant effect on biochemical parameters but reduced renal tissue SOD level and reversed immunocytochemical staining of inducible nitric oxide synthase (i-NOS) and neurotrophin-3.	Acetylcysteine	0-3	neurotrophin 3	Rattus norvegicus	185-199
33010248-7	2021	Mice were given N-acetylcysteine (NAC) to prevent loss of CD4+ T cells from liver.	Acetylcysteine	16-32	CD4 antigen	Mus musculus	58-61
33010248-7	2021	Mice were given N-acetylcysteine (NAC) to prevent loss of CD4+ T cells from liver.	Acetylcysteine	34-37	CD4 antigen	Mus musculus	58-61
22129741-5	2011	The mRNAs of members of the phase II nuclear factor, erythroid derived 2, like 2 (Nrf2) gene batteries, whose promoter region is called as antioxidant response element (ARE), were down-regulated in the DEN-I3C-NAC group compared to the DEN-I3C group, but Cyp1a1 was not suppressed in the DEN-I3C-NAC group compared to the DEN-I3C group.	Acetylcysteine	210-213	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	255-261
33010248-11	2021	In mice with steatohepatitis given NAC, which prevents loss of CD4+ T cells, M30 and aOX40 were able slow growth of hepatic tumors.	Acetylcysteine	35-38	CD4 antigen	Mus musculus	63-66
22129741-5	2011	The mRNAs of members of the phase II nuclear factor, erythroid derived 2, like 2 (Nrf2) gene batteries, whose promoter region is called as antioxidant response element (ARE), were down-regulated in the DEN-I3C-NAC group compared to the DEN-I3C group, but Cyp1a1 was not suppressed in the DEN-I3C-NAC group compared to the DEN-I3C group.	Acetylcysteine	296-299	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	255-261
33035499-7	2020	In striatum and cortex, NAC prevented glial cells activation (GFAP and Iba-1), decreased NGF, Bcl-2 and NeuN, the increase of lipid peroxidation and PARP induced by GA in both ages.	Acetylcysteine	24-27	poly (ADP-ribose) polymerase family, member 1	Mus musculus	149-153
22132160-8	2011	The pretreatment of cells with N-acetyl-cysteine prevented the loss of intracellular GSH and subsequently DJ-1 oxidation induced by 6-OHDA.	Acetylcysteine	31-48	Parkinsonism associated deglycase	Homo sapiens	106-110
32736244-6	2020	Moreover, the down regulating of p-Akt/Akt, p-mTOR/mTOR and subsequent up-regulation of p-AMPK/AMPK induced by NP can be rescued by pretreatment of NAC.	Acetylcysteine	148-151	mechanistic target of rapamycin kinase	Rattus norvegicus	46-50
32736244-6	2020	Moreover, the down regulating of p-Akt/Akt, p-mTOR/mTOR and subsequent up-regulation of p-AMPK/AMPK induced by NP can be rescued by pretreatment of NAC.	Acetylcysteine	148-151	mechanistic target of rapamycin kinase	Rattus norvegicus	51-55
21912612-7	2011	NAC but not ALP increased cardiac APN concentrations and AdipoR2 expression in diabetic rats.	Acetylcysteine	0-3	adiponectin receptor 2	Rattus norvegicus	57-64
32949789-6	2020	RESULTS: mRNA and protein levels of HO-1 in KMY-J cells were increased significantly at 3, 6, and 9 h after laser irradiation and the increased mRNA level of HO-1 was decreased by antioxidant N-acetyl cysteine treatment.	Acetylcysteine	192-209	heme oxygenase 1	Rattus norvegicus	36-40
32949789-6	2020	RESULTS: mRNA and protein levels of HO-1 in KMY-J cells were increased significantly at 3, 6, and 9 h after laser irradiation and the increased mRNA level of HO-1 was decreased by antioxidant N-acetyl cysteine treatment.	Acetylcysteine	192-209	heme oxygenase 1	Rattus norvegicus	158-162
21912612-8	2011	ALP enhanced the effects of NAC in restoring cardiac AdipoR2 and phosphorylation of Akt, STAT3 and eNOS in diabetic rats.	Acetylcysteine	28-31	adiponectin receptor 2	Rattus norvegicus	53-60
21912612-8	2011	ALP enhanced the effects of NAC in restoring cardiac AdipoR2 and phosphorylation of Akt, STAT3 and eNOS in diabetic rats.	Acetylcysteine	28-31	signal transducer and activator of transcription 3	Rattus norvegicus	89-94
32946259-14	2020	Autophagy inhibition by chloroquine and ROS inhibition by N-acetylcysteine attenuated the proliferation and migration of PASMCs caused by TIGAR knockdown and hypoxia exposure.	Acetylcysteine	58-74	Trp53 induced glycolysis regulatory phosphatase	Mus musculus	138-143
21912612-12	2011	CONCLUSIONS/SIGNIFICANCE: NAC and ALP synergistically restore myocardial APN and AdipoR2 mediated eNOS activation.	Acetylcysteine	26-29	adiponectin receptor 2	Rattus norvegicus	81-88
21121367-6	2010	SWCNT induced nuclear NF-kB/P65 translocation can be inhibited by N-acetylcysteine, indicating elevated ICAM-1 and VCAM-1 expression is mediated by oxidative stress in RAECs, and may play important inflammatory roles in SWCNT-induced vascular endothelium damage.	Acetylcysteine	66-82	RELA proto-oncogene, NF-kB subunit	Rattus norvegicus	22-27
32684241-8	2020	Upregulation of RRAGC was limited by the reactive oxygen species (ROS) scavenger N-acetyl cysteine (NAC), suggesting that ROS are involved in EHMT2-mediated transcriptional regulation of stress-response genes in HCC cells.	Acetylcysteine	81-98	euchromatic histone lysine methyltransferase 2	Homo sapiens	142-147
32684241-8	2020	Upregulation of RRAGC was limited by the reactive oxygen species (ROS) scavenger N-acetyl cysteine (NAC), suggesting that ROS are involved in EHMT2-mediated transcriptional regulation of stress-response genes in HCC cells.	Acetylcysteine	100-103	euchromatic histone lysine methyltransferase 2	Homo sapiens	142-147
20958994-5	2010	The pre-treatment with poly I or carrageenan or NAC significantly inhibited the LOX-1 expression, alpha-SMA expression, the lipid intake and ROS generation and reversed decrease of E-cadherin expression induced by ox-LDL.	Acetylcysteine	48-51	oxidized low density lipoprotein receptor 1	Rattus norvegicus	80-85
33117193-9	2020	The protein expression of HIF-1alpha (an index of HIF-1 activation) and p47phox subunit in the membrane fraction (an index of NADPH oxidase activation) in the laryngeal tissues increased in 14 days IH rats; the former was reduced by NAC, whereas the latter was inhibited by YC-1.	Acetylcysteine	233-236	hypoxia inducible factor 1 subunit alpha	Rattus norvegicus	26-36
20958994-5	2010	The pre-treatment with poly I or carrageenan or NAC significantly inhibited the LOX-1 expression, alpha-SMA expression, the lipid intake and ROS generation and reversed decrease of E-cadherin expression induced by ox-LDL.	Acetylcysteine	48-51	actin gamma 2, smooth muscle	Rattus norvegicus	98-107
32619679-14	2020	Furthermore, data from treatment of reactive oxygen species inhibitor N-acetyl-L-cysteine or NOXs inhibitor diphenyleneiodonium in fructose-exposed HepG2 cells showed that fructose enhanced NOX1, NOX2 and NOX4 expression to increase reactive oxygen species generation, causing oxidative stress and inflammation, more importantly, these disturbances were significantly attenuated by magnesium isoglycyrrhizinate.	Acetylcysteine	70-89	cytochrome b-245 beta chain	Homo sapiens	196-200
20958994-5	2010	The pre-treatment with poly I or carrageenan or NAC significantly inhibited the LOX-1 expression, alpha-SMA expression, the lipid intake and ROS generation and reversed decrease of E-cadherin expression induced by ox-LDL.	Acetylcysteine	48-51	cadherin 1	Rattus norvegicus	181-191
32098455-0	2020	N-acetylcysteine decreases airway inflammation and responsiveness in asthma by modulating claudin 18 expression.	Acetylcysteine	0-16	claudin 18	Mus musculus	90-100
20674558-6	2010	DP increased the levels of reactive oxygen species (ROS) in HepG2 cells, and antioxidant N-acetylcysteine (NAC) completely blocked DP-induced ROS accumulation and the disruption of the balance between Bax and Bcl-2 proteins, and effectively blocked the decreased MMP and apoptosis, but had no effect on the activation of caspase-8 and the up-regulations of DR4 and DR5 induced by DP.	Acetylcysteine	89-105	TNF receptor superfamily member 10b	Homo sapiens	365-368
32098455-7	2020	Levels of CLDN18 protein were higher in lung tissue from OVA mice than tissue from control mice, and were increased by treatment with NAC or dexamethasone.	Acetylcysteine	134-137	claudin 18	Mus musculus	10-16
32534099-5	2020	While SFN significantly (p < 0.05) induced NRF2, KEAP1 and BACH1, NAC attenuated SFN-induced NRF2, KEAP1 and BACH1.	Acetylcysteine	66-69	kelch-like ECH-associated protein 1	Mus musculus	99-104
20674558-6	2010	DP increased the levels of reactive oxygen species (ROS) in HepG2 cells, and antioxidant N-acetylcysteine (NAC) completely blocked DP-induced ROS accumulation and the disruption of the balance between Bax and Bcl-2 proteins, and effectively blocked the decreased MMP and apoptosis, but had no effect on the activation of caspase-8 and the up-regulations of DR4 and DR5 induced by DP.	Acetylcysteine	107-110	TNF receptor superfamily member 10b	Homo sapiens	365-368
32534099-6	2020	The down-regulation of KEAP1 by NAC was of interest, as Keap1 is markedly increased in the MCK conditional frataxin knockout (MCK KO) mouse model and this could lead to the decreased Nrf2 levels.	Acetylcysteine	32-35	kelch-like ECH-associated protein 1	Mus musculus	23-28
32534099-6	2020	The down-regulation of KEAP1 by NAC was of interest, as Keap1 is markedly increased in the MCK conditional frataxin knockout (MCK KO) mouse model and this could lead to the decreased Nrf2 levels.	Acetylcysteine	32-35	kelch-like ECH-associated protein 1	Mus musculus	56-61
20443032-5	2010	At the same time, ERK and c-Jun N-terminal kinase (JNK) as well as cell division control protein 2 homolog (Cdc2) were found to be highly phosphorylated, which could be counteracted with the antioxidant N-acetylcysteine (NAC).	Acetylcysteine	203-219	cyclin dependent kinase 1	Homo sapiens	108-112
20443032-5	2010	At the same time, ERK and c-Jun N-terminal kinase (JNK) as well as cell division control protein 2 homolog (Cdc2) were found to be highly phosphorylated, which could be counteracted with the antioxidant N-acetylcysteine (NAC).	Acetylcysteine	221-224	cyclin dependent kinase 1	Homo sapiens	108-112
20045538-10	2010	Finally, treatment of obese db/db mice with N-acetyl cysteine augmented the expression of AGT in the adipose tissue, but not in the liver.	Acetylcysteine	44-61	WD and tetratricopeptide repeats 1	Mus musculus	101-108
32554304-7	2020	Importantly, antioxidant N-acetylcysteine (NAC) significantly attenuated the induction of DNA damage and the perturbation of proliferation caused by RAD51 depletion.	Acetylcysteine	25-41	RAD51 recombinase	Homo sapiens	149-154
32554304-7	2020	Importantly, antioxidant N-acetylcysteine (NAC) significantly attenuated the induction of DNA damage and the perturbation of proliferation caused by RAD51 depletion.	Acetylcysteine	43-46	RAD51 recombinase	Homo sapiens	149-154
20808797-0	2010	Oral N-acetyl-cysteine attenuates loss of dopaminergic terminals in alpha-synuclein overexpressing mice.	Acetylcysteine	5-22	synuclein, alpha	Mus musculus	68-83
20808797-3	2010	We hypothesized that supplementation with n-acetylcysteine (NAC), a source of cysteine--the limiting amino acid in glutathione synthesis, would protect against alpha-synuclein toxicity.	Acetylcysteine	42-58	synuclein, alpha	Mus musculus	160-175
20808797-3	2010	We hypothesized that supplementation with n-acetylcysteine (NAC), a source of cysteine--the limiting amino acid in glutathione synthesis, would protect against alpha-synuclein toxicity.	Acetylcysteine	60-63	synuclein, alpha	Mus musculus	160-175
32817784-6	2020	Confocal microscopy revealed that diazoxide also led to nuclear translocation of the transcription factors c-Fos and NFkappaB, which was also blocked by NAC or 5-HD.	Acetylcysteine	153-156	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	107-112
20808797-6	2010	Despite the transient nature of the impact of NAC on brain glutathione, the loss of dopaminergic terminals at 1 year associated with SNCA overexpression was significantly attenuated by NAC supplementation, as measured by immunoreactivity for tyrosine hydroxylase in the striatum (p = 0.007; unpaired, two-tailed t-test), with a similar but nonsignificant trend for dopamine transporter (DAT) immunoreactivity.	Acetylcysteine	185-188	synuclein alpha	Homo sapiens	133-137
20808797-7	2010	NAC significantly decreased the levels of human SNCA in the brains of PDGFb-SNCA transgenic mice compared to alanine treated transgenics.	Acetylcysteine	0-3	synuclein alpha	Homo sapiens	48-52
32347295-0	2020	Mechanism of N-acetylcysteine in alleviating diabetic myocardial ischemia reperfusion injury by regulating PTEN/Akt pathway through promoting DJ-1.	Acetylcysteine	13-29	phosphatase and tensin homolog	Rattus norvegicus	107-111
32545880-11	2020	Meanwhile, NAC pretreatment also blocked the phosphorylation of ERK1/2 and p38 induced by NEFA, and the nucleation of Nrf2 and p53, suggesting that ROS plays a crucial role in regulating the NEFA-induced apoptosis of GCs.	Acetylcysteine	11-14	mitogen-activated protein kinase 14	Bos taurus	75-78
20808797-7	2010	NAC significantly decreased the levels of human SNCA in the brains of PDGFb-SNCA transgenic mice compared to alanine treated transgenics.	Acetylcysteine	0-3	synuclein alpha	Homo sapiens	76-80
32551386-6	2020	NAC-related increase in glutathione was associated with significant alterations in tumor necrosis factor-alpha (TNF-alpha), interleukin (IL)-6, IL-8 and IL-10 levels secreted in the culture medium.	Acetylcysteine	0-3	interleukin 10	Homo sapiens	153-158
20489149-7	2010	In vitro, NAC not only reduced ROS production below control levels, but further decreased the expression of thyroid-specific proteins in addition to IL-1alpha/IFNgamma-inhibitory effects.	Acetylcysteine	10-13	interleukin 1 alpha	Homo sapiens	149-158
32551386-8	2020	In contrast, the secretary IL-10 was significantly increased as a result of NAC treatments.	Acetylcysteine	76-79	interleukin 10	Homo sapiens	27-32
20479336-7	2010	Antioxidants ebselen and N-acetylcysteine decreased the association of Axl with MHC-IIB in response to both Gas6 and reactive oxygen species.	Acetylcysteine	25-41	Axl receptor tyrosine kinase	Rattus norvegicus	71-74
31769880-6	2020	Of note, mice with TAL haploinsufficiency are also predisposed to HCC and APAP-induced liver failure which are preventable with oral N-acetylcysteine (NAC) administration.	Acetylcysteine	133-149	transaldolase 1	Homo sapiens	19-22
31769880-6	2020	Of note, mice with TAL haploinsufficiency are also predisposed to HCC and APAP-induced liver failure which are preventable with oral N-acetylcysteine (NAC) administration.	Acetylcysteine	151-154	transaldolase 1	Homo sapiens	19-22
31769880-9	2020	All four patients with TAL haplo-insufficiency with APAP-induced liver failure were successfully treated with NAC.	Acetylcysteine	110-113	transaldolase 1	Homo sapiens	23-26
20571742-10	2010	The phosphorylation of c-jun N-terminal protein kinase (JNK) was increased markedly when stimulated with high glucose for 30 and 60 min, which was abolished when pretreated with CLT or NAC.	Acetylcysteine	185-188	mitogen-activated protein kinase 8	Rattus norvegicus	23-54
31769880-12	2020	These findings suggest an unexpected prevalence and variety of genetic changes in human TALDO1 with relevance for liver injury that may be preventable by treatment with NAC.	Acetylcysteine	169-172	transaldolase 1	Homo sapiens	88-94
32188759-8	2020	The endoplasmic reticulum stress response in the TLR9/RP105-stimulated cells was higher in IgG+ than in IgG- cells and was reduced by NAC in IgG+ cells only.	Acetylcysteine	134-137	CD180 molecule	Homo sapiens	54-59
32023790-9	2020	BPA and its substitutes showed significant cytotoxicity and ROS production, which were attenuated by the treatment with N-acetylcysteine(NAC), a ROS scavenger.	Acetylcysteine	120-136	X-linked Kx blood group	Homo sapiens	137-140
20571742-10	2010	The phosphorylation of c-jun N-terminal protein kinase (JNK) was increased markedly when stimulated with high glucose for 30 and 60 min, which was abolished when pretreated with CLT or NAC.	Acetylcysteine	185-188	mitogen-activated protein kinase 8	Rattus norvegicus	56-59
20399762-0	2010	N-acetylcysteine prevents memory deficits, the decrease in acetylcholinesterase activity and oxidative stress in rats exposed to cadmium.	Acetylcysteine	0-16	acetylcholinesterase	Rattus norvegicus	59-79
32155788-2	2020	L-N-acetylcysteine (L-NAC) and dexamethasone (Dex) have been individually shown to provide otoprotection albeit at higher concentrations that may be associated with adverse effects.	Acetylcysteine	0-18	X-linked Kx blood group	Homo sapiens	22-25
32155766-8	2020	N-acetyl-L-cysteine (NAC) markedly decreased PCV2-induced ROS, down-regulated Drp1 phosphorylation, and lessened PINK1 expression and mitochondrial accumulation of Parkin.	Acetylcysteine	0-19	parkin RBR E3 ubiquitin protein ligase	Sus scrofa	164-170
32155766-8	2020	N-acetyl-L-cysteine (NAC) markedly decreased PCV2-induced ROS, down-regulated Drp1 phosphorylation, and lessened PINK1 expression and mitochondrial accumulation of Parkin.	Acetylcysteine	21-24	parkin RBR E3 ubiquitin protein ligase	Sus scrofa	164-170
20399762-6	2010	Decreased AChE activity was found in hippocampus, cerebellum and hypothalamus in the Cd-group but NAC reversed this effect totally or partially while in cortex synaptosomes and striatum there was no alteration in AChE activity.	Acetylcysteine	98-101	acetylcholinesterase	Rattus norvegicus	213-217
32132577-7	2020	Both SB225002, an inhibitor of CXCR2, and antioxidant N-acetylcysteine suppressed the TGF-beta2-induced EMT in ARPE-19 cells.	Acetylcysteine	54-70	transforming growth factor beta 2	Homo sapiens	86-95
20399762-9	2010	The present findings show that treatment with NAC prevented the Cd-mediated decrease in AChE activity, as well as oxidative stress and consequent memory impairment in Cd-exposed rats, demonstrating that this compound may modulate cholinergic neurotransmission and consequently improve cognition.	Acetylcysteine	46-49	acetylcholinesterase	Rattus norvegicus	88-92
20117100-9	2010	The inactivation of recombinant CYP1A1 and human liver microsomes by CBD required NADPH, was not influenced by dialysis and by glutathione, N-acetylcysteine, and superoxide dismutase as trapping agents.	Acetylcysteine	140-156	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	32-38
32068662-5	2020	MMP-9 expression is blunted by a diverse array of molecular factors, such as tissue inhibitors of metalloproteinases, cyclosporine A (CyA), PES_103, epigalloccatechin-3-gallate (EGCG), N-acetylcysteine (NaC), ascorbate, tetracyclines, and corticosteroids.	Acetylcysteine	185-201	matrix metallopeptidase 9	Homo sapiens	0-5
32068662-5	2020	MMP-9 expression is blunted by a diverse array of molecular factors, such as tissue inhibitors of metalloproteinases, cyclosporine A (CyA), PES_103, epigalloccatechin-3-gallate (EGCG), N-acetylcysteine (NaC), ascorbate, tetracyclines, and corticosteroids.	Acetylcysteine	203-206	matrix metallopeptidase 9	Homo sapiens	0-5
31631367-10	2020	ALI-induced lung morphological damage, edema and aberrant MPO activity can be attenuated by NAC or DEX and mostly by NAC+DEX.	Acetylcysteine	92-95	myeloperoxidase	Mus musculus	58-61
31631367-10	2020	ALI-induced lung morphological damage, edema and aberrant MPO activity can be attenuated by NAC or DEX and mostly by NAC+DEX.	Acetylcysteine	117-120	myeloperoxidase	Mus musculus	58-61
20356045-7	2010	Pretreatment with N-acetyl-l-cysteine (NAC) attenuated 6-DG-induced DR5 expression and inhibited TRAIL-induced apoptosis.	Acetylcysteine	18-37	TNF receptor superfamily member 10b	Homo sapiens	68-71
20356045-7	2010	Pretreatment with N-acetyl-l-cysteine (NAC) attenuated 6-DG-induced DR5 expression and inhibited TRAIL-induced apoptosis.	Acetylcysteine	39-42	TNF receptor superfamily member 10b	Homo sapiens	68-71
31245853-5	2020	In contrast, NAC reduced the vitamin D receptor (VDR) abundance and its signaling of ECD.	Acetylcysteine	13-16	vitamin D receptor	Homo sapiens	29-47
20037173-10	2010	However, NAC pretreatment significantly improved renal function and decreased the activation of ERK, JNK, Bax and Bad, whereas it increased Bcl-2 and Bcl-xL.	Acetylcysteine	9-12	mitogen-activated protein kinase 8	Rattus norvegicus	101-104
31245853-5	2020	In contrast, NAC reduced the vitamin D receptor (VDR) abundance and its signaling of ECD.	Acetylcysteine	13-16	vitamin D receptor	Homo sapiens	49-52
20037173-10	2010	However, NAC pretreatment significantly improved renal function and decreased the activation of ERK, JNK, Bax and Bad, whereas it increased Bcl-2 and Bcl-xL.	Acetylcysteine	9-12	BCL2 associated X, apoptosis regulator	Rattus norvegicus	106-109
31556775-13	2020	Two-hit induced hippocampal alterations in females, namely expression of GPER-1, alpha7-nAChR and parvalbumin, were prevented by NAC.	Acetylcysteine	129-132	parvalbumin	Rattus norvegicus	98-109
20233320-8	2010	Pharmacological agents NAC, U0126, and PD98059 were found to decrease the CsA-induced PAI-1 mRNA and protein expression (P &lt; 0.05).	Acetylcysteine	23-26	serpin family E member 1	Homo sapiens	86-91
31948545-4	2020	We describe a procedure for the differentiation of TCF-1+ stem-like CD8+ memory T cells from peripheral blood naive precursors that takes advantage of the use of antioxidants, in particular N-acetylcysteine (NAC), in combination with T cell receptor stimulation and proinflammatory cytokines.	Acetylcysteine	190-206	CD8a molecule	Homo sapiens	68-71
31948545-4	2020	We describe a procedure for the differentiation of TCF-1+ stem-like CD8+ memory T cells from peripheral blood naive precursors that takes advantage of the use of antioxidants, in particular N-acetylcysteine (NAC), in combination with T cell receptor stimulation and proinflammatory cytokines.	Acetylcysteine	208-211	CD8a molecule	Homo sapiens	68-71
19903460-8	2010	Induction of OPN expression by FGF-2 was inhibited not only by PD98059 (MEK1 inhibitor) and PP1 (c-Src inhibitor), but also by an antioxidant, N-acetyl cysteine.	Acetylcysteine	143-160	secreted phosphoprotein 1	Homo sapiens	13-16
32882411-0	2020	N-acetyl-cysteine mediates protection against Mycobacterium avium through induction of human beta-defensin-2 in a mouse lung infection model.	Acetylcysteine	0-17	defensin beta 4B	Homo sapiens	93-108
20080177-7	2010	NAC treatment suppressed the contraction-mediated increase in 2-DG uptake; lactate production; hexokinase, PFK, and G6PDH activities; and gene expression of GLUT4, HKII, and PFK.	Acetylcysteine	0-3	solute carrier family 2 member 4	Rattus norvegicus	157-162
20198323-6	2010	Moreover, pre-treatment of transfected cells with N-acetyl L-cysteine blocked the silencing of uPA and uPAR, which further confirmed the oxidative damage-mediated downregulation.	Acetylcysteine	50-69	plasminogen activator, urokinase receptor	Homo sapiens	103-107
31822750-6	2019	MMP13 expression and down-regulation of type II collagen in chondrocytes, both of which indicate osteoarthritis, as well as chondrocyte apoptosis in osteoarthritis rats were inhibited by NAC.	Acetylcysteine	187-190	matrix metallopeptidase 13	Rattus norvegicus	0-5
31867003-6	2019	Using the HSG cell line, our results showed that both ICAM-1 and PD-L1 are induced by ROS through pSTAT3, and that this activation pathway is reversed by the use of JAK inhibitors, AG490 and ruxolitinib, as well as by N-acetylcysteine, which is a direct inhibitor of ROS.	Acetylcysteine	218-234	intercellular adhesion molecule 1	Homo sapiens	54-60
31871537-8	2019	In H9c2 cells pretreated with ROS scavenger N-acetylcysteine, or transfected with miR-15b mimic and inhibitor, fructose-induced cardiac ROS overload could drive Pitx2c-mediated miR-15b low expression, then cause p-p53-activated TGF-beta1/Smads signaling and CTGF induction in myocardial fibrosis.	Acetylcysteine	44-60	microRNA 15b	Rattus norvegicus	177-184
20093493-8	2010	In addition, NAC reduced PCNA and cyclin D1 immunostainings, as well as thyroid weight, whereas 15dPGJ2 influenced neither thyroid weight nor cell proliferation.	Acetylcysteine	13-16	proliferating cell nuclear antigen	Homo sapiens	25-29
31493144-14	2019	Importantly, we found that activation of the p38 and JNK signaling pathways prompted by PL and oxaliplatin was also reversed by NAC pretreatment.	Acetylcysteine	128-131	mitogen-activated protein kinase 8	Mus musculus	53-56
20179891-6	2010	Furthermore, NAC increased the protein expression of p-ERK, while inhibited protein expression of p-JNK, NF-kappaB in gastric mucosa.	Acetylcysteine	13-16	mitogen-activated protein kinase 8	Rattus norvegicus	100-103
30676497-6	2019	NAC ameliorated the gentamicin-induced decreases in the levels of autophagy-related proteins, such as LC3 (microtubule-associated protein 1 light chain 3), PINK1 (phosphatase and tensin homologue deleted on chromosome10-induced kinase 1), phospho-parkin, AMBRA1 (activatingmolecule in Beclin 1-regulated autophagy), p62/SQSTM1 (sequestosome protein 1), and polyubiquitinated protein aggregates.	Acetylcysteine	0-3	parkin RBR E3 ubiquitin protein ligase	Sus scrofa	247-253
31890447-0	2019	Novel Use of N-Acetylcysteine in Management of Tyrosine Kinase Inhibitor Induced Acute Liver Injury.	Acetylcysteine	13-29	TXK tyrosine kinase	Homo sapiens	47-62
20193479-18	2010	NAC might provide protection of the Clara cells from oxidative damage and possibly through the elevation of the synthesis and secretion of CC16.	Acetylcysteine	0-3	secretoglobin family 1A member 1	Homo sapiens	139-143
31611307-7	2019	N-acetyl-L-cysteine and mito-TEMPO blocked the induction of IL-1beta by inhibiting reactive oxygen species (ROS) with SAA treatment.	Acetylcysteine	0-19	serum amyloid A cluster	Mus musculus	118-121
20193479-19	2010	These data indicate that NAC decreases airway inflammation induced by CS via induction of CC16.	Acetylcysteine	25-28	secretoglobin family 1A member 1	Homo sapiens	90-94
31542478-3	2019	Antioxidants N-acetylcysteine and butylated hydroxyanisole suppressed MPP+-induced cytotoxicity, AMPK, and Akt activation.	Acetylcysteine	13-29	protein kinase AMP-activated non-catalytic subunit beta 1	Homo sapiens	97-101
19833168-5	2010	Rottlerin-mediated HO-1 induction was abrogated in the presence of N-acetylcysteine (NAC) or glutathione (GSH).	Acetylcysteine	67-83	heme oxygenase 1	Homo sapiens	19-23
31521245-7	2019	Additionally, we also observed that N-Acetylcysteine (NAC, a ROS scavenger) pretreatment inhibited NLRP3 inflammasome activation as evidenced by suppressing the upregulation of NLRP3, ASC, cleaved-caspase-1, GSDMD-N, IL-1beta and IL-18 protein levels in CSE-treated ECs.	Acetylcysteine	36-52	interleukin 18	Homo sapiens	230-235
31521245-7	2019	Additionally, we also observed that N-Acetylcysteine (NAC, a ROS scavenger) pretreatment inhibited NLRP3 inflammasome activation as evidenced by suppressing the upregulation of NLRP3, ASC, cleaved-caspase-1, GSDMD-N, IL-1beta and IL-18 protein levels in CSE-treated ECs.	Acetylcysteine	54-57	interleukin 18	Homo sapiens	230-235
31704836-6	2019	G3BP1 depletion impaired the intracellular ROS scavenging system and NAC abolished the radiation-sensitive phenotypes caused by G3BP1 depletion.	Acetylcysteine	69-72	G3BP stress granule assembly factor 1	Homo sapiens	128-133
19833168-5	2010	Rottlerin-mediated HO-1 induction was abrogated in the presence of N-acetylcysteine (NAC) or glutathione (GSH).	Acetylcysteine	85-88	heme oxygenase 1	Homo sapiens	19-23
22272000-1	2009	To clarify the modifying effect of N-Acetyl-L-Cysteine (NAC), which has antioxidative ability, on hepatocarcinogenesis promoted by fenofibrate (FF), a peroxisome proliferator-activated receptor (PPAR) alpha agonist , male F344/N rats were administered a single intraperitoneal injection of N-diethylnitrosamine (DEN) as an initiator followed by administration of a diet containing 3,000 ppm of FF for 16 weeks.	Acetylcysteine	35-54	peroxisome proliferator activated receptor alpha	Rattus norvegicus	195-199
31442556-5	2019	Accordingly, general antioxidants such as ascorbic acid, alpha-tocopherol, gallic acid, and N-acetylcysteine partially protected mice from PAF-induced death.	Acetylcysteine	92-108	patchy fur	Mus musculus	139-142
31442556-8	2019	PAF stimulated all three (ERK, JNK, and p38) of the MAP-kinases, which were also inhibited by N-acetylcysteine.	Acetylcysteine	94-110	patchy fur	Mus musculus	0-3
31583053-5	2019	Pretreatment with the antioxidant N-acetylcysteine (NAC) attenuated hyperglycemia-induced reduction of Cav-3 expression and Akt and STAT3 activation and restored RPC-mediated cardioprotection in diabetes, which was abolished by cardiac-specific knockdown of Cav-3 by AAV9-shRNA-Cav-3, PI3K/Akt inhibitor wortmannin, or JAK2/STAT3 inhibitor AG490, respectively.	Acetylcysteine	34-50	Janus kinase 2	Rattus norvegicus	319-323
31583053-5	2019	Pretreatment with the antioxidant N-acetylcysteine (NAC) attenuated hyperglycemia-induced reduction of Cav-3 expression and Akt and STAT3 activation and restored RPC-mediated cardioprotection in diabetes, which was abolished by cardiac-specific knockdown of Cav-3 by AAV9-shRNA-Cav-3, PI3K/Akt inhibitor wortmannin, or JAK2/STAT3 inhibitor AG490, respectively.	Acetylcysteine	52-55	Janus kinase 2	Rattus norvegicus	319-323
30982974-11	2019	Furthermore, ROS inhibitor N-acetyl-L-cysteine (NAC) also suppressed BaP co-exposure-induced expression of epithelial TSLP, IL-33, and IL-25.	Acetylcysteine	27-46	interleukin 33	Mus musculus	124-129
22272000-1	2009	To clarify the modifying effect of N-Acetyl-L-Cysteine (NAC), which has antioxidative ability, on hepatocarcinogenesis promoted by fenofibrate (FF), a peroxisome proliferator-activated receptor (PPAR) alpha agonist , male F344/N rats were administered a single intraperitoneal injection of N-diethylnitrosamine (DEN) as an initiator followed by administration of a diet containing 3,000 ppm of FF for 16 weeks.	Acetylcysteine	56-59	peroxisome proliferator activated receptor alpha	Rattus norvegicus	151-193
30982974-11	2019	Furthermore, ROS inhibitor N-acetyl-L-cysteine (NAC) also suppressed BaP co-exposure-induced expression of epithelial TSLP, IL-33, and IL-25.	Acetylcysteine	48-51	interleukin 33	Mus musculus	124-129
22272000-1	2009	To clarify the modifying effect of N-Acetyl-L-Cysteine (NAC), which has antioxidative ability, on hepatocarcinogenesis promoted by fenofibrate (FF), a peroxisome proliferator-activated receptor (PPAR) alpha agonist , male F344/N rats were administered a single intraperitoneal injection of N-diethylnitrosamine (DEN) as an initiator followed by administration of a diet containing 3,000 ppm of FF for 16 weeks.	Acetylcysteine	56-59	peroxisome proliferator activated receptor alpha	Rattus norvegicus	195-199
31447555-5	2019	NAC can effectively mitigate iron-induced oxidative injury of cardiomyocytes, evidenced by reduced production of MDA, 8-iso-PGF2alpha, and 8-OHDG and maintained concentrations of SOD, CAT, GSH-Px, and GSH in ELISA and biochemical tests; downregulated expression of CHOP, GRP78, p62, and LC3-II proteins in Western Blot, and less cardiomyocytes apoptosis in flow cytometric analysis.	Acetylcysteine	0-3	heat shock protein family A (Hsp70) member 5	Rattus norvegicus	271-276
20104683-8	2009	The level of TNF-alpha and ALT declined significantly in the group pretreated by NAC.	Acetylcysteine	81-84	glutamic pyruvic transaminase, soluble	Mus musculus	27-30
31206177-14	2019	We also found that treatment with the antioxidant N-acetylcysteine (NAC) improved fetal survival in DHT+insulin-treated pregnant rats, an effect related to changes in Keap1/Nrf2 and nuclear factor-kappaB signalling.	Acetylcysteine	50-66	Kelch-like ECH-associated protein 1	Rattus norvegicus	167-172
31206177-14	2019	We also found that treatment with the antioxidant N-acetylcysteine (NAC) improved fetal survival in DHT+insulin-treated pregnant rats, an effect related to changes in Keap1/Nrf2 and nuclear factor-kappaB signalling.	Acetylcysteine	68-71	Kelch-like ECH-associated protein 1	Rattus norvegicus	167-172
19625608-6	2009	The HOCl-mediated induction of Nrf2 or HO-1 was blocked by the glutathione donor N-acetyl-l-cysteine but was unaffected by ascorbic or uric acid.	Acetylcysteine	81-100	heme oxygenase 1	Homo sapiens	39-43
31229567-8	2019	Pretreatment with N-acetyl-L-cysteine (NAC), a ROS scavenger and antioxidant, suppressed maduramicin-induced inhibition of PP5 and activation of JNK as well as apoptosis.	Acetylcysteine	18-37	mitogen-activated protein kinase 8	Mus musculus	145-148
31229567-8	2019	Pretreatment with N-acetyl-L-cysteine (NAC), a ROS scavenger and antioxidant, suppressed maduramicin-induced inhibition of PP5 and activation of JNK as well as apoptosis.	Acetylcysteine	39-42	mitogen-activated protein kinase 8	Mus musculus	145-148
31360201-10	2019	Leukotriene B4 production and 5-lipoxygenase expression were decreased by blocking the UII receptor (UT) with urantide, eliminating ROS with N-acetylcysteine and diphenyliodonium, and inhibiting Akt phosphorylation with LY294002.	Acetylcysteine	141-157	arachidonate 5-lipoxygenase	Mus musculus	30-44
2548765-5	1989	Endothelial cells stimulated with bradykinin or exposed to stirred medium expressed a dose-dependent inhibition of platelet aggregation that was potentiated by the reduced thiol, N-acetylcysteine.	Acetylcysteine	179-195	kininogen 1	Bos taurus	34-44
19346170-6	2009	Rapid hydrolysis of the BA-NAC conjugates by rabbit liver carboxylesterase was found, demonstrating the possible labile nature of the NAC conjugates formed in the liver.	Acetylcysteine	27-30	liver carboxylesterase 1	Oryctolagus cuniculus	52-74
2658458-1	1989	In a randomized, double-blind study, 131 consecutive patients, subjected to elective upper laparotomy, were prophylactically given the recommended dose of N-acetylcysteine (NAC) (Mucomyst, ASTRA) (200 mg x 3) or placebo against postoperative pulmonary complications.	Acetylcysteine	179-187	X-linked Kx blood group	Homo sapiens	155-177
31289608-3	2019	NAC, the ROS inhibitor, significantly inhibited the up-regulation of protein expression of integrin alphav, integrin beta3 and laminin by palmitate (P &lt; 0.05).	Acetylcysteine	0-3	integrin subunit alpha V	Homo sapiens	91-122
19953933-13	2009	CONCLUSION: NAC inhibits the atherosclerotic formation, suppresses the levels of ox-LDL, MMP-9 and MMP-2 and downgrades the expression of matrix metalloproteinase mRNA.	Acetylcysteine	12-15	72 kDa type IV collagenase	Oryctolagus cuniculus	99-104
19551668-1	2009	PURPOSE: To evaluate the effect of topical N-acetylcysteine (NAC) on interleukin 1-alpha (IL-1alpha) levels in tear fluid after myopic laser subepithelial keratectomy (LASEK) and its possible role in modulating corneal wound healing.	Acetylcysteine	43-59	interleukin 1 alpha	Homo sapiens	69-88
31316651-2	2019	Nitroglycerin, N-acetyl cysteine and Metoprolol in acute liver injury induced by CCL4.	Acetylcysteine	15-32	C-C motif chemokine 4	Oryctolagus cuniculus	81-85
31285782-10	2019	Interestingly, treatment with either N-acetyl-L-cysteine (NAC) or diphenyleneiodonium (DPI) reduced the PMA-stimulated phosphorylation of these PTKs, implicating a potential role in cellular ROS signaling.	Acetylcysteine	37-56	X-linked Kx blood group	Homo sapiens	58-61
3242443-8	1988	Covalent binding of radioactivity from [14C]-PCBD-NAC to cytosolic protein could be detected after 5 min incubation, and although the extent of binding was similar for both male and female cytosol at early time periods, after 60 min incubation more binding was found in the presence of male cytosol.	Acetylcysteine	50-53	pterin-4 alpha-carbinolamine dehydratase 1	Rattus norvegicus	45-49
3242443-10	1988	These results indicate that the sex differences in the nephrotoxicity of HCBD and PCBD-NAC in the rat are not attributable to differences in the rate of deacetylation of PCBD-NAC to give the proximate nephrotoxin PCBD-CYS.	Acetylcysteine	87-90	pterin-4 alpha-carbinolamine dehydratase 1	Rattus norvegicus	82-86
3946094-8	1986	At doses up to 30 mg of 1,3-DBP, excretion of mercapturic acids was virtually complete in 24 h urine and amounted to about 19% of the dose (11.3% MA I, 4.9% MA II, 2.6% MA III and 0.2% MA IV).	Acetylcysteine	46-63	D-box binding PAR bZIP transcription factor	Rattus norvegicus	28-31
33402029-7	2021	Both N-acetyl-L-cysteine (NAC, an ROS antagonist) and Wnt3a (an activator of the Wnt/beta-catenin pathway) attenuated the poor osteogenic ability of osteoblasts.	Acetylcysteine	5-24	catenin (cadherin associated protein), beta 1	Mus musculus	85-97
19551668-1	2009	PURPOSE: To evaluate the effect of topical N-acetylcysteine (NAC) on interleukin 1-alpha (IL-1alpha) levels in tear fluid after myopic laser subepithelial keratectomy (LASEK) and its possible role in modulating corneal wound healing.	Acetylcysteine	43-59	interleukin 1 alpha	Homo sapiens	90-99
33402029-8	2021	In addition, NAC reactivated the Wnt/beta-catenin pathway in osteoblasts under high-fat stimulation.	Acetylcysteine	13-16	catenin (cadherin associated protein), beta 1	Mus musculus	37-49
31293646-6	2019	Cisplatin exposure induced ROS stress in Hep-2 cells in a time-dependent manner and was accompanied by increased Nrf2 and SENP3 protein accumulations, an effect reversed by the addition of the antioxidant N-acetyl-cysteine (NAC).	Acetylcysteine	205-222	SUMO specific peptidase 3	Homo sapiens	122-127
19551668-1	2009	PURPOSE: To evaluate the effect of topical N-acetylcysteine (NAC) on interleukin 1-alpha (IL-1alpha) levels in tear fluid after myopic laser subepithelial keratectomy (LASEK) and its possible role in modulating corneal wound healing.	Acetylcysteine	61-64	interleukin 1 alpha	Homo sapiens	69-88
19551668-1	2009	PURPOSE: To evaluate the effect of topical N-acetylcysteine (NAC) on interleukin 1-alpha (IL-1alpha) levels in tear fluid after myopic laser subepithelial keratectomy (LASEK) and its possible role in modulating corneal wound healing.	Acetylcysteine	61-64	interleukin 1 alpha	Homo sapiens	90-99
19551668-14	2009	CONCLUSIONS: NAC seems to have an additive effect to steroids in suppressing IL-1alpha levels in tear fluid and may be clinically advantageous in modulating corneal wound healing during the early postoperative period after LASEK.	Acetylcysteine	13-16	interleukin 1 alpha	Homo sapiens	77-86
19551139-10	2009	Our further study revealed that antioxidant N-acetylcysteine attenuated the contractile dysfunction in APP/PS1 mice.	Acetylcysteine	44-60	presenilin 1	Mus musculus	107-110
30998386-6	2019	In Xrcc1-deficienct SSCs, elevated oxidative stress and mitochondrial dysfunction could be partially reversed by treatment with the antioxidant N-acetylcysteine (NAC), whereas NAC treatment did not restore the fertility or ameliorate the apoptosis caused by loss of Xrcc1.	Acetylcysteine	144-160	X-ray repair complementing defective repair in Chinese hamster cells 1	Mus musculus	3-8
33957094-6	2021	Mitochondrial reactive oxygen species (ROS) production is critical in this process, as eliminating ROS with N-acetylcysteine (NAC) efficiently inhibits PINK1 signaling-mediated mitophagy initiation and alleviates lysosomal dysfunction.	Acetylcysteine	108-124	PTEN induced kinase 1	Homo sapiens	152-157
33957094-6	2021	Mitochondrial reactive oxygen species (ROS) production is critical in this process, as eliminating ROS with N-acetylcysteine (NAC) efficiently inhibits PINK1 signaling-mediated mitophagy initiation and alleviates lysosomal dysfunction.	Acetylcysteine	126-129	PTEN induced kinase 1	Homo sapiens	152-157
30998386-6	2019	In Xrcc1-deficienct SSCs, elevated oxidative stress and mitochondrial dysfunction could be partially reversed by treatment with the antioxidant N-acetylcysteine (NAC), whereas NAC treatment did not restore the fertility or ameliorate the apoptosis caused by loss of Xrcc1.	Acetylcysteine	162-165	X-ray repair complementing defective repair in Chinese hamster cells 1	Mus musculus	3-8
19328227-7	2009	The antioxidant N-acetylcysteine abolished As(3+)-induced Gclc expression and attenuated induction of Gclm.	Acetylcysteine	16-32	glutamate-cysteine ligase, modifier subunit	Mus musculus	102-106
30838890-5	2019	We assessed miR-122 expression in patients receiving the two acetylcysteine regimens and in a separate group with acute liver injury (ALI).	Acetylcysteine	61-75	microRNA 122	Homo sapiens	12-19
33247942-14	2021	The most pronounced decrease was demonstrated within the NAC-NEC-NAC group CONCLUSIONS: NAC treatment can attenuate newborn inflammatory response syndrome and decrease offspring brain neuro apoptosis and inflammation in a rat model of NEC by inhibition of NFkB, nNOS and Caspase 3 pathways.	Acetylcysteine	57-60	nitric oxide synthase 1	Rattus norvegicus	262-266
33919218-7	2021	Treating C2C12 cells with antioxidant N-acetylcysteine also promoted osteoblast differentiation, and upregulated Runx2/Osterix/Dlx5, while ROS generator antimycin A treatment performed the opposite.	Acetylcysteine	38-54	Sp7 transcription factor 7	Mus musculus	119-126
30838890-8	2019	Median normalized miR-122 Ct after 20 h of acetylcysteine was 2.2 (IQR 1.9, 6.4), 1.1 (0.7, 2.9), 63.9 (2.5, 168), 123.2 (40.9, 207.8) in the NACSTOP-abbreviated, NACSTOP-control, ALI and hepatotoxicity groups, respectively.	Acetylcysteine	43-57	microRNA 122	Homo sapiens	18-25
19326266-6	2009	Treatment of the ROS scavenger N-acetyl-cysteine (NAC) inhibited EGFR transactivation and ERK phosphorylation induced by hUII.	Acetylcysteine	31-48	urotensin 2	Homo sapiens	121-125
33388248-7	2021	Investigation observations revealed that PCs with NAC showed reduced platelet activation, annexin V binding, ROS production, and sialic acid levels.	Acetylcysteine	50-53	annexin A5	Mus musculus	90-99
19326266-6	2009	Treatment of the ROS scavenger N-acetyl-cysteine (NAC) inhibited EGFR transactivation and ERK phosphorylation induced by hUII.	Acetylcysteine	50-53	urotensin 2	Homo sapiens	121-125
19350554-7	2009	In contrast, N-acetylcysteine, a potent cysteine reductive compound, significantly prevents up-regulation of HMOX1, GCLM, and CXCL2 genes, and repression of MMP9 and CCL22 genes induced by As(2)O(3).	Acetylcysteine	13-29	heme oxygenase 1	Homo sapiens	109-114
33649207-8	2021	ROS scavenging by N-acetylcysteine reverted the Ido1 -/-Gr-1+CD11b+ composition and function to an MDSC state, as well as improved the survival of GVHD hosts with Ido1 -/- BM.	Acetylcysteine	18-34	integrin subunit alpha M	Homo sapiens	61-66
30350305-9	2019	Using antioxidant N-acetyl cysteine, we detected increased level of reactive oxygen species generation that was found responsible for induced cathepsin B expression by DA and resultant APP degradation.	Acetylcysteine	18-35	cathepsin B	Homo sapiens	142-153
19350554-7	2009	In contrast, N-acetylcysteine, a potent cysteine reductive compound, significantly prevents up-regulation of HMOX1, GCLM, and CXCL2 genes, and repression of MMP9 and CCL22 genes induced by As(2)O(3).	Acetylcysteine	13-29	C-X-C motif chemokine ligand 2	Homo sapiens	126-131
33360347-10	2021	Both the antioxidants N-acetylcysteine and folic acid reversed the arsenic-mediated repression of Sp1, GDF1 and SIRT1.	Acetylcysteine	22-38	sirtuin 1	Danio rerio	112-117
19350554-8	2009	In addition, we demonstrate that As(2)O(3) markedly alters nuclear levels of Nrf2 and Bach1, two redox-sensitive regulators of stress genes, and represses expression of the transcription factor EGR2 which is involved in mouse macrophage differentiation; such effects are reduced by N-acetylcysteine.	Acetylcysteine	282-298	early growth response 2	Mus musculus	194-198
19412010-6	2009	There was a slightly higher activity of cytochrome P450 (CYP1A1/2 activity) in cultures treated with ALF and ALF + NAC than with normal sera treated hepatocyte cultures.	Acetylcysteine	115-118	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	57-63
33570605-7	2021	Adding NAC into NAg-containing cement greatly reduced the biofilm metabolic activity and lactic acid production (P < .05) and lowered the colony unit-forming counts by approximately 1 log (P < .05).	Acetylcysteine	7-10	NBAS subunit of NRZ tethering complex	Homo sapiens	16-19
33570605-8	2021	The cell viability against NAg-containing cement was improved by NAC (P < .05).	Acetylcysteine	65-68	NBAS subunit of NRZ tethering complex	Homo sapiens	27-30
33570605-9	2021	CONCLUSIONS: The incorporation of NAC into NAg-containing cement achieved stronger antibacterial capability and better biocompatibility, without compromising the enamel SBS.	Acetylcysteine	34-37	NBAS subunit of NRZ tethering complex	Homo sapiens	43-46
30692515-7	2019	In EAAC1 KO mice, oxidative stress and autophagy were suppressed with increased glutathione levels by NAC treatment.	Acetylcysteine	102-105	solute carrier family 1 (neuronal/epithelial high affinity glutamate transporter, system Xag), member 1	Mus musculus	3-8
30294906-7	2018	RESULTS: NAC prevented hemin-induced ferroptosis by neutralizing toxic lipids generated by arachidonate-dependent ALOX5 activity.	Acetylcysteine	9-12	arachidonate 5-lipoxygenase	Mus musculus	114-119
30294906-11	2018	INTERPRETATION: NAC is a promising, protective therapy for ICH, which acted to inhibit toxic arachidonic acid products of nuclear ALOX5 that synergized with exogenously delivered protective PGE2 in vitro and in vivo.	Acetylcysteine	16-19	arachidonate 5-lipoxygenase	Mus musculus	130-135
19475715-6	2009	In contrast, treatment with N-acetyl cysteine (NAC) can prevent cell cycle arrest and p21 up-regulation at early hours.	Acetylcysteine	28-45	H3 histone pseudogene 16	Homo sapiens	86-89
30355525-10	2018	Notably, pretreating the cells with an antioxidant N-acetyl-L-cysteine (NAC) dramatically decreased apoptosis in cells treated by He-CAP, but not by IR.	Acetylcysteine	51-70	X-linked Kx blood group	Homo sapiens	72-75
30257333-10	2018	IL-17A-induced oxidative stress/IL-6 expression and neutrophilic inflammation was attenuated by NAC treatment, whereas there was no effect on chemokines.	Acetylcysteine	96-99	interleukin 17A	Mus musculus	0-6
30257333-11	2018	This suggests that antioxidant NAC attenuates IL-17A-induced pulmonary inflammation by restoring oxidant-antioxidant balance and attenuation of IL-6 in the lung.	Acetylcysteine	31-34	interleukin 17A	Mus musculus	46-52
33407994-3	2021	However, Kv2.1 expression was significantly decreased when the cells were treated with anti-oxidants, such as N-acetylcysteine or ascorbic acid, implying that the highly expressed Kv2.1 could detect reactive oxygen species (ROS) in malignant prostate cancer cells.	Acetylcysteine	110-126	potassium voltage-gated channel subfamily B member 1	Homo sapiens	9-14
33407994-3	2021	However, Kv2.1 expression was significantly decreased when the cells were treated with anti-oxidants, such as N-acetylcysteine or ascorbic acid, implying that the highly expressed Kv2.1 could detect reactive oxygen species (ROS) in malignant prostate cancer cells.	Acetylcysteine	110-126	potassium voltage-gated channel subfamily B member 1	Homo sapiens	180-185
33507837-6	2021	Additionally, NAC down-regulated CT-1 expression in the heart and aorta.	Acetylcysteine	14-17	cardiotrophin 1	Rattus norvegicus	33-37
30257333-12	2018	Further, our study suggests that inflammatory pulmonary disorders which involve increase in IL-17 A may be ameliorated by NAC treatment.	Acetylcysteine	122-125	interleukin 17A	Mus musculus	92-99
19475715-6	2009	In contrast, treatment with N-acetyl cysteine (NAC) can prevent cell cycle arrest and p21 up-regulation at early hours.	Acetylcysteine	47-50	H3 histone pseudogene 16	Homo sapiens	86-89
29964331-7	2018	Moreover, inhibition of reactive oxygen species by N-acetyl-L-cysteine efficiently blocked BIX-01294-induced DR5 upregulation by inhibiting ATF4/CHOP expression, leading to diminished sensitization to TRAIL.	Acetylcysteine	51-70	activating transcription factor 4	Homo sapiens	140-144
33507837-7	2021	These findings demonstrated the protective effect of NAC against aortic and myocardial degeneration and fibrosis through down-regulation of CT-1 in fructose induced MS animal model.	Acetylcysteine	53-56	cardiotrophin 1	Rattus norvegicus	140-144
19276353-3	2009	GD3-induced apoptosis of activated T cells was dose dependent and inhibitable by pretreating the lymphocytes with N-acetylcysteine, cyclosporin A, or bongkrekic acid, emphasizing the essential role of ROS and mitochondrial permeability to the process.	Acetylcysteine	114-130	GRDX	Homo sapiens	0-3
33530504-0	2021	Activation of NRF2 and ATF4 Signaling by the Pro-Glutathione Molecule I-152, a Co-Drug of N-Acetyl-Cysteine and Cysteamine.	Acetylcysteine	90-107	activating transcription factor 4	Homo sapiens	23-27
30416532-5	2018	Additionally, exposure of bone marrow stromal cells (HS-5) to NAC increased adiponectin, PPARgamma, HO-1, and SIRT-1 and increased beta-oxidation markers such as PPARalpha and PPARdelta mRNA levels.	Acetylcysteine	62-65	sirtuin 1	Homo sapiens	110-116
30416532-5	2018	Additionally, exposure of bone marrow stromal cells (HS-5) to NAC increased adiponectin, PPARgamma, HO-1, and SIRT-1 and increased beta-oxidation markers such as PPARalpha and PPARdelta mRNA levels.	Acetylcysteine	62-65	peroxisome proliferator activated receptor delta	Homo sapiens	176-185
30055241-8	2018	Subsequent analyses demonstrated that antioxidant N-acetylcysteine (NAC) attenuated SIRT1 repression, increased SIRT1 mRNA levels and decreased SIRT1 protein degradation in Sb-treated cells.	Acetylcysteine	50-66	sirtuin 1	Homo sapiens	84-89
30055241-8	2018	Subsequent analyses demonstrated that antioxidant N-acetylcysteine (NAC) attenuated SIRT1 repression, increased SIRT1 mRNA levels and decreased SIRT1 protein degradation in Sb-treated cells.	Acetylcysteine	50-66	sirtuin 1	Homo sapiens	112-117
30055241-8	2018	Subsequent analyses demonstrated that antioxidant N-acetylcysteine (NAC) attenuated SIRT1 repression, increased SIRT1 mRNA levels and decreased SIRT1 protein degradation in Sb-treated cells.	Acetylcysteine	50-66	sirtuin 1	Homo sapiens	112-117
19154785-8	2009	UFP also up-regulated heme oxygenase-1 (HO-1) and tissue factor (TF) mRNA expression, and pretreatment with the antioxidant N-acetylcysteine significantly decreased their expression.	Acetylcysteine	124-140	heme oxygenase 1	Homo sapiens	22-38
30055241-8	2018	Subsequent analyses demonstrated that antioxidant N-acetylcysteine (NAC) attenuated SIRT1 repression, increased SIRT1 mRNA levels and decreased SIRT1 protein degradation in Sb-treated cells.	Acetylcysteine	68-71	sirtuin 1	Homo sapiens	84-89
30055241-8	2018	Subsequent analyses demonstrated that antioxidant N-acetylcysteine (NAC) attenuated SIRT1 repression, increased SIRT1 mRNA levels and decreased SIRT1 protein degradation in Sb-treated cells.	Acetylcysteine	68-71	sirtuin 1	Homo sapiens	112-117
30055241-8	2018	Subsequent analyses demonstrated that antioxidant N-acetylcysteine (NAC) attenuated SIRT1 repression, increased SIRT1 mRNA levels and decreased SIRT1 protein degradation in Sb-treated cells.	Acetylcysteine	68-71	sirtuin 1	Homo sapiens	112-117
33227289-10	2021	Furthermore, N-acetylcysteine, a potential ROS scavenger, substantially suppressed the expression of mitophagy-regulated proteins and LC3 puncta by coptisine.	Acetylcysteine	13-29	microtubule associated protein 1 light chain 3 alpha	Homo sapiens	134-137
33310292-5	2021	Further investigation suggested that tribulosaponin A up-regulated the expression of NCF1 and NOX1 to accumulate ROS for triggering apoptosis in GSCs, but not in untransformed cells, and it was further supported by the assay that N-acetyl-l-cysteine (NAC) clearing ROS delayed GSCs apoptosis.	Acetylcysteine	230-249	neutrophil cytosolic factor 1	Homo sapiens	85-89
33310292-5	2021	Further investigation suggested that tribulosaponin A up-regulated the expression of NCF1 and NOX1 to accumulate ROS for triggering apoptosis in GSCs, but not in untransformed cells, and it was further supported by the assay that N-acetyl-l-cysteine (NAC) clearing ROS delayed GSCs apoptosis.	Acetylcysteine	251-254	neutrophil cytosolic factor 1	Homo sapiens	85-89
33130472-16	2021	Both the inhibition of 4EBP1 phosphorylation (Ser 65) and activation of PERK-eIF2alpha axis triggered by LCA was restored by co-treatment with NAC.	Acetylcysteine	143-146	eukaryotic translation initiation factor 2A	Homo sapiens	77-86
30338789-12	2018	NAC inhibited ROS level and enhanced TERT expression.	Acetylcysteine	0-3	telomerase reverse transcriptase	Rattus norvegicus	37-41
30139658-9	2018	RESULTS: We identified a number of novel genes, including Regulator of calcineurin 1 (Rcan1) and Sestrin 2 (Sesn2) and demonstrated that they are induced by oxidative stress, by stimulation with H2O2 and by inhibiting caerulein stimulated expression with the antioxidant N-acetylcysteine.	Acetylcysteine	271-287	sestrin 2	Mus musculus	97-106
30139658-9	2018	RESULTS: We identified a number of novel genes, including Regulator of calcineurin 1 (Rcan1) and Sestrin 2 (Sesn2) and demonstrated that they are induced by oxidative stress, by stimulation with H2O2 and by inhibiting caerulein stimulated expression with the antioxidant N-acetylcysteine.	Acetylcysteine	271-287	sestrin 2	Mus musculus	108-113
30217943-9	2018	The levels of TNF-alpha, IL-8, CC16, and ICAM-1 in EBC were significantly lower, and SOD activity was higher, at T2 in the NAC group; similar data were found in serum at T2, T3, and T4.	Acetylcysteine	123-126	intercellular adhesion molecule 1	Homo sapiens	41-47
19154785-8	2009	UFP also up-regulated heme oxygenase-1 (HO-1) and tissue factor (TF) mRNA expression, and pretreatment with the antioxidant N-acetylcysteine significantly decreased their expression.	Acetylcysteine	124-140	coagulation factor III, tissue factor	Homo sapiens	50-63
29655793-9	2018	Pre-treatment of MLE-12 cells with ROS scavenger of N-acetylcysteine (NAC) remarkably decreased lipopolysaccharide (LPS)- and rMuNLRP9-induced production of ROS, and the secretion of inflammatory cytokines or chemokine, as well as the activity of IkappaBalpha/NF-kappaB, ASC/Casapse-1 and Caspase-3/PARP signaling pathways.	Acetylcysteine	70-73	caspase 3	Mus musculus	289-298
19154785-8	2009	UFP also up-regulated heme oxygenase-1 (HO-1) and tissue factor (TF) mRNA expression, and pretreatment with the antioxidant N-acetylcysteine significantly decreased their expression.	Acetylcysteine	124-140	coagulation factor III, tissue factor	Homo sapiens	65-67
29655793-9	2018	Pre-treatment of MLE-12 cells with ROS scavenger of N-acetylcysteine (NAC) remarkably decreased lipopolysaccharide (LPS)- and rMuNLRP9-induced production of ROS, and the secretion of inflammatory cytokines or chemokine, as well as the activity of IkappaBalpha/NF-kappaB, ASC/Casapse-1 and Caspase-3/PARP signaling pathways.	Acetylcysteine	70-73	poly (ADP-ribose) polymerase family, member 1	Mus musculus	299-303
33316776-4	2020	Furthermore, the production of intracellular reactive oxygen species (ROS) in the TRL group increased significantly, while pretreatment with the ROS scavenger N-acetyl-L-cysteine effectively attenuated the premature senescence of AMSCs by decreasing ROS production and upregulating SIRT1 level.	Acetylcysteine	159-178	sirtuin 1	Homo sapiens	282-287
19034402-4	2009	We find that glutathione (GSH), cysteine, homocysteine, and N-acetylcysteine at physiological concentrations competitively reduce MMP-1 activity up to 75% with an efficiency of cysteine &gt; or = GSH &gt; homocysteine &gt; N-acetylcysteine.	Acetylcysteine	60-76	matrix metallopeptidase 1	Homo sapiens	130-135
33139577-4	2020	As a result, Akt3-expressing cells activate the DNA damage response pathway, express high levels of p53 and its direct transcriptional target miR-34, and exhibit a proliferation defect, which is rescued by the antioxidant N-acetylcysteine.	Acetylcysteine	222-238	AKT serine/threonine kinase 3	Homo sapiens	13-17
19034402-4	2009	We find that glutathione (GSH), cysteine, homocysteine, and N-acetylcysteine at physiological concentrations competitively reduce MMP-1 activity up to 75% with an efficiency of cysteine &gt; or = GSH &gt; homocysteine &gt; N-acetylcysteine.	Acetylcysteine	223-239	matrix metallopeptidase 1	Homo sapiens	130-135
29683755-0	2018	N-acetylcysteine decreases urinary level of neutrophil gelatinase-associated lipocalin in deceased-donor renal transplant recipients: a randomized clinical trial.	Acetylcysteine	0-16	lipocalin 2	Homo sapiens	44-86
29683755-3	2018	OBJECTIVES: We assessed the renoprotective effect of N-acetylcysteine (NAC) on u-NGAL levels as an early prognostic marker of graft function immediately after transplantation.	Acetylcysteine	53-69	lipocalin 2	Homo sapiens	81-85
19202317-9	2009	We also confirmed that PDGF-induced JNK and Akt activations were inhibited by antioxidants, N-acetylcysteine and diphenyleneiodonium chloride, in RASMCs.	Acetylcysteine	92-108	mitogen-activated protein kinase 8	Rattus norvegicus	36-39
29683755-3	2018	OBJECTIVES: We assessed the renoprotective effect of N-acetylcysteine (NAC) on u-NGAL levels as an early prognostic marker of graft function immediately after transplantation.	Acetylcysteine	71-74	lipocalin 2	Homo sapiens	81-85
29683755-7	2018	RESULTS: NAC significantly reduced u-NGAL levels compared to placebo (p value = 0.02), while improvement in early graft function with NAC did not reach statistical significance.	Acetylcysteine	9-12	lipocalin 2	Homo sapiens	37-41
29683755-8	2018	CONCLUSIONS: This study showed that NAC administration in deceased-donor KT recipients can reduce tubular kidney injury, evidenced by u-NGAL measurements.	Acetylcysteine	36-39	lipocalin 2	Homo sapiens	136-140
33037139-7	2020	ROS generation and spleen tyrosine kinase (Syk) activation induced by heme were critical for most proinflammatory signaling pathways, as the antioxidant N-acetyl-l-cysteine and a Syk inhibitor differentially blocked heme-induced ROS, MAPK phosphorylation, and cytokine production in macrophages.	Acetylcysteine	153-172	spleen tyrosine kinase	Mus musculus	19-41
33037139-7	2020	ROS generation and spleen tyrosine kinase (Syk) activation induced by heme were critical for most proinflammatory signaling pathways, as the antioxidant N-acetyl-l-cysteine and a Syk inhibitor differentially blocked heme-induced ROS, MAPK phosphorylation, and cytokine production in macrophages.	Acetylcysteine	153-172	spleen tyrosine kinase	Mus musculus	43-46
33198336-10	2020	In the duodenum, NQO1, TXNRD, and SOD activities were upregulated by NAC.	Acetylcysteine	69-72	NAD(P)H dehydrogenase, quinone 1	Mus musculus	17-21
33146789-10	2021	In addition, using the ROS inhibitor N-acetyl-L-cysteine (NAC), we observed abrogated mRNA expression of several ARPs and production of inflammatory cytokines/chemokines (IL-6, IL-8, MCP-1, and CCL-5) in the CSE-challenged cells suggesting an important role of ROS in regulating CSE-induced autophagy.	Acetylcysteine	37-56	C-C motif chemokine ligand 5	Homo sapiens	194-199
33146789-10	2021	In addition, using the ROS inhibitor N-acetyl-L-cysteine (NAC), we observed abrogated mRNA expression of several ARPs and production of inflammatory cytokines/chemokines (IL-6, IL-8, MCP-1, and CCL-5) in the CSE-challenged cells suggesting an important role of ROS in regulating CSE-induced autophagy.	Acetylcysteine	58-61	C-C motif chemokine ligand 5	Homo sapiens	194-199
33051453-10	2020	Antioxidant N-acetylcysteine (NAC) could inhibit the expression of PERK phosphorylation, osteoclast-related proteins and autophagy-related proteins, but the use of PERK activator CCT020312 can reverse inhibition effect of NAC.	Acetylcysteine	12-28	eukaryotic translation initiation factor 2 alpha kinase 3	Mus musculus	67-71
29613836-13	2018	NAC or 3-MA pretreatments inhibited IL-17-mediated cell apoptosis.	Acetylcysteine	0-3	interleukin 17A	Mus musculus	36-41
30081847-9	2018	We further demonstrated that the NH4Cl/NAC inhibited intermittent high glucose-induced autophage by altered level of LC3 and p62.	Acetylcysteine	39-42	microtubule associated protein 1 light chain 3 alpha	Homo sapiens	117-120
30081847-9	2018	We further demonstrated that the NH4Cl/NAC inhibited intermittent high glucose-induced autophage by altered level of LC3 and p62.	Acetylcysteine	39-42	nucleoporin 62	Homo sapiens	125-128
33051453-10	2020	Antioxidant N-acetylcysteine (NAC) could inhibit the expression of PERK phosphorylation, osteoclast-related proteins and autophagy-related proteins, but the use of PERK activator CCT020312 can reverse inhibition effect of NAC.	Acetylcysteine	30-33	eukaryotic translation initiation factor 2 alpha kinase 3	Mus musculus	67-71
19033392-9	2009	A significant inhibition of the expression of hmox1 and nqo1 mRNAs and CD86 expression was found in 1-chloro 2,4-dinitrobenzene-treated THP-1 cells preincubated with N-acetyl cysteine, a glutathione precursor.	Acetylcysteine	166-183	heme oxygenase 1	Homo sapiens	46-51
19372642-5	2009	RESULTS: HPMC exposed to PDF resulted in a significant decrease in cell survival in a time-dependent manner, which was reversed by NAC.	Acetylcysteine	131-134	peptide deformylase, mitochondrial	Homo sapiens	25-28
32929153-7	2020	Treatment of pancreatic cancer cells with the antioxidant N-acetyl-L-cysteine decreased ROS activity and expression level of NRF2 and ITGB7.	Acetylcysteine	58-77	integrin subunit beta 7	Homo sapiens	134-139
33162896-9	2020	The pretreatments of antioxidant N-acetylcysteine (NAC) and apocynin (APO) abolished the drop of the levels of PP2Ac Tyr307 and eNOS Ser1177 induced by AngII in HUVECs.	Acetylcysteine	33-49	nitric oxide synthase 3	Rattus norvegicus	128-132
33162896-9	2020	The pretreatments of antioxidant N-acetylcysteine (NAC) and apocynin (APO) abolished the drop of the levels of PP2Ac Tyr307 and eNOS Ser1177 induced by AngII in HUVECs.	Acetylcysteine	51-54	nitric oxide synthase 3	Rattus norvegicus	128-132
30344285-0	2018	Serum and Tissue HIF-2 Alpha Expression in CIN, N-Acetyl Cysteine, and Sildenafil-Treated Rat Models: An Experimental Study.	Acetylcysteine	48-65	endothelial PAS domain protein 1	Rattus norvegicus	17-28
30344285-11	2018	Similarly, after treatment with sildenafil and NAC, HIF-2alpha levels were significantly decreased (p &lt; 0.05).	Acetylcysteine	47-50	endothelial PAS domain protein 1	Rattus norvegicus	52-62
30344285-13	2018	Besides, the levels and tissue expression of HIF-2alpha decrease with both NAC and sildenafil treatments.	Acetylcysteine	75-78	endothelial PAS domain protein 1	Rattus norvegicus	45-55
29635121-9	2018	Binary logistic regression analysis indicated that the modulatory effect of NAC on NKA levels was associated with a reduction of pro-oxidant factors and IL-6, and selectively blocking the NK2 receptor abolished such an association.	Acetylcysteine	76-79	tachykinin receptor 2	Homo sapiens	188-200
29604266-8	2018	N-acetyl-l-cysteine (NAC), a ROS inhibitor, protected against PAT-induced cytotoxicity, decreased the protein expression of LC3-II, and up-regulated the level of p-Akt1 and p-MTOR.	Acetylcysteine	0-19	X-linked Kx blood group	Homo sapiens	21-24
19372642-9	2009	NAC treatment preserved the content of intracellular reduced glutathione, and also attenuated the PDF-induced superoxide accumulation and Deltapsim collapse.	Acetylcysteine	0-3	peptide deformylase, mitochondrial	Homo sapiens	98-101
32998228-4	2020	The knockdown of HOXB13 reduced hydrogen peroxide-induced cytotoxicity; however, this phenomenon was largely absent in the presence of antioxidants (Trolox or N-acetyl cysteine (NAC)).	Acetylcysteine	159-176	homeobox B13	Homo sapiens	17-23
32998228-4	2020	The knockdown of HOXB13 reduced hydrogen peroxide-induced cytotoxicity; however, this phenomenon was largely absent in the presence of antioxidants (Trolox or N-acetyl cysteine (NAC)).	Acetylcysteine	178-181	homeobox B13	Homo sapiens	17-23
19372642-10	2009	Moreover, the enhanced expression of HSP72 induced by PDF exposure was also reversed by NAC.	Acetylcysteine	88-91	peptide deformylase, mitochondrial	Homo sapiens	54-57
19372642-12	2009	NAC protects HPMCs from PDF-induced cellular damage by preserving the reduced glutathione.	Acetylcysteine	0-3	peptide deformylase, mitochondrial	Homo sapiens	24-27
19530032-3	2009	It complicates interpretation of results that the antidote, acetylcysteine (NAC) depresses this activity.	Acetylcysteine	60-74	synuclein alpha	Homo sapiens	76-79
32916895-7	2020	In addition, well-known antioxidants, trolox and N-acetyl cysteine, significantly attenuated the BBB permeability increase, disruption of claudin-5 and ZO-1, and FoxO3a activation during hypoxia, suggesting that ROS are important mediators of BBB dysfunction during hypoxia.	Acetylcysteine	49-66	claudin 5	Mus musculus	138-147
32640348-4	2020	Furthermore, RT-qPCR and immunofluorescence assay results indicated that NAC restored the expression of Gclc, reduced the expression of ATF4, JNK and Caspase-12, and decreased the expression of eNOS and IGF-1, in the placenta.	Acetylcysteine	73-76	glutamate-cysteine ligase, catalytic subunit	Mus musculus	104-108
32640348-4	2020	Furthermore, RT-qPCR and immunofluorescence assay results indicated that NAC restored the expression of Gclc, reduced the expression of ATF4, JNK and Caspase-12, and decreased the expression of eNOS and IGF-1, in the placenta.	Acetylcysteine	73-76	mitogen-activated protein kinase 8	Mus musculus	142-145
29636531-7	2018	Both NAC and SP600125 inhibited JNK phosphorylation and reduced cell viability in TBT-treated beta-cells.	Acetylcysteine	5-8	mitogen-activated protein kinase 8	Mus musculus	32-35
29636531-8	2018	Four-week exposure of TBT (0.25 mg/kg) to mice revealed the decreased plasma insulin, increased blood glucose and plasma malondialdehyde, suppressed islet insulin secretion, and increased islet caspase-3 activity, which could be reversed by NAC treatment.	Acetylcysteine	241-244	caspase 3	Mus musculus	194-203
29335220-6	2018	Treatment with Z-DEVD-fmk, a caspase-3 inhibitor, or N-acetyl-L-cysteine, an antioxidant, blocked PKCdelta activation and subsequently inhibited inflammation, thereby improving learning and memory deficits in BDE-47-treated mice.	Acetylcysteine	53-72	protein kinase C, delta	Mus musculus	98-106
19122686-6	2008	Tissue MPO activities of R+NAC and R+WR-2721 rats were higher than those of R rats (p&lt;0.001).	Acetylcysteine	27-30	myeloperoxidase	Rattus norvegicus	7-10
29396710-7	2018	Interestingly, NAC did not affect memory subsets, but diminished up-regulation of senescence (CD57) and exhaustion (PD-1) markers and significantly decreased expression of the transcription factors EOMES and Foxo1.	Acetylcysteine	15-18	eomesodermin	Homo sapiens	198-203
29396710-9	2018	This suggests a model in which NAC through PI3K/Akt activation suppresses Foxo1 expression, thereby impacting its transcriptional targets EOMES, PD-1, and granzyme B.	Acetylcysteine	31-34	eomesodermin	Homo sapiens	138-143
32825703-0	2020	Transient Receptor Potential Melastatin 2 (TRPM2) Inhibition by Antioxidant, N-Acetyl-l-Cysteine, Reduces Global Cerebral Ischemia-Induced Neuronal Death.	Acetylcysteine	77-96	transient receptor potential cation channel subfamily M member 2	Homo sapiens	0-41
32825703-0	2020	Transient Receptor Potential Melastatin 2 (TRPM2) Inhibition by Antioxidant, N-Acetyl-l-Cysteine, Reduces Global Cerebral Ischemia-Induced Neuronal Death.	Acetylcysteine	77-96	transient receptor potential cation channel subfamily M member 2	Homo sapiens	43-48
32825703-5	2020	Therefore, we examined whether anti-oxidant treatment, such as with N-acetyl-l-cysteine (NAC), provides neuroprotection via regulation of TRPM2, following global cerebral ischemia (GCI).	Acetylcysteine	68-87	transient receptor potential cation channel subfamily M member 2	Homo sapiens	138-143
32825703-5	2020	Therefore, we examined whether anti-oxidant treatment, such as with N-acetyl-l-cysteine (NAC), provides neuroprotection via regulation of TRPM2, following global cerebral ischemia (GCI).	Acetylcysteine	89-92	transient receptor potential cation channel subfamily M member 2	Homo sapiens	138-143
32825703-7	2020	We demonstrated that NAC administration reduced activation of GCI-induced neuronal death cascades, such as lipid peroxidation, microglia and astroglia activation, free zinc accumulation, and TRPM2 over-activation.	Acetylcysteine	21-24	transient receptor potential cation channel subfamily M member 2	Homo sapiens	191-196
32574682-7	2020	Rosiglitazone also significantly reversed the NAC-induced increase in the MC2R expression in adrenal, but not steroidogenic acute regulatory protein (StAR).	Acetylcysteine	46-49	melanocortin 2 receptor	Mus musculus	74-78
32418903-6	2020	IDR-1018 peptide was encapsulated with/without an anti-TB drug in N-acetyl cysteine(NAC) decorated porous PLGA microspheres.	Acetylcysteine	66-83	NLR family, pyrin domain containing 1A	Mus musculus	84-87
29996215-11	2018	Furthermore, the protein levels of hormone sensitive lipase (HSL) did not significantly differ among 3 groups, whereas NAC prevented binge drinking-induced increase of HSL phosphorylation at ser563 and ser660.	Acetylcysteine	119-122	lipase, hormone sensitive	Mus musculus	168-171
29996215-12	2018	Conclusion: NAC could effectively attenuate binge drinking-induced fatty liver, which might be associated with the inhibition of lipid mobilization by suppressing the phosphorylation of HSL.	Acetylcysteine	12-15	lipase, hormone sensitive	Mus musculus	186-189
19548360-5	2008	The increases in reactive species and HO-1 protein are inhibited by agonists of glucocorticoid receptors (GR), such as RU28362, prednisolone, and dexamethasone, as well as by N-acetyl-L-cysteine and SB203580 (a p38 inhibitor), suggesting a role of GR in NF-induced increases in reactive species and HO-1.	Acetylcysteine	175-194	heme oxygenase 1	Homo sapiens	38-42
29378912-8	2018	In addition, inhibition of reactive oxygen species using N-acetylcysteine attenuated ER stress, expression of osteoclast-specific marker genes, and RANKL-induced CREBH activation.	Acetylcysteine	57-73	TNF superfamily member 11	Homo sapiens	148-153
29174818-7	2018	In vitro study revealed that methylglyoxal-derived AGE (MG-AGE) incubation in isolated cardiomyocytes promoted oxidation of sarco(endo)plasmic reticulum Ca2+-ATPase (SERCA2a) and production of superoxide, the effects of which were negated by the autophagy inducer rapamycin, the ER stress chaperone TUDCA or the antioxidant N-acetylcysteine.	Acetylcysteine	324-340	ATPase, Ca++ transporting, cardiac muscle, slow twitch 2	Mus musculus	166-173
32724493-15	2020	As expected, the addition of NAC efficiently suppresses the TNF-alpha and IL-6 secretion stimulated from PQ and also downregulated ERK, JNK, and p65 phosphorylation (ERK/JNK MAPK and NF-kappaB pathways) as well as MUC5B expression.	Acetylcysteine	29-32	mitogen-activated protein kinase 8	Mus musculus	136-139
32674468-8	2020	These chemical species seem to be an important signal in activating the melanogenic process since the antioxidants N-acetyl-l-cysteine and glutathione decreased both the level and activity of tyrosinase stimulated by melatonin.	Acetylcysteine	115-134	tyrosinase	Homo sapiens	192-202
19548360-5	2008	The increases in reactive species and HO-1 protein are inhibited by agonists of glucocorticoid receptors (GR), such as RU28362, prednisolone, and dexamethasone, as well as by N-acetyl-L-cysteine and SB203580 (a p38 inhibitor), suggesting a role of GR in NF-induced increases in reactive species and HO-1.	Acetylcysteine	175-194	heme oxygenase 1	Homo sapiens	299-303
18603603-2	2008	We investigated whether enhanced ROS scavenging induced with the antioxidant N-acetylcysteine (NAC) blunted the increase in Na(+)-K(+) pump mRNA during repeated contractions in human and rat muscle.	Acetylcysteine	77-93	synuclein alpha	Homo sapiens	95-98
32409143-9	2020	The HO-1 induction was inhibited by a ROS scavenger N-acetylcysteine (NAC), thiol-containing antioxidants (glutathione [GSH] and dithiothreitol [DTT]), JNK and p38 MAPK inhibitors, and nuclear transport inhibitor leptomycin.	Acetylcysteine	52-68	heme oxygenase 1	Rattus norvegicus	4-8
32409143-9	2020	The HO-1 induction was inhibited by a ROS scavenger N-acetylcysteine (NAC), thiol-containing antioxidants (glutathione [GSH] and dithiothreitol [DTT]), JNK and p38 MAPK inhibitors, and nuclear transport inhibitor leptomycin.	Acetylcysteine	70-73	heme oxygenase 1	Rattus norvegicus	4-8
29079519-7	2018	The adaptation to chronic ischemia in this model included an increase in muscle VEGF and HIF levels, and NAC was able to decrease VEGF, but not HIF levels.	Acetylcysteine	105-108	vascular endothelial growth factor A	Mus musculus	130-134
29382173-12	2018	However, pretreatment with N-acetyl-l-cysteine (NAC) could not attenuate WSPIS-induced apoptosis.	Acetylcysteine	27-46	X-linked Kx blood group	Homo sapiens	48-51
32647651-7	2020	15d-PGJ2-mediated inhibition of IKKbeta and nuclear translocation of phospho-p65 was blocked by NAC treatment.	Acetylcysteine	96-99	component of inhibitor of nuclear factor kappa B kinase complex	Homo sapiens	32-39
18713279-6	2008	RESULTS: N-acetylcysteine treatment significantly improved liver function parameters including the plasma levels of aspartate aminotransferase, alkaline phosphatase, gamma-glutamyl transpeptidase and bilirubin.	Acetylcysteine	9-25	gamma-glutamyltransferase 1	Rattus norvegicus	166-195
32347295-6	2020	However, in the groups of HG-N, DM, HG-N+I/R and DM+I/R, NAC can significantly reduce oxidative stress injury and apoptosis rate of myocytes, promote the Bcl-2 and DJ-1 molecules, inhibit BAX and c-caspase-3 protein and PTEN/Akt pathway.	Acetylcysteine	57-60	phosphatase and tensin homolog	Rattus norvegicus	220-224
32347295-8	2020	Taken together, the findings suggest that NAC can reduce ischemia reperfusion injury in diabetic myocardium by up-regulating the PTEN/Akt pathway through the level of DJ-1.	Acetylcysteine	42-45	phosphatase and tensin homolog	Rattus norvegicus	129-133
18689604-8	2008	Treatment with the antioxidants N-acetyl-l-cysteine or GSH reduced the expression of HO-1 induced by CSE.	Acetylcysteine	32-51	heme oxygenase 1	Homo sapiens	85-89
18625331-6	2008	Meanwhile more primary CD34(+)CD38(-) cells were obtained when cultivation was performed under hypoxia or with N-acetyl cysteine (the precursor of GSH) under normoxia.	Acetylcysteine	111-128	CD38 molecule	Homo sapiens	30-34
32461996-7	2020	We observed that JMJD1A reduced the production of total cellular and mitochondrial levels of reactive oxygen species (ROS), which was critically involved in the effects of JMJD1A because either N-acetylcysteine or MitoTEMPO treatment blocked the effects of JMJD1A deficiency on cardiomyocyte hypertrophy.	Acetylcysteine	194-210	lysine demethylase 3A	Rattus norvegicus	17-23
32461996-7	2020	We observed that JMJD1A reduced the production of total cellular and mitochondrial levels of reactive oxygen species (ROS), which was critically involved in the effects of JMJD1A because either N-acetylcysteine or MitoTEMPO treatment blocked the effects of JMJD1A deficiency on cardiomyocyte hypertrophy.	Acetylcysteine	194-210	lysine demethylase 3A	Rattus norvegicus	172-178
32461996-7	2020	We observed that JMJD1A reduced the production of total cellular and mitochondrial levels of reactive oxygen species (ROS), which was critically involved in the effects of JMJD1A because either N-acetylcysteine or MitoTEMPO treatment blocked the effects of JMJD1A deficiency on cardiomyocyte hypertrophy.	Acetylcysteine	194-210	lysine demethylase 3A	Rattus norvegicus	172-178
18469310-9	2008	Post-BUO downregulation of AQP2 protein expression was averted in the BUO + NAC-pre group rats.	Acetylcysteine	76-79	aquaporin 2	Rattus norvegicus	27-31
32106375-9	2020	Post-insult treatment with the antioxidant N-acetylcysteine also resulted in suppressed activation of AMPK/JNK, mitigated apoptosis and alleviated liver injury.	Acetylcysteine	43-59	mitogen-activated protein kinase 8	Mus musculus	107-110
32392918-6	2020	Pretreating cells with either NAC or DPI significantly enhanced the oncogenic H-Ras-mediated down-regulation of mdr1b expression and markedly prevented doxorubicin-induced cell death.	Acetylcysteine	30-33	Harvey rat sarcoma virus oncogene	Mus musculus	78-83
18538675-4	2008	Supplementation of PUVA-treated fibroblasts with alpha-tocopherol (alpha-Toc), N-acetylcysteine (NAC), or alpha-lipoic acid (alpha-LA) abrogated the increased ROS generation and rescued fibroblasts from the ROS-dependent changes into the cellular senescence phenotype, such as cytoplasmic enlargement, enhanced expression of senescence-associated-beta-galactosidase and matrix-metalloproteinase-1, hallmarks of photoaging and intrinsic aging.	Acetylcysteine	79-95	matrix metallopeptidase 1	Homo sapiens	370-396
32191241-4	2020	In this study, we use CdTe QDs capped with short ligands of N-acetyl-l cysteine (NAC) to fabricate three-dimensional QD assemblies by utilizing chemical bonding between NACs.	Acetylcysteine	169-173	X-linked Kx blood group	Homo sapiens	81-84
18538675-4	2008	Supplementation of PUVA-treated fibroblasts with alpha-tocopherol (alpha-Toc), N-acetylcysteine (NAC), or alpha-lipoic acid (alpha-LA) abrogated the increased ROS generation and rescued fibroblasts from the ROS-dependent changes into the cellular senescence phenotype, such as cytoplasmic enlargement, enhanced expression of senescence-associated-beta-galactosidase and matrix-metalloproteinase-1, hallmarks of photoaging and intrinsic aging.	Acetylcysteine	97-100	matrix metallopeptidase 1	Homo sapiens	370-396
18554678-6	2008	An inhibitor of NF-kappaB, IKK-NBD, and the anti-inflammatory antioxidant N-acetylcysteine (NAC) were both effective in suppressing styrene-induced MCP-1 secretion.	Acetylcysteine	74-90	C-C motif chemokine ligand 2	Homo sapiens	148-153
32155190-9	2020	nsPEF-induced eIF2alpha phosphorylation was blocked by treatment with the ROS scavenger N-acetyl-L-cysteine (NAC).	Acetylcysteine	88-107	eukaryotic translation initiation factor 2-alpha kinase 2	Mus musculus	14-23
32155190-9	2020	nsPEF-induced eIF2alpha phosphorylation was blocked by treatment with the ROS scavenger N-acetyl-L-cysteine (NAC).	Acetylcysteine	109-112	eukaryotic translation initiation factor 2-alpha kinase 2	Mus musculus	14-23
32131874-9	2020	RESULTS: Low-dose NAC (1000 muM) increased the expression of Nrf2 and phospho-p62 in MH7A cells, activating antioxidant genes, suppressing the expression of MMP-3, and inhibiting the phosphorylation of JNK.	Acetylcysteine	18-21	sequestosome 1	Homo sapiens	78-81
32440328-9	2020	Indeed, there was decrease in the MMP-9/TIMP ratio in bleomycin-instilled rats, which increased with NAC treatment.	Acetylcysteine	101-104	TIMP metallopeptidase inhibitor 1	Rattus norvegicus	40-44
18554678-6	2008	An inhibitor of NF-kappaB, IKK-NBD, and the anti-inflammatory antioxidant N-acetylcysteine (NAC) were both effective in suppressing styrene-induced MCP-1 secretion.	Acetylcysteine	92-95	C-C motif chemokine ligand 2	Homo sapiens	148-153
18554678-7	2008	In addition, NAC was capable of inhibiting the upregulation of GST expression.	Acetylcysteine	13-16	glutathione S-transferase kappa 1	Homo sapiens	63-66
18332044-9	2008	Pretreating the fibroblasts with N-acetyl cysteine also significantly reduced the Cr(VI)-induced cytotoxicity and overexpression of the HO-1 gene.	Acetylcysteine	33-50	heme oxygenase 1	Homo sapiens	136-140
32337366-6	2020	Pretreatment with N-acetyl-L-cysteine reversed ARS- and PAM-induced inhibition of PTPase activity.	Acetylcysteine	18-37	protein tyrosine phosphatase non-receptor type 22	Homo sapiens	82-88
31838118-11	2020	Furthermore, NAC improved redox and inflammatory status; decreased levels of RIPK3, MLKL, NLRP3, IL-18; down-regulated ASC, iNOS, GFAP and MMP-9 expression; and decreased myeloperoxidase activity in cerebral cortex.	Acetylcysteine	13-16	receptor-interacting serine-threonine kinase 3	Rattus norvegicus	77-82
31838118-11	2020	Furthermore, NAC improved redox and inflammatory status; decreased levels of RIPK3, MLKL, NLRP3, IL-18; down-regulated ASC, iNOS, GFAP and MMP-9 expression; and decreased myeloperoxidase activity in cerebral cortex.	Acetylcysteine	13-16	glial fibrillary acidic protein	Rattus norvegicus	130-134
31838118-11	2020	Furthermore, NAC improved redox and inflammatory status; decreased levels of RIPK3, MLKL, NLRP3, IL-18; down-regulated ASC, iNOS, GFAP and MMP-9 expression; and decreased myeloperoxidase activity in cerebral cortex.	Acetylcysteine	13-16	matrix metallopeptidase 9	Rattus norvegicus	139-144
18275980-7	2008	Berberine-induced apoptosis was blocked in the presence of antioxidant, N-acetylcysteine, through the prevention of disruption of mitochondrial membrane potential and subsequently release of cytochrome c and Smac/DIABLO.	Acetylcysteine	72-88	diablo IAP-binding mitochondrial protein	Homo sapiens	208-212
31756435-7	2020	Results showed that in the presence of either NAC, rotenone, or antimycin A, bombyxin-stimulated phosphorylation of insulin receptor, Akt, and 4E-binding protein (4E-BP) was blocked and bombyxin-stimulated ecdysteroidogenesis in PGs was greatly inhibited.	Acetylcysteine	46-49	RAC serine/threonine-protein kinase	Bombyx mori	134-137
18275980-7	2008	Berberine-induced apoptosis was blocked in the presence of antioxidant, N-acetylcysteine, through the prevention of disruption of mitochondrial membrane potential and subsequently release of cytochrome c and Smac/DIABLO.	Acetylcysteine	72-88	diablo IAP-binding mitochondrial protein	Homo sapiens	213-219
18456507-5	2008	N-acetylcysteine (NAC), a thiol reducing agent, but not reactive oxygen species scavengers, prevented 15d-PGJ(2)-induced COX-2 up-regulation.	Acetylcysteine	0-16	synuclein alpha	Homo sapiens	18-21
31872920-4	2020	The discovery of kisspeptin and its receptor within the posterodorsal medial amygdala (MePD), and our recent finding showing that intra-MePD administration of kisspeptin or a kisspeptin receptor antagonist results in increased LH secretion and decreased LH pulse frequency, respectively, suggests an important role for amygdala kisspeptin signalling in the regulation of the GnRH pulse generator.	Acetylcysteine	130-140	KiSS-1 metastasis-suppressor	Mus musculus	159-169
31872920-4	2020	The discovery of kisspeptin and its receptor within the posterodorsal medial amygdala (MePD), and our recent finding showing that intra-MePD administration of kisspeptin or a kisspeptin receptor antagonist results in increased LH secretion and decreased LH pulse frequency, respectively, suggests an important role for amygdala kisspeptin signalling in the regulation of the GnRH pulse generator.	Acetylcysteine	130-140	KiSS-1 metastasis-suppressor	Mus musculus	159-169
31872920-4	2020	The discovery of kisspeptin and its receptor within the posterodorsal medial amygdala (MePD), and our recent finding showing that intra-MePD administration of kisspeptin or a kisspeptin receptor antagonist results in increased LH secretion and decreased LH pulse frequency, respectively, suggests an important role for amygdala kisspeptin signalling in the regulation of the GnRH pulse generator.	Acetylcysteine	130-140	KiSS-1 metastasis-suppressor	Mus musculus	159-169
18464885-7	2008	N-acetyl-L-cysteine (L-NAC) at 1 mM significantly suppressed the glyoxal-induced embryonal toxicity.	Acetylcysteine	0-19	synuclein alpha	Homo sapiens	23-26
31721616-10	2020	Furthermore, the induction of Pdk4 and Pck1 in WAT culture by CL316,243 was markedly reduced in the presence of antioxidants N-acetylcysteine or vitamin E.	Acetylcysteine	125-141	phosphoenolpyruvate carboxykinase 1, cytosolic	Mus musculus	39-43
18291369-12	2008	Collectively, these data provide unprecedented evidence that LPS-induced peroxisomal dysfunction exacerbates cerebral white matter injury and its attenuation by NAC via a PPAR-alpha dependent mechanism expands therapeutic avenues for CP and related demyelinating diseases.	Acetylcysteine	161-164	peroxisome proliferator activated receptor alpha	Homo sapiens	171-181
31479873-8	2020	The results showed that while palmitate stimulates ROS production, pretreatment of the cells with N-acetyl cysteine (NAC), a ROS scavenger, reduced inflammatory responses and also improved LC3-BII and P62 protein in the C2C12 cells exposed to palmitate.	Acetylcysteine	98-115	nucleoporin 62	Mus musculus	201-204
31479873-8	2020	The results showed that while palmitate stimulates ROS production, pretreatment of the cells with N-acetyl cysteine (NAC), a ROS scavenger, reduced inflammatory responses and also improved LC3-BII and P62 protein in the C2C12 cells exposed to palmitate.	Acetylcysteine	117-120	nucleoporin 62	Mus musculus	201-204
31790150-7	2019	The ATP7B increase in TMEM16A-overexpressing cells was reversed by suppression of NADPH oxidase 2 (NOX2), by the antioxidant N-Acetyl-Cysteine (NAC) and by copper chelation using cuprizone and bathocuproine sulphonate (BCS).	Acetylcysteine	125-142	ATPase copper transporting beta	Homo sapiens	4-9
31790150-7	2019	The ATP7B increase in TMEM16A-overexpressing cells was reversed by suppression of NADPH oxidase 2 (NOX2), by the antioxidant N-Acetyl-Cysteine (NAC) and by copper chelation using cuprizone and bathocuproine sulphonate (BCS).	Acetylcysteine	144-147	ATPase copper transporting beta	Homo sapiens	4-9
18404532-0	2008	The differential NF-kB modulation by S-adenosyl-L-methionine, N-acetylcysteine and quercetin on the promotion stage of chemical hepatocarcinogenesis.	Acetylcysteine	62-78	RELA proto-oncogene, NF-kB subunit	Rattus norvegicus	17-22
31850806-19	2019	NAC and Trolox, two established antioxidants, reversed the MeHg-induced decline in HIF-1alpha protein levels and the decrease in cell proliferation (p&lt;0.05).	Acetylcysteine	0-3	hypoxia inducible factor 1 subunit alpha	Rattus norvegicus	83-93
31368586-10	2019	NAC-pretreated cells showed increased anti-apoptotic protein Bcl-2 and decreased pro-apoptotic protein Bax expression.	Acetylcysteine	0-3	BCL2-associated X protein	Mus musculus	103-106
18404532-7	2008	NAC decreased IKK and IkB-a phosphorylation, and Rel-A/p65 and NF-kB binding, though the last two were affected with less intensity compared to the NF-kB inhibitor.	Acetylcysteine	0-3	RELA proto-oncogene, NF-kB subunit	Rattus norvegicus	49-54
31542421-6	2019	In both WT and HT iron-overloaded mice, DFP and NAC had similar efficacy in decreasing plasma non-transferrin-bound iron, decreasing cardiac iron concentration (CIC) and relieving systolic dysfunction.	Acetylcysteine	48-51	transferrin	Mus musculus	98-109
18404532-7	2008	NAC decreased IKK and IkB-a phosphorylation, and Rel-A/p65 and NF-kB binding, though the last two were affected with less intensity compared to the NF-kB inhibitor.	Acetylcysteine	0-3	RELA proto-oncogene, NF-kB subunit	Rattus norvegicus	148-153
18642776-14	2008	The intrapancreatic MPO levels at the time points 3 h, 6 h, and 12 h of the NAC group were 0.63 +/- 0.03, 0.88 +/- 0.05, and 1.31 +/- 0.09 respectively, all significantly lower than those of the ANP groups (0.89 +/- 0.03, 1.42 +/- 0.14, and 1.94 +/- 0.07, all P &lt; 0.05).	Acetylcysteine	76-79	myeloperoxidase	Rattus norvegicus	20-23
18642776-15	2008	The MCP-1 mRNA expression levels at different time points the NAC group were 0.2497 +/- 0.0168, 0.4457 +/- 0.0097, and 0.6306 +/- 0.0423 respectively, and the MIP-2 mRNA expression levels at the time points 3 h, 6 h, and 12 h of the NAC group were 0.2436 +/- 0.0099, 0.4312 +/- 0.0221, and 0.6302 +/- 0.0288 respectively, all significantly lower than those of the ANP group (all P &lt; 0.05).	Acetylcysteine	62-65	C-C motif chemokine ligand 2	Rattus norvegicus	4-9
31772713-11	2019	Moreover, in CMECs treated with HG-HFFAs, both ablation and phosphorylation of Plin5 reduced LDs content, increased intracellular FFAs, stimulated mitochondrial beta-oxidation, added ROS generation, and reduced the expression and activity of endothelial nitric oxide synthase (eNOS), eventually leading to increased apoptotic rate and decreased NO content, all of which were reversed by N-acetyl-L-cysteine.	Acetylcysteine	387-406	perilipin 5	Mus musculus	79-84
18642776-15	2008	The MCP-1 mRNA expression levels at different time points the NAC group were 0.2497 +/- 0.0168, 0.4457 +/- 0.0097, and 0.6306 +/- 0.0423 respectively, and the MIP-2 mRNA expression levels at the time points 3 h, 6 h, and 12 h of the NAC group were 0.2436 +/- 0.0099, 0.4312 +/- 0.0221, and 0.6302 +/- 0.0288 respectively, all significantly lower than those of the ANP group (all P &lt; 0.05).	Acetylcysteine	233-236	C-C motif chemokine ligand 2	Rattus norvegicus	4-9
31578313-5	2019	We found that combination of PDK1 knockdown or inhibition by dichloroacetic acid (DCA) with ASCT2 knockdown or with cetuximab treatment induced ROS overproduction and apoptosis in HNSCC cells, and this effect was independent of effective inhibition of EGFR downstream pathways but could be lessened by N-acetyl cysteine, an anti-oxidative agent.	Acetylcysteine	302-319	pyruvate dehydrogenase kinase 1	Homo sapiens	29-33
18642776-20	2008	NAC may have beneficial effects on AP through downregulation of the expression of MCP-1 and MIP-2.	Acetylcysteine	0-3	C-C motif chemokine ligand 2	Rattus norvegicus	82-87
31578313-5	2019	We found that combination of PDK1 knockdown or inhibition by dichloroacetic acid (DCA) with ASCT2 knockdown or with cetuximab treatment induced ROS overproduction and apoptosis in HNSCC cells, and this effect was independent of effective inhibition of EGFR downstream pathways but could be lessened by N-acetyl cysteine, an anti-oxidative agent.	Acetylcysteine	302-319	solute carrier family 1 member 5	Homo sapiens	92-97
18155175-6	2008	Enhanced MIP-1beta mRNA expression was completely suppressed by the ROS scavenger N-acetyl-l-cysteine, the NADPH oxidase inhibitors diphenylene iodonium and apocynin, and the protein kinase C (PKC)-delta inhibitor rottlerin.	Acetylcysteine	82-101	C-C motif chemokine ligand 4	Homo sapiens	9-18
31390228-6	2019	Selective angiotensin II type 1 receptor (AT1R) blocker losartan suppressed ROS production and ROS scavenger N-Acetyl-L-cysteine (NAC) prevented p38 MAPK phosphorylation.	Acetylcysteine	109-128	X-linked Kx blood group	Homo sapiens	130-133
17651528-6	2008	NAC, SEC or SPC treatment also significantly suppressed high saturated fat-induced hepatic mRNA expression of sterol regulatory element-binding protein (SREBP)-1c and SREBP-2 (P &lt; 0.05).	Acetylcysteine	0-3	sterol regulatory element binding transcription factor 1	Mus musculus	110-162
31206613-4	2019	In the NAC group, significantly increased DAT binding was found in the caudate and putamen (mean increase from 3.4% to 8.3%) compared with controls (P < 0.05), along with significantly improved PD symptoms (P < 0.0001).	Acetylcysteine	7-10	solute carrier family 6 member 3	Homo sapiens	42-45
31422095-10	2019	In high glucose-cultured cardiomyocytes, Klotho and N-acetylcysteine significantly downregulated intracellular reactive oxygen species generation and TXNIP/NLRP3 inflammasome activation.	Acetylcysteine	52-68	thioredoxin interacting protein	Rattus norvegicus	150-155
18062818-0	2007	N-acetylcysteine prevents HIV gp 120-related damage of human cultured astrocytes: correlation with glutamine synthase dysfunction.	Acetylcysteine	0-16	inter-alpha-trypsin inhibitor heavy chain 4	Homo sapiens	30-36
18062818-3	2007	Here we investigated on the effect of N-acetylcysteine (NAC), on gp120-induced damage in human cultured astroglial cells and the possible contribution of gp120-related reacting oxygen species (ROS) in the imbalanced activity of glutamine synthase (GS), the enzyme that metabolizes glutamate into glutamine within astroglial cells playing a neuroprotective role in brain disorders.	Acetylcysteine	38-54	inter-alpha-trypsin inhibitor heavy chain 4	Homo sapiens	65-70
17904098-7	2007	N-acetylcysteine (NAC), a well-known ROS scavenger, suppressed caspase-8 activation and the subsequent cleavage of caspase-9 and caspase-3, indicating the role of ROS in caspase-8-mediated apoptosis.	Acetylcysteine	0-16	caspase 9	Homo sapiens	115-124
31077745-7	2019	Additionally, the ROS scavenger, N-Acetyl-L-cysteine (NAC), partially prevented prodigiosin-induced apoptosis but did not reduce prodigiosin-inhibited autophagy in K562 cells.	Acetylcysteine	33-52	X-linked Kx blood group	Homo sapiens	54-57
31251971-6	2019	Treatment with the antioxidants N-acetyl-L-cysteine (NAC) and superoxide dismutase (SOD) prevented PCB118-induced effects on PKM2, cell proliferation and glycolysis.	Acetylcysteine	32-51	X-linked Kx blood group	Homo sapiens	53-56
17904098-7	2007	N-acetylcysteine (NAC), a well-known ROS scavenger, suppressed caspase-8 activation and the subsequent cleavage of caspase-9 and caspase-3, indicating the role of ROS in caspase-8-mediated apoptosis.	Acetylcysteine	18-21	caspase 9	Homo sapiens	115-124
17596533-6	2007	Moreover, NAC and taurine increased cyclin D1/cdk4 activation and suppressed p21(Waf1/Cip1) and p27(Kip1) expression in HG-treated cells.	Acetylcysteine	10-13	interferon alpha inducible protein 27	Homo sapiens	96-99
31636802-1	2019	The present study investigated the antiapoptotic and antigenotoxic capabilities of N-acetyl cysteine- (NAC-) containing polymethyl methacrylate (PMMA) resin.	Acetylcysteine	83-100	X-linked Kx blood group	Homo sapiens	103-106
17596533-6	2007	Moreover, NAC and taurine increased cyclin D1/cdk4 activation and suppressed p21(Waf1/Cip1) and p27(Kip1) expression in HG-treated cells.	Acetylcysteine	10-13	cyclin dependent kinase inhibitor 1B	Homo sapiens	100-104
31273057-13	2019	Moreover, E-cadherin expression was increased while vimentin and Cytochrome C expressions were decreased by NAC.	Acetylcysteine	108-111	vimentin	Mus musculus	52-60
17705945-2	2007	OBJECTIVE: To provide descriptive data on the safety and efficacy of intravenous N-acetylcysteine (IV-NAC) in the treatment of APAP toxicity, based on information in the Hunter Area Toxicology Service (HATS) database involving residents of the Greater Newcastle Area of New South Wales, Australia.	Acetylcysteine	81-97	synuclein alpha	Homo sapiens	102-105
31172724-5	2019	Claudin-1 was degraded by GCE, and was restored by PAR2-ant or NAC in the cells.	Acetylcysteine	63-66	claudin 1	Mus musculus	0-9
31222000-7	2019	Like NAC, ADM dose-dependently reduced LPS-induced cytotoxicity and ROS overproduction.	Acetylcysteine	5-8	adrenomedullin	Rattus norvegicus	10-13
17584759-11	2007	Cotreatment with either NAC or GSHee mitigated the effects of APAP in Gclm wild-type and heterozygous mice, but not in Gclm null mice.	Acetylcysteine	24-27	glutamate-cysteine ligase, modifier subunit	Mus musculus	70-74
31207966-7	2019	Trauma-induced hypocellularity, MMP-13 expression, and cell cluster formation were reduced in NAC-treated animals.	Acetylcysteine	94-97	collagenase 3	Oryctolagus cuniculus	32-38
31207966-9	2019	Moreover, synovial concentrations of COL2 carboxy propeptide (CPII) and proteoglycan staining intensities were enhanced in NAC- and NAC+BMP7-treated joints.	Acetylcysteine	132-135	bone morphogenetic protein 7	Oryctolagus cuniculus	136-140
17478559-9	2007	MFG-E8 in the microvesicles was reduced when cultured in the low-glucose medium or cultured in the high-glucose medium with antioxidant N-acetyl cysteine.	Acetylcysteine	136-153	milk fat globule EGF and factor V/VIII domain containing	Mus musculus	0-6
31196186-15	2019	Treatment of leukemic cell lines with NAC prevented the DFX-mediated phosphorylation of STAT1 as well as the expression of the IFN-stimulated genes.	Acetylcysteine	38-41	signal transducer and activator of transcription 1	Homo sapiens	88-93
30956032-9	2019	Pretreatment with N-acetylcysteine (NAC) abrogate the difference between HI and LIUVA radiation on fibroblasts in terms of intracellular ROS, JNK phosphorylation, MMP-1 expression and type I collagen expression.	Acetylcysteine	18-34	mitogen-activated protein kinase 8	Mus musculus	142-145
30956032-9	2019	Pretreatment with N-acetylcysteine (NAC) abrogate the difference between HI and LIUVA radiation on fibroblasts in terms of intracellular ROS, JNK phosphorylation, MMP-1 expression and type I collagen expression.	Acetylcysteine	36-39	mitogen-activated protein kinase 8	Mus musculus	142-145
17884964-8	2007	NAC and vitamin E significantly reduced the increases in the local production of TNF-alpha and VEGF, and perivascular MPO activity.	Acetylcysteine	0-3	vascular endothelial growth factor A	Rattus norvegicus	95-99
30496017-9	2019	Expressions of Brca2, Xpc, Mlh3, Rad51, Xrcc2, Hus1, Rad9a, Cdkn1a, Gadd45a which are the DNA-repair genes were found to be significantly higher in NAC + ALC + IR group than those in individual treatment of ALC or NAC.	Acetylcysteine	214-217	RAD51 recombinase	Homo sapiens	33-38
29773887-8	2019	Pretreatment of N-acetyl cysteine (an antioxidant), rather than z-VAD (specific caspase inhibitor), markedly prevented XIAP reduction, suggesting that XIAP reduction may be resulted from oxidative stress.	Acetylcysteine	16-33	X-linked inhibitor of apoptosis	Homo sapiens	119-123
29076434-9	2018	Furthermore, exposure to ROS scavengers (N-acetyl-l-cysteine (NAC), and JNK-specific inhibitor SP600125) significantly reversed the effects of CJK-7 by down-regulating apoptosis and autophagy signatures in HCT-116 cancer cells.	Acetylcysteine	41-60	X-linked Kx blood group	Homo sapiens	62-65
29313384-5	2018	CS NPs significantly triggered the occurrence of autophagy by increasing the ratio of LC3 II to LC3 I and CS NPs-mediated autophagy was implicated in reactive oxygen species (ROS) generation and the ROS scavenger N-acetylcysteine (NAC) attenuated CS-induced autophagy.	Acetylcysteine	213-229	microtubule associated protein 1 light chain 3 alpha	Homo sapiens	86-89
29313384-5	2018	CS NPs significantly triggered the occurrence of autophagy by increasing the ratio of LC3 II to LC3 I and CS NPs-mediated autophagy was implicated in reactive oxygen species (ROS) generation and the ROS scavenger N-acetylcysteine (NAC) attenuated CS-induced autophagy.	Acetylcysteine	213-229	microtubule associated protein 1 light chain 3 alpha	Homo sapiens	96-99
17884964-8	2007	NAC and vitamin E significantly reduced the increases in the local production of TNF-alpha and VEGF, and perivascular MPO activity.	Acetylcysteine	0-3	myeloperoxidase	Rattus norvegicus	118-121
29313384-5	2018	CS NPs significantly triggered the occurrence of autophagy by increasing the ratio of LC3 II to LC3 I and CS NPs-mediated autophagy was implicated in reactive oxygen species (ROS) generation and the ROS scavenger N-acetylcysteine (NAC) attenuated CS-induced autophagy.	Acetylcysteine	231-234	microtubule associated protein 1 light chain 3 alpha	Homo sapiens	86-89
29313384-5	2018	CS NPs significantly triggered the occurrence of autophagy by increasing the ratio of LC3 II to LC3 I and CS NPs-mediated autophagy was implicated in reactive oxygen species (ROS) generation and the ROS scavenger N-acetylcysteine (NAC) attenuated CS-induced autophagy.	Acetylcysteine	231-234	microtubule associated protein 1 light chain 3 alpha	Homo sapiens	96-99
17400565-9	2007	RESULTS: NAC significantly attenuated deterioration of renal function in diclofenac-treated rats: cystatin C dropped from 2.8+/-0.35 to 2.2+/-0.67 mg/l, P=0.016; creatinine from 1.2+/-0.97 to 0.96+/-0.19 mg/dl, P=0.02; urea from 208.4+/-57.9 to 157.6+/-33.7 mg/dl, P=0.028.	Acetylcysteine	9-12	cystatin C	Rattus norvegicus	98-108
30481789-6	2018	Quercetin, the AEM and NAC showed a significant inhibitory effect on both ICAM-1 expression and ROS generation (p&lt;0.05).	Acetylcysteine	23-26	intercellular adhesion molecule 1	Homo sapiens	74-80
28966297-7	2017	In addition, NAC (N-acetylcysteine, a reactive oxygen species (ROS) scavenger) treatment dramatically decreased ROS generation in H1299 cells; both of NAC and 4-PBA (4-phenylbutyrate, a specific endoplasmic reticulum (ER) stress inhibitor) administration impaired apoptosis and expression levels of ATF4, CHOP and caspase-4 in G-Rh2 incubated H1299 cells.	Acetylcysteine	18-34	activating transcription factor 4	Homo sapiens	299-303
28880428-7	2017	Pretreatment with N-Acetyl L-Cysteine, a ROS scavenger, could fully reverse SZC017-induced ROS and increase the expression of Akt, p-STAT3, and procaspase-3, while decrease the ratio of LC3-II/I and the expression of Beclin-1.	Acetylcysteine	18-37	beclin 1	Homo sapiens	217-225
30774333-10	2019	The release kinetic curve indicated that NAC was released from (PLGA + NAC)/(NAC@MSN) in a biphasic pattern, that featured an initial burst release stage and a later sustained release stage.	Acetylcysteine	41-44	moesin	Rattus norvegicus	81-84
30774333-11	2019	This release pattern of NAC encapsulated on the (PLGA + NAC)/(NAC@MSN) scaffolds enabled to prolong the high concentrations of release of NAC, thus drastically affecting the osteogenic differentiation of rBMSCs.	Acetylcysteine	24-27	moesin	Rattus norvegicus	66-69
30774333-12	2019	Conclusion: A PLGA electrospun scaffold was developed, and MSNs were used as separate nanocarriers for recharging NAC concentration, demonstrating the promising use of (PLGA + NAC)/(NAC@MSN) for bone tissue engineering.	Acetylcysteine	114-117	moesin	Rattus norvegicus	59-62
30774333-12	2019	Conclusion: A PLGA electrospun scaffold was developed, and MSNs were used as separate nanocarriers for recharging NAC concentration, demonstrating the promising use of (PLGA + NAC)/(NAC@MSN) for bone tissue engineering.	Acetylcysteine	176-179	moesin	Rattus norvegicus	59-62
30774333-12	2019	Conclusion: A PLGA electrospun scaffold was developed, and MSNs were used as separate nanocarriers for recharging NAC concentration, demonstrating the promising use of (PLGA + NAC)/(NAC@MSN) for bone tissue engineering.	Acetylcysteine	176-179	moesin	Rattus norvegicus	59-62
30774430-4	2019	Intracellular ROS level was detected by DCFH-DA fluorescence assay, and N-Acetyl-L-cysteine (NAC) was used to scavenge intracellular ROS.	Acetylcysteine	72-91	X-linked Kx blood group	Homo sapiens	93-96
17531120-11	2007	Preincubation with N-acetylcysteine or ginkgo biloba extract increased GSH level, suppressed AGEs-induced oxidative stress and TGF-beta1, CTGF and Fn mRNA overexpression.	Acetylcysteine	19-35	cellular communication network factor 2	Rattus norvegicus	138-142
30654800-2	2019	Our aim was to alleviate ROS stress in vitrified mice oocytes using N-acetylcysteine (NAC at 1 mM), to improve the oocyte"s developmental competence.	Acetylcysteine	68-84	NLR family, pyrin domain containing 1A	Mus musculus	86-89
30641872-7	2019	The benefits of NAC were associated with enhanced AMPK-PGC-1alpha-SIRT3 signaling protein expressions, which led to decreased acetylation of superoxide dismutase 2 (SOD2) and increased expression of mitochondrial antioxidant manganese superoxide dismutase (MnSOD).	Acetylcysteine	16-19	superoxide dismutase 2	Rattus norvegicus	141-163
30641872-7	2019	The benefits of NAC were associated with enhanced AMPK-PGC-1alpha-SIRT3 signaling protein expressions, which led to decreased acetylation of superoxide dismutase 2 (SOD2) and increased expression of mitochondrial antioxidant manganese superoxide dismutase (MnSOD).	Acetylcysteine	16-19	superoxide dismutase 2	Rattus norvegicus	165-169
30641872-7	2019	The benefits of NAC were associated with enhanced AMPK-PGC-1alpha-SIRT3 signaling protein expressions, which led to decreased acetylation of superoxide dismutase 2 (SOD2) and increased expression of mitochondrial antioxidant manganese superoxide dismutase (MnSOD).	Acetylcysteine	16-19	superoxide dismutase 2	Rattus norvegicus	225-255
30641872-7	2019	The benefits of NAC were associated with enhanced AMPK-PGC-1alpha-SIRT3 signaling protein expressions, which led to decreased acetylation of superoxide dismutase 2 (SOD2) and increased expression of mitochondrial antioxidant manganese superoxide dismutase (MnSOD).	Acetylcysteine	16-19	superoxide dismutase 2	Rattus norvegicus	257-262
30387809-7	2019	The results revealed that the reduced form of Trx1 was markedly increased, and the oxidized forms of Prx1, GSR and PTEN were decreased following NAC pretreatment.	Acetylcysteine	145-148	phosphatase and tensin homolog	Rattus norvegicus	115-119
17291459-7	2007	Dimethylthiourea (DMTU) and N-acetyl-cysteine (NAC) attenuated hydroxyl radical accumulation, and importantly, diminished p53 activation during cisplatin treatment.	Acetylcysteine	28-45	transformation related protein 53, pseudogene	Mus musculus	122-125
30959503-10	2019	Also, secretion of the studied solutes, with the exception of ICAM-1, was reduced in the presence of NAC: IL6 -34%, p &lt; 0.01; VEGF -40%, p &lt; 0.005; vWF -25%, p &lt; 0.001; t-PA -47%, p &lt; 0.01, and MMP9 -37%, p &lt; 0.001.	Acetylcysteine	101-104	intercellular adhesion molecule 1	Homo sapiens	62-68
30959503-10	2019	Also, secretion of the studied solutes, with the exception of ICAM-1, was reduced in the presence of NAC: IL6 -34%, p &lt; 0.01; VEGF -40%, p &lt; 0.005; vWF -25%, p &lt; 0.001; t-PA -47%, p &lt; 0.01, and MMP9 -37%, p &lt; 0.001.	Acetylcysteine	101-104	matrix metallopeptidase 9	Homo sapiens	206-210
30315841-8	2019	Interestingly, NAC supplementation not only attenuated elevated 8-OHdG, PARP-1, caspase-3, cleaved caspase-9, and Bax, but also the TCE-mediated autoimmune response supported by significantly reduced serum anti-ssDNA antibodies.	Acetylcysteine	15-18	poly (ADP-ribose) polymerase family, member 1	Mus musculus	72-78
30315841-8	2019	Interestingly, NAC supplementation not only attenuated elevated 8-OHdG, PARP-1, caspase-3, cleaved caspase-9, and Bax, but also the TCE-mediated autoimmune response supported by significantly reduced serum anti-ssDNA antibodies.	Acetylcysteine	15-18	caspase 3	Mus musculus	80-89
30315841-8	2019	Interestingly, NAC supplementation not only attenuated elevated 8-OHdG, PARP-1, caspase-3, cleaved caspase-9, and Bax, but also the TCE-mediated autoimmune response supported by significantly reduced serum anti-ssDNA antibodies.	Acetylcysteine	15-18	BCL2-associated X protein	Mus musculus	114-117
17291459-7	2007	Dimethylthiourea (DMTU) and N-acetyl-cysteine (NAC) attenuated hydroxyl radical accumulation, and importantly, diminished p53 activation during cisplatin treatment.	Acetylcysteine	47-50	transformation related protein 53, pseudogene	Mus musculus	122-125
17291459-10	2007	Notably, DMTU and NAC, when added post-cisplatin treatment, were also inhibitory to p53 activation and apoptosis.	Acetylcysteine	18-21	transformation related protein 53, pseudogene	Mus musculus	84-87
17216608-10	2007	Erdosteine, NAC and vitamin E significantly reduced the increases in the local production of TNF-alpha and heart MPO activity.	Acetylcysteine	12-15	myeloperoxidase	Rattus norvegicus	113-116
30187827-4	2018	This study investigated the effectiveness of ex vivo antioxidant treatment [N-acetylcysteine (7.5 mM NAC) and Ascorbic acid 2-phosphate (0.6 mM AAP)] to restore the paracrine function of diabetic MSCs.	Acetylcysteine	76-92	NLR family, pyrin domain containing 1A	Mus musculus	101-104
30011378-9	2018	Coadministration of NAC and GEN has an additive gastroprotective effect in IND-induced gastric injury, which may be through interaction of their potential cytoprotective, antioxidant, anti-inflammatory, and antiapoptotic mechanisms together with regulation of MMP-9 expression.	Acetylcysteine	20-23	matrix metallopeptidase 9	Rattus norvegicus	260-265
17466927-6	2007	AGE-induced Hsp70 was attenuated by AG-490 (a JAK2 inhibitor) and N-acetylcysteine.	Acetylcysteine	66-82	heat shock protein family A (Hsp70) member 1B	Rattus norvegicus	12-17
17466927-10	2007	AGE-induced Hsp70 and mitogenesis were also attenuated by N-acetylcysteine.	Acetylcysteine	58-74	heat shock protein family A (Hsp70) member 1B	Rattus norvegicus	12-17
29859004-9	2018	Notably, in the presence of NAC, Rb1 expression was normalized and a normal cell proliferation pattern could be restored.	Acetylcysteine	28-31	RB transcriptional corepressor 1	Rattus norvegicus	33-36
17384488-7	2007	On the other hand, daily administration of an antioxidant, N-acetylcysteine significantly reduced the level of AR mRNA in the heart with a concomitant elevation in the enzyme activity.	Acetylcysteine	59-75	aldo-keto reductase family 1, member B3 (aldose reductase)	Mus musculus	111-113
29357673-5	2018	RyR2 downregulation or inhibitors of N-methyl-d-aspartate (NMDA) receptors, or NOS or of NADPH oxidase type-2 (NOX2) prevented RyR2 upregulation and the spine remodeling induced by BDNF, as did incubation with the antioxidant agent N-acetyl l-cysteine.	Acetylcysteine	232-251	cytochrome b-245 beta chain	Homo sapiens	89-109
29357673-5	2018	RyR2 downregulation or inhibitors of N-methyl-d-aspartate (NMDA) receptors, or NOS or of NADPH oxidase type-2 (NOX2) prevented RyR2 upregulation and the spine remodeling induced by BDNF, as did incubation with the antioxidant agent N-acetyl l-cysteine.	Acetylcysteine	232-251	cytochrome b-245 beta chain	Homo sapiens	111-115
30025894-9	2018	Besides, administration of the antioxidant N-acetyl-l-cysteine (NAC) normalized the increased ROS levels in FoxO1-deficient osteoblasts, restoring the decreased osteoblasts differentiation, suppressing apoptosis-related caspase-3 activity, and promoting the expression of osteogenic markers in FoxO1-deficient osteoblasts.	Acetylcysteine	43-62	caspase 3	Mus musculus	220-229
30025894-9	2018	Besides, administration of the antioxidant N-acetyl-l-cysteine (NAC) normalized the increased ROS levels in FoxO1-deficient osteoblasts, restoring the decreased osteoblasts differentiation, suppressing apoptosis-related caspase-3 activity, and promoting the expression of osteogenic markers in FoxO1-deficient osteoblasts.	Acetylcysteine	64-67	caspase 3	Mus musculus	220-229
30131715-6	2018	Furthermore, NAC pretreatment partly inhibited MC-LR-induced ERs and autophagy via the PERK/ATG12 and XBP1/Beclin1 pathways.	Acetylcysteine	13-16	eukaryotic translation initiation factor 2 alpha kinase 3	Mus musculus	87-91
17178255-9	2007	Pitavastatin, DPI, and an anti-oxidant N-acetylcysteine inhibited the LPA-induced proliferation and MCP-1 gene expression in SMCs.	Acetylcysteine	39-55	C-C motif chemokine ligand 2	Homo sapiens	100-105
30008899-1	2018	N-acetyl-L-cysteine (NAC) is the most abundant water-soluble component of garlic.	Acetylcysteine	0-19	X-linked Kx blood group	Homo sapiens	21-24
17174578-0	2007	Antioxidant N-acetyl-L-cysteine inhibits erythropoietin-induced differentiation of erythroid progenitors derived from mouse fetal liver.	Acetylcysteine	12-31	erythropoietin	Mus musculus	41-55
29741731-13	2018	Finally, N-acetylcysteine (NAC) was used to decrease the intracellular ROS level, and the expression of p-mTOR was measured.	Acetylcysteine	9-25	X-linked Kx blood group	Homo sapiens	27-30
17192422-5	2007	The stimulation of OKL38 by OxPAPC depends on superoxide production, because the NADPH oxidase (Nox) inhibitor apocynin and the superoxide scavenger N-acetyl cysteine block this stimulation.	Acetylcysteine	149-166	oxidative stress induced growth inhibitor 1	Homo sapiens	19-24
17279683-2	2007	The objective of this work was to assess the intracellular Cd2+ concentration in human breast cancer MCF-7 cells treated with cadmium telluride (CdTe) and core/shell cadmium selenide/zinc sulfide (CdSe/ZnS) nanoparticles capped with mercaptopropionic acid (MPA), cysteamine (Cys), or N-acetylcysteine (NAC) conjugated to cysteamine.	Acetylcysteine	284-300	CD2 molecule	Homo sapiens	59-62
29923297-6	2018	In addition, oxidative stress regulated autophagy, reflected by the results that NAC decreased the mRNA and protein expression of LC3, Beclin1, and p62.	Acetylcysteine	81-84	microtubule associated protein 1 light chain 3 alpha	Homo sapiens	130-133
29923297-6	2018	In addition, oxidative stress regulated autophagy, reflected by the results that NAC decreased the mRNA and protein expression of LC3, Beclin1, and p62.	Acetylcysteine	81-84	beclin 1	Homo sapiens	135-142
29923297-6	2018	In addition, oxidative stress regulated autophagy, reflected by the results that NAC decreased the mRNA and protein expression of LC3, Beclin1, and p62.	Acetylcysteine	81-84	nucleoporin 62	Homo sapiens	148-151
29660332-11	2018	Intriguingly, pre-treatment of ROS scavenger, N-acetylcysteine (NAC), markedly abolished DUSP14-KD-augmented NF-kappaB and MAPKs activation in HR-stimulated primary cardiomyocytes.	Acetylcysteine	46-62	dual specificity phosphatase 14	Mus musculus	89-95
29660332-11	2018	Intriguingly, pre-treatment of ROS scavenger, N-acetylcysteine (NAC), markedly abolished DUSP14-KD-augmented NF-kappaB and MAPKs activation in HR-stimulated primary cardiomyocytes.	Acetylcysteine	64-67	dual specificity phosphatase 14	Mus musculus	89-95
17279683-2	2007	The objective of this work was to assess the intracellular Cd2+ concentration in human breast cancer MCF-7 cells treated with cadmium telluride (CdTe) and core/shell cadmium selenide/zinc sulfide (CdSe/ZnS) nanoparticles capped with mercaptopropionic acid (MPA), cysteamine (Cys), or N-acetylcysteine (NAC) conjugated to cysteamine.	Acetylcysteine	302-305	CD2 molecule	Homo sapiens	59-62
29292543-8	2018	Moreover, Abeta upregulated ROS accumulation, while ROS scavengers N-acetyl-l-cysteine impaired Abeta-mediated autophagy.	Acetylcysteine	67-86	amyloid beta precursor protein	Rattus norvegicus	96-101
17188792-9	2007	Cytochrome P450 enzymes present in microsomes bioactivate APAP to NAPQI, which binds the electrophile trapping agent, N-acetyl cysteine (NAC).	Acetylcysteine	118-135	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	0-15
29904431-1	2018	The aim of the present study was to investigate the impact of N-acetylcysteine (NAC) on the expression of activin receptor-like kinase-1 (ALK-1) and mothers against decapentaplegic homolog 1 (Smad1) in the pulmonary artery of rats with pulmonary arterial hypertension (PAH), and to explore the possible mechanisms underlying its effects on pulmonary vascular remodeling (PVR).	Acetylcysteine	62-78	SMAD family member 1	Rattus norvegicus	192-197
29904431-1	2018	The aim of the present study was to investigate the impact of N-acetylcysteine (NAC) on the expression of activin receptor-like kinase-1 (ALK-1) and mothers against decapentaplegic homolog 1 (Smad1) in the pulmonary artery of rats with pulmonary arterial hypertension (PAH), and to explore the possible mechanisms underlying its effects on pulmonary vascular remodeling (PVR).	Acetylcysteine	80-83	SMAD family member 1	Rattus norvegicus	192-197
29904431-7	2018	In addition, NAC reduced the MCT-induced PVR, pulmonary inflammation score and upregulation of ALK-1 and Smad1.	Acetylcysteine	13-16	SMAD family member 1	Rattus norvegicus	105-110
29904431-8	2018	These results indicate that ALK-1 and Smad1 participate in the formation of PAH and the process of PVR, and suggest that NAC may inhibit PAH by inhibiting the expression of ALK-1 and Smad1 in the pulmonary artery.	Acetylcysteine	121-124	SMAD family member 1	Rattus norvegicus	183-188
17188792-9	2007	Cytochrome P450 enzymes present in microsomes bioactivate APAP to NAPQI, which binds the electrophile trapping agent, N-acetyl cysteine (NAC).	Acetylcysteine	137-140	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	0-15
17189831-6	2007	Incubation with the thiol antioxidant N-acetylcysteine strongly inhibited both the Nrf2 accumulation and the expression of Nrf2-regulated genes such as HO-1, GCLM, and SQSTM1.	Acetylcysteine	38-54	heme oxygenase 1	Homo sapiens	152-156
17612979-10	2007	Transient decreases in glutathione reductase (GR) activity were measured in the skin and kidney in association with repeat administration of 1,200 mg/kg NAC.	Acetylcysteine	153-156	glutathione-disulfide reductase	Rattus norvegicus	46-48
29561203-4	2018	N-acetylcysteine resulted in a rapid and significant GSH increase to 1 93 +- 0.23 mM within 12-30 min after completion of infusion ( n = 21, p &lt; 0.0001, paired t-test), compared with those who did not receive N-acetylcysteine ( n = 3, GSH = 1.66 +- 0.06 mM and 1.64 +- 0.09 mM).	Acetylcysteine	0-16	GS homeobox 1	Homo sapiens	238-245
29734752-6	2018	Moreover, putative protective drugs, namely the antioxidants N-acetyl-l-cysteine (NAC; 1 mM) and 100 &amp;mu;M tiron, the inhibitor of caspase-3/7, Ac-DEVD-CHO (100 &amp;mu;M), and a protein synthesis inhibitor, cycloheximide (CHX; 10 nM), were tested to prevent DOX- or MTX-induced toxicity.	Acetylcysteine	61-80	X-linked Kx blood group	Homo sapiens	82-85
29436612-6	2018	Furthermore, blocking ROS with NAC inhibited SW-induced ER stress, as evidenced by the downregulation of GRP78, phosphorylated (p)-protein kinase R-like ER kinase (PERK), p-inositol-requiring kinase 1alpha (IRE1alpha), p-50 activating transcription factor 6alpha and CHOP.	Acetylcysteine	31-34	heat shock protein family A (Hsp70) member 5	Rattus norvegicus	105-110
28942246-14	2017	N-acetylcysteine (NAC) suppressed HNF1b knockdown-induced ER stress, TG formation and insulin resistance.	Acetylcysteine	0-16	HNF1 homeobox B	Mus musculus	34-39
28942246-14	2017	N-acetylcysteine (NAC) suppressed HNF1b knockdown-induced ER stress, TG formation and insulin resistance.	Acetylcysteine	18-21	HNF1 homeobox B	Mus musculus	34-39
17612979-12	2007	Overall, the results of this study present the possibility that NAC could provide some benefit in preventing or reducing toxicity related to exposure to chemical irritants (particularly sulfur mustard) in some tissues by increasing tissue NAC and/or cysteine levels, GSH concentrations, and GST activity.	Acetylcysteine	64-67	hematopoietic prostaglandin D synthase	Rattus norvegicus	291-294
28942246-15	2017	Palmitic acid (PA) decreased HNF1b expression which was inhibited by NAC.	Acetylcysteine	69-72	HNF1 homeobox B	Mus musculus	29-34
17760653-3	2007	N-acetylcysteine ((NAC) has been shown to have oxygen scavenging abilities.	Acetylcysteine	0-16	synuclein alpha	Homo sapiens	19-22
28986255-7	2017	Analysis of mTORC2, the complex responsible for phosphorylating Akt at S473, reveals increased cysteine oxidation of Rictor in Prdx3 KD cells that can be rescued with NAC.	Acetylcysteine	167-170	peroxiredoxin 3	Homo sapiens	127-132
29686303-7	2018	In our study we observed that the high levels of mtDNA and elevated TLR9/NF-kappaB activity were ameliorated in the CQ/NAC-coated FC group.	Acetylcysteine	119-122	toll-like receptor 9	Sus scrofa	68-72
30788945-8	2018	Compared with TCP group, serum levels of TNF-alpha, IL-1beta and IL-6, and osteolysis area were decreased markedly in NAC group (P&lt;0.05), serum level of T-AOC and SOD activity were increased obviously in NAC group (P&lt;0.05), and GRP78 expression, the ratio of p-PERK/PERK and p-eIF2alpha/eIF2alpha were obviously down-regulated.	Acetylcysteine	118-121	eukaryotic translation initiation factor 2 alpha kinase 3	Mus musculus	267-271
17046137-10	2006	Posttreatment with erdosteine and NAC significantly reduced the increases in the local production of TNF-alpha and VEGF, and epithelial MPO activity.	Acetylcysteine	34-37	vascular endothelial growth factor A	Rattus norvegicus	115-119
30788945-8	2018	Compared with TCP group, serum levels of TNF-alpha, IL-1beta and IL-6, and osteolysis area were decreased markedly in NAC group (P&lt;0.05), serum level of T-AOC and SOD activity were increased obviously in NAC group (P&lt;0.05), and GRP78 expression, the ratio of p-PERK/PERK and p-eIF2alpha/eIF2alpha were obviously down-regulated.	Acetylcysteine	118-121	eukaryotic translation initiation factor 2 alpha kinase 3	Mus musculus	272-276
29170479-6	2017	Moreover, heme degradation products, except iron and N-acetylcysteine prevented H2O2-mediated miR-155-5p biogenesis and eNOS downregulation.	Acetylcysteine	53-69	microRNA 155	Homo sapiens	94-101
17046137-10	2006	Posttreatment with erdosteine and NAC significantly reduced the increases in the local production of TNF-alpha and VEGF, and epithelial MPO activity.	Acetylcysteine	34-37	myeloperoxidase	Rattus norvegicus	136-139
17046137-11	2006	The effects of NAC on apoptosis, the increases in the local production of TNF-alpha and VEGF, were weaker than the effects of erdosteine.	Acetylcysteine	15-18	vascular endothelial growth factor A	Rattus norvegicus	88-92
17008589-5	2006	Treatment with polyethylene-glycol-conjugated superoxide dismutase, N-acetylcysteine (NAC), diphenylene iodonium (DPI), or apocynin significantly decreased LPS-induced TLR4 expression.	Acetylcysteine	68-84	toll like receptor 4	Homo sapiens	168-172
28918123-5	2017	Pre-incubation of HCC cells with N-Acetyl-l-cysteine (NAC), a ROS inhibitor, strongly suppressed CA-induced apoptotic phenomena, including reduced cell viability, excessive ROS levels, MMP decreases, and abnormal protein expression, suggesting an association of CA-induced apoptosis with oxidative stress-mediated mitochondrial pathways.	Acetylcysteine	33-52	X-linked Kx blood group	Homo sapiens	54-57
29416235-10	2017	Lower serum CRP and ICAM 1 with NAC versus C on day 3 (44.2 +- 13.4 vs. 68.7 +- 48.2 mg/l, P = 0.003), (308.8 +- 38.2 vs. 352.8 +- 59.4 ng/ml, P = 0.002), respectively.	Acetylcysteine	32-35	intercellular adhesion molecule 1	Homo sapiens	20-26
29416235-13	2017	Conclusion: Prophylactic NAC in hepatic patients undergoing liver surgery attenuated postoperative increase in transaminases, ICAM 1, and CRP blood levels.	Acetylcysteine	25-28	intercellular adhesion molecule 1	Homo sapiens	126-132
28497199-8	2018	AA-induced HO-1 expression was mediated through Nox/ROS generation, which was inhibited by Nox inhibitors (diphenyleneiodonium and apocynin) and ROS scavengers (N-acetyl cysteine).	Acetylcysteine	161-178	heme oxygenase 1	Rattus norvegicus	11-15
30261511-5	2018	Using quantitative PCR, we showed that NAC administration normalized the LPS induced expression of Keap1-Nrf2 signaling and oxidative stress key enzyme gene expressions (SOD, GPx and YAP1).	Acetylcysteine	39-42	kelch like ECH associated protein 1	Gallus gallus	99-104
30261511-5	2018	Using quantitative PCR, we showed that NAC administration normalized the LPS induced expression of Keap1-Nrf2 signaling and oxidative stress key enzyme gene expressions (SOD, GPx and YAP1).	Acetylcysteine	39-42	Yes associated protein 1	Gallus gallus	183-187
17008589-5	2006	Treatment with polyethylene-glycol-conjugated superoxide dismutase, N-acetylcysteine (NAC), diphenylene iodonium (DPI), or apocynin significantly decreased LPS-induced TLR4 expression.	Acetylcysteine	86-89	toll like receptor 4	Homo sapiens	168-172
29550818-11	2018	In TCMK-1 cells, Klotho and NAC attenuated the elevation in RIP1, RIP3, and LDH release induced by H/R or H2O2.	Acetylcysteine	28-31	receptor-interacting serine-threonine kinase 3	Mus musculus	66-70
28655635-7	2017	N-acetyl-l-cysteine (NAC), a ROS inhibitor, protected against MEHP-induced cytotoxicity and decreased the protein expression of LC3-II.	Acetylcysteine	0-19	X-linked Kx blood group	Homo sapiens	21-24
17008589-7	2006	Inhibition of NADPH oxidase activity by DPI, apocynin, or NAC significantly decreased TLR4 mRNA stability, as did the knock-down of RAC1 gene expression by RNA interference.	Acetylcysteine	58-61	toll like receptor 4	Homo sapiens	86-90
16973888-2	2006	Addition of antioxidants such as N-acetyl-l-cysteine or catalase attenuates G-Rh2-induced ROS generation, JNK1 activation, and apoptosis.	Acetylcysteine	33-52	Rh associated glycoprotein	Homo sapiens	78-81
28812437-9	2017	A ROS inhibitor, N-acetylcysteine, abolished KDR phosphorylation and the formation of VM by GSCs.	Acetylcysteine	17-33	kinase insert domain receptor	Homo sapiens	45-48
28577929-10	2017	Adding the antioxidant N-acetyl-l-cysteine significantly reduced MRP-1 and BCRP expression.	Acetylcysteine	23-42	ATP binding cassette subfamily C member 1	Rattus norvegicus	65-70
29843152-10	2018	Conversely, the antioxidant N-Acetyl-L-cysteine (NAC) and pan-caspase inhibitor z-VAD-fmk attenuated RA-induced apoptosis by scavenging ROS and inactivating caspase-3.	Acetylcysteine	28-47	caspase 3	Mus musculus	157-166
29843152-10	2018	Conversely, the antioxidant N-Acetyl-L-cysteine (NAC) and pan-caspase inhibitor z-VAD-fmk attenuated RA-induced apoptosis by scavenging ROS and inactivating caspase-3.	Acetylcysteine	49-52	caspase 3	Mus musculus	157-166
28504001-12	2018	Moreover, mutant strains in ABC transporters Pdr5, Yor1, Bpt1 or Pdr15, were more sensitive to DCF; while mutant strains in Pdr5, Vmr1 or Pdr12 were more sensitive to NAC/DCF interaction.	Acetylcysteine	167-170	ATP-binding cassette multidrug transporter PDR5	Saccharomyces cerevisiae S288C	45-49
28504001-12	2018	Moreover, mutant strains in ABC transporters Pdr5, Yor1, Bpt1 or Pdr15, were more sensitive to DCF; while mutant strains in Pdr5, Vmr1 or Pdr12 were more sensitive to NAC/DCF interaction.	Acetylcysteine	167-170	ATP-binding cassette multidrug transporter PDR5	Saccharomyces cerevisiae S288C	124-128
28504001-12	2018	Moreover, mutant strains in ABC transporters Pdr5, Yor1, Bpt1 or Pdr15, were more sensitive to DCF; while mutant strains in Pdr5, Vmr1 or Pdr12 were more sensitive to NAC/DCF interaction.	Acetylcysteine	167-170	putative ATP-binding cassette multidrug transporter VMR1	Saccharomyces cerevisiae S288C	130-134
29043702-0	2018	N-Acetylcysteine Compared to Metformin, Improves The Expression Profile of Growth Differentiation Factor-9 and Receptor Tyrosine Kinase c-Kit in The Oocytes of Patients with Polycystic Ovarian Syndrome.	Acetylcysteine	0-16	growth differentiation factor 9	Homo sapiens	75-106
28341391-8	2017	Addition of NAC to drinking water protected KO +Fe from hepatic steatosis, injury and fibrosis, and prevented activation of AKT, ERK, NF-kappaB and reappearance of beta-catenin.	Acetylcysteine	12-15	catenin (cadherin associated protein), beta 1	Mus musculus	164-176
28422158-9	2017	When oxidative stress was blocked by exposing mice to N-acetylcysteine, induction of liver UGT1A1 and CYP2B10 by PEITC was prevented.	Acetylcysteine	54-70	UDP glucuronosyltransferase 1 family, polypeptide A1	Mus musculus	91-97
29043702-2	2018	The aim of this study was to investigate the effects of metformin (MET), N-acetylcysteine (NAC) and their combination on the hormonal levels and expression profile of GDF-9, BMP-15 and c-kit, as hallmarks of oocyte quality, in PCOS patients.	Acetylcysteine	73-89	growth differentiation factor 9	Homo sapiens	167-172
29043702-2	2018	The aim of this study was to investigate the effects of metformin (MET), N-acetylcysteine (NAC) and their combination on the hormonal levels and expression profile of GDF-9, BMP-15 and c-kit, as hallmarks of oocyte quality, in PCOS patients.	Acetylcysteine	91-94	growth differentiation factor 9	Homo sapiens	167-172
16860347-12	2006	We conclude that post-treatment with NAC suppresses the release of plasma TNF-alpha, IL-6, and IL-10 in endotoxin shock, and decreases the markers of organ injury.	Acetylcysteine	37-40	interleukin 10	Rattus norvegicus	95-100
29043702-3	2018	MATERIALS AND METHODS: This prospective randomized, double-blind, placebo controlled trial aims to study the effects of MET, NAC and their combination (MET+NAC) on expression of GDF-9, BMP-15 and c-kit mRNA in oocytes [10 at the germinal vesicle (GV) stage, 10 at the MI stage, and 10 at the MII stage from per group] derived following ovulation induction in PCOS.	Acetylcysteine	125-128	growth differentiation factor 9	Homo sapiens	178-183
29043702-3	2018	MATERIALS AND METHODS: This prospective randomized, double-blind, placebo controlled trial aims to study the effects of MET, NAC and their combination (MET+NAC) on expression of GDF-9, BMP-15 and c-kit mRNA in oocytes [10 at the germinal vesicle (GV) stage, 10 at the MI stage, and 10 at the MII stage from per group] derived following ovulation induction in PCOS.	Acetylcysteine	156-159	growth differentiation factor 9	Homo sapiens	178-183
16802348-10	2006	Moreover, we found that the activation of the ARE and the induction of HO-1 mRNA caused by Apo were suppressed in the presence of the antioxidant N-acetylcysteine and also that Apo produced intracellular reactive oxygen species (ROS), indicating that the low level of ROS produced by Apo may play a critical role in this phenomenon.	Acetylcysteine	146-162	heme oxygenase 1	Homo sapiens	71-75
27957685-7	2018	On the other hand, quenching of H2O2 by antioxidants, resveratrol (RSV), or N-acetylcysteine (NAC) effectively blocked TRPM2-mediated Ca2+ influx, decreased intracellular Ca2+ overload, and increased cell survival.	Acetylcysteine	76-92	transient receptor potential cation channel subfamily M member 2	Homo sapiens	119-124
27957685-7	2018	On the other hand, quenching of H2O2 by antioxidants, resveratrol (RSV), or N-acetylcysteine (NAC) effectively blocked TRPM2-mediated Ca2+ influx, decreased intracellular Ca2+ overload, and increased cell survival.	Acetylcysteine	94-97	transient receptor potential cation channel subfamily M member 2	Homo sapiens	119-124
28237877-5	2017	In addition, OSI increased reactive oxygen species (ROS) generation and scavenge of ROS via pretreatment with N-acetyl-l-cysteine (NAC), catalase (CAT), or vitamin E (Vita E) significantly inhibited OSI-induced the accumulations of cytoplasmic vacuoles, the expression of LC3-II, as well as the formation of GFP-LC3 puncta.	Acetylcysteine	110-129	X-linked Kx blood group	Homo sapiens	131-134
28469982-9	2017	No early antioxidant action of 17beta-E2 has been found but the estrogen effect is similar to N-acetylcysteine which, by increasing the intracellular redox state, maintains JNK bound to GSTP1-1.	Acetylcysteine	94-110	mitogen-activated protein kinase 8	Mus musculus	173-176
16788090-5	2006	Suppression of CYP1A1 mRNA expression in TCDD-treated Huh.8 cells was partially reversed after pretreatment with the antioxidants N-acetylcysteine and nordihydroguaiaretic acid, suggesting a role for oxidative stress.	Acetylcysteine	130-146	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	15-21
28129433-5	2017	Also, N-acetyl-l-cysteine, a ROS scavenger, potentiated celastrol"s inhibition of the events in the cells triggered by Cd, implying neuroprotection by celastrol via blocking Cd-evoked NOX2-derived ROS.	Acetylcysteine	6-25	cytochrome b-245 beta chain	Rattus norvegicus	184-188
28187322-7	2017	N-acetylcysteine prevented the aspartame-induced liver injury and the increase in plasma ALT activity as well as the decrease in GSH, gamma-GC, cysteine, SAM and SAH levels and GCLc protein levels.	Acetylcysteine	0-16	glutamate-cysteine ligase, catalytic subunit	Mus musculus	177-181
28823537-13	2018	Moreover, ROS generation occurred upon treatment of SH-SY5Y cells with HPO-DAEE, and the antioxidants N-acetylcysteine and glutathione suppressed HPO-DAEE-induced activation of the Nrf2-ARE and eIF2alpha-ATF4 pathways.	Acetylcysteine	102-118	eukaryotic translation initiation factor 2A	Homo sapiens	194-203
28823537-13	2018	Moreover, ROS generation occurred upon treatment of SH-SY5Y cells with HPO-DAEE, and the antioxidants N-acetylcysteine and glutathione suppressed HPO-DAEE-induced activation of the Nrf2-ARE and eIF2alpha-ATF4 pathways.	Acetylcysteine	102-118	activating transcription factor 4	Homo sapiens	204-208
16847070-3	2006	These studies show that alveolar macrophages recovered from rodents subjected to hemorrhagic shock/resuscitation expressed increased surface levels of Toll-like receptor 4 (TLR4), an effect inhibited by adding the antioxidant N-acetylcysteine to the resuscitation fluid.	Acetylcysteine	226-242	toll like receptor 4	Homo sapiens	151-171
29326556-5	2017	First, we showed that H2O2 induces a significant increase in AQP4 protein levels and that this is inhibited by the antioxidant N-acetylcysteine (NAC).	Acetylcysteine	127-143	aquaporin 4	Homo sapiens	61-65
29326556-5	2017	First, we showed that H2O2 induces a significant increase in AQP4 protein levels and that this is inhibited by the antioxidant N-acetylcysteine (NAC).	Acetylcysteine	145-148	aquaporin 4	Homo sapiens	61-65
28902442-1	2017	The effect of N-acetyl-l-cysteine-capped CdTe quantum dots (NAC-CdTe QDs) with different sizes on lysozyme was investigated by isothermal titration calorimetry (ITC), enzyme activity assays, and multi-spectroscopic methods.	Acetylcysteine	14-33	X-linked Kx blood group	Homo sapiens	60-63
28204833-11	2017	H2O2 treatment decreased SHP luciferase activity, which was recovered by treatment with the NF-kappaB inhibitor Bay11-7082, transfection with dominant-negative c-Jun or treatment with N-acetyl cysteine (NAC).	Acetylcysteine	184-201	nuclear receptor subfamily 0, group B, member 2	Mus musculus	25-28
28204833-11	2017	H2O2 treatment decreased SHP luciferase activity, which was recovered by treatment with the NF-kappaB inhibitor Bay11-7082, transfection with dominant-negative c-Jun or treatment with N-acetyl cysteine (NAC).	Acetylcysteine	203-206	nuclear receptor subfamily 0, group B, member 2	Mus musculus	25-28
27994012-6	2017	Furthermore, the loss of enzymatic activity of prmt-1 induces food avoidance behavior due to mitochondrial dysfunction, but treatment with the antioxidant N-acetylcysteine significantly ameliorates this phenotype.	Acetylcysteine	155-171	Protein arginine N-methyltransferase 1	Caenorhabditis elegans	47-53
28905500-11	2017	Furthermore, the pharmacological effect of Sal associated with the ROS-mediated PI3K/Akt/mTOR pathway was proved by the use of ROS scavenger, N-acetyl-l-cysteine, in LPS-stimulated H9C2 cells.	Acetylcysteine	142-161	mechanistic target of rapamycin kinase	Rattus norvegicus	89-93
16847070-3	2006	These studies show that alveolar macrophages recovered from rodents subjected to hemorrhagic shock/resuscitation expressed increased surface levels of Toll-like receptor 4 (TLR4), an effect inhibited by adding the antioxidant N-acetylcysteine to the resuscitation fluid.	Acetylcysteine	226-242	toll like receptor 4	Homo sapiens	173-177
28057718-3	2017	N-Acetyl l-cysteine (NAC) and l-NG-Nitroarginine methyl ester (l-NAME) blocked stress-induced TJ disruption and barrier dysfunction.	Acetylcysteine	0-19	X-linked Kx blood group	Homo sapiens	21-24
16928829-5	2006	Pretreatment with N-acetylcysteine, a GSH precursor, blocked the down-regulation of AR mRNA and protein expression by selenite and restored AR ligand binding and prostate-specific antigen expression to control levels.	Acetylcysteine	18-34	kallikrein related peptidase 3	Homo sapiens	162-187
27981650-4	2017	Further studies showed that reactive oxygen species (ROS) induced apoptosis of A549 in the presence of rosbin as apoptosis was inhibited by N-acetyl cysteine (NAC).	Acetylcysteine	140-157	round spermatid basic protein 1	Homo sapiens	103-109
27981650-4	2017	Further studies showed that reactive oxygen species (ROS) induced apoptosis of A549 in the presence of rosbin as apoptosis was inhibited by N-acetyl cysteine (NAC).	Acetylcysteine	159-162	round spermatid basic protein 1	Homo sapiens	103-109
28983589-9	2017	Importantly, honokiol significantly increased the intracellular ROS levels as determined by a 2",7"-dichlorofluorescin diacetate assay, while ROS scavenger N-acetyl cysteine significantly prevented the induction of ROS and RIP3 by honokiol.	Acetylcysteine	156-173	receptor-interacting serine-threonine kinase 3	Mus musculus	223-227
29296199-8	2017	Further studies showed that N-acetyl cysteine blocked JNK and p38 phosphorylation, suggesting that ROS were upstream activators of JNK and p38.	Acetylcysteine	28-45	mitogen-activated protein kinase 8	Mus musculus	54-57
29296199-8	2017	Further studies showed that N-acetyl cysteine blocked JNK and p38 phosphorylation, suggesting that ROS were upstream activators of JNK and p38.	Acetylcysteine	28-45	mitogen-activated protein kinase 8	Mus musculus	131-134
29123322-3	2017	In this study, using the antioxidant N-acetylcysteine (NAC), we show that hypoxia-induced reactive oxygen species (ROS) in MDA-MB-468 breast cancer cells, selectively regulate hypoxia-induced increases in N-cadherin and SERPINE1, two proteins involved in cell adhesion.	Acetylcysteine	37-53	cadherin 2	Homo sapiens	205-215
29123322-3	2017	In this study, using the antioxidant N-acetylcysteine (NAC), we show that hypoxia-induced reactive oxygen species (ROS) in MDA-MB-468 breast cancer cells, selectively regulate hypoxia-induced increases in N-cadherin and SERPINE1, two proteins involved in cell adhesion.	Acetylcysteine	55-58	cadherin 2	Homo sapiens	205-215
28116245-7	2017	In conclusion, we demonstrated that 7KCHO induced apoptosis of MC3T3-E1 cells associated with ROS generation, ER stress, and caspase-3/7 activity, and the effects of 7KCHO were abolished by the ROS inhibitor NAC.	Acetylcysteine	208-211	caspase 3	Mus musculus	125-134
16135398-7	2006	Exogenous addition of antioxidants, glutathione (GSH) and N-Acetyl-Cysteine (NAC) inhibited the anti-proliferative ability of TPL in both MCF 7 and T47 D. Annexin-V and propidium iodide double staining of cells treated with TPL for 2h revealed that TPL induced significant apoptosis in both the cell lines in a dose dependant manner but magnitude of apoptosis was significantly higher in MCF 7 than in T 47-D cells.	Acetylcysteine	58-75	annexin A5	Homo sapiens	155-164
28214842-12	2017	Importantly, before the exposure to MGO, the preconditioning with NAC significantly attenuated MGO-induced AGEs generation, improved cellular viability and mitochondrial function, partially reversed the overexpression of proinflammatory factors and MMP-9, as well as the activation of NF-kappaB.	Acetylcysteine	66-69	matrix metallopeptidase 9	Homo sapiens	249-254
28214842-13	2017	Lastly, NAC blocked MGO-induced RAGE upregulation, and inhibition of RAGE with its neutralizing antibody significantly alleviated MGO-induced NF-kappaB activation, MMP-9 upregulation and inflammatory injury in HaCaT cells.	Acetylcysteine	8-11	long intergenic non-protein coding RNA 914	Homo sapiens	32-36
28849167-0	2017	Mechanisms of N-acetylcysteine in reducing monocrotaline-induced pulmonary hypertension in rats: Inhibiting the expression of Nox1 in pulmonary vascular smooth muscle cells.	Acetylcysteine	14-30	NADPH oxidase 1	Rattus norvegicus	126-130
28849167-1	2017	The aim of the present study was to investigate the impact of N-acetylcysteine (NAC) on the expression of reduced nicotinamide adenine dinucleotide phosphate oxidase 1 (Nox1), and the proliferation and apoptosis of pulmonary artery smooth muscle cells (PASMCs) in rats exhibiting monocrotaline (MCT)-induced pulmonary hypertension, and to investigate the possible mechanisms and treatment roles of NAC in pulmonary vascular remodeling (PVR).	Acetylcysteine	62-78	NADPH oxidase 1	Rattus norvegicus	114-167
28214842-14	2017	CONCLUSION: The present work indicates the administration of NAC can prevent MGO-induced dermal inflammatory injury through inhibition of AGEs/RAGE signal, which may provide a basal support for the treatment of diabetic skin complications with NAC-containing medicines in the future.	Acetylcysteine	61-64	long intergenic non-protein coding RNA 914	Homo sapiens	143-147
28849167-1	2017	The aim of the present study was to investigate the impact of N-acetylcysteine (NAC) on the expression of reduced nicotinamide adenine dinucleotide phosphate oxidase 1 (Nox1), and the proliferation and apoptosis of pulmonary artery smooth muscle cells (PASMCs) in rats exhibiting monocrotaline (MCT)-induced pulmonary hypertension, and to investigate the possible mechanisms and treatment roles of NAC in pulmonary vascular remodeling (PVR).	Acetylcysteine	62-78	NADPH oxidase 1	Rattus norvegicus	169-173
16135398-7	2006	Exogenous addition of antioxidants, glutathione (GSH) and N-Acetyl-Cysteine (NAC) inhibited the anti-proliferative ability of TPL in both MCF 7 and T47 D. Annexin-V and propidium iodide double staining of cells treated with TPL for 2h revealed that TPL induced significant apoptosis in both the cell lines in a dose dependant manner but magnitude of apoptosis was significantly higher in MCF 7 than in T 47-D cells.	Acetylcysteine	77-80	annexin A5	Homo sapiens	155-164
28849167-1	2017	The aim of the present study was to investigate the impact of N-acetylcysteine (NAC) on the expression of reduced nicotinamide adenine dinucleotide phosphate oxidase 1 (Nox1), and the proliferation and apoptosis of pulmonary artery smooth muscle cells (PASMCs) in rats exhibiting monocrotaline (MCT)-induced pulmonary hypertension, and to investigate the possible mechanisms and treatment roles of NAC in pulmonary vascular remodeling (PVR).	Acetylcysteine	80-83	NADPH oxidase 1	Rattus norvegicus	114-167
28849167-1	2017	The aim of the present study was to investigate the impact of N-acetylcysteine (NAC) on the expression of reduced nicotinamide adenine dinucleotide phosphate oxidase 1 (Nox1), and the proliferation and apoptosis of pulmonary artery smooth muscle cells (PASMCs) in rats exhibiting monocrotaline (MCT)-induced pulmonary hypertension, and to investigate the possible mechanisms and treatment roles of NAC in pulmonary vascular remodeling (PVR).	Acetylcysteine	80-83	NADPH oxidase 1	Rattus norvegicus	169-173
28849167-11	2017	NAC was able to decrease Nox1-derived reactive oxygen species in PASMCs, thereby improving PVR.	Acetylcysteine	0-3	NADPH oxidase 1	Rattus norvegicus	25-29
27639126-10	2016	ROS scavenger N-acetylcysteine (NAC) and NF-kappaB inhibitor PDTC showed similar effect on PA-induced secretion of TNF-alpha, IL-6, and expression of ICAM-1.	Acetylcysteine	14-30	intercellular adhesion molecule 1	Homo sapiens	150-156
27639126-10	2016	ROS scavenger N-acetylcysteine (NAC) and NF-kappaB inhibitor PDTC showed similar effect on PA-induced secretion of TNF-alpha, IL-6, and expression of ICAM-1.	Acetylcysteine	32-35	intercellular adhesion molecule 1	Homo sapiens	150-156
16609688-8	2006	Plasma MCP-1 concentration fell from 164 +/- 17.7 to 135 +/- 17.7 pg/ml with NAC, whereas it remained unchanged from 133 +/- 12.5 to 132 +/- 17.7 pg/ml with placebo (P=0.001 for visit x antioxidant drug interaction).	Acetylcysteine	77-80	C-C motif chemokine ligand 2	Homo sapiens	7-12
27665314-5	2016	Elevated inositol 1,4,5-trisphosphate (IP3) levels with up-regulated IP3 receptor (IP3R) protein levels were shown in Cd-exposed cells, confirming that IP3R-mediated ER Ca2+ release results in the elevation of [Ca2+]c. Up-regulated sequestosome 1 (p62) protein levels and autophagic flux assay demonstrated that Cd impaired autophagic degradation, while N-acetylcysteine (NAC) markedly attenuated Cd-induced p62 and microtubule-associated protein 1 light chain 3-II (LC3-II) accumulation, implying that the inhibition of autophagic flux was due to oxidative stress.	Acetylcysteine	354-370	inositol 1,4,5-trisphosphate receptor, type 1	Rattus norvegicus	152-156
27665314-5	2016	Elevated inositol 1,4,5-trisphosphate (IP3) levels with up-regulated IP3 receptor (IP3R) protein levels were shown in Cd-exposed cells, confirming that IP3R-mediated ER Ca2+ release results in the elevation of [Ca2+]c. Up-regulated sequestosome 1 (p62) protein levels and autophagic flux assay demonstrated that Cd impaired autophagic degradation, while N-acetylcysteine (NAC) markedly attenuated Cd-induced p62 and microtubule-associated protein 1 light chain 3-II (LC3-II) accumulation, implying that the inhibition of autophagic flux was due to oxidative stress.	Acetylcysteine	372-375	inositol 1,4,5-trisphosphate receptor, type 1	Rattus norvegicus	152-156
27634458-6	2016	Treatments of SH-SY5Y cells with the chemical chaperone, 4-phenylbutyric acid and the ROS scavenger, N-acetyl-cysteine reduced the AA-induced expression of ATF4 protein and CHOP mRNA, and resulted in the suppression of apoptosis.	Acetylcysteine	101-118	activating transcription factor 4	Homo sapiens	156-160
28848050-5	2017	Supporting this, combinatorial treatment with N-acetyl-l-cysteine and catalase substantially inhibited the ROS upsurge and PINK1-dependent Parkin translocation to mitochondria in response to carbonyl cyanide m-chlorophenylhydrazone treatment.	Acetylcysteine	46-65	PTEN induced kinase 1	Homo sapiens	123-128
28273344-8	2017	ROS scavengers, such as glutathione (GSH) and N-acetyl cysteine, prevented extracellular secretion of ATP and increases in intracellular calcium concentrations that precede IL-33 release.	Acetylcysteine	46-63	interleukin 33	Mus musculus	173-178
16609688-12	2006	In conclusion, iron sucrose causes rapid and transient generation and/or release of MCP-1 plasma concentration and increases urinary excretion rate, and systemic MCP-1 level but the urinary excretion rate is not abrogated with the antioxidant NAC.	Acetylcysteine	243-246	C-C motif chemokine ligand 2	Homo sapiens	84-89
27572094-6	2016	In addition, the present study demonstrated that S1PR1 suppressed the generation of reactive oxygen species (ROS) in AML cells, and that the apoptosis mediated by the downregulation of S1PR1 was partially reversed by treatment with N-acetyl-L-cysteine, a ROS scavenging agent, suggesting that the S1PR1-induced resistance of cell apoptosis resulted, at least partially, from the suppression of ROS generation.	Acetylcysteine	232-251	sphingosine-1-phosphate receptor 1	Homo sapiens	49-54
27572094-6	2016	In addition, the present study demonstrated that S1PR1 suppressed the generation of reactive oxygen species (ROS) in AML cells, and that the apoptosis mediated by the downregulation of S1PR1 was partially reversed by treatment with N-acetyl-L-cysteine, a ROS scavenging agent, suggesting that the S1PR1-induced resistance of cell apoptosis resulted, at least partially, from the suppression of ROS generation.	Acetylcysteine	232-251	sphingosine-1-phosphate receptor 1	Homo sapiens	185-190
27572094-6	2016	In addition, the present study demonstrated that S1PR1 suppressed the generation of reactive oxygen species (ROS) in AML cells, and that the apoptosis mediated by the downregulation of S1PR1 was partially reversed by treatment with N-acetyl-L-cysteine, a ROS scavenging agent, suggesting that the S1PR1-induced resistance of cell apoptosis resulted, at least partially, from the suppression of ROS generation.	Acetylcysteine	232-251	sphingosine-1-phosphate receptor 1	Homo sapiens	185-190
28843610-8	2017	In contrast, inhibitors of the MAP kinases p38 and JNK as well as the antioxidant N-acetylcysteine attenuated the LPS-stimulated TNF-alpha expression both in the absence and presence of OGG1.	Acetylcysteine	82-98	8-oxoguanine DNA-glycosylase 1	Mus musculus	186-190
16520658-1	2006	Isothiocyanates (ITCs) are a class of well-known cancerpreventive phytochemicals, but are primarily disposed of and concentrated in the urine as N-acetylcysteine conjugates (NAC-ITCs) in vivo.	Acetylcysteine	145-161	synuclein alpha	Homo sapiens	174-177
28669854-5	2017	We conjugated N-acetyl-L-cysteine to Cy5-labeled PAMAM dendrimer (Cy5-D-NAC) and used a mouse model of perinatal HIE to study effects of timing of administration, hypothermia, brain injury, and microglial activation on uptake.	Acetylcysteine	14-33	NLR family, pyrin domain containing 1A	Mus musculus	72-75
27557522-6	2016	In addition, Ca2+ levels and the expression of the Ca2+ channels, RyR1, SERCA, CACNA1S, TRPC1, and TRPC3 were recovered to normal levels by N-acetyl-L-cysteine (NAC) treatment compared with SelW knockdown cells.	Acetylcysteine	140-159	selenoprotein W	Gallus gallus	190-194
16282349-11	2006	The antioxidant N-acetyl-L-cysteine diminished G-CSF-induced ROS production and cell proliferation by inhibiting Akt activation.	Acetylcysteine	16-35	colony stimulating factor 3	Homo sapiens	47-52
27264312-11	2016	Furthermore, LGH00168 (10 and 20 mumol/L) dose-dependently induced mito-ROS production in A549 cells, which was reversed by the ROS scavenger N-acetyl-L-cysteine (NAC, 10 mmol/L).	Acetylcysteine	142-161	X-linked Kx blood group	Homo sapiens	163-166
29416738-9	2018	Overexpression of TrxR1 or application of antioxidant N-acetyl-L-cysteine (NAC) depletes the ROS increase, reduces DNA damage, and decreases cell death triggered by APR-246/PHEN in HNSCC cells.	Acetylcysteine	54-73	X-linked Kx blood group	Homo sapiens	75-78
28705740-5	2017	Especially, the glutamine metabolic process related molecules, GPX1, GPX3, SMS, GGCT, GSTK1, NFkappaB, GSTT2, SOD1 and GCLM, are involved in the switching process from oxidized glutathione (GSSG) conversion to the reduced glutathione (GSH) by glutathione, mercapturic acid and arginine metabolism process.	Acetylcysteine	256-272	glutathione peroxidase 1	Homo sapiens	63-67
28705740-5	2017	Especially, the glutamine metabolic process related molecules, GPX1, GPX3, SMS, GGCT, GSTK1, NFkappaB, GSTT2, SOD1 and GCLM, are involved in the switching process from oxidized glutathione (GSSG) conversion to the reduced glutathione (GSH) by glutathione, mercapturic acid and arginine metabolism process.	Acetylcysteine	256-272	gamma-glutamylcyclotransferase	Homo sapiens	80-84
27328773-5	2016	Increased LC3 processing upon knockdown of RPIA can be reversed by treatment with the antioxidant N-acetyl cysteine.	Acetylcysteine	98-115	microtubule associated protein 1 light chain 3 alpha	Homo sapiens	10-13
28580603-7	2017	In addition, high glucose-stimulated melatonin receptor 1B (MTNR1B) mRNA and PINK1 expressions were reversed by ROS scavenger N-acetyl cysteine pretreatment.	Acetylcysteine	126-143	PTEN induced kinase 1	Homo sapiens	77-82
27277612-6	2006	When a potent antioxidant, N-acetyl-L-cysteine, was added to the culture medium before or after sonication, the induction was attenuated, indicating that reactive oxygen species are involved in HO-1 induction.	Acetylcysteine	27-46	heme oxygenase 1	Homo sapiens	194-198
29179463-7	2017	Pre-treatment with antioxidant N-acetylcysteine effectively ameliorated olaquindox-induced exhaustion of ZO-1 and N-Cadherin proteins, DNA damage and apoptosis.	Acetylcysteine	31-47	cadherin 2	Homo sapiens	114-124
27435854-6	2016	The PAPV-mediated growth arrest was significantly abrogated in cells pre-treated with the N-acetylcysteine, Rac1 knocked down by siRNA and DPI an inhibitor of NADPH oxidase.	Acetylcysteine	90-106	Rac family small GTPase 1	Homo sapiens	108-112
27288489-7	2016	Moreover, adiponectin-upregulated cPLA2 and COX-2 expression was significantly abrogated by ROS scavenger (N-acetylcysteine) or the inhibitors of NADPH oxidase (apocynin), mitochondrial complex I (rotenone), PKC (Ro31-8220, Go-6976, and rottlerin), and p300 (garcinol).	Acetylcysteine	107-123	phospholipase A2 group IVA	Homo sapiens	34-39
16449798-6	2006	This mechanism is supported by the ability of N-acetyl cysteine (NAC) to prevent dissociation of Trx-ASK1 and activation of the p38 MAPK pathway.	Acetylcysteine	46-63	mitogen-activated protein kinase kinase kinase 5	Mus musculus	101-105
28560421-6	2017	Furthermore, treatment of the cells with 1 mM N-acetyl-L-cysteine (a scavenger of ROS) for 60 min prior to exposure to HG significantly reduced the HG-induced increase in the RIP3 expression level, as well as the injury and inflammatory response described above.	Acetylcysteine	46-65	receptor-interacting serine-threonine kinase 3	Rattus norvegicus	175-179
28380464-7	2017	N-Acetyl-L-Cysteine was shown to inhibit ROS generation, suppress permeabilization of lysosomal membranes, decrease levels of cathepsin B and cytochrome C in the cytosol, and inhibit Bax/Bcl2 ratio, caspase-9 and caspase-3 activity both in vitro and in vivo.	Acetylcysteine	0-19	cathepsin B	Homo sapiens	126-137
16507747-5	2006	Interestingly, administration of the antioxidant compound N-acetylcysteine (NAC) inhibited the growth of tumor volume in p53-depleted injected cells, and NAC supplementation of p53(-/-) mice from birth greatly decreased the number of karyotype abnormalities and tumors formed in these mice by six months of age.	Acetylcysteine	58-74	transformation related protein 53, pseudogene	Mus musculus	121-124
28632169-6	2017	Pre-treatment with astaxanthin or with N-acetyl-cysteine (NAC) which is an antioxidant drug, significantly attenuated the palmitate-induced MCP-1 release through downregulation of phosphorylated c-Jun NH2-terminal protein kinase (JNK) pathways, and suppressed VEGF120 through the PI3K/Akt pathways relative to the cells stimulated with palmitate alone.	Acetylcysteine	39-56	chemokine (C-C motif) ligand 2	Mus musculus	140-145
28632169-6	2017	Pre-treatment with astaxanthin or with N-acetyl-cysteine (NAC) which is an antioxidant drug, significantly attenuated the palmitate-induced MCP-1 release through downregulation of phosphorylated c-Jun NH2-terminal protein kinase (JNK) pathways, and suppressed VEGF120 through the PI3K/Akt pathways relative to the cells stimulated with palmitate alone.	Acetylcysteine	39-56	mitogen-activated protein kinase 8	Mus musculus	195-228
28632169-6	2017	Pre-treatment with astaxanthin or with N-acetyl-cysteine (NAC) which is an antioxidant drug, significantly attenuated the palmitate-induced MCP-1 release through downregulation of phosphorylated c-Jun NH2-terminal protein kinase (JNK) pathways, and suppressed VEGF120 through the PI3K/Akt pathways relative to the cells stimulated with palmitate alone.	Acetylcysteine	39-56	mitogen-activated protein kinase 8	Mus musculus	230-233
28632169-6	2017	Pre-treatment with astaxanthin or with N-acetyl-cysteine (NAC) which is an antioxidant drug, significantly attenuated the palmitate-induced MCP-1 release through downregulation of phosphorylated c-Jun NH2-terminal protein kinase (JNK) pathways, and suppressed VEGF120 through the PI3K/Akt pathways relative to the cells stimulated with palmitate alone.	Acetylcysteine	58-61	chemokine (C-C motif) ligand 2	Mus musculus	140-145
28632169-6	2017	Pre-treatment with astaxanthin or with N-acetyl-cysteine (NAC) which is an antioxidant drug, significantly attenuated the palmitate-induced MCP-1 release through downregulation of phosphorylated c-Jun NH2-terminal protein kinase (JNK) pathways, and suppressed VEGF120 through the PI3K/Akt pathways relative to the cells stimulated with palmitate alone.	Acetylcysteine	58-61	mitogen-activated protein kinase 8	Mus musculus	195-228
28632169-6	2017	Pre-treatment with astaxanthin or with N-acetyl-cysteine (NAC) which is an antioxidant drug, significantly attenuated the palmitate-induced MCP-1 release through downregulation of phosphorylated c-Jun NH2-terminal protein kinase (JNK) pathways, and suppressed VEGF120 through the PI3K/Akt pathways relative to the cells stimulated with palmitate alone.	Acetylcysteine	58-61	mitogen-activated protein kinase 8	Mus musculus	230-233
30263604-4	2017	NAC further increased the lifespan of age-1 and clk-1 mutants, which have increased lifespan owing to reduced insulin/IGF-1-like signaling and mitochondrial function, respectively.	Acetylcysteine	0-3	Phosphatidylinositol 3-kinase age-1	Caenorhabditis elegans	38-43
26678254-3	2016	We assessed the ability of purified human gamma-glutamyl transpeptidase-1 (GGT-1), a primary enzyme of the mercapturic acid pathway, to cleave S-linked GSH conjugates of 4,4"-methylene diphenyl diisocyanate (MDI) and 1,6-hexamethylene diisocyanate (HDI), two widely used industrial chemicals.	Acetylcysteine	107-123	gamma-glutamyltransferase 1	Homo sapiens	42-80
27004703-2	2016	The aim of this study was to evaluate the renal effects of NAC using neutrophil gelatinase-associated lipocalin (NGAL) blood levels in elderly patients undergoing coronary artery bypass grafting (CABG).	Acetylcysteine	59-62	lipocalin 2	Homo sapiens	113-117
27004703-10	2016	The mean serum NGAL levels at 3 h postoperatively were higher in the placebo group than in the NAC group (104.94+-30.51 vs. 87.82+-25.18; p&lt;0.05).	Acetylcysteine	95-98	lipocalin 2	Homo sapiens	15-19
27004703-14	2016	NAC infusion in elderly patients undergoing CABG reduced the incidence of acute kidney injury as determined by blood NGAL and creatinine levels.	Acetylcysteine	0-3	lipocalin 2	Homo sapiens	117-121
16507747-5	2006	Interestingly, administration of the antioxidant compound N-acetylcysteine (NAC) inhibited the growth of tumor volume in p53-depleted injected cells, and NAC supplementation of p53(-/-) mice from birth greatly decreased the number of karyotype abnormalities and tumors formed in these mice by six months of age.	Acetylcysteine	76-79	transformation related protein 53, pseudogene	Mus musculus	121-124
16507747-5	2006	Interestingly, administration of the antioxidant compound N-acetylcysteine (NAC) inhibited the growth of tumor volume in p53-depleted injected cells, and NAC supplementation of p53(-/-) mice from birth greatly decreased the number of karyotype abnormalities and tumors formed in these mice by six months of age.	Acetylcysteine	154-157	transformation related protein 53, pseudogene	Mus musculus	177-180
16201965-8	2006	Inhibition of the generation of longchain ceramide in response to C6-cer by FB1 or NAC significantly blocked the modulation of the c-Myc/Max function.	Acetylcysteine	83-86	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	131-136
27364593-5	2016	Pretreatment with lipid raft disruptor (Methyl-beta-cyclodextrin, MbetaCD) and oxidative stress inhibitor (N-acetyl-L-cysteine, NAC) slightly rescued the viability of cells damaged by C12-HSL exposure, while the paraoxonase 2 (PON2) inhibitor (Triazolo[4,3-a]quinolone, TQ416) significantly affected recovering cells viability and mucin secretion.	Acetylcysteine	107-126	lipase E, hormone sensitive type	Homo sapiens	188-191
27364593-5	2016	Pretreatment with lipid raft disruptor (Methyl-beta-cyclodextrin, MbetaCD) and oxidative stress inhibitor (N-acetyl-L-cysteine, NAC) slightly rescued the viability of cells damaged by C12-HSL exposure, while the paraoxonase 2 (PON2) inhibitor (Triazolo[4,3-a]quinolone, TQ416) significantly affected recovering cells viability and mucin secretion.	Acetylcysteine	107-126	paraoxonase 2	Homo sapiens	212-225
27364593-5	2016	Pretreatment with lipid raft disruptor (Methyl-beta-cyclodextrin, MbetaCD) and oxidative stress inhibitor (N-acetyl-L-cysteine, NAC) slightly rescued the viability of cells damaged by C12-HSL exposure, while the paraoxonase 2 (PON2) inhibitor (Triazolo[4,3-a]quinolone, TQ416) significantly affected recovering cells viability and mucin secretion.	Acetylcysteine	107-126	paraoxonase 2	Homo sapiens	227-231
28445141-9	2017	Finally, the ROS scavenger N-acetyl-L-cysteine significantly counteracts the lifespan shortening and lipofuscin accumulation induced by kin-10 knockdown.	Acetylcysteine	27-46	Casein kinase II subunit beta	Caenorhabditis elegans	136-142
16189296-5	2006	The free radical scavenger N-acetyl cysteine blocked LAQ824-mediated ROS generation, mitochondrial injury, Mcl-1 down-regulation, ceramide generation, and apoptosis, suggesting a primary role for oxidative injury in LAQ824 lethality.	Acetylcysteine	27-44	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	107-112
28280002-7	2017	Additionally, NAC stimulated HUVEC migration and proliferation in a phospholipase C beta-dependent fashion and decreased Galphaq palmitoylation.	Acetylcysteine	14-17	guanine nucleotide binding protein, alpha q polypeptide	Mus musculus	121-128
28280002-8	2017	Similarly, NAC treatment also decreased Galphaq palmitoylation in ischemic and nonischemic hindlimbs in vivo In summary, we demonstrate that NAC accelerates healing of amputation stumps in the setting of diabetes and ischemia.	Acetylcysteine	11-14	guanine nucleotide binding protein, alpha q polypeptide	Mus musculus	40-47
28280002-8	2017	Similarly, NAC treatment also decreased Galphaq palmitoylation in ischemic and nonischemic hindlimbs in vivo In summary, we demonstrate that NAC accelerates healing of amputation stumps in the setting of diabetes and ischemia.	Acetylcysteine	141-144	guanine nucleotide binding protein, alpha q polypeptide	Mus musculus	40-47
28280002-9	2017	The underlying mechanism appears to involve a previously unrecognized effect of NAC on Galphaq palmitoylation and phospholipase C beta-mediated signaling in endothelial cells.-Zayed, M. A., Wei, X., Park, K., Belaygorod, L., Naim, U., Harvey, J., Yin, L., Blumer, K., Semenkovich, C. F. N-acetylcysteine accelerates amputation stump healing in the setting of diabetes.	Acetylcysteine	80-83	guanine nucleotide binding protein, alpha q polypeptide	Mus musculus	87-94
28280002-9	2017	The underlying mechanism appears to involve a previously unrecognized effect of NAC on Galphaq palmitoylation and phospholipase C beta-mediated signaling in endothelial cells.-Zayed, M. A., Wei, X., Park, K., Belaygorod, L., Naim, U., Harvey, J., Yin, L., Blumer, K., Semenkovich, C. F. N-acetylcysteine accelerates amputation stump healing in the setting of diabetes.	Acetylcysteine	287-303	guanine nucleotide binding protein, alpha q polypeptide	Mus musculus	87-94
27309537-8	2016	The clinical study showed significantly increased DAT binding in the caudate and putamen (mean increase ranging from 4.4% to 7.8%; p<0.05 for all values) in the PD group treated with NAC, and no measurable changes in the control group.	Acetylcysteine	183-186	solute carrier family 6 member 3	Homo sapiens	50-53
27206739-6	2016	Incubation of gLDL-exposed cells with the anti-oxidant N-acetyl-cysteine (NAC) reduced ERS, revealed by decreased eIF2alpha phosphorylation and CHOP gene expression and increased GRP78 expression, thus validating the interconnection between ERS and oxidative stress.	Acetylcysteine	55-72	eukaryotic translation initiation factor 2A	Homo sapiens	114-123
27206739-6	2016	Incubation of gLDL-exposed cells with the anti-oxidant N-acetyl-cysteine (NAC) reduced ERS, revealed by decreased eIF2alpha phosphorylation and CHOP gene expression and increased GRP78 expression, thus validating the interconnection between ERS and oxidative stress.	Acetylcysteine	74-77	eukaryotic translation initiation factor 2A	Homo sapiens	114-123
16489261-1	2005	The aim of the present study was to evaluate the effects of N-acetylcysteine (NAC) and L-carnitine (LCAR) supplementations on polymorphonuclear leukocytes myeloperoxidase (MPO) and Cu/Zn-superoxide dismutase (Cu/Zn-SOD) and plasma malondialdehyde (MDA) in acetic acid (AA)-induced ulcerative colitis model.	Acetylcysteine	60-76	myeloperoxidase	Rattus norvegicus	155-170
16489261-1	2005	The aim of the present study was to evaluate the effects of N-acetylcysteine (NAC) and L-carnitine (LCAR) supplementations on polymorphonuclear leukocytes myeloperoxidase (MPO) and Cu/Zn-superoxide dismutase (Cu/Zn-SOD) and plasma malondialdehyde (MDA) in acetic acid (AA)-induced ulcerative colitis model.	Acetylcysteine	78-81	myeloperoxidase	Rattus norvegicus	155-170
27135742-10	2016	Consistently, homologous recombination-defective cells accumulate spontaneous gammaH2AX or XRCC1 foci that are abolished by treatment with N-acetyl-cysteine or maintenance at 3% O2.	Acetylcysteine	139-156	X-ray repair cross complementing 1	Homo sapiens	91-96
28478937-8	2017	Treatment with the powerful antioxidant N-acetylcysteine inhibited GDF11-induced EMT and cell migration.	Acetylcysteine	40-56	growth differentiation factor 11	Homo sapiens	67-72
16489261-1	2005	The aim of the present study was to evaluate the effects of N-acetylcysteine (NAC) and L-carnitine (LCAR) supplementations on polymorphonuclear leukocytes myeloperoxidase (MPO) and Cu/Zn-superoxide dismutase (Cu/Zn-SOD) and plasma malondialdehyde (MDA) in acetic acid (AA)-induced ulcerative colitis model.	Acetylcysteine	78-81	myeloperoxidase	Rattus norvegicus	172-175
28399781-6	2017	N-acetyl-l-cysteine (NAC), a ROS scavenger, partially reduced PCB 118-induced apoptosis and Bax/Bcl-2 ratios in HUVECs.	Acetylcysteine	0-19	X-linked Kx blood group	Homo sapiens	21-24
16192891-11	2005	Exogenous H2O2 enhanced IL-8 secretion and N-acetyl cysteine (NAC) prevented IL-1alpha-induced ROS production and IL-8 secretion.	Acetylcysteine	43-60	interleukin 1 alpha	Homo sapiens	77-86
16309591-7	2005	The MMPs mRNA expression was unaffected by the p38 MAPK inhibitor SB203580, but in the case of MMP-1 was reversed by the antioxidant N-acetylcysteine.	Acetylcysteine	133-149	matrix metallopeptidase 1	Homo sapiens	4-8
28281643-6	2017	Following knock-down of the p47phox expression, which is required for ROS activation, or co-treatment with the ROS inhibitor, N-acetyl-L-cysteine, ZA-induced apoptosis was significantly suppressed in both osteoclast precursors and mature osteoclast-like cells.	Acetylcysteine	126-145	neutrophil cytosolic factor 1	Homo sapiens	28-35
26655501-8	2016	Accordingly, NGR-peptide"s downregulation of 88 kDa progranulin protein was prevented by BAPTA and NAC.	Acetylcysteine	99-102	reticulon 4 receptor	Homo sapiens	13-16
26620190-9	2016	Furthermore, phenotypes induced by complex II activity knockdown were abolished by pretreatment with N-acetyl cysteine (an ROS scavenger) and by prior HIF1alpha knockdown, indicating an ROS- and HIF1alpha-dependent mechanism.	Acetylcysteine	101-118	hypoxia inducible factor 1 subunit alpha	Rattus norvegicus	195-204
16309591-7	2005	The MMPs mRNA expression was unaffected by the p38 MAPK inhibitor SB203580, but in the case of MMP-1 was reversed by the antioxidant N-acetylcysteine.	Acetylcysteine	133-149	matrix metallopeptidase 1	Homo sapiens	95-100
28199982-0	2017	N-acetyl-cysteine attenuates remifentanil-induced postoperative hyperalgesia via inhibiting matrix metalloproteinase-9 in dorsal root ganglia.	Acetylcysteine	0-17	matrix metallopeptidase 9	Rattus norvegicus	92-118
16042792-12	2005	Glutathione S-Transferase activity was decreased by NAC.	Acetylcysteine	52-55	glutathione S-transferase kappa 1	Homo sapiens	0-25
28199982-8	2017	Intraperitoneal injection of N-acetyl-cysteine (NAC), a broadly used safe drug, significantly attenuated RIH via suppressing the activation of MMP-9 in DRGs.	Acetylcysteine	29-46	matrix metallopeptidase 9	Rattus norvegicus	143-148
28199982-8	2017	Intraperitoneal injection of N-acetyl-cysteine (NAC), a broadly used safe drug, significantly attenuated RIH via suppressing the activation of MMP-9 in DRGs.	Acetylcysteine	48-51	matrix metallopeptidase 9	Rattus norvegicus	143-148
28199982-9	2017	NAC inhibited the cleavage of IL-1beta in DRGs, which is a critical substrate of MMP-9, and markedly suppressed glial activation and neuron excitability in spinal dorsal horn induced by remifentanil.	Acetylcysteine	0-3	matrix metallopeptidase 9	Rattus norvegicus	81-86
28199982-10	2017	These results demonstrated that NAC can effectively alleviate RIH via powerfully inhibiting MMP-9 activation in DRGs.	Acetylcysteine	32-35	matrix metallopeptidase 9	Rattus norvegicus	92-97
26548866-11	2016	Moreover, when N-acetylcysteine was present, increase of cell proliferation induced by downregulation of FoxO1, and upregulation of miR-155 was significantly inhibited.	Acetylcysteine	15-31	microRNA 155	Homo sapiens	132-139
26923123-6	2016	NAC preconditioning improved cell viability, decreased lactate dehydrogenase release, beta-galactosidase activity, and Annexin-V-positive cells.	Acetylcysteine	0-3	annexin A5	Mus musculus	119-128
25386730-4	2016	Pretreatment with N-acetylcysteine partially inhibited alpha-Syn expression induced by a 200 mug/ml dose of TiO2-NPs.	Acetylcysteine	18-34	synuclein alpha	Rattus norvegicus	55-64
15880142-7	2005	CORM-2 or CORM-3 did not cause any evident cytotoxicity and produced an increase in HO-1 expression and heme oxygenase activity; this effect was completely prevented by the thiol donor N-acetylcysteine.	Acetylcysteine	185-201	heme oxygenase 1	Homo sapiens	84-88
26783539-9	2016	N-Acetylcysteine restored Sevo-postC cardioprotection in diabetes possibly through enhancing cardiac p-STAT3 and adiponectin and reducing Fox1 and CD36.	Acetylcysteine	0-16	adiponectin, C1Q and collagen domain containing	Rattus norvegicus	113-124
28086233-6	2017	The depletion of ROS by N-Acetyl cysteine (NAC) partially blocked MBIC-induced apoptosis and JNK activation in HCC cells.	Acetylcysteine	24-41	mitogen-activated protein kinase 8	Mus musculus	93-96
28086233-6	2017	The depletion of ROS by N-Acetyl cysteine (NAC) partially blocked MBIC-induced apoptosis and JNK activation in HCC cells.	Acetylcysteine	43-46	mitogen-activated protein kinase 8	Mus musculus	93-96
27929749-8	2017	In addition, ROS scavenger (N-acetyl-L-cysteine, NAC) and NOX4 inhibitor GKT137831 reduced ROS generation and alleviated activation of Xbp1 and RIPK1-related NF-kappaB signaling.	Acetylcysteine	28-47	receptor interacting serine/threonine kinase 1	Rattus norvegicus	144-149
27929749-8	2017	In addition, ROS scavenger (N-acetyl-L-cysteine, NAC) and NOX4 inhibitor GKT137831 reduced ROS generation and alleviated activation of Xbp1 and RIPK1-related NF-kappaB signaling.	Acetylcysteine	49-52	receptor interacting serine/threonine kinase 1	Rattus norvegicus	144-149
26497050-5	2015	In addition, the expression levels of MMP-2 and MMP-9 were inhibited by NAC, IAA-94 and SB203580.	Acetylcysteine	72-75	matrix metallopeptidase 9	Homo sapiens	48-53
16117612-0	2005	Induction of quinone reductase by sulforaphane and sulforaphane N-acetylcysteine conjugate in murine hepatoma cells.	Acetylcysteine	64-80	crystallin, zeta	Mus musculus	13-30
26447155-8	2015	Moreover, NAC significantly decreased systolic (P = 0.003) and diastolic (P = 0.017) blood pressure within all subjects with a significant reduction in diastolic pressure in the HYL group (P = 0.008) but not in the NOL group.	Acetylcysteine	10-13	megakaryocyte-associated tyrosine kinase	Homo sapiens	178-181
26447155-10	2015	CONCLUSIONS: Four weeks of oral NAC treatment significantly decreased plasma tHcy concentrations, irrespective of lipid or smoking status, and lowered systolic blood pressure in both normolipidemic and hyperlipidemic men, with significant diastolic blood pressure reductions in the HYL group only.	Acetylcysteine	32-35	megakaryocyte-associated tyrosine kinase	Homo sapiens	282-285
26341012-12	2015	Plumbagin increased TrxR-1 and heme oxygenase (HO)-1 expression and pretreatment with NAC significantly attenuated the plumbagin-induced increase of TrxR-1 and HO-1 expression in HepG2 cells, LLC cells and SiHa cells.	Acetylcysteine	86-89	thioredoxin reductase 1	Homo sapiens	149-155
27912102-9	2017	Pretreatment with N-acetyl-l-cysteine (NAC) recovered the Toyocamycin-induced mitochondrial dysfunction, ROS, and apoptosis.	Acetylcysteine	18-37	X-linked Kx blood group	Homo sapiens	39-42
15965045-4	2005	A further study revealed that the expression of MMP1 could be further induced by treatment of the skin fibroblasts with 200 microM hydrogen peroxide (H2O2) and inhibited by 1 mM N-acetylcysteine.	Acetylcysteine	178-194	matrix metallopeptidase 1	Homo sapiens	48-52
28007593-7	2017	Treatment of MsrB3-depleted cells with N-acetylcysteine, an ROS scavenger, prevented cell death, suggesting that MsrB3 deficiency-induced cell death is associated with increased ROS production.	Acetylcysteine	39-55	methionine sulfoxide reductase B3	Homo sapiens	13-18
15965068-7	2005	N-acetylcysteine, a free radical scavenger, strongly decreased HO-1 expression, suggesting the involvement of reactive oxygen species (ROS).	Acetylcysteine	0-16	heme oxygenase 1	Homo sapiens	63-67
28007593-7	2017	Treatment of MsrB3-depleted cells with N-acetylcysteine, an ROS scavenger, prevented cell death, suggesting that MsrB3 deficiency-induced cell death is associated with increased ROS production.	Acetylcysteine	39-55	methionine sulfoxide reductase B3	Homo sapiens	113-118
26334094-9	2015	Pretreatment with N-acetyl cysteine blocked cell-growth inhibition induced by ATP1A1 downregulation.	Acetylcysteine	18-35	ATPase Na+/K+ transporting subunit alpha 1	Homo sapiens	78-84
15965068-10	2005	N-acetylcysteine reduced the stimulatory effect of celecoxib on stress kinase activities, suggesting an involvement of JNK in HO-1 expression.	Acetylcysteine	0-16	heme oxygenase 1	Homo sapiens	126-130
26093296-3	2015	In this study, we found that angiotensin II dose-dependently increased the expression of Col1a1, Col3a1 and alpha-smooth muscle actin, which were blocked by ROS (reactive oxygen species) scavenger N-acetyl cysteine (NAC).	Acetylcysteine	197-214	collagen type I alpha 1 chain	Homo sapiens	89-95
26093296-3	2015	In this study, we found that angiotensin II dose-dependently increased the expression of Col1a1, Col3a1 and alpha-smooth muscle actin, which were blocked by ROS (reactive oxygen species) scavenger N-acetyl cysteine (NAC).	Acetylcysteine	216-219	collagen type I alpha 1 chain	Homo sapiens	89-95
16088183-3	2005	The use of NAC inhibited the changes in urine output, pO(2), tissue activity of MPO and MDA in pancreas and lungs, and the serum activity of IL-6, ALT, and serum concentrations of urea and calcium.	Acetylcysteine	11-14	myeloperoxidase	Rattus norvegicus	80-83
25575547-6	2015	AAP (0.5-1.0 mM) and NAC (0.5-1.0 mM) used individually or in combination could down-regulate protein expression of cleaved caspase-1 and mRNA expression of IL-1beta, IL-18 and NLRP3.	Acetylcysteine	21-24	interleukin 18	Homo sapiens	167-172
26002468-6	2015	The antioxidant N-Acety-l-Cysteine (NAC) was found to attenuate the JNK and p38 MAPK activation with a concomitant reduction of PA-induced autophagy and apoptosis.	Acetylcysteine	16-34	X-linked Kx blood group	Homo sapiens	36-39
27729002-11	2017	Downregulation of P53 and N-acetyl-cysteine suppressed miR-30 inhibitors-activated mitochondrial dysfunction and apoptotic events.	Acetylcysteine	26-43	membrane associated ring-CH-type finger 8	Homo sapiens	55-58
15725085-8	2005	Inhibition of HO-1 with tin protoporphyrin enhances ROS in MM cells in ATO, and addition of N-acetylcysteine increases MT-2A.	Acetylcysteine	92-108	metallothionein 2A	Homo sapiens	119-124
28291959-8	2017	Diazoxide (DZ, a mitochondrial KATP channel opener) or pinacidil (Pin, a non-selective KATP channel opener) or N-acetyl-L-cysteine (NAC, a ROS scavenger) pre-treatment blocked the up-regulation of TLR4 and RIP3.	Acetylcysteine	111-130	receptor-interacting serine-threonine kinase 3	Rattus norvegicus	206-210
25964188-7	2015	N-acetyl-l-cysteine (NAC), a ROS scavenger, could reverse SC-III3-caused ROS accumulation, but it did not affect SC-III3-induced autophagy, suggesting that ROS was not involved in SC-III3-mediated autophagy in HepG2 cells.	Acetylcysteine	0-19	X-linked Kx blood group	Homo sapiens	21-24
26057728-7	2015	We identified enhancement of STAT1 activity as a potential strategy to treat EGFR-hyperactive cancers and PTEN as a target of the antioxidant, N-acetylcysteine.	Acetylcysteine	143-159	signal transducer and activator of transcription 1	Homo sapiens	29-34
25972196-6	2015	Furthermore, the attenuation of ATO-induced ROS and the resulting oxidative DNA damage by N-acetyl-L-cysteine (NAC), a potent antioxidant, significantly reduced the activation of PARP-1 and NF-kappaB in ATO-treated cells.	Acetylcysteine	90-109	X-linked Kx blood group	Homo sapiens	111-114
27693243-4	2016	BITC-induced cell death was completely prevented by pretreatment with thiol-containing redox compounds including N-acetyl-l-cysteine (NAC), glutathione (GSH), dithiothreitol, and 2-mercaptoethanol, but not free radical scavengers mito-TEMPO, catalase, apocynin, l-NAME and mannitol.	Acetylcysteine	113-132	X-linked Kx blood group	Homo sapiens	134-137
15680334-0	2005	N-acetylcysteine attenuates early induction of heme oxygenase-1 following traumatic brain injury.	Acetylcysteine	0-16	heme oxygenase 1	Homo sapiens	47-63
27325640-11	2016	NAC also restored Abeta-induced annexin V/PI-positive cell populations.	Acetylcysteine	0-3	annexin A5	Mus musculus	32-41
26006712-6	2015	Moreover, our findings indicated that the pretreatment of Molt 4 cells with N-acetyl-l-cysteine (NAC), a reactive oxygen species (ROS) scavenger, diminished MMP disruption and apoptosis induced by HQ, suggesting that ROS overproduction plays a crucial rule in the cytotoxic activity of HQ.	Acetylcysteine	76-95	X-linked Kx blood group	Homo sapiens	97-100
15680334-3	2005	We have studied the temporal and spatial effects of the antioxidant N-acetylcysteine (NAC) on HO-1 levels following lateral fluid-percussion injury by immunoblotting and immunohistochemistry.	Acetylcysteine	68-84	heme oxygenase 1	Homo sapiens	94-98
27613482-5	2016	We showed that SiO2-NPs up-regulated alpha-synuclein expression, and N-acetyl cysteine reduced alpha-synuclein.	Acetylcysteine	69-86	synuclein alpha	Rattus norvegicus	95-110
15680334-3	2005	We have studied the temporal and spatial effects of the antioxidant N-acetylcysteine (NAC) on HO-1 levels following lateral fluid-percussion injury by immunoblotting and immunohistochemistry.	Acetylcysteine	86-89	heme oxygenase 1	Homo sapiens	94-98
25373316-8	2015	ROS inhibition by N-acetyl-L-cysteine prevented the inhibition of PTP1B phosphatase activity induced by PAR1-AP and the PAR4-AP, but had no effect on PAR1/4-mediated activation of Met and PDGFR in Hep3B cells.	Acetylcysteine	18-37	protein tyrosine phosphatase non-receptor type 1	Homo sapiens	66-71
25373316-8	2015	ROS inhibition by N-acetyl-L-cysteine prevented the inhibition of PTP1B phosphatase activity induced by PAR1-AP and the PAR4-AP, but had no effect on PAR1/4-mediated activation of Met and PDGFR in Hep3B cells.	Acetylcysteine	18-37	F2R like thrombin or trypsin receptor 3	Homo sapiens	120-124
15680334-7	2005	The administration of NAC 5 min following TBI resulted in a marked reduction in this widespread induction of HO-1, concomitant with a decrease in the volume of injury in all three brain regions.	Acetylcysteine	22-25	heme oxygenase 1	Homo sapiens	109-113
25666878-3	2015	We aimed to investigate the effects of NAC on apoptosis, oxidative stress, and Ca(2+) entry through transient receptor potential vanilloid 1 (TRPV1) and TRP melastatin 2 (TRPM2) channels in neutrophils from patients with PCOS.	Acetylcysteine	39-42	transient receptor potential cation channel subfamily M member 2	Homo sapiens	153-169
27329155-5	2016	We describe a stimulatory effect of PGD2 on lactate dehydrogenase (LDH) expression via DP1/DP2 receptors, which is prevented by the antioxidant N-acetyl-L-cysteine and the PI3K/Akt pathway inhibitor LY 294002.	Acetylcysteine	144-163	transcription factor Dp 1	Mus musculus	87-104
25666878-3	2015	We aimed to investigate the effects of NAC on apoptosis, oxidative stress, and Ca(2+) entry through transient receptor potential vanilloid 1 (TRPV1) and TRP melastatin 2 (TRPM2) channels in neutrophils from patients with PCOS.	Acetylcysteine	39-42	transient receptor potential cation channel subfamily M member 2	Homo sapiens	171-176
15496615-0	2005	The chemoprotective agent N-acetylcysteine blocks cisplatin-induced apoptosis through caspase signaling pathway.	Acetylcysteine	26-42	caspase 9	Homo sapiens	86-93
15496615-6	2005	Expression of tumor suppressor p53 and the cell cycle regulatory protein p21 was stimulated within 5 to 10 min by cisplatin in p53-positive LX-1 small cell lung carcinoma cells, and this effect was blocked by NAC.	Acetylcysteine	209-212	H3 histone pseudogene 16	Homo sapiens	73-76
15841722-5	2005	RESULTS: AP results in significant increases in plasma levels of IL-6 at 6 h and IL-10 at 3 and 6 h. Plasma levels of IL-6 were significantly decreased after administration of NAC.	Acetylcysteine	176-179	interleukin 10	Rattus norvegicus	81-86
27577752-0	2016	N-acetylcysteine attenuates lipopolysaccharide-induced impairment in lamination of Ctip2-and Tbr1- expressing cortical neurons in the developing rat fetal brain.	Acetylcysteine	0-16	T-box brain transcription factor 1	Rattus norvegicus	93-97
15841722-6	2005	NAC pretreatment also increased the ratio of IL-10/IL-6.	Acetylcysteine	0-3	interleukin 10	Rattus norvegicus	45-50
25147347-8	2015	Expression of intercellular adhesion molecule 1 was reduced by NAC treatment.	Acetylcysteine	63-66	intercellular adhesion molecule 1	Rattus norvegicus	14-47
15841722-8	2005	Pretreatment with NAC, PDTC, PD98059 or Genistein significantly decreased MPO levels in the pancreas at 3 and 6 h and following the administration of PD-98059 or NAC at 6 h. Pretreatment with NAC significantly decreased MPO levels in the lungs at 3 h. CONCLUSIONS: Pretreatment with NAC could regulate the pro-and anti-inflammatory cytokine balance, probably through NF-kappaB and ROS signaling pathways.	Acetylcysteine	18-21	myeloperoxidase	Rattus norvegicus	74-77
15841722-8	2005	Pretreatment with NAC, PDTC, PD98059 or Genistein significantly decreased MPO levels in the pancreas at 3 and 6 h and following the administration of PD-98059 or NAC at 6 h. Pretreatment with NAC significantly decreased MPO levels in the lungs at 3 h. CONCLUSIONS: Pretreatment with NAC could regulate the pro-and anti-inflammatory cytokine balance, probably through NF-kappaB and ROS signaling pathways.	Acetylcysteine	18-21	myeloperoxidase	Rattus norvegicus	220-223
15619135-1	2004	OBJECTIVE: We aimed to determine the pharmacokinetics (PK) of N-acetylcysteine (NAC) at rest and during exercise when given by continuous intravenous infusion intended to maintain relatively constant plasma concentrations.	Acetylcysteine	62-78	solute carrier family 13 member 5	Homo sapiens	80-83
25161103-8	2015	We evaluated the overall MPs activity in FA complementation group A (FANCA) cells by exposing them to the antioxidants N-acetyl cysteine (NAC) and resveratrol (RV).	Acetylcysteine	119-136	FA complementation group A	Homo sapiens	69-74
25161103-8	2015	We evaluated the overall MPs activity in FA complementation group A (FANCA) cells by exposing them to the antioxidants N-acetyl cysteine (NAC) and resveratrol (RV).	Acetylcysteine	138-141	FA complementation group A	Homo sapiens	69-74
25607831-8	2015	Pretreatment with N-acetyl-cysteine (NAC), the inhibitor of ROS, or with SP600125, the inhibitor of JNK, prevented the apoptosis and the high expression of p-JNK, p53, caspase-9 and caspase-3 in CDK5RAP1-deficient MCF-7 cells.	Acetylcysteine	18-35	CDK5 regulatory subunit associated protein 1	Homo sapiens	195-203
25607831-8	2015	Pretreatment with N-acetyl-cysteine (NAC), the inhibitor of ROS, or with SP600125, the inhibitor of JNK, prevented the apoptosis and the high expression of p-JNK, p53, caspase-9 and caspase-3 in CDK5RAP1-deficient MCF-7 cells.	Acetylcysteine	37-40	CDK5 regulatory subunit associated protein 1	Homo sapiens	195-203
25767408-6	2015	An excessive dosage of NAC over a short period of time can lead to hemolysis, thrombocytopenia, and acute renal failure in patients with normal glucose-6-phosphate dehydrogenase, and finally to death.	Acetylcysteine	23-26	glucose-6-phosphate dehydrogenase	Homo sapiens	144-177
27177453-8	2016	Moreover, the increase of activated caspase-3 and PARP was blocked by the ROS inhibitor antioxidant N-acetyl cysteine (NAC).	Acetylcysteine	100-117	caspase 3	Mus musculus	36-45
27177453-8	2016	Moreover, the increase of activated caspase-3 and PARP was blocked by the ROS inhibitor antioxidant N-acetyl cysteine (NAC).	Acetylcysteine	100-117	poly (ADP-ribose) polymerase family, member 1	Mus musculus	50-54
27177453-8	2016	Moreover, the increase of activated caspase-3 and PARP was blocked by the ROS inhibitor antioxidant N-acetyl cysteine (NAC).	Acetylcysteine	119-122	caspase 3	Mus musculus	36-45
27177453-8	2016	Moreover, the increase of activated caspase-3 and PARP was blocked by the ROS inhibitor antioxidant N-acetyl cysteine (NAC).	Acetylcysteine	119-122	poly (ADP-ribose) polymerase family, member 1	Mus musculus	50-54
27179791-3	2016	The aim of the present study was to establish whether cysteine supplementation, using N-acetylcysteine (NAC) could ameliorate glutamate pathology through the cystine-dependent transporters, system xc- and GLT-1.	Acetylcysteine	104-107	solute carrier family 1 (glial high affinity glutamate transporter), member 2	Mus musculus	205-210
27179791-6	2016	This effect was blocked by co-administration of the system xc- and GLT-1 inhibitors CPG and DHK, showing that glutamate transporter activity was required for the antidepressant effects of NAC.	Acetylcysteine	188-191	solute carrier family 1 (glial high affinity glutamate transporter), member 2	Mus musculus	67-72
27177023-8	2016	Cedrol induced autophagy, which was confirmed by TEM analysis, by increasing intracellular ROS formation in a concentration-dependent manner, which was almost completely reversed by N-acetyl-L-cysteine (NAC) and tocopherol.	Acetylcysteine	182-201	X-linked Kx blood group	Homo sapiens	203-206
27220372-9	2016	The in vitro experiments demonstrated that Ang II upregulated the expression levels of periostin and alpha-SMA compared with the control, whereas, pretreatment with NAC inhibited oxidative stress, periostin and alpha-SMA expression in fibroblasts.	Acetylcysteine	165-168	periostin	Rattus norvegicus	87-96
27220372-9	2016	The in vitro experiments demonstrated that Ang II upregulated the expression levels of periostin and alpha-SMA compared with the control, whereas, pretreatment with NAC inhibited oxidative stress, periostin and alpha-SMA expression in fibroblasts.	Acetylcysteine	165-168	periostin	Rattus norvegicus	197-206
15648272-5	2004	Therefore, the different effects of free methionine, acetylcysteine, and glutathione on the rates of oxidation of methionine residues in G-CSF are consistent with their different reactivity toward oxidation by H2O2.	Acetylcysteine	53-67	colony stimulating factor 3	Homo sapiens	137-142
25591758-13	2015	NAC decreased NOX4 and p22(phox) expression.	Acetylcysteine	0-3	NADPH oxidase 4	Rattus norvegicus	14-18
15382040-5	2004	N-acetyl-L-cysteine, a specific scavenger of reactive oxygen species, abrogated As2O3-induced upregulation of CD95/Fas and enhancement of CD95/Fas-mediated apoptosis.	Acetylcysteine	0-19	Fas cell surface death receptor	Homo sapiens	110-114
25599738-9	2015	Although the levels of NGAL and IL-18 decreased in the NAC and NAC and vitamin C groups, these reductions were not significant.	Acetylcysteine	55-58	lipocalin 2	Homo sapiens	23-27
25599738-9	2015	Although the levels of NGAL and IL-18 decreased in the NAC and NAC and vitamin C groups, these reductions were not significant.	Acetylcysteine	55-58	interleukin 18	Homo sapiens	32-37
25599738-9	2015	Although the levels of NGAL and IL-18 decreased in the NAC and NAC and vitamin C groups, these reductions were not significant.	Acetylcysteine	63-66	lipocalin 2	Homo sapiens	23-27
25599738-9	2015	Although the levels of NGAL and IL-18 decreased in the NAC and NAC and vitamin C groups, these reductions were not significant.	Acetylcysteine	63-66	interleukin 18	Homo sapiens	32-37
27138352-9	2016	Inhibition of ROS production by N-acetyl-l-cysteine (NAC) effectively reduced the over-expression of VEGF.	Acetylcysteine	32-51	vascular endothelial growth factor A	Mus musculus	101-105
27138352-9	2016	Inhibition of ROS production by N-acetyl-l-cysteine (NAC) effectively reduced the over-expression of VEGF.	Acetylcysteine	53-56	vascular endothelial growth factor A	Mus musculus	101-105
26206603-8	2016	The ROS increase and OCT4 downregulation after BDE-209 exposure could be reversed partly by antioxidant N-acetylcysteine supplement.	Acetylcysteine	104-120	homeobox D13	Homo sapiens	47-50
27162477-9	2016	When ROS was cleared by N-acetylcysteine (NAC), OA-induced LC3-II convertsion and cell death were all reversed.	Acetylcysteine	24-40	microtubule associated protein 1 light chain 3 alpha	Homo sapiens	59-62
27162477-9	2016	When ROS was cleared by N-acetylcysteine (NAC), OA-induced LC3-II convertsion and cell death were all reversed.	Acetylcysteine	42-45	microtubule associated protein 1 light chain 3 alpha	Homo sapiens	59-62
15382040-5	2004	N-acetyl-L-cysteine, a specific scavenger of reactive oxygen species, abrogated As2O3-induced upregulation of CD95/Fas and enhancement of CD95/Fas-mediated apoptosis.	Acetylcysteine	0-19	Fas cell surface death receptor	Homo sapiens	138-142
15467911-9	2004	Unexpectedly, N-acetylcysteine was found to inhibit VKOR activity at concentrations that are obtained during rescue therapy of paracetamol intoxication.	Acetylcysteine	14-30	vitamin K epoxide reductase complex subunit 1	Homo sapiens	52-56
26859778-1	2016	The mercapturic acid pathway (MAP) is a major phase II detoxification route, comprising the conjugation of electrophilic substances to glutathione (GSH) in a reaction catalyzed by glutathione S-transferase (GST) enzymes.	Acetylcysteine	4-20	Glutathione S-transferase	Crassostrea gigas	180-205
26859778-1	2016	The mercapturic acid pathway (MAP) is a major phase II detoxification route, comprising the conjugation of electrophilic substances to glutathione (GSH) in a reaction catalyzed by glutathione S-transferase (GST) enzymes.	Acetylcysteine	4-20	Glutathione S-transferase	Crassostrea gigas	207-210
26747500-4	2016	The increased expression of Gqalpha/PLCbeta1 proteins, increased protein synthesis, and augmented cell volume exhibited by VSMCs from SHRs were significantly attenuated by antioxidants N-acetyl-cysteine (NAC), a scavenger of superoxide anion, DPI, an inhibitor of NAD(P)H oxidase.	Acetylcysteine	185-202	phospholipase C beta 1	Rattus norvegicus	36-44
26747500-4	2016	The increased expression of Gqalpha/PLCbeta1 proteins, increased protein synthesis, and augmented cell volume exhibited by VSMCs from SHRs were significantly attenuated by antioxidants N-acetyl-cysteine (NAC), a scavenger of superoxide anion, DPI, an inhibitor of NAD(P)H oxidase.	Acetylcysteine	204-207	phospholipase C beta 1	Rattus norvegicus	36-44
25185584-7	2015	N-acetylcysteine or GSH cotreatment protected TSC2-null cells from chelerythrine"s effects, indicating that chelerythrine-induced cell death is ROS dependent.	Acetylcysteine	0-16	TSC complex subunit 2	Homo sapiens	46-50
25426938-8	2014	Acetylcysteine (NAC) as an inhibitor of the dimerization of PAC1 inhibited the anti-apoptotic activities that were endowed by PAC1 and decreased the Wnt/beta-catenin signal in Top-flash assays.	Acetylcysteine	0-14	adenylate cyclase activating polypeptide 1 receptor 1	Mus musculus	60-64
26747500-6	2016	Furthermore, the levels of IGF-1R and EGFR proteins and not of PDGFR were also enhanced in VSMCs from SHRs, which were attenuated significantly by NAC, DPI, and PP2.	Acetylcysteine	147-150	epidermal growth factor receptor	Rattus norvegicus	38-42
26747500-7	2016	In addition, NAC, DPI, and PP2 also attenuated the enhanced phosphorylation of IGF-1R, PDGFR, EGFR, c-Src, and EKR1/2 in VSMCs from SHRs.	Acetylcysteine	13-16	epidermal growth factor receptor	Rattus norvegicus	94-98
26747500-7	2016	In addition, NAC, DPI, and PP2 also attenuated the enhanced phosphorylation of IGF-1R, PDGFR, EGFR, c-Src, and EKR1/2 in VSMCs from SHRs.	Acetylcysteine	13-16	SRC proto-oncogene, non-receptor tyrosine kinase	Rattus norvegicus	100-105
25426938-8	2014	Acetylcysteine (NAC) as an inhibitor of the dimerization of PAC1 inhibited the anti-apoptotic activities that were endowed by PAC1 and decreased the Wnt/beta-catenin signal in Top-flash assays.	Acetylcysteine	0-14	adenylate cyclase activating polypeptide 1 receptor 1	Mus musculus	126-130
25426938-8	2014	Acetylcysteine (NAC) as an inhibitor of the dimerization of PAC1 inhibited the anti-apoptotic activities that were endowed by PAC1 and decreased the Wnt/beta-catenin signal in Top-flash assays.	Acetylcysteine	16-19	adenylate cyclase activating polypeptide 1 receptor 1	Mus musculus	60-64
25426938-8	2014	Acetylcysteine (NAC) as an inhibitor of the dimerization of PAC1 inhibited the anti-apoptotic activities that were endowed by PAC1 and decreased the Wnt/beta-catenin signal in Top-flash assays.	Acetylcysteine	16-19	adenylate cyclase activating polypeptide 1 receptor 1	Mus musculus	126-130
25386077-7	2014	In addition, NAC treatment significantly reduced caspase-3 activity and apoptosis after reperfusion, which correlated with the protein expression of Bcl-2 and Bcl-xl.	Acetylcysteine	13-16	caspase 3	Mus musculus	49-58
25106704-5	2014	Using N-acetylcysteine (NAC) as an antioxidant, we demonstrated further that oxidative stress was thoroughly responsible for the increased expression of HSP70.	Acetylcysteine	6-22	heat shock protein family A (Hsp70) member 4	Homo sapiens	153-158
26158396-8	2016	Monocyte chemoattractant protein-1 (MCP-1) gene expression and apoptotic cell death were induced by 4 h- and 8 day-exposure to high glucose, respectively, both of which were also blocked by tofogliflozin or NAC.	Acetylcysteine	207-210	chemokine (C-C motif) ligand 2	Mus musculus	0-34
15197348-5	2004	The reduction in cell growth and enhancement in cell killing by the combination of GST-MDA-7 and radiation were blocked by an ROS scavenger, N-acetyl cysteine (NAC), a JNK1/2/3 inhibitor SP600125, a pan-caspase inhibitor (zVAD) and by an inhibitor of caspase 9 (LEHD), but not by an inhibitor of caspase 8 (IETD).	Acetylcysteine	143-158	interleukin 24	Homo sapiens	87-92
26158396-8	2016	Monocyte chemoattractant protein-1 (MCP-1) gene expression and apoptotic cell death were induced by 4 h- and 8 day-exposure to high glucose, respectively, both of which were also blocked by tofogliflozin or NAC.	Acetylcysteine	207-210	chemokine (C-C motif) ligand 2	Mus musculus	36-41
25106704-5	2014	Using N-acetylcysteine (NAC) as an antioxidant, we demonstrated further that oxidative stress was thoroughly responsible for the increased expression of HSP70.	Acetylcysteine	24-27	heat shock protein family A (Hsp70) member 4	Homo sapiens	153-158
15197348-5	2004	The reduction in cell growth and enhancement in cell killing by the combination of GST-MDA-7 and radiation were blocked by an ROS scavenger, N-acetyl cysteine (NAC), a JNK1/2/3 inhibitor SP600125, a pan-caspase inhibitor (zVAD) and by an inhibitor of caspase 9 (LEHD), but not by an inhibitor of caspase 8 (IETD).	Acetylcysteine	160-163	interleukin 24	Homo sapiens	87-92
15284390-4	2004	Ingested ITCs are almost exclusively excreted and highly concentrated in the urine as N-acetylcysteine conjugates (NAC-ITC).	Acetylcysteine	86-102	synuclein alpha	Homo sapiens	115-118
25151118-9	2014	We observed that N-acetylcysteine reduced (i) Syk activation, (ii) band 3 clusterization, (iii) HSP27 membrane association, and (iv) erythroid microparticle release, resulting in increased Prx2(-/-) mouse red cell survival.	Acetylcysteine	17-33	spleen tyrosine kinase	Mus musculus	46-49
25151118-9	2014	We observed that N-acetylcysteine reduced (i) Syk activation, (ii) band 3 clusterization, (iii) HSP27 membrane association, and (iv) erythroid microparticle release, resulting in increased Prx2(-/-) mouse red cell survival.	Acetylcysteine	17-33	heat shock protein 1	Mus musculus	96-101
26890139-13	2016	Antioxidant treatment with N-Acetyl-Cysteine was found to rescue Kv2.1-dependent currents and decreased spontaneous hyperexcitability in 3xTg-AD neurons.	Acetylcysteine	27-44	potassium voltage gated channel, Shab-related subfamily, member 1	Mus musculus	65-70
15158123-7	2004	In addition, the induction of COX-2 and HO-1 expression by TGD was prevented by pretreatment with NAC or SB203580, a p38 MAPK inhibitor.	Acetylcysteine	98-101	heme oxygenase 1	Homo sapiens	40-44
25350110-7	2014	Pre-treatment of N-acetyl cysteine, a membrane-permeant cysteine prodrug, increased basal glutathione levels in the EAAC1-/- female mice and reduced ischemic neuronal death, BBB disruption and vessel disorganization.	Acetylcysteine	17-34	solute carrier family 1 (neuronal/epithelial high affinity glutamate transporter, system Xag), member 1	Mus musculus	116-121
26820738-7	2016	The oxidative stress-mediated cell death after silencing of PTGR2 or addition of 15-keto-PGE2 was further abolished after restoring intracellular GSH concentrations and cysteine supply by N-acetyl-L-cysteine and 2-Mercaptomethanol.	Acetylcysteine	188-207	prostaglandin reductase 2	Homo sapiens	60-65
14747612-6	2004	Administration of free radical scavengers N-acetylcysteine (4 mM) or N-(2-mercaptopropionyl)-glycine (1 mM) also abolished the protective effects of IL-2 and U50,488H [(trans)-3,4-dichloro-N-methyl-N-[2-(1-pyrrolidinyl)-cyclohexyl]benzeneacetamide], a selective kappa-OR agonist.	Acetylcysteine	42-58	interleukin 2	Rattus norvegicus	149-153
25876056-6	2016	However, N-acetylcysteine (NAC), a scavenger of ROS, prevented the increase of ROS generation, attenuated the phosphorylation of the above kinases, and decreased the NF-kappaB activation as well as the expression of ICAM-1 and VCAM-1.	Acetylcysteine	9-25	intercellular adhesion molecule 1	Homo sapiens	216-222
25876056-6	2016	However, N-acetylcysteine (NAC), a scavenger of ROS, prevented the increase of ROS generation, attenuated the phosphorylation of the above kinases, and decreased the NF-kappaB activation as well as the expression of ICAM-1 and VCAM-1.	Acetylcysteine	27-30	intercellular adhesion molecule 1	Homo sapiens	216-222
27405163-12	2016	The expression levels of HIF-1alpha, Beclin-1 and Bnip3 (mitophagy marker molecular) increased remarkably after sodium nitrite treatment, which were reversed by NAC.	Acetylcysteine	161-164	beclin 1	Homo sapiens	37-45
26431905-10	2015	NAC decreased fluoride-induced ROS generation and attenuated JNK and c-Jun phosphorylation.	Acetylcysteine	0-3	mitogen-activated protein kinase 8	Mus musculus	61-64
26431905-11	2015	NAC decreased SIRT1 phosphorylation and formation of the autophagy marker LC3II, which resulted in an increase in the apoptosis mediators gammaH2AX and cleaved/activated caspase-3.	Acetylcysteine	0-3	caspase 3	Mus musculus	170-179
25147340-8	2014	P66(Shc)-induced beta-catenin dephosphorylation was inhibited by antioxidants N-acetyl cysteine and catalase.	Acetylcysteine	78-95	src homology 2 domain-containing transforming protein C1	Mus musculus	0-9
25147340-8	2014	P66(Shc)-induced beta-catenin dephosphorylation was inhibited by antioxidants N-acetyl cysteine and catalase.	Acetylcysteine	78-95	catenin (cadherin associated protein), beta 1	Mus musculus	17-29
24973647-0	2014	Redox activation of DUSP4 by N-acetylcysteine protects endothelial cells from Cd2+-induced apoptosis.	Acetylcysteine	29-45	dual specificity phosphatase 4	Homo sapiens	20-25
24973647-6	2014	Immunoblotting of endothelial NO synthase (eNOS) and DUSP4, a dual-specificity phosphatase with a cysteine as its active residue, revealed that both enzymes are upregulated by NAC.	Acetylcysteine	176-179	dual specificity phosphatase 4	Homo sapiens	53-58
24973647-9	2014	Treatment with NAC prevents DUSP4 degradation and protects cells against Cd(2+)-induced apoptosis.	Acetylcysteine	15-18	dual specificity phosphatase 4	Homo sapiens	28-33
24973647-14	2014	Therefore, the identification of DUSP4 activation by NAC provides a novel target for future drug design.	Acetylcysteine	53-56	dual specificity phosphatase 4	Homo sapiens	33-38
26364141-8	2015	Pretreatment with N-acetyl-l-cysteine (NAC) significantly inhibited intracellular ROS generation and increased cell viability, accompanied by a significant NF-kappaB inhibition and suppression of TLR4 and inflammatory cytokine MCP-1 expression.	Acetylcysteine	18-37	chemokine (C-C motif) ligand 2	Mus musculus	227-232
26364141-8	2015	Pretreatment with N-acetyl-l-cysteine (NAC) significantly inhibited intracellular ROS generation and increased cell viability, accompanied by a significant NF-kappaB inhibition and suppression of TLR4 and inflammatory cytokine MCP-1 expression.	Acetylcysteine	39-42	chemokine (C-C motif) ligand 2	Mus musculus	227-232
14688353-4	2004	The level of TRX release is augmented upon the addition of H2O2, but suppressed upon the addition of N-acetylcysteine.	Acetylcysteine	101-117	thioredoxin	Homo sapiens	13-16
26536834-9	2015	Intracellular and extracellular reactive oxidative species (ROS) production was significantly increased in the animals treated with native LDL, or ox-LDL and in hyperlipidemic LDL receptor knockout (LDLR(-/-)) mice that was effectively prevented with NAC treatment.	Acetylcysteine	251-254	low density lipoprotein receptor	Mus musculus	199-203
26536834-10	2015	NAC also significantly reduced atherosclerotic plaque formation in hyperlipidemic LDLR(-/-) mice.	Acetylcysteine	0-3	low density lipoprotein receptor	Mus musculus	82-86
25101674-7	2014	N-acetyl-L-cysteine (NAC) and 3-methyladenine (3-MA) attenuated DSTD-induced autophagy but promoted cell death, suggesting that DSTD induced ROS-mediated autophagy to rescue cell death.	Acetylcysteine	0-19	X-linked Kx blood group	Homo sapiens	21-24
14615069-6	2003	Fas receptor activation also increased the generation of reactive oxygen species, and N-acetylcysteine, a well-known antioxidant, could block Fas-mediated iNOS induction.	Acetylcysteine	86-102	inositol-3-phosphate synthase 1	Homo sapiens	155-159
24938881-9	2014	Abrin also shown to increase in stress factor associated proteins SAPK/JNK, c-fos and c-jun levels which were effectively suppressed by NAC and trolox.	Acetylcysteine	136-139	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	76-81
24938881-9	2014	Abrin also shown to increase in stress factor associated proteins SAPK/JNK, c-fos and c-jun levels which were effectively suppressed by NAC and trolox.	Acetylcysteine	136-139	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	86-91
26254540-9	2015	The synergistic effect of SSZ and CDDP was reversed by antioxidant N-acetyl-L-cysteine (NAC).	Acetylcysteine	67-86	X-linked Kx blood group	Homo sapiens	88-91
12966092-7	2003	Experiments with the Src inhibitor, PP2, and the antioxidant N-acetyl-L-cysteine revealed critical roles for Src and reactive oxygen species as upstream mediators of EGFR transactivation in response to PPAR ligands.	Acetylcysteine	61-80	peroxisome proliferator activated receptor alpha	Homo sapiens	202-206
26722260-9	2015	Notably, the ROS scavenger, N-acetyl-L-cysteine, almost fully reversed the cell death and Bcr-Abl downregulation that was induced by the combination of SAHA and MG-132.	Acetylcysteine	28-47	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	90-97
26350099-5	2015	Furthermore, with the addition of N-acetylcysteine, a scavenger of reactive oxygen species (ROS), it was found that NGAL depletion was sufficient to cause apoptosis of lung adenocarcinoma cells by generating ROS through the inhibition of the nuclear factor E2-related factor 2/heme oxygenase-1 anti-oxidant pathway.	Acetylcysteine	34-50	lipocalin 2	Homo sapiens	116-120
24792639-5	2014	The current study evaluated a novel, cell permeant amide form of N-acetylcysteine (NACA), which has high permeability through cellular and mitochondrial membranes resulting in increased CNS bioavailability.	Acetylcysteine	65-81	nascent polypeptide associated complex subunit alpha	Rattus norvegicus	83-87
14521937-3	2003	Pretreatment with N-acetylcysteine suppressed the oxLDL-induced fibronectin production as well as ROS generation.	Acetylcysteine	18-34	fibronectin 1	Rattus norvegicus	64-75
25182817-12	2014	Compared with the dust group, the dust plus NAC group showed significant decreases in the content of ROS on the 14th, 28th, and 56th days (P &lt; 0.05), significant decreases in the content of protein carbonyl on the 28th and 56th days (P &lt; 0.05), and significant decreases in the protein expression of caspase-12 and apoptosis rate (P &lt; 0.05).	Acetylcysteine	44-47	caspase 12	Rattus norvegicus	306-316
26206888-3	2015	In this work, we used the dtd mouse model to study the role of N-acetyl-l-cysteine (NAC), a well-known drug with antioxidant properties, as an intracellular sulfate source for macromolecular sulfation.	Acetylcysteine	63-82	X-linked Kx blood group	Homo sapiens	84-87
26206453-5	2015	RESULTS: Treatment with NAC inhibited apoptosis of penile tissue, the expressions of ERS-related products: BIP, CHOP, caspase12, and Bax, NO, and endothelial NOS.	Acetylcysteine	24-27	heat shock protein family A (Hsp70) member 5	Rattus norvegicus	107-110
26206453-5	2015	RESULTS: Treatment with NAC inhibited apoptosis of penile tissue, the expressions of ERS-related products: BIP, CHOP, caspase12, and Bax, NO, and endothelial NOS.	Acetylcysteine	24-27	caspase 12	Rattus norvegicus	118-127
14511644-7	2003	Furthermore, antioxidants, N-acetyl-cysteine and pyrrolidinedithiocarbamate (PDTC), completely abolished the increase of HBx protein induced by adriamycin, indicating that adriamycin modulates the intracellular HBx level via ROS generation.	Acetylcysteine	27-44	X protein	Hepatitis B virus	121-124
26206453-7	2015	CONCLUSION: Our results show that pre-CIH NAC administration ameliorates the ED following CIH partly by alleviating CIH-induced ERS and cell apoptosis via regulating the expressions of BIP, CHOP, caspase12, and Bax.	Acetylcysteine	42-45	heat shock protein family A (Hsp70) member 5	Rattus norvegicus	185-188
26206453-7	2015	CONCLUSION: Our results show that pre-CIH NAC administration ameliorates the ED following CIH partly by alleviating CIH-induced ERS and cell apoptosis via regulating the expressions of BIP, CHOP, caspase12, and Bax.	Acetylcysteine	42-45	caspase 12	Rattus norvegicus	196-205
26317351-7	2015	We found that GSH-AITC and NAC-AITC effectively inhibit adipogenic differentiation of 3T3-L1 preadipocytes and suppress expression of PPAR-gamma, C/EBPalpha, and FAS, which are up-regulated during adipogenesis.	Acetylcysteine	27-30	peroxisome proliferator-activated receptor gamma	Rattus norvegicus	134-144
24915933-14	2014	N-acetyl-L-cysteine (NAC), an antioxidant, can partially attenuate DS/Cu complex-induced apoptosis and block JNK activation in vitro.	Acetylcysteine	0-19	X-linked Kx blood group	Homo sapiens	21-24
24601883-8	2014	N-acetylcysteine, an antioxidant, and diphenyleneiodonium, an inhibitor of nicotinamide adenine dinucleotide phosphate oxidase, suppressed indoxyl sulfate-induced PRR expression in proximal tubular cells.	Acetylcysteine	0-16	ATPase H+ transporting accessory protein 2	Homo sapiens	163-166
24686172-5	2014	Notably, SASP sensitized breast cancer cells to inhibitors of the type I IGF receptor (IGF-IR) in a manner reversed by the reactive oxygen species (ROS) scavenger N-acetyl-L-cysteine.	Acetylcysteine	163-182	insulin like growth factor 1 receptor	Homo sapiens	87-93
14511644-7	2003	Furthermore, antioxidants, N-acetyl-cysteine and pyrrolidinedithiocarbamate (PDTC), completely abolished the increase of HBx protein induced by adriamycin, indicating that adriamycin modulates the intracellular HBx level via ROS generation.	Acetylcysteine	27-44	X protein	Hepatitis B virus	211-214
24115584-6	2014	In addition, when given to Fancd2(-/-) mice, NAC helped maintain Fancd2(-/-) KSL cells in quiescence while tempol did not.	Acetylcysteine	45-48	Fanconi anemia, complementation group D2	Mus musculus	27-33
24115584-6	2014	In addition, when given to Fancd2(-/-) mice, NAC helped maintain Fancd2(-/-) KSL cells in quiescence while tempol did not.	Acetylcysteine	45-48	Fanconi anemia, complementation group D2	Mus musculus	65-71
26230185-0	2015	Organic Anion Transporter 5 (Oat5) Urinary Excretion Is a Specific Biomarker of Kidney Injury: Evaluation of Urinary Excretion of Exosomal Oat5 after N-Acetylcysteine Prevention of Cisplatin Induced Nephrotoxicity.	Acetylcysteine	150-166	solute carrier family 22, member 24	Rattus norvegicus	0-27
26230185-0	2015	Organic Anion Transporter 5 (Oat5) Urinary Excretion Is a Specific Biomarker of Kidney Injury: Evaluation of Urinary Excretion of Exosomal Oat5 after N-Acetylcysteine Prevention of Cisplatin Induced Nephrotoxicity.	Acetylcysteine	150-166	solute carrier family 22, member 24	Rattus norvegicus	29-33
26230185-0	2015	Organic Anion Transporter 5 (Oat5) Urinary Excretion Is a Specific Biomarker of Kidney Injury: Evaluation of Urinary Excretion of Exosomal Oat5 after N-Acetylcysteine Prevention of Cisplatin Induced Nephrotoxicity.	Acetylcysteine	150-166	solute carrier family 22, member 24	Rattus norvegicus	139-143
26230185-6	2015	To accomplish that aim, we evaluated if urinary excretion of exosomal Oat5 returns to its basal levels when cisplatin renal damage is prevented by the coadministration of the renoprotective compound N-acetylcysteine.	Acetylcysteine	199-215	solute carrier family 22, member 24	Rattus norvegicus	70-74
24533448-10	2014	Furthermore, pregestational diabetes increased ROS, impaired cell proliferation, and altered Gata4, Gata5 and Vegf-a expression in the fetal heart of diabetic offspring, which were all prevented by NAC treatment.	Acetylcysteine	198-201	vascular endothelial growth factor A	Mus musculus	110-116
24157283-8	2014	NAC and the specific JNK inhibitor (SP600125) and ERK1/2 inhibitor (PD98059) abrogated iAs-induced cell cytotoxicity, caspase-3/-7 activity, and JNK and ERK1/2 activation.	Acetylcysteine	0-3	caspase 3	Mus musculus	118-130
13679067-5	2003	We further demonstrated that H(2)O(2) stimulates PAI-1 expression and suppresses plasmin activity and that N-acetylcysteine effectively reverses TGF-beta1- and H(2)O(2)-induced changes in PAI-1 expression and plasmin activity.	Acetylcysteine	107-123	serpin family E member 1	Homo sapiens	188-193
24157283-8	2014	NAC and the specific JNK inhibitor (SP600125) and ERK1/2 inhibitor (PD98059) abrogated iAs-induced cell cytotoxicity, caspase-3/-7 activity, and JNK and ERK1/2 activation.	Acetylcysteine	0-3	mitogen-activated protein kinase 8	Mus musculus	145-148
26028291-8	2015	N-acetyl cysteine or melatonin treatments, significantly dampened the Bmal1 promoter activity suggesting that sustained scavenging of ROS impairs clock synchronization.	Acetylcysteine	0-17	aryl hydrocarbon receptor nuclear translocator like	Homo sapiens	70-75
12957649-8	2003	The reduction in NMDAR-mediated migration observed in Ts16 neurons was returned to normal littermate values by NAC or DTT.	Acetylcysteine	111-114	glutamate receptor, ionotropic, NMDA1 (zeta 1)	Mus musculus	17-22
26203910-2	2015	OBJECTIVES: In this study, we evaluated morphological and functional changes in human corneas exposed for 2 minutes (min) to APCP and tested if the antioxidant n-acetyl l-cysteine (NAC) was able to inhibit or prevent damage and cell death.	Acetylcysteine	160-179	X-linked Kx blood group	Homo sapiens	181-184
25431587-8	2014	The rate of bridging fibrosis was higher (100% versus 20%, P = .025), but the intensity of e-NOS in liver was lower in rats that received NAC (1.3 versus 2.7, P = .046).	Acetylcysteine	138-141	nitric oxide synthase 3	Rattus norvegicus	91-96
25431587-13	2014	Our study showed that e-NOS expression increased in liver tissue of rats with CC and that this was reversed by NAC.	Acetylcysteine	111-114	nitric oxide synthase 3	Rattus norvegicus	22-27
25431587-14	2014	Treatment with NAC might restore e-NOS protein expression and prevent liver injury in CC.	Acetylcysteine	15-18	nitric oxide synthase 3	Rattus norvegicus	33-38
25359386-12	2014	Significantly increased expressions of GRP78 and CHOP were observed in the NRK-52E cells exposed to iopromide for 4 h; NAC attenuated iopromide-induced NRK-52E cell apoptosis by inhibiting the overproduction of intracellular ROS and subsequently suppressing the overexpression of GRP78 and CHOP.	Acetylcysteine	119-122	heat shock protein family A (Hsp70) member 5	Rattus norvegicus	39-44
25359386-12	2014	Significantly increased expressions of GRP78 and CHOP were observed in the NRK-52E cells exposed to iopromide for 4 h; NAC attenuated iopromide-induced NRK-52E cell apoptosis by inhibiting the overproduction of intracellular ROS and subsequently suppressing the overexpression of GRP78 and CHOP.	Acetylcysteine	119-122	heat shock protein family A (Hsp70) member 5	Rattus norvegicus	280-285
12743010-7	2003	The ability of both n-acetyl-cysteine and diphenyleneionium (antioxidants) to inhibit uric acid-induced MCP-1 production suggested involvement of intracellular redox pathways.	Acetylcysteine	20-37	C-C motif chemokine ligand 2	Homo sapiens	104-109
24322755-9	2013	Treatment with N-acetyl-L-cysteine (NAC) or diphenyleneiodonium chloride (DPI) decreased BIX-induced LC3-II, GFP-LC3 puncta, and cell death, indicating that ROS instigated autophagy-dependent cell death triggered by BIX.	Acetylcysteine	15-34	X-linked Kx blood group	Homo sapiens	36-39
24322755-9	2013	Treatment with N-acetyl-L-cysteine (NAC) or diphenyleneiodonium chloride (DPI) decreased BIX-induced LC3-II, GFP-LC3 puncta, and cell death, indicating that ROS instigated autophagy-dependent cell death triggered by BIX.	Acetylcysteine	15-34	microtubule associated protein 1 light chain 3 alpha	Homo sapiens	101-104
26073049-5	2015	N-Acetyl-l-cysteine blocked anti-CD3-induced T-cell suppression by AFB1 through increasing intracellular concentrations of GSH levels, decreasing MDA levels, and down-regulated p-ERK1/2 expression, respectively.	Acetylcysteine	0-19	mitogen-activated protein kinase 3	Sus scrofa	179-185
26339453-0	2015	N-acetylcysteine protects against liver injure induced by carbon tetrachloride via activation of the Nrf2/HO-1 pathway.	Acetylcysteine	0-16	heme oxygenase 1	Rattus norvegicus	106-110
26339453-9	2015	Treatment with NAC had been shown to an increase in nuclear factor erythroid 2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1) mRNA levels.	Acetylcysteine	15-18	heme oxygenase 1	Rattus norvegicus	107-123
26339453-9	2015	Treatment with NAC had been shown to an increase in nuclear factor erythroid 2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1) mRNA levels.	Acetylcysteine	15-18	heme oxygenase 1	Rattus norvegicus	125-129
26339453-10	2015	In conclusion, these results suggested that NAC upregulated HO-1 through the activation of Nrf2 pathway and protected rat against CCl4-induced liver injure.	Acetylcysteine	44-47	heme oxygenase 1	Rattus norvegicus	60-64
24322755-9	2013	Treatment with N-acetyl-L-cysteine (NAC) or diphenyleneiodonium chloride (DPI) decreased BIX-induced LC3-II, GFP-LC3 puncta, and cell death, indicating that ROS instigated autophagy-dependent cell death triggered by BIX.	Acetylcysteine	15-34	microtubule associated protein 1 light chain 3 alpha	Homo sapiens	113-116
12754095-5	2003	Compared to treatment with UV radiation alone, combination treatment with NAC doubled the ratio of activated caspase-3 to pro-caspase-3 and produced greater fragmentation of the retinoblastoma protein and the E2F-4 transcription factor without affecting the E2F-1 protein.	Acetylcysteine	74-77	E2F transcription factor 1	Homo sapiens	258-263
12529245-3	2003	Levels of extracellular Trx are decreased by the antioxidant N-acetylcysteine.	Acetylcysteine	61-77	thioredoxin	Homo sapiens	24-27
24090735-8	2013	Pre-treatment with antioxidant n-acetyl-l-cysteine (NAC) reduced ROS generation and DNA DSBs, inhibited apoptosis, and increased cell viability in AFG1-treated cells.	Acetylcysteine	31-50	X-linked Kx blood group	Homo sapiens	52-55
24090735-8	2013	Pre-treatment with antioxidant n-acetyl-l-cysteine (NAC) reduced ROS generation and DNA DSBs, inhibited apoptosis, and increased cell viability in AFG1-treated cells.	Acetylcysteine	31-50	AFG1 like ATPase	Homo sapiens	147-151
25950987-12	2015	N-Acetyl-l-cysteine (NAC) scavenged ROS formation and consequently alleviated PCB29-pQ-induced expression of ER stress-related genes.	Acetylcysteine	0-19	X-linked Kx blood group	Homo sapiens	21-24
25955698-9	2015	The decrease in IGF-1R and increase in IGFBP-3, as well as apoptosis, were also antagonized by pre-treatment with the antioxidant agents, N-acetylcysteine, dexrazoxane, and carvedilol.	Acetylcysteine	138-154	insulin like growth factor 1 receptor	Homo sapiens	16-22
12529245-7	2003	We demonstrate that N-acetylcysteine reduces the cellular level of Trx but not the proportion secreted; thus this chemical does not block the nonclassic pathway for Trx secretion.	Acetylcysteine	20-36	thioredoxin	Homo sapiens	67-70
23770272-4	2013	The pretreatment of N-acetyl-l-cysteine (NAC, an ROS scavenger) also prevents OGD/R-induced activation of caspase-3.	Acetylcysteine	20-39	caspase 3	Mus musculus	106-115
12826064-2	2003	The dinitrosyl-iron complexes had the ligands glutathione (DNIC-GS) or N-acetylcysteine (DNIC-NAC).	Acetylcysteine	71-87	synuclein alpha	Homo sapiens	94-97
23770272-4	2013	The pretreatment of N-acetyl-l-cysteine (NAC, an ROS scavenger) also prevents OGD/R-induced activation of caspase-3.	Acetylcysteine	41-44	caspase 3	Mus musculus	106-115
12466149-5	2003	Fibronectin and bFGF also significantly augmented invasion of myoblasts across a Matrigel barrier, and plasmin cotreatment potentiated whereas N-acetyl cysteine suppressed the effects of bFGF and fibronectin on myoblast migration and invasion.	Acetylcysteine	143-160	fibronectin 1	Mus musculus	0-11
24008345-7	2013	NAC, but not SPL, suppressed oxidative stress in MIN6 cells, as revealed by the decrease in inducible NOS levels and expression of the proteins p22-phox and p67-phox.	Acetylcysteine	0-3	neutrophil cytosolic factor 2	Mus musculus	157-165
23948373-8	2013	Following treatment with the antioxidant NAC, cybrid B4 cells showed significantly reduced insulin-induced phosphorylation of P38 and increased GLUT1/GLUT4 translocation to the cell membrane, suggesting that NAC may divert insulin signaling from pro-inflammation to glucose uptake.	Acetylcysteine	41-44	solute carrier family 2 member 1	Homo sapiens	144-149
23948373-8	2013	Following treatment with the antioxidant NAC, cybrid B4 cells showed significantly reduced insulin-induced phosphorylation of P38 and increased GLUT1/GLUT4 translocation to the cell membrane, suggesting that NAC may divert insulin signaling from pro-inflammation to glucose uptake.	Acetylcysteine	208-211	solute carrier family 2 member 1	Homo sapiens	144-149
12466149-5	2003	Fibronectin and bFGF also significantly augmented invasion of myoblasts across a Matrigel barrier, and plasmin cotreatment potentiated whereas N-acetyl cysteine suppressed the effects of bFGF and fibronectin on myoblast migration and invasion.	Acetylcysteine	143-160	fibronectin 1	Mus musculus	196-207
12556365-5	2003	N-acetylcysteine completely blocked hemin-induced expression of HO-1 and MCP-1 mRNA, thereby providing added evidence for redox regulation of expression of these genes.	Acetylcysteine	0-16	C-C motif chemokine ligand 2	Rattus norvegicus	73-78
23249342-4	2013	The intravenous application of NAC during a hemodialysis session resulted in a substantial increase of native TTR from median 15% (range 8.8%-30%) to median 40% (37-50) and reduction of S-cysteinylated TTR [51% (44-60) vs. 6.6% (2.4-10)].	Acetylcysteine	31-34	transthyretin	Homo sapiens	110-113
12606766-11	2003	Probenecid-sensitive transport of the NAC-Hg(2+) conjugate was also shown to occur in Xenopus laevis oocytes expressing the hOAT1 or the rOAT3 transporters, suggesting that OAT3 may also transport thiol-Hg(2+) conjugates.	Acetylcysteine	38-41	solute carrier family 22 member 6	Homo sapiens	124-129
23249342-4	2013	The intravenous application of NAC during a hemodialysis session resulted in a substantial increase of native TTR from median 15% (range 8.8%-30%) to median 40% (37-50) and reduction of S-cysteinylated TTR [51% (44-60) vs. 6.6% (2.4-10)].	Acetylcysteine	31-34	transthyretin	Homo sapiens	202-205
23249342-5	2013	Additionally the pronounced formation of a TTR-NAC adduct was detected.	Acetylcysteine	47-50	transthyretin	Homo sapiens	43-46
23249342-7	2013	Additionally, in vitro incubation of plasma with NAC confirmed the in vivo results and indicated that changes in post-translational modification pattern of TTR were a function of NAC concentration.	Acetylcysteine	49-52	transthyretin	Homo sapiens	156-159
23249342-7	2013	Additionally, in vitro incubation of plasma with NAC confirmed the in vivo results and indicated that changes in post-translational modification pattern of TTR were a function of NAC concentration.	Acetylcysteine	179-182	transthyretin	Homo sapiens	156-159
12606766-11	2003	Probenecid-sensitive transport of the NAC-Hg(2+) conjugate was also shown to occur in Xenopus laevis oocytes expressing the hOAT1 or the rOAT3 transporters, suggesting that OAT3 may also transport thiol-Hg(2+) conjugates.	Acetylcysteine	38-41	solute carrier family 22 member 8	Rattus norvegicus	137-142
12606766-11	2003	Probenecid-sensitive transport of the NAC-Hg(2+) conjugate was also shown to occur in Xenopus laevis oocytes expressing the hOAT1 or the rOAT3 transporters, suggesting that OAT3 may also transport thiol-Hg(2+) conjugates.	Acetylcysteine	38-41	solute carrier family 22 member 8	Rattus norvegicus	138-142
23732519-9	2013	Pretreatments with VEGF, VEGF-B, or the antioxidant N-acetylcysteine (NAC) rescued SU1498 or siRNA-treated neurons from the mitochondrial dysfunction and oxidative stress induced by VEGFR-2 inhibition in a timely fashion.	Acetylcysteine	70-73	kinase insert domain receptor	Homo sapiens	182-189
12627328-11	2003	An anti-oxidant, N-acetylcysteine, or pigment epithelium-derived factor completely prevented the AGE-induced up-regulation of MCP-1 mRNA contents as well as protein production in microvascular endothelial cells.	Acetylcysteine	17-33	C-C motif chemokine ligand 2	Homo sapiens	126-131
23876822-8	2013	However, the elimination of R-scy-induced ROS by treatment with N-acetyl-L-cysteine (NAC) markedly opposed R-scy-induced PCDII.	Acetylcysteine	64-83	X-linked Kx blood group	Homo sapiens	85-88
12566471-7	2003	In all cell lines studied, alpha-tocopherol and N-acetylcysteine inhibited the effects of beta-carotene on NF-kappaB, cell growth and apoptosis, and normalized the increased expression of c-myc induced by the carotenoid.	Acetylcysteine	48-64	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	188-193
12206715-11	2002	Taken together these results strongly suggest that EGCG executed apoptotic cell death via an ASK1, MKK and JNK/p38 cascade which is triggered by NAC-sensitive intracellular oxidative events in a manner distinct from chemically induced or receptor-mediated apoptosis.	Acetylcysteine	145-148	mitogen-activated protein kinase kinase kinase 5	Homo sapiens	93-97
24137468-4	2013	Notably, the pre-treatment with N-acetyl-L-cysteine (NAC) abolished the TPL-induced ROS generation, NF-kappaB inhibition and cell apoptosis, but did not affect the inhibitory effect of TPL on complex I activity.	Acetylcysteine	32-51	X-linked Kx blood group	Homo sapiens	53-56
24086766-7	2013	Additionally, although the ROS scavenger N-acetyl-l-cysteine abrogated 5-HT-induced PDGFbeta and TrkB receptor transactivation, it was unable to prevent 5-HT-induced ERK1/2 phosphorylation.	Acetylcysteine	41-60	platelet derived growth factor subunit B	Homo sapiens	84-92
12359264-6	2002	Activation of caspase-3 in TPEN-treated AEC was inhibited strongly by N-acetylcysteine and partially by vitamin C and vitamin E.	Acetylcysteine	70-86	caspase-3	Ovis aries	14-23
23666527-4	2013	NAC was able to partially suppress phenotypes in both antisense-induced (NPC1ASO) and germline (Npc1-/-) knockout genetic mouse models, confirming the presence of an oxidative stress-related mechanism in progression of NPC1 phenotypes and suggesting NAC as a potential molecule for treatment.	Acetylcysteine	0-3	NPC1 like intracellular cholesterol transporter 1	Mus musculus	73-77
23666527-5	2013	Gene expression analyses of NAC-treated NPC1ASO mice suggested NAC affects pathways distinct from those initially altered by Npc1 knockdown, data consistent with NAC achieving partial disease phenotype suppression.	Acetylcysteine	28-31	NPC1 like intracellular cholesterol transporter 1	Mus musculus	40-44
23666527-5	2013	Gene expression analyses of NAC-treated NPC1ASO mice suggested NAC affects pathways distinct from those initially altered by Npc1 knockdown, data consistent with NAC achieving partial disease phenotype suppression.	Acetylcysteine	63-66	NPC1 like intracellular cholesterol transporter 1	Mus musculus	40-44
23666527-5	2013	Gene expression analyses of NAC-treated NPC1ASO mice suggested NAC affects pathways distinct from those initially altered by Npc1 knockdown, data consistent with NAC achieving partial disease phenotype suppression.	Acetylcysteine	63-66	NPC1 like intracellular cholesterol transporter 1	Mus musculus	40-44
23704321-8	2013	RESULTS: Our AKU model allowed us to prove the efficacy of ascorbic acid combined with N-acetylcysteine, taurine, phytic acid and lipoic acid in significantly inhibiting SAA production, pro-inflammatory cytokine release and membrane lipid peroxidation.	Acetylcysteine	87-103	serum amyloid A1 cluster	Homo sapiens	170-173
23765110-0	2013	Influence of N-acetylcysteine on Klotho expression and its signaling pathway in experimental model of chronic cyclosporine nephropathy in mice.	Acetylcysteine	13-29	klotho	Mus musculus	33-39
23765110-2	2013	This study was designed to examine whether N-acetylcysteine (NAC), a well-known antioxidant, affects Klotho, antiaging gene, expression and its signaling pathway in an experimental model of chronic CsA nephropathy.	Acetylcysteine	43-59	klotho	Mus musculus	101-107
23765110-2	2013	This study was designed to examine whether N-acetylcysteine (NAC), a well-known antioxidant, affects Klotho, antiaging gene, expression and its signaling pathway in an experimental model of chronic CsA nephropathy.	Acetylcysteine	61-64	klotho	Mus musculus	101-107
23765110-5	2013	The influence of NAC on Klotho and its signal pathway (p-AKT and p-FoxO1) in CsA-treated mouse kidney was evaluated with immunohistochemistry and/or immunoblot.	Acetylcysteine	17-20	klotho	Mus musculus	24-30
23765110-7	2013	NAC treatment preserved Klotho gene expression compared with CsA treatment alone (P &lt; 0.05), and this correlated with urinary 8-OHdG excretion (r = -0.934) and MnSOD expression (r = 0.873, P &lt; 0.001 for both).	Acetylcysteine	0-3	klotho	Mus musculus	24-30
23765110-9	2013	CONCLUSION: NAC treatment preserves Klotho expression and modifies p-AKT/p-FoxO1 pathway in chronic CsA nephropathy.	Acetylcysteine	12-15	klotho	Mus musculus	36-42
23740244-4	2013	Gemcitabine-induced CXCR4 expression is dependent on reactive oxygen species (ROS) generation because it is abrogated by pretreatment of PC cells with the free radical scavenger N-acetyl-L-cysteine.	Acetylcysteine	178-197	C-X-C motif chemokine receptor 4	Homo sapiens	20-25
23660503-10	2013	Alcohol-induced and H2O2-induced increases in intestinal cell CLOCK and PER2 were significantly inhibited by treatment with NAC.	Acetylcysteine	124-127	period circadian regulator 2	Homo sapiens	72-76
23703906-6	2013	Treatment with the sulphydryl anti-oxidant N-acetylcysteine reversed the abnormalities in the Miner1 deficient cells, suggesting that sulphydryl reducing agents should be explored as a treatment for this rare genetic disease.	Acetylcysteine	43-59	CDGSH iron sulfur domain 2	Mus musculus	94-100
23613809-4	2013	Subsequent studies demonstrated that the electrotaxis of glioma cells were abolished by the superoxide inhibitor N-acetyl-l-cysteine (NAC) or overexpression of mitochondrial superoxide dismutase (MnSOD), but was not affected by inhibition of hydrogen peroxide through the overexpression of catalase.	Acetylcysteine	113-132	X-linked Kx blood group	Homo sapiens	134-137
23434081-9	2013	IL-10 was significantly decreased in the NAC group at 24h after LPS stimulation (P&lt;0.05).	Acetylcysteine	41-44	interleukin 10	Homo sapiens	0-5
23434081-12	2013	The level of IL-10 in the group with AAP plus NAC was significantly lower (P&lt;0.05) at 24h after LPS stimulation, while the rest of the inflammatory cytokines were returned to the original levels.	Acetylcysteine	46-49	interleukin 10	Homo sapiens	13-18
23490067-7	2013	AA clearly increased TPA-induced HL-60 cell differentiation, as evidenced by a marked increase in CD11b expression, which was inhibited by NAC and PD98059 addition.	Acetylcysteine	139-142	integrin subunit alpha M	Homo sapiens	98-103
22665050-9	2013	In addition, treatment with N-acetyl-L-cysteine, a reactive oxygen species (ROS) scavenger, suppressed the induction of beclin-1 and LC3 II, implying that the differential SVCT-2 protein-dependent L-ascorbate uptake was attributable to intracellular ROS induced by L-ascorbate, subsequently leading to autophagy.	Acetylcysteine	28-47	beclin 1	Homo sapiens	120-128
23457180-5	2013	Converseley, an understanding of the common mechanisms of sensitisation (such as regionally selective alterations in brain derived neurotrophic factor (BDNF) and hyperactivity of striatally based habit memories), could also result in single therapies (such as N-acetylcysteine) having positive effects in all three domains.	Acetylcysteine	260-276	brain derived neurotrophic factor	Homo sapiens	117-150
23283970-9	2013	Sodium arsenite, an agent that induces oxidative stress, promoted nuclear export of ectopically expressed Nurr1 in HEK293T cells, and the antioxidant N-acetylcysteine rescued from this effect.	Acetylcysteine	150-166	nuclear receptor subfamily 4 group A member 2	Homo sapiens	106-111
23426507-14	2013	In accordance with this, ISO+NAC group rats also showed marked reductions in the expressions of NOX(4) and p-CaMKII/CaMKII compared to ISO group rats (P &lt; 0.05).	Acetylcysteine	29-32	NADPH oxidase 4	Rattus norvegicus	96-102
23183129-7	2013	In addition, NAC-treated rats showed upregulated expression of NKCC2, AQP2, and UT-A1; elevated Klotho protein expression, low p53 expression, and few ED-1 positive cells.	Acetylcysteine	13-16	solute carrier family 12 member 1	Rattus norvegicus	63-68
23183129-8	2013	In conclusion, we attribute these beneficial effects of NAC (the significant improvements in inulin clearance and in the expression of NKCC2, AQP2, and UT-A1) to its ability to decrease oxidative stress, inhibit p53 expression, minimize kidney inflammation, and stimulate Klotho expression.	Acetylcysteine	56-59	solute carrier family 12 member 1	Rattus norvegicus	135-140
23175375-7	2013	In addition, NAC inhibited KSHV infection-induced translocation of alphaVbeta3 integrin into lipid rafts, actin-dependent membrane perturbations, such as blebs, observed during macropinocytosis, and activation of the signal molecules ephrin-A2 receptor, FAK, Src, and Rac1.	Acetylcysteine	13-16	Rac family small GTPase 1	Homo sapiens	268-272
23143036-8	2013	Whole mount in situ hybridization revealed a wide distribution of msh6 mRNA in the head regions of 10 hpf embryos and pretreatment of embryos with antioxidants butylhydroxytoluene (BHT), d-mannitol or N-acetylcysteine (NAC) at 1-10 muM restored Cd-suppressed msh6 expression.	Acetylcysteine	201-217	mutS homolog 6 (E. coli)	Danio rerio	66-70
23143036-8	2013	Whole mount in situ hybridization revealed a wide distribution of msh6 mRNA in the head regions of 10 hpf embryos and pretreatment of embryos with antioxidants butylhydroxytoluene (BHT), d-mannitol or N-acetylcysteine (NAC) at 1-10 muM restored Cd-suppressed msh6 expression.	Acetylcysteine	219-222	mutS homolog 6 (E. coli)	Danio rerio	66-70
23103613-9	2013	Pretreatment with NAC and specific p38-MAPK inhibitor (SB203580), but not JNK inhibitor (SP600125) effectively abrogated the phosphorylation of p38-MAPK and attenuated the apoptotic signals (including: decrease in cytotoxicity, caspase-3/-7 activation, the cytosolic cytochrome c release, and the reversed alteration of Bcl-2 and Bax mRNA) in CA-treated Neuro-2a cells.	Acetylcysteine	18-21	caspase 3	Mus musculus	228-237
23103613-9	2013	Pretreatment with NAC and specific p38-MAPK inhibitor (SB203580), but not JNK inhibitor (SP600125) effectively abrogated the phosphorylation of p38-MAPK and attenuated the apoptotic signals (including: decrease in cytotoxicity, caspase-3/-7 activation, the cytosolic cytochrome c release, and the reversed alteration of Bcl-2 and Bax mRNA) in CA-treated Neuro-2a cells.	Acetylcysteine	18-21	BCL2-associated X protein	Mus musculus	330-333
22746102-3	2013	We used an animal model of KSHV-induced Kaposi"s sarcomagenesis (mECK36) to study the role of ROS in KS and the efficacy of N-acetyl l-cysteine (NAC) in inhibiting or preventing KS.	Acetylcysteine	124-143	X-linked Kx blood group	Homo sapiens	145-148
23902724-8	2013	Furthermore, PCV2 replication in PK15 cells was significantly impaired after the elevation of intracellular GSH through treatment with the antioxidant N-acetyl-l-cysteine (NAC), a precursor in GSH synthesis.	Acetylcysteine	151-170	X-linked Kx blood group	Homo sapiens	172-175
24398995-0	2013	Valproic acid substantially downregulated genes folr1, IGF2R, RGS2, COL6A3, EDNRB, KLF6, and pax-3, N-acetylcysteine alleviated most of the induced gene alterations in chicken embryo model.	Acetylcysteine	100-116	collagen type VI alpha 3 chain	Gallus gallus	68-74
24398995-0	2013	Valproic acid substantially downregulated genes folr1, IGF2R, RGS2, COL6A3, EDNRB, KLF6, and pax-3, N-acetylcysteine alleviated most of the induced gene alterations in chicken embryo model.	Acetylcysteine	100-116	Kruppel like factor 6	Gallus gallus	83-87
22824115-11	2012	These results demonstrate that NAC has a protective effect against hepatic lipid accumulation in rats exposed to PCB 126.	Acetylcysteine	31-34	pyruvate carboxylase	Rattus norvegicus	113-116
22991071-1	2012	The present study aimed to investigate the influence of N-acetylcysteine (NAC) on cadmium (Cd) poisoning by evaluating Cd concentration in tissues, hematological indices as well as the activity of NTPDase, acetylcholinesterase (AChE) and butyrylcholinesterase (BChE) enzymes of rats exposed to Cd and co-treated with NAC.	Acetylcysteine	74-77	butyrylcholinesterase	Rattus norvegicus	238-259
22991071-1	2012	The present study aimed to investigate the influence of N-acetylcysteine (NAC) on cadmium (Cd) poisoning by evaluating Cd concentration in tissues, hematological indices as well as the activity of NTPDase, acetylcholinesterase (AChE) and butyrylcholinesterase (BChE) enzymes of rats exposed to Cd and co-treated with NAC.	Acetylcysteine	74-77	butyrylcholinesterase	Rattus norvegicus	261-265
23047606-3	2012	Our results directly show that BRCA1-null ovarian cancer cells produce large amounts of hydrogen peroxide, which can be abolished either by administration of simple antioxidants (N-acetyl-cysteine; NAC) or by replacement of the BRCA1 gene.	Acetylcysteine	179-196	BRCA1 DNA repair associated	Homo sapiens	31-36
22925809-11	2012	Chloroquine (lysosomal inhibitor), N-acetyl-l-cysteine (reactive oxygen species scavenger) and wortmannin (a phosphatidylinositol-3-kinase inhibitor), fully or partially, rescued GLP1R protein in OA-pretreated, glucose-stimulated ductal cells.	Acetylcysteine	35-54	glucagon-like peptide 1 receptor	Rattus norvegicus	179-184
22842544-6	2012	Pretreatment with N-acetyl-l-cysteine (NAC) partly recovered the expression levels of c-FLIPL and c-FLIPs proteins were downregulated by the AMA treatment, suggesting that AMA appears to be partially dependent on the generation of ROS for downregulation of c-FLIPL and c-FLIPs.	Acetylcysteine	18-37	X-linked Kx blood group	Homo sapiens	39-42
22732503-3	2012	Here, 12-month-old male EAAT3 knockout mice received intraperitoneal injection of N-acetylcysteine (NAC) at 150 mg/kg once every day for 4 weeks.	Acetylcysteine	82-98	solute carrier family 1 (neuronal/epithelial high affinity glutamate transporter, system Xag), member 1	Mus musculus	24-29
22732503-8	2012	NAC but not saline injection attenuated these behavioral and biochemical changes in the EAAT3 knockout mice.	Acetylcysteine	0-3	solute carrier family 1 (neuronal/epithelial high affinity glutamate transporter, system Xag), member 1	Mus musculus	88-93
22732651-7	2012	Interestingly, the moderate impact of NAC on lipids and proteins oxidation correlated with myeloperoxidase and nitric oxide levels.NAC as a mucoregulator and a thiol restoring agent is protective on oxidative crypt alterations, mucin depletion, epithelial cell hyperplasia and apoptosis.	Acetylcysteine	38-41	myeloperoxidase	Mus musculus	91-106
22732651-7	2012	Interestingly, the moderate impact of NAC on lipids and proteins oxidation correlated with myeloperoxidase and nitric oxide levels.NAC as a mucoregulator and a thiol restoring agent is protective on oxidative crypt alterations, mucin depletion, epithelial cell hyperplasia and apoptosis.	Acetylcysteine	131-134	myeloperoxidase	Mus musculus	91-106
22822083-5	2012	Citreoviridin-enhanced eIF2alpha phosphorylation could be reversed by siRNA-mediated attenuation of the UPR kinase PKR-like endoplasmic reticulum kinase (PERK) combined with treatment with the antioxidant N-acetylcysteine, establishing that reactive oxygen species (ROS) boost UPR after citreoviridin treatment.	Acetylcysteine	205-221	eukaryotic translation initiation factor 2A	Homo sapiens	23-32
22549432-10	2012	NAC increased Deltapsim (P = 0.0001) in all T cells, profoundly reduced mTOR activity (P = 0.0009), enhanced apoptosis (P = 0.0004), reversed expansion of CD4-CD8- T cells (mean +- SEM 1.35 +- 0.12-fold change; P = 0.008), stimulated FoxP3 expression in CD4+CD25+ T cells (P = 0.045), and reduced anti-DNA production (P = 0.049).	Acetylcysteine	0-3	CD8a molecule	Homo sapiens	159-162
22710416-7	2012	NAC successfully blocked the inhibition             of HSP70 and HSP90 as well as the activation of caspase-3, suggesting that ROS             is essential in Cr(VI)-induced caspase-3 activation.	Acetylcysteine	0-3	heat shock protein family A (Hsp70) member 4	Homo sapiens	55-60
23156673-0	2012	N-acetylcysteine enhances neuronal differentiation of P19 embryonic stem cells via Akt and N-cadherin activation.	Acetylcysteine	0-16	cadherin 2	Homo sapiens	91-101
23156673-1	2012	We examined whether N-acetylcysteine (NAC) enhanced embryonic body (EB) formation and neuronal differentiation in terms of EB formation, neuronal marker (microtubule-associated protein 2; MAP-2) expression, and neuron maturation using P19 embryonic stem cells.	Acetylcysteine	20-36	microtubule associated protein 2	Homo sapiens	154-186
23156673-1	2012	We examined whether N-acetylcysteine (NAC) enhanced embryonic body (EB) formation and neuronal differentiation in terms of EB formation, neuronal marker (microtubule-associated protein 2; MAP-2) expression, and neuron maturation using P19 embryonic stem cells.	Acetylcysteine	20-36	microtubule associated protein 2	Homo sapiens	188-193
23156673-1	2012	We examined whether N-acetylcysteine (NAC) enhanced embryonic body (EB) formation and neuronal differentiation in terms of EB formation, neuronal marker (microtubule-associated protein 2; MAP-2) expression, and neuron maturation using P19 embryonic stem cells.	Acetylcysteine	38-41	microtubule associated protein 2	Homo sapiens	154-186
23156673-1	2012	We examined whether N-acetylcysteine (NAC) enhanced embryonic body (EB) formation and neuronal differentiation in terms of EB formation, neuronal marker (microtubule-associated protein 2; MAP-2) expression, and neuron maturation using P19 embryonic stem cells.	Acetylcysteine	38-41	microtubule associated protein 2	Homo sapiens	188-193
23156673-4	2012	Our results suggested that NAC increased EB formation by up-regulating the N-cadherin expression.	Acetylcysteine	27-30	cadherin 2	Homo sapiens	75-85
22790389-12	2012	Concurrent pravastatin or N-acetylcysteine treatment reduced urinary excretion of 8-hydroxy-2"-deoxyguanosine and subsequently decreased LC3-II expression and the number of p62-positive cells compared with the CsA group.	Acetylcysteine	26-42	nucleoporin 62	Mus musculus	173-176
22522044-11	2012	Treatment of infected animals with anti-oxidants alpha-lipoic acid and N-acetylcysteine and HO inhibitor stannous protoporphyrin (SnPPIX) showed only selective beneficial effects on HO-1 and COX-2 expression in the liver and spleen and serum levels of KC and MCP-1.	Acetylcysteine	71-87	chemokine (C-C motif) ligand 2	Mus musculus	259-264
22581648-9	2012	In addition, an antioxidant N-acetylcysteine mimicked the effects of GIP on RAGE and VCAM-1 gene expression in HUVECs.	Acetylcysteine	28-44	long intergenic non-protein coding RNA 914	Homo sapiens	76-80
22472608-8	2012	Administration of N-acetyl-cysteine during hypoxic conditions improved neuronal survival by preventing Ngb oxidation and degradation.	Acetylcysteine	18-35	neuroglobin	Homo sapiens	103-106
22575539-11	2012	N-acetylcysteine, a membrane-permeant cysteine pro-drug, normalized basal zinc levels, reduced TSQ (+) neurons and reduced ischemic neuronal death in the EAAC1(-/-) mice when delivered in a pre-treatment fashion.	Acetylcysteine	0-16	solute carrier family 1 (neuronal/epithelial high affinity glutamate transporter, system Xag), member 1	Mus musculus	154-159
22503982-5	2012	Such discharge of Dectin-1-reactive beta-glucan from macrophage cells was inhibited by either NADPH oxidase inhibitors (apocynin and diphenylene iodonium) or radical scavengers (N-acetyl cysteine and MCI-186).	Acetylcysteine	178-195	C-type lectin domain family 7, member a	Mus musculus	18-26
22343340-14	2012	Treatment with N-acetyl-l-cysteine, a reducing agent, improved NF-kappaB DNA-binding capacity and restored HIF1alpha induction.	Acetylcysteine	15-34	hypoxia inducible factor 1 subunit alpha	Rattus norvegicus	107-116
21986891-5	2012	In conclusion, curcumin, alpha-lipoic acid, and N-acetylcysteine protect rats against CCl(4)-induced liver fibrosis most possibly through their antioxidant activities and their capacities to induce MMP-13 and to inhibit TGF-alpha levels.	Acetylcysteine	48-64	matrix metallopeptidase 13	Rattus norvegicus	198-204
21986891-5	2012	In conclusion, curcumin, alpha-lipoic acid, and N-acetylcysteine protect rats against CCl(4)-induced liver fibrosis most possibly through their antioxidant activities and their capacities to induce MMP-13 and to inhibit TGF-alpha levels.	Acetylcysteine	48-64	transforming growth factor alpha	Rattus norvegicus	220-229
22281495-7	2012	Additionally, siRNA knockdown of CHOP and antioxidant N-acetyl-l-cysteine (NAC) attenuated ER stress-mediated apoptosis.	Acetylcysteine	54-73	X-linked Kx blood group	Homo sapiens	75-78
21975875-8	2012	The ROS scavenger N-acetylcysteine (NAC) or NADPH oxidase inhibitors apocynin and DPI prevented glucose-induced RhoA activation.	Acetylcysteine	18-34	ras homolog family member A	Rattus norvegicus	112-116
21975875-8	2012	The ROS scavenger N-acetylcysteine (NAC) or NADPH oxidase inhibitors apocynin and DPI prevented glucose-induced RhoA activation.	Acetylcysteine	36-39	ras homolog family member A	Rattus norvegicus	112-116
22217266-8	2012	The antioxidant N-acetyl-L-cysteine reduced ROS production and STAT1 activity induced by Ang II, indicating that Ang II uses ROS as a second messenger to regulate STAT1 activity.	Acetylcysteine	16-35	signal transducer and activator of transcription 1	Homo sapiens	63-68
22217266-8	2012	The antioxidant N-acetyl-L-cysteine reduced ROS production and STAT1 activity induced by Ang II, indicating that Ang II uses ROS as a second messenger to regulate STAT1 activity.	Acetylcysteine	16-35	signal transducer and activator of transcription 1	Homo sapiens	163-168
22927877-6	2012	Both DBT and NAC reduced HIF-1alpha gene and protein expression in fibrotic livers, with DBT being more effective.	Acetylcysteine	13-16	hypoxia inducible factor 1 subunit alpha	Rattus norvegicus	25-35
23319348-10	2012	NAC administration also improved hematopoietic differentiation of iPSCs in terms of production of CD34, CD45 and CD43 positive cells.	Acetylcysteine	0-3	protein tyrosine phosphatase receptor type C	Homo sapiens	104-108
22078209-6	2012	The NAC-induced homoaggregation phenotype is paralleled with increased expressions of CD54, CD11a, CD27 and CD38.	Acetylcysteine	4-7	intercellular adhesion molecule 1	Homo sapiens	86-90
22019925-9	2011	In addition, DNA strand breaks were attenuated when cells were pre-treated with N-acetyl-l-cysteine (NAC) and oxidative base modifications were revealed when a lesion specific endonuclease, human 8-hydroxyguanine DNA glycosylase 1 (hOGG1) was introduced into the comet assay.	Acetylcysteine	80-99	X-linked Kx blood group	Homo sapiens	101-104
21985290-3	2011	The HO-1 inhibitor or CO scavenger significantly reversed the inhibitory effect of Alk-8/9 on TNF-alpha expression, whereas N-acetyl-L-cysteine was observed to reduce Alk-8/9-induced HO-1 expression in LPS-treated macrophages.	Acetylcysteine	124-143	activin A receptor, type 1	Mus musculus	167-172
21843499-3	2011	We found that pretreatment of SP600125, an inhibitor of c-Jun N-terminal kinase (JNK), or an anti-oxidant, N-acetylcysteine (NAC), could not only prevent Daxx from trafficking but also increase the number of the surviving CA1 pyramidal cells of hippocampus at 5days of reperfusion.	Acetylcysteine	107-123	death-domain associated protein	Rattus norvegicus	154-158
21843499-3	2011	We found that pretreatment of SP600125, an inhibitor of c-Jun N-terminal kinase (JNK), or an anti-oxidant, N-acetylcysteine (NAC), could not only prevent Daxx from trafficking but also increase the number of the surviving CA1 pyramidal cells of hippocampus at 5days of reperfusion.	Acetylcysteine	125-128	death-domain associated protein	Rattus norvegicus	154-158
21843499-5	2011	We found the treatment of SP600125 or NAC could decrease the activation of Ask1 during ischemia/reperfusion and suppress the assembly of the Fas Daxx Ask1 signaling module, and in succession inhibit JNK activation and c-Jun phosphorylation.	Acetylcysteine	38-41	death-domain associated protein	Rattus norvegicus	145-149
21799126-7	2011	We, therefore, evaluated lung injury and apoptosis in the presence of N-acetyl-cysteine (NAC) in both mouse and cell culture models, and we provide evidence that NAC significantly inhibited lung injury and apoptosis by reducing the production of ROS, activation of JNK, and apoptosis.	Acetylcysteine	162-165	mitogen-activated protein kinase 8	Mus musculus	265-268
21799126-10	2011	NAC protects lung injury and apoptosis by inhibiting ROS-mediated activation of JNK and downstream proapoptotic signaling.	Acetylcysteine	0-3	mitogen-activated protein kinase 8	Mus musculus	80-83
21615215-4	2011	PURPOSE: To examine the effectiveness of conventional or liposome-encapsulated N-acetylcysteine (Lipo-NAC) in ameliorating RTA-induced hepatotoxicity.	Acetylcysteine	79-95	RT1 class I, locus A	Rattus norvegicus	123-126
21615215-8	2011	Treatment of animals with the antioxidant formulations reversed the RTA-induced hepatotoxicity, being most evident following the administration of Lipo-NAC.	Acetylcysteine	152-155	RT1 class I, locus A	Rattus norvegicus	68-71
21615215-9	2011	CONCLUSION: NAC, administered in a liposomal form, may serve as a potentially effective pharmacological agent in the treatment of RTA-induced liver injuries.	Acetylcysteine	12-15	RT1 class I, locus A	Rattus norvegicus	130-133
21782974-6	2011	Conditioned media from GPx1(+/-) SMCs caused increased NF-kappaB activation of quiescent WT SMCs, and this was inhibited by the antioxidant N-acetyl-l-cysteine or by cyclosporine A (CsA).	Acetylcysteine	140-159	glutathione peroxidase 1	Homo sapiens	23-27
21384399-7	2011	Pretreatment with N-acetyl cysteine, a scavenger of reactive oxygen species, suppressed MnCl(2) -induced Nrf2 activation, increase in Nrf2-ARE binding and subsequent upregulation of HO-1 expression.	Acetylcysteine	18-35	heme oxygenase 1	Rattus norvegicus	182-186
21777666-13	2011	Pretreatment of cells with N-acetyl-l-cysteine (NAC) attenuated intracellular ROS generation, the Bax/Bcl-2 protein expression, and apoptosis.	Acetylcysteine	27-46	X-linked Kx blood group	Homo sapiens	48-51
21844206-6	2011	The loss of lymphoid progenitors was likely due the increased levels of ROS in LT-HSCs caused by treatment of Paf(-/-) mice with the anti-oxidant N-acetylcysteine restored lymphoid progenitor numbers to that of Paf(+/+) mice.	Acetylcysteine	146-162	patchy fur	Mus musculus	110-113
21844206-6	2011	The loss of lymphoid progenitors was likely due the increased levels of ROS in LT-HSCs caused by treatment of Paf(-/-) mice with the anti-oxidant N-acetylcysteine restored lymphoid progenitor numbers to that of Paf(+/+) mice.	Acetylcysteine	146-162	patchy fur	Mus musculus	211-214
21424515-4	2011	OBJECTIVE: To evaluate the anti-inflammatory effect of N-acetylcysteine (NAC) on the expression and secretion of inflammatory cytokines and interleukin (IL)-10 in lipopolysaccharide (LPS)-activated THP-1 macrophages under mild oxidative conditions.	Acetylcysteine	55-71	interleukin 10	Homo sapiens	140-159
21424515-4	2011	OBJECTIVE: To evaluate the anti-inflammatory effect of N-acetylcysteine (NAC) on the expression and secretion of inflammatory cytokines and interleukin (IL)-10 in lipopolysaccharide (LPS)-activated THP-1 macrophages under mild oxidative conditions.	Acetylcysteine	73-76	interleukin 10	Homo sapiens	140-159
21424515-8	2011	IL-10 mRNA and protein expression are strongly downregulated in NAC-treated cells, which may further modify the inflammatory cytokine profile.	Acetylcysteine	64-67	interleukin 10	Homo sapiens	0-5
21536676-6	2011	15(S)-HETE induced the production of H(2)O(2) via an NADPH oxidase-dependent manner and its scavengers, N-acetyl cysteine (NAC) and catalase suppressed 15(S)-HETE-stimulated EGFR, Src, Jak2, and STAT3 phosphorylation and MCP-1 expression.	Acetylcysteine	104-121	chemokine (C-C motif) ligand 2	Mus musculus	221-226
25449180-10	2015	Furthermore, NAC restored liver GP and PEPCK expression.	Acetylcysteine	13-16	phosphoenolpyruvate carboxykinase 1	Rattus norvegicus	39-44
25660312-0	2015	Glutathione, N-acetylcysteine and lipoic acid down-regulate starvation-induced apoptosis, RANKL/OPG ratio and sclerostin in osteocytes: involvement of JNK and ERK1/2 signalling.	Acetylcysteine	13-29	tumor necrosis factor receptor superfamily, member 11b (osteoprotegerin)	Mus musculus	96-99
25660312-0	2015	Glutathione, N-acetylcysteine and lipoic acid down-regulate starvation-induced apoptosis, RANKL/OPG ratio and sclerostin in osteocytes: involvement of JNK and ERK1/2 signalling.	Acetylcysteine	13-29	sclerostin	Mus musculus	110-120
25660312-0	2015	Glutathione, N-acetylcysteine and lipoic acid down-regulate starvation-induced apoptosis, RANKL/OPG ratio and sclerostin in osteocytes: involvement of JNK and ERK1/2 signalling.	Acetylcysteine	13-29	mitogen-activated protein kinase 8	Mus musculus	151-154
25147052-5	2015	Antioxidants MCI-186 and N-acetyl cysteine prevented E-FABP"s induction in expression by PAM-LTx, while tert-butyl hydroperoxide increased ROS and E-FABP expression.	Acetylcysteine	25-42	peptidylglycine alpha-amidating monooxygenase	Homo sapiens	89-92
25541714-10	2014	Pretreatment with NAC decreased the levels of intestinal alpha-defensins and plasma I-FABP, as well as lung MPO and cytokines.	Acetylcysteine	18-21	fatty acid binding protein 2, intestinal	Mus musculus	84-90
25541714-10	2014	Pretreatment with NAC decreased the levels of intestinal alpha-defensins and plasma I-FABP, as well as lung MPO and cytokines.	Acetylcysteine	18-21	myeloperoxidase	Mus musculus	108-111
25336634-9	2014	The glutathione level was lower in SelH shRNA than scrambled shRNA HeLa cells, and the H2O2-induced cell death was rescued in the presence of N-acetylcysteine, a glutathione precursor.	Acetylcysteine	142-158	selenoprotein H	Homo sapiens	35-39
24861666-6	2014	In order to mitigate such toxicity, N-acetylcysteine (NAC) was administered before (3 d) and simultaneously with (PhTe)2 (7 d).	Acetylcysteine	36-52	NLR family, pyrin domain containing 1A	Mus musculus	54-57
25264893-0	2014	N-acetylcysteine attenuates ischemia-reperfusion-induced apoptosis and autophagy in mouse liver via regulation of the ROS/JNK/Bcl-2 pathway.	Acetylcysteine	0-16	mitogen-activated protein kinase 8	Mus musculus	122-125
25264893-8	2014	We hypothesized that the mechanism of NAC may involve the ROS/JNK/Bcl-2 pathway.	Acetylcysteine	38-41	mitogen-activated protein kinase 8	Mus musculus	62-65
25264893-13	2014	In addition, JNK, p-JNK, Bax, TNF-alpha, NF-kappaB, IL2, IL6 and levels were also decreased in NAC-treated mice.	Acetylcysteine	95-98	mitogen-activated protein kinase 8	Mus musculus	13-16
25264893-13	2014	In addition, JNK, p-JNK, Bax, TNF-alpha, NF-kappaB, IL2, IL6 and levels were also decreased in NAC-treated mice.	Acetylcysteine	95-98	mitogen-activated protein kinase 8	Mus musculus	20-23
25264893-13	2014	In addition, JNK, p-JNK, Bax, TNF-alpha, NF-kappaB, IL2, IL6 and levels were also decreased in NAC-treated mice.	Acetylcysteine	95-98	BCL2-associated X protein	Mus musculus	25-28
25264893-14	2014	CONCLUSION: NAC can prevent HIRI-induced autophagy and apoptosis by influencing the JNK signal pathway.	Acetylcysteine	12-15	mitogen-activated protein kinase 8	Mus musculus	84-87
24902638-10	2014	Treatment with the antioxidants N-acetylcysteine or ascorbic acid reduced sensitivity to anoikis in human cells and inhibited AA-PCD in yeast cells expressing BRCA2.	Acetylcysteine	32-48	BRCA2 DNA repair associated	Homo sapiens	159-164
25002068-8	2014	N-acetylcysteine suppressed the augmentation of ROS levels and the enhanced expression of COQ2, COQ4, COQ7, and COQ9 induced by oligomycin, but did not modulate the changes in CoQ10 levels.	Acetylcysteine	0-16	coenzyme Q4	Homo sapiens	96-100
25002068-8	2014	N-acetylcysteine suppressed the augmentation of ROS levels and the enhanced expression of COQ2, COQ4, COQ7, and COQ9 induced by oligomycin, but did not modulate the changes in CoQ10 levels.	Acetylcysteine	0-16	coenzyme Q9	Homo sapiens	112-116
25511268-1	2014	OBJECTIVE: To study the protective effects of N-acetylcysteine (NAC) against oxidative injury in the brain tissue of mice induced by decabromodiphenyl ether (PBDE-209) and the expression of mitogen activated protein kinase (MAPK)-related proteins in the hippocampus.	Acetylcysteine	46-62	NLR family, pyrin domain containing 1A	Mus musculus	64-67
25126945-0	2014	Treatment of FANCA cells with resveratrol and N-acetylcysteine: a comparative study.	Acetylcysteine	46-62	FA complementation group A	Homo sapiens	13-18
25126945-5	2014	We have characterized from the structural and biochemical point of view the response of FANCA lymphocytes to N-acetyl-cysteine (NAC) and resveratrol (RV).	Acetylcysteine	109-126	FA complementation group A	Homo sapiens	88-93
25126945-5	2014	We have characterized from the structural and biochemical point of view the response of FANCA lymphocytes to N-acetyl-cysteine (NAC) and resveratrol (RV).	Acetylcysteine	128-131	FA complementation group A	Homo sapiens	88-93
25090113-1	2014	We have previously shown that carboplatin induces inflammation and apoptosis in renal tubular cells (RTCs) through the activation of the nuclear factor of activated T cells-3 (NFAT3) protein by reactive oxygen species (ROS), and that the ROS-mediated activation of NFAT3 is prevented by N-acetyl cysteine and heme oxygenase-1 treatment.	Acetylcysteine	287-304	nuclear factor of activated T cells, cytoplasmic, calcineurin dependent 4	Mus musculus	137-174
25090113-1	2014	We have previously shown that carboplatin induces inflammation and apoptosis in renal tubular cells (RTCs) through the activation of the nuclear factor of activated T cells-3 (NFAT3) protein by reactive oxygen species (ROS), and that the ROS-mediated activation of NFAT3 is prevented by N-acetyl cysteine and heme oxygenase-1 treatment.	Acetylcysteine	287-304	nuclear factor of activated T cells, cytoplasmic, calcineurin dependent 4	Mus musculus	176-181
24913818-7	2014	Excretion of the benzene-derived mercapturic acid was higher in participants who were GSTT1-positive than in the null genotype, irrespective of study arm assignment.	Acetylcysteine	33-49	glutathione S-transferase theta 1	Homo sapiens	86-91
24907397-9	2014	Moreover, N-acetyl-L-cysteine significantly inhibited reactive oxygen/nitrogen species generation, elevated antioxidants levels, inhibited Akt, ERK1/2, tuberin phosphorylation, decreased 8-hydroxydeoxyguanosine accumulation and upregulated 8-oxoG-DNA glycosylase expression.	Acetylcysteine	10-29	TSC complex subunit 2	Homo sapiens	152-159
24718901-8	2014	WA demonstrated induction of N-acetyl-L-cysteine-repressible oxidative stress as measured directly and through a subsequent heat shock response with HSP32 and HSP70 upregulation and decreased HSF1.	Acetylcysteine	29-48	heat shock protein family A (Hsp70) member 4	Homo sapiens	159-164
24909514-10	2014	Pretreatment with N-acetyl-cysteine abrogated the increased sensitivity of RIP3-transfected MCF-7 and MDA-MB-231 cells to parthenolide.	Acetylcysteine	18-35	receptor interacting serine/threonine kinase 3	Homo sapiens	75-79
24959718-5	2014	Application of the antioxidant N-acetyl-L-cysteine (NAC) inhibited H2O2-induced reactive oxygen species (ROS) production and apoptosis, but did not affect EVO-induced apoptosis of COLO205 or HT-29 cells.	Acetylcysteine	31-50	X-linked Kx blood group	Homo sapiens	52-55
24919544-10	2014	N-acetyl-L-cysteine (NAC), a free radical scavenger, also reduced ROS production and AKT phosphorylation, resulting in apoptotic cell death.	Acetylcysteine	0-19	X-linked Kx blood group	Homo sapiens	21-24
24251357-7	2014	In contrast, NAC + GL decreased the biliary excretion of APAP and AG leading to accumulation of APAP in the liver and systemic circulation whereas NAC + SL [multidrug resistance associated 2 (Mrp2) inducer] increased the biliary excretion of AG and decreased the hepatic exposure to APAP and AG.	Acetylcysteine	147-150	ATP binding cassette subfamily C member 2	Rattus norvegicus	192-196
24583029-9	2014	N-acetyl-L-cysteine (NAC), however, did not produce a reduction in viral load or promote expression of HO-1.	Acetylcysteine	0-19	X-linked Kx blood group	Homo sapiens	21-24
23644946-8	2014	NAC lowered serum baseline TBARS levels in controls and increased serum PON1 activity but lowered liver PON1 activities in animals treated with 1 mumol/kg PCB 126, suggesting antioxidant activity by NAC primarily in serum.	Acetylcysteine	0-3	paraoxonase 1	Rattus norvegicus	72-76
23644946-8	2014	NAC lowered serum baseline TBARS levels in controls and increased serum PON1 activity but lowered liver PON1 activities in animals treated with 1 mumol/kg PCB 126, suggesting antioxidant activity by NAC primarily in serum.	Acetylcysteine	0-3	paraoxonase 1	Rattus norvegicus	104-108
23644946-8	2014	NAC lowered serum baseline TBARS levels in controls and increased serum PON1 activity but lowered liver PON1 activities in animals treated with 1 mumol/kg PCB 126, suggesting antioxidant activity by NAC primarily in serum.	Acetylcysteine	0-3	pyruvate carboxylase	Rattus norvegicus	155-158
23644946-8	2014	NAC lowered serum baseline TBARS levels in controls and increased serum PON1 activity but lowered liver PON1 activities in animals treated with 1 mumol/kg PCB 126, suggesting antioxidant activity by NAC primarily in serum.	Acetylcysteine	199-202	pyruvate carboxylase	Rattus norvegicus	155-158
23644946-9	2014	These results also show an unexpected predominantly inverse relationship between Se or NAC and PON1 during control and PCB 126 exposure conditions.	Acetylcysteine	87-90	paraoxonase 1	Rattus norvegicus	95-99
24412703-7	2014	Blocking ROS generation using the antioxidant N-acetyl-l-cysteine abolished the apoptosis and caspase-3 activities induced by POMC gene delivery and hypoxia.	Acetylcysteine	46-65	caspase 3	Mus musculus	94-103
24651440-10	2014	Moreover, the antioxidant N-acetylcysteine prevented phosphorylation of both JNK and c-Jun.	Acetylcysteine	26-42	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	85-90
24361613-6	2014	RESULTS: Compared to saline, Trx or N-acetylcysteine, an intravenous administration of HSA-Trx attenuated the cisplatin-induced elevation in serum creatinine, blood urea nitrogen and urinary N-acetyl-beta-d-glucosaminidase along with the decrease in creatinine clearance.	Acetylcysteine	36-52	thioredoxin 1	Mus musculus	91-94
24431405-8	2014	We also demonstrate that curcumin-mediated caspase-1 activation is oxidant dependent by using N-acetyl-L-cysteine (NAC) to inhibit pyroptosis.	Acetylcysteine	94-113	X-linked Kx blood group	Homo sapiens	115-118
24296245-4	2014	Our results demonstrated that pretreatment with NAC increased protein levels of hypoxia-inducible factor-1alpha (HIF-1alpha), the regulatable subunit of HIF-1, and its target proteins erythropoietin (EPO) and glucose transporter (GLUT)-3, in the ipsilateral hemispheres of rodents subjected to 90min middle cerebral artery occlusion (MCAO) and 24h reperfusion.	Acetylcysteine	48-51	solute carrier family 2 member 3	Homo sapiens	209-237
24296245-6	2014	Suppressing HIF-1 activity with two widely used pharmacological inhibitors, YC-1 and 2ME2, and specific knockout of neuronal HIF-1alpha abolished NAC"s neuroprotective effects.	Acetylcysteine	146-149	RNA binding motif single stranded interacting protein 1	Homo sapiens	76-89
24296245-7	2014	The results also showed that YC-1 and 2ME2 massively enlarged infarcts, indicating that their toxic effect was larger than just abolishing NAC"s neuroprotective effects.	Acetylcysteine	139-142	RNA binding motif single stranded interacting protein 1	Homo sapiens	29-42
24504121-4	2014	Furthermore, long-time N-acetyl-L-cysteine treatment decreases expressions of protein phosphatases, catalytic subunit of protein phosphatase-2A and dual specificity phosphatase 1.	Acetylcysteine	23-42	dual specificity phosphatase 1	Mus musculus	148-178
24105017-4	2014	RESULTS: In patients who received NAC, the serum levels of matrix metalloproteinase (MMP)-9 and MMP-2 after 72 h were significantly lower than those in the placebo group (p = 0.014 and p = 0.045, respectively).	Acetylcysteine	34-37	matrix metallopeptidase 9	Homo sapiens	59-91
24105017-8	2014	CONCLUSION: NAC can be beneficial in preventing early remodeling by reducing the level of MMP-2 and MMP-9.	Acetylcysteine	12-15	matrix metallopeptidase 9	Homo sapiens	100-105
24284796-8	2014	The protection provided by HSS to the SERCA is identical to that observed with N-acetyl-l-cysteine (NAC) and sodium dimercaptopropane sulfonate (Na-DMPS), which are two typical free radical scavengers.	Acetylcysteine	79-98	ATPase sarcoplasmic/endoplasmic reticulum Ca2+ transporting 3	Homo sapiens	38-43
24284796-8	2014	The protection provided by HSS to the SERCA is identical to that observed with N-acetyl-l-cysteine (NAC) and sodium dimercaptopropane sulfonate (Na-DMPS), which are two typical free radical scavengers.	Acetylcysteine	100-103	ATPase sarcoplasmic/endoplasmic reticulum Ca2+ transporting 3	Homo sapiens	38-43
24337227-7	2014	Although the exogenous ROS donor, H(2)O(2), triggered similar degrees of proliferation to CoCl(2), the ROS scavenger, N-acetyl-L-cysteine (NAC), markedly abolished the H(2)O(2)-induced cell proliferation, as opposed to the CoCl(2)-induced proliferation.	Acetylcysteine	118-137	X-linked Kx blood group	Homo sapiens	139-142
24489685-7	2014	Pretreatment of AGS cells with N-acetylcysteine or dithiothreitol attenuated DATS-induced nuclear localization of Nrf2 and the expression of HO-1 and NQO1.	Acetylcysteine	31-47	NAD(P)H dehydrogenase, quinone 1	Mus musculus	150-154
24913775-8	2014	Mechanistically, we show that auranofin-induced VEGFR3 downregulation is blocked by antioxidant N-acetyl-L-cysteine (NAC) and lysosome inhibitor chloroquine, but is promoted by proteasomal inhibitor MG132.	Acetylcysteine	96-115	fms related receptor tyrosine kinase 4	Homo sapiens	48-54
24075930-8	2014	The antioxidant N-acetyl-l-cysteine (NAC) acts synergistically with CAP to reduce ROS generation, without affecting CAP-induced toxicity.	Acetylcysteine	16-35	X-linked Kx blood group	Homo sapiens	37-40
25711080-1	2014	We have shown that antioxidant N-acetylcysteine (NAC, 2-10 mM) quickly (for 2 hours) and completely inactivates the activity of matrix metalloproteinases (gelatinases MMP-2 and MMP-9, and collagenases MMP-1 and MMP-8) secreted by transformed mouse fibroblasts 3T3-SV40 into the medium.	Acetylcysteine	31-47	matrix metallopeptidase 2	Mus musculus	167-172
25711080-1	2014	We have shown that antioxidant N-acetylcysteine (NAC, 2-10 mM) quickly (for 2 hours) and completely inactivates the activity of matrix metalloproteinases (gelatinases MMP-2 and MMP-9, and collagenases MMP-1 and MMP-8) secreted by transformed mouse fibroblasts 3T3-SV40 into the medium.	Acetylcysteine	31-47	matrix metallopeptidase 8	Mus musculus	211-216
25711080-1	2014	We have shown that antioxidant N-acetylcysteine (NAC, 2-10 mM) quickly (for 2 hours) and completely inactivates the activity of matrix metalloproteinases (gelatinases MMP-2 and MMP-9, and collagenases MMP-1 and MMP-8) secreted by transformed mouse fibroblasts 3T3-SV40 into the medium.	Acetylcysteine	49-52	matrix metallopeptidase 2	Mus musculus	167-172
25711080-1	2014	We have shown that antioxidant N-acetylcysteine (NAC, 2-10 mM) quickly (for 2 hours) and completely inactivates the activity of matrix metalloproteinases (gelatinases MMP-2 and MMP-9, and collagenases MMP-1 and MMP-8) secreted by transformed mouse fibroblasts 3T3-SV40 into the medium.	Acetylcysteine	49-52	matrix metallopeptidase 8	Mus musculus	211-216
23993974-4	2013	The current study was undertaken to further assess the role of oxidative stress in TCE-induced autoimmunity by supplementing with an antioxidant N-acetylcysteine (NAC).	Acetylcysteine	145-161	NLR family, pyrin domain containing 1A	Mus musculus	163-166
24244749-7	2013	Acetaldehyde, a metabolic product of alcohol dehydrogenase, induced significant cell death, depolarization of MMP, and caspase-3 activation as ethanol and this damage was also averted by NAC.	Acetylcysteine	187-190	aldo-keto reductase family 1 member A1	Homo sapiens	37-58
21300145-5	2011	Antioxidants, including Tiron, N-acetyl-l-cysteine (NAC) and glutathione (GSH), effectively suppressed the AAI-induced ROS and AAI-elicited genotoxicity, indicating that AAI induced the DNA damage through oxidative stress.	Acetylcysteine	31-50	X-linked Kx blood group	Homo sapiens	52-55
21217061-6	2011	High-glucose-induced upregulation of NQO1, GCLC, and HMOX1 was also prevented by pretreatment with polyethylene glycol (PEG)-catalase or N-acetylcysteine, whereas administration of H(2)O(2) mimicked the effect of high glucose.	Acetylcysteine	137-153	NAD(P)H dehydrogenase, quinone 1	Mus musculus	37-41
21217061-6	2011	High-glucose-induced upregulation of NQO1, GCLC, and HMOX1 was also prevented by pretreatment with polyethylene glycol (PEG)-catalase or N-acetylcysteine, whereas administration of H(2)O(2) mimicked the effect of high glucose.	Acetylcysteine	137-153	glutamate-cysteine ligase, catalytic subunit	Mus musculus	43-47
20667012-6	2011	Pretreatment of Ra2 cells with the antioxidant N-acetylcysteine, the extracellular signal-regulated kinase (ERK) inhibitor PD98059 or the p38 mitogen-activated protein kinase (MAPK) inhibitor SB203580 prevented the HNE-induced increased expression of cPLA(2) and p-cPLA(2).	Acetylcysteine	47-63	phospholipase A2 group IVA	Homo sapiens	251-258
20667012-6	2011	Pretreatment of Ra2 cells with the antioxidant N-acetylcysteine, the extracellular signal-regulated kinase (ERK) inhibitor PD98059 or the p38 mitogen-activated protein kinase (MAPK) inhibitor SB203580 prevented the HNE-induced increased expression of cPLA(2) and p-cPLA(2).	Acetylcysteine	47-63	phospholipase A2 group IVA	Homo sapiens	265-272
20865757-6	2011	Furthermore, our data indicated that 7-AI-b triggers apoptosis through reactive oxygen species (ROS): cellular ROS levels were increased after 3 h exposure of 7-AI-b, which was reversed by the ROS scavenger N-acetyl-L-cysteine.	Acetylcysteine	207-226	ANIB1	Homo sapiens	39-43
20865757-6	2011	Furthermore, our data indicated that 7-AI-b triggers apoptosis through reactive oxygen species (ROS): cellular ROS levels were increased after 3 h exposure of 7-AI-b, which was reversed by the ROS scavenger N-acetyl-L-cysteine.	Acetylcysteine	207-226	ANIB1	Homo sapiens	161-165
20865757-7	2011	As a consequence, 7-AI-b-mediated cell death, mitochondrial transmembrane potential collapse and ATP level were partly blocked by N-acetyl-L-cysteine.	Acetylcysteine	130-149	ANIB1	Homo sapiens	20-24
21190955-6	2011	Furthermore, aldosterone induced similar changes in senescence-associated beta-galactosidase, p21, and SIRT1 expression in cultured human proximal tubular cells, which were normalized by an antioxidant, N-acetyl L-cysteine, or gene silencing of MR. Aldosterone significantly delayed wound healing and reduced the number of proliferating human proximal tubular cells, while gene silencing of p21 diminished the effects, suggesting impaired recovery from tubular damage.	Acetylcysteine	203-222	sirtuin 1	Homo sapiens	103-108
23979599-7	2013	Administration of the antioxidant N-acetylcysteine (NAC) restored structural abnormality of TM tissue in Cyp1b1(-/-) mice.	Acetylcysteine	34-50	cytochrome P450, family 1, subfamily b, polypeptide 1	Mus musculus	105-111
12117417-4	2002	Oocytes expressing LAT1-4F2hc or LAT2-4F2hc demonstrated enhanced uptake of [(14)C]MeHg when administered as the L-cysteine or D,L-homocysteine complexes, but not when administered as the D-cysteine, N -acetyl-L-cysteine, penicillamine or GSH complexes.	Acetylcysteine	200-220	solute carrier family 7 member 5	Homo sapiens	19-23
23979599-7	2013	Administration of the antioxidant N-acetylcysteine (NAC) restored structural abnormality of TM tissue in Cyp1b1(-/-) mice.	Acetylcysteine	52-55	cytochrome P450, family 1, subfamily b, polypeptide 1	Mus musculus	105-111
12117417-4	2002	Oocytes expressing LAT1-4F2hc or LAT2-4F2hc demonstrated enhanced uptake of [(14)C]MeHg when administered as the L-cysteine or D,L-homocysteine complexes, but not when administered as the D-cysteine, N -acetyl-L-cysteine, penicillamine or GSH complexes.	Acetylcysteine	200-220	solute carrier family 3 member 2	Homo sapiens	24-29
23249342-0	2013	Does N-acetylcysteine modulate post-translational modifications of transthyretin in hemodialysis patients?	Acetylcysteine	5-21	transthyretin	Homo sapiens	67-80
12117417-4	2002	Oocytes expressing LAT1-4F2hc or LAT2-4F2hc demonstrated enhanced uptake of [(14)C]MeHg when administered as the L-cysteine or D,L-homocysteine complexes, but not when administered as the D-cysteine, N -acetyl-L-cysteine, penicillamine or GSH complexes.	Acetylcysteine	200-220	solute carrier family 3 member 2	Homo sapiens	38-43
23249342-2	2013	Therefore, we analyzed NAC-induced modifications of the protein transthyretin (TTR) in plasma of hemodialysis patients in a randomized, placebo-controlled study.	Acetylcysteine	23-26	transthyretin	Homo sapiens	64-77
23249342-2	2013	Therefore, we analyzed NAC-induced modifications of the protein transthyretin (TTR) in plasma of hemodialysis patients in a randomized, placebo-controlled study.	Acetylcysteine	23-26	transthyretin	Homo sapiens	79-82
21069346-0	2011	Pre-treatment with N-acetylcysteine upregulates superoxide dismutase 2 and catalase genes in cadmium-induced oxidative stress in the chick omphalocele model.	Acetylcysteine	19-35	catalase	Gallus gallus	75-83
21069346-14	2011	In addition, gene expression levels of SOD2 and CAT were significantly increased in NAC + Cd(-) as compared to Cd(+) and NAC + Cd(+) (p &lt; 0.05 vs. controls).	Acetylcysteine	84-87	superoxide dismutase 2, mitochondrial	Gallus gallus	39-43
12237255-9	2002	4 Antioxidants (pyrrolidine dithiocarbamate and N-acetyl-L-cysteine) inhibited GPI-80 release by TNF-alpha stimulation, but superoxide dismutase did not.	Acetylcysteine	48-67	vanin 2	Homo sapiens	79-85
21069346-14	2011	In addition, gene expression levels of SOD2 and CAT were significantly increased in NAC + Cd(-) as compared to Cd(+) and NAC + Cd(+) (p &lt; 0.05 vs. controls).	Acetylcysteine	84-87	catalase	Gallus gallus	48-51
21069346-14	2011	In addition, gene expression levels of SOD2 and CAT were significantly increased in NAC + Cd(-) as compared to Cd(+) and NAC + Cd(+) (p &lt; 0.05 vs. controls).	Acetylcysteine	121-124	superoxide dismutase 2, mitochondrial	Gallus gallus	39-43
21069346-16	2011	Increased immunoreactivity of SOD2 and CAT was also observed in NAC + Cd(-) as compared to Cd(+) and NAC + Cd(+).	Acetylcysteine	64-67	superoxide dismutase 2, mitochondrial	Gallus gallus	30-34
21069346-16	2011	Increased immunoreactivity of SOD2 and CAT was also observed in NAC + Cd(-) as compared to Cd(+) and NAC + Cd(+).	Acetylcysteine	64-67	catalase	Gallus gallus	39-42
21980400-8	2011	N-acetyl-L-cysteine, a scavenger of ROS, inhibited hypoxia-induced ROS generation, PI3K, ERK and Rac1 activation as well as HIF-1alpha expression.	Acetylcysteine	0-19	Rac family small GTPase 1	Homo sapiens	97-101
21203535-9	2010	Accompanied with the hemodynamic improvement, NAC-treated piglets had significantly lower plasma cardiac troponin-I, myocardial lipid hydroperoxides, activated caspase-3 and lactate levels (vs. H-R controls).	Acetylcysteine	46-49	troponin I, cardiac muscle	Sus scrofa	97-115
24098333-6	2013	Moreover, the NAC treatment significantly reduced the enhanced aggregation of p62 and Mallory-Denk bodies in the DEN-induced HCC liver tissue, suggesting that NAC treatment improves the suppressive autophagic flux in the TLR2-deficient liver.	Acetylcysteine	14-17	nucleoporin 62	Mus musculus	78-81
24098333-6	2013	Moreover, the NAC treatment significantly reduced the enhanced aggregation of p62 and Mallory-Denk bodies in the DEN-induced HCC liver tissue, suggesting that NAC treatment improves the suppressive autophagic flux in the TLR2-deficient liver.	Acetylcysteine	159-162	nucleoporin 62	Mus musculus	78-81
23850346-10	2013	Moreover, the results of reactive oxygen species (ROS) scavenging by N-acetyl cysteine (NAC) indicated that ROS were required in the Nox4-mediated upregulation of ADAM17 expression.	Acetylcysteine	69-86	ADAM metallopeptidase domain 17	Homo sapiens	163-169
23850346-10	2013	Moreover, the results of reactive oxygen species (ROS) scavenging by N-acetyl cysteine (NAC) indicated that ROS were required in the Nox4-mediated upregulation of ADAM17 expression.	Acetylcysteine	88-91	ADAM metallopeptidase domain 17	Homo sapiens	163-169
20920557-5	2010	The same results were obtained in the cells treated with N-acetyl-L-cysteine, suggesting that the prolonged activation of JNK and p38 by ISA is mediated by reactive oxygen species generated from mitochondria.	Acetylcysteine	57-76	annexin A13	Homo sapiens	137-140
12242087-5	2002	Pepstatin A restored DNA synthesis of stellate cells stimulated by either platelet-derived growth factor-BB (PDGF-BB) or insulin-like growth factor-I (IGF-I), an effect that was attenuated by N-acetyl-L-cysteine.	Acetylcysteine	192-211	insulin-like growth factor 1	Rattus norvegicus	121-149
20718735-7	2010	Additionally, NAC blocked NFAT3 activation by inhibition of NADPH oxidase activation, and ERK/JNK and PKC pathways, resulting in a decrease in cell apoptosis; the therapeutic effect of NAC was verified in vivo.	Acetylcysteine	14-17	nuclear factor of activated T cells, cytoplasmic, calcineurin dependent 4	Mus musculus	26-31
20718735-7	2010	Additionally, NAC blocked NFAT3 activation by inhibition of NADPH oxidase activation, and ERK/JNK and PKC pathways, resulting in a decrease in cell apoptosis; the therapeutic effect of NAC was verified in vivo.	Acetylcysteine	185-188	nuclear factor of activated T cells, cytoplasmic, calcineurin dependent 4	Mus musculus	26-31
23900080-4	2013	This phenomenon was potentiated in radiation-treated EB1-knockdown cells and was largely blocked by N-acetyl-L-cysteine, a scavenger of ROS.	Acetylcysteine	100-119	microtubule associated protein RP/EB family member 1	Homo sapiens	53-56
23732519-9	2013	Pretreatments with VEGF, VEGF-B, or the antioxidant N-acetylcysteine (NAC) rescued SU1498 or siRNA-treated neurons from the mitochondrial dysfunction and oxidative stress induced by VEGFR-2 inhibition in a timely fashion.	Acetylcysteine	52-68	kinase insert domain receptor	Homo sapiens	182-189
20718735-7	2010	Additionally, NAC blocked NFAT3 activation by inhibition of NADPH oxidase activation, and ERK/JNK and PKC pathways, resulting in a decrease in cell apoptosis; the therapeutic effect of NAC was verified in vivo.	Acetylcysteine	185-188	mitogen-activated protein kinase 8	Mus musculus	94-97
12242087-5	2002	Pepstatin A restored DNA synthesis of stellate cells stimulated by either platelet-derived growth factor-BB (PDGF-BB) or insulin-like growth factor-I (IGF-I), an effect that was attenuated by N-acetyl-L-cysteine.	Acetylcysteine	192-211	insulin-like growth factor 1	Rattus norvegicus	151-156
12242087-6	2002	This agent induced the recovery of both the expression of PDGF receptor beta and IGF-I receptor beta and the phosphorylation of p42/44 mitogen-activated protein kinase (MAPK) and Akt under stimulation with either PDGF-BB or IGF-I, which were downregulated by N-acetyl-L-cysteine.	Acetylcysteine	259-278	insulin-like growth factor 1	Rattus norvegicus	224-229
12095135-7	2002	A dose response inhibition of both TNF and PCA production was demonstrated after both NAC and BHA pretreatment but not with VC, Trolox, or SOD.	Acetylcysteine	86-89	tumor necrosis factor	Oryctolagus cuniculus	35-38
20508647-9	2010	The addition of N-acetyl-L-cysteine (ROS scavenger) to As(2)O(3)-treated cells reversed changes in SnoN protein and the autophagic/apoptotic response.	Acetylcysteine	16-35	SKI like proto-oncogene	Homo sapiens	99-103
20388917-8	2010	In the NAC group, the levels of ALP, GGT, WBC, CRP, and NE% decreased significantly (P &lt; .001), whereas a significant decrease did not occur in the placebo group.	Acetylcysteine	7-10	inactive glutathione hydrolase 2	Homo sapiens	37-40
23782487-9	2013	In patients with detectable IL-17 concentrations on admission, 78% of those who received NAC vs. 44% of those who received placebo had undetectable levels by day 3-5 (P = 0.042), and the mean decrease in IL-17 concentrations between admission and late samples was significantly greater in patients who received NAC vs. placebo (P = 0.045).	Acetylcysteine	89-92	interleukin 17A	Homo sapiens	28-33
23782487-9	2013	In patients with detectable IL-17 concentrations on admission, 78% of those who received NAC vs. 44% of those who received placebo had undetectable levels by day 3-5 (P = 0.042), and the mean decrease in IL-17 concentrations between admission and late samples was significantly greater in patients who received NAC vs. placebo (P = 0.045).	Acetylcysteine	89-92	interleukin 17A	Homo sapiens	204-209
23782487-10	2013	CONCLUSIONS: N-acetylcysteine (NAC) may improve transplant-free survival in patients with non-acetaminophen ALF by ameliorating the production of IL-17, which is associated with progression of hepatic encephalopathy and poor outcome.	Acetylcysteine	13-29	interleukin 17A	Homo sapiens	146-151
23782487-10	2013	CONCLUSIONS: N-acetylcysteine (NAC) may improve transplant-free survival in patients with non-acetaminophen ALF by ameliorating the production of IL-17, which is associated with progression of hepatic encephalopathy and poor outcome.	Acetylcysteine	31-34	interleukin 17A	Homo sapiens	146-151
23640046-14	2013	Our results indicate that NAC blocked CAPE-mediated AKT/XIAP inhibition and protected the cells from apoptosis.	Acetylcysteine	26-29	X-linked inhibitor of apoptosis	Homo sapiens	56-60
12095135-8	2002	In addition, northern blots revealed inhibition of TNF mRNA production by both NAC and BHA.	Acetylcysteine	79-82	tumor necrosis factor	Oryctolagus cuniculus	51-54
20810184-0	2010	Oral N-acetylcysteine rescues lethality of hepatocyte-specific Gclc-knockout mice, providing a model for hepatic cirrhosis.	Acetylcysteine	5-21	glutamate-cysteine ligase, catalytic subunit	Mus musculus	63-67
23666527-0	2013	Efficacy of N-acetylcysteine in phenotypic suppression of mouse models of Niemann-Pick disease, type C1.	Acetylcysteine	12-28	NPC1 like intracellular cholesterol transporter 1	Mus musculus	74-103
11994482-8	2002	Oxidant stress related to shock/resuscitation appeared to contribute to the regulation of TLR4 mRNA, because supplementation of the resuscitation fluid with the antioxidant N-acetylcysteine reversed the ability of shock/resuscitation to preserve TLR4 mRNA levels following LPS.	Acetylcysteine	173-189	toll like receptor 4	Homo sapiens	90-94
23109061-8	2013	Treatment with N-acetylcysteine and deferoxamine prevented both the memory deficit and the increase in the BDNF levels induced by BCAA administration.	Acetylcysteine	15-31	brain-derived neurotrophic factor	Rattus norvegicus	107-111
20810184-5	2010	RESULTS: Gclc(h/h) mice were rescued by use of NAC supplementation, and survived until adulthood.	Acetylcysteine	47-50	glutamate-cysteine ligase, catalytic subunit	Mus musculus	9-13
20810184-10	2010	Thus, with NAC supplementation, Gclc(h/h) mice provide a model for the development of liver fibrosis and cirrhosis.	Acetylcysteine	11-14	glutamate-cysteine ligase, catalytic subunit	Mus musculus	32-36
20815781-4	2010	In contrast, reducing chemicals, such as dithiothreitol, 2,3-dimercapto-1-propanol and N-acetylcysteine inhibited CD11b expression.	Acetylcysteine	87-103	integrin subunit alpha M	Homo sapiens	114-119
11994482-8	2002	Oxidant stress related to shock/resuscitation appeared to contribute to the regulation of TLR4 mRNA, because supplementation of the resuscitation fluid with the antioxidant N-acetylcysteine reversed the ability of shock/resuscitation to preserve TLR4 mRNA levels following LPS.	Acetylcysteine	173-189	toll like receptor 4	Homo sapiens	246-250
20638463-3	2010	We conducted a study to determine whether N-Acetyl-cysteine (NAC) protected men against noise-induced temporary threshold shift (TTS), and whether subgroups with genetic polymorphisms of glutathione S-transferase (GST) T1 and M1 responded to NAC differently.	Acetylcysteine	242-245	glutathione S-transferase theta 1	Homo sapiens	187-228
11982744-3	2002	We investigated the effect of the antioxidant N-acetylcysteine on the expression of the class A scavenger receptor (SR-A) types I and II in human macrophages.	Acetylcysteine	46-62	macrophage scavenger receptor 1	Homo sapiens	116-120
20638463-11	2010	When the participants were grouped by GST M1/T1 genotypes, the NAC effect was only significant among workers with null genotypes in both GSTM1 and GSTT1 (p = 0.004).	Acetylcysteine	63-66	glutathione S-transferase theta 1	Homo sapiens	147-152
20638463-13	2010	The protective effect of NAC was more prominent in subjects with both GSTM1-null and GSTT1-null genotypes.	Acetylcysteine	25-28	glutathione S-transferase theta 1	Homo sapiens	85-90
23424090-0	2013	Studies of the metabotropic glutamate receptor 5 radioligand [11C]ABP688 with N-acetylcysteine challenge in rhesus monkeys.	Acetylcysteine	78-94	glutamate metabotropic receptor 5	Macaca mulatta	15-48
23731375-9	2013	Erythrocyte G6PD activity was significantly elevated in workers receiving 200, 400, and 800 mg of NAC compared to those in baseline by 24%, 14%, and 14%, respectively.	Acetylcysteine	98-101	glucose-6-phosphate dehydrogenase	Homo sapiens	12-16
11982744-6	2002	RESULTS: Incubation of monocytes and monocyte-derived macrophages with N-acetylcysteine decreased both SR-A I and II mRNA expression.	Acetylcysteine	71-87	macrophage scavenger receptor 1	Homo sapiens	103-107
20633688-12	2010	Expression of Runx2 was upregulated by Ox-LDL and H(2)O(2), and these effects were suppressed by NAC pretreatment.	Acetylcysteine	97-100	RUNX family transcription factor 2	Bos taurus	14-19
11982744-7	2002	N-Acetylcysteine also reduced SR-A mRNA in lesion-derived cells.	Acetylcysteine	0-16	macrophage scavenger receptor 1	Homo sapiens	30-34
20557081-10	2010	Additionally, pretreatment of Huh7 cells with antioxidants ascorbic acid and N-acetyl cysteine markedly attenuated the MAA-induced apoptosis by upregulation of Bax, Bak, and PUMA, mitochondrial translocation of cofilin, activation of caspase-3, and cell death.	Acetylcysteine	77-94	BCL2 antagonist/killer 1	Homo sapiens	165-168
23163860-5	2013	Pretreatment with antioxidant N-acetyl-l-cysteine (NAC) and ERK inhibitor PD98059, but not NF-kappaB inhibitor Bay 11-7082, JNK inhibitor SP600125, p38 MAPK inhibitor SB203580, and PI3-K inhibitor LY294002, significantly reduced arecoline-induced PlGF protein synthesis.	Acetylcysteine	30-49	X-linked Kx blood group	Homo sapiens	51-54
11982744-10	2002	CONCLUSIONS: Our results imply that N-acetylcysteine leads to a decrease in SR-A mRNA and initially also to an attenuated uptake of modified lipoproteins.	Acetylcysteine	36-52	macrophage scavenger receptor 1	Homo sapiens	76-80
20138851-8	2010	In addition, co-treatment of the Bv-2 cells with LPS and NAC surprisingly further increased the iNOS expression, an effect also found to be mediated through the JNK MAPK pathway.	Acetylcysteine	57-60	mitogen-activated protein kinase 8	Mus musculus	161-164
12086016-6	2002	However, such severe cell death was effectively (approximately 85%) prevented with N-acetylcysteine (NAC), a precursor of reduced glutathione (GSH) that is an essential cofactor for Gly-I, accompanied by the intact Gly-I and G3PDH activities.	Acetylcysteine	83-99	glyoxalase I	Homo sapiens	182-187
20138851-9	2010	The level of phosphorylated JNK MAPK (p46) was strongly increased by LPS alone and was further increased when combined with NAC.	Acetylcysteine	124-127	mitogen-activated protein kinase 8	Mus musculus	28-31
23568032-5	2013	Mechanistically, the lack of Cyp1B1 was associated with increased oxidative stress and sustained NF-kappaB activation, which was reversed by the antioxidant N-acetylcysteine.	Acetylcysteine	157-173	cytochrome P450, family 1, subfamily b, polypeptide 1	Mus musculus	29-35
12086016-6	2002	However, such severe cell death was effectively (approximately 85%) prevented with N-acetylcysteine (NAC), a precursor of reduced glutathione (GSH) that is an essential cofactor for Gly-I, accompanied by the intact Gly-I and G3PDH activities.	Acetylcysteine	83-99	glyoxalase I	Homo sapiens	215-220
12086016-6	2002	However, such severe cell death was effectively (approximately 85%) prevented with N-acetylcysteine (NAC), a precursor of reduced glutathione (GSH) that is an essential cofactor for Gly-I, accompanied by the intact Gly-I and G3PDH activities.	Acetylcysteine	101-104	glyoxalase I	Homo sapiens	182-187
12086016-6	2002	However, such severe cell death was effectively (approximately 85%) prevented with N-acetylcysteine (NAC), a precursor of reduced glutathione (GSH) that is an essential cofactor for Gly-I, accompanied by the intact Gly-I and G3PDH activities.	Acetylcysteine	101-104	glyoxalase I	Homo sapiens	215-220
19833500-0	2010	Near-infrared luminescence quenching method for the detection of phenolic compounds using N-acetyl-L-cysteine-protected gold nanoparticles-tyrosinase hybrid material.	Acetylcysteine	90-109	tyrosinase	Homo sapiens	139-149
11814408-6	2002	Induction of uPAR surface expression by microglia was inhibited by the antioxidant N-acetyl-cysteine, indicating that this gene may be induced as a result of oxidative stress-related mechanisms.	Acetylcysteine	83-100	plasminogen activator, urokinase receptor	Homo sapiens	13-17
19833500-1	2010	A rapid and simple near-infrared (NIR) luminescence quenching method for the detection of phenolic compounds based on combining the unique property of N-acetyl-L-cysteine-protected gold nanoparticles (NAC-AuNPs) and tyrosinase (Tyr) enzymatic reactions is described.	Acetylcysteine	151-170	tyrosinase	Homo sapiens	228-231
20054154-7	2010	Co-administration of N-Acetylcysteine (NAC) exerted a strong protective effect against CdCl(2) induced barrier damage and stress related genes, while other antioxidants only attenuated CdCl(2) induced HSP70 and HMOX-1 and showed no protective effect on the barrier collapse.	Acetylcysteine	21-37	heat shock protein family A (Hsp70) member 4	Homo sapiens	201-206
23478644-0	2013	N-acetyl-cysteine prevents pyramidal cell disarray and reelin-immunoreactive neuron deficiency in CA3 after prenatal immune challenge in rats.	Acetylcysteine	0-17	carbonic anhydrase 3	Rattus norvegicus	98-101
23478644-9	2013	These disorders, more pronounced in the CA3 area, were prevented by NAC.	Acetylcysteine	68-71	carbonic anhydrase 3	Rattus norvegicus	40-43
23583403-6	2013	The inhibitory effect of SFN on the interaction of LPS and MD2 was reversed by thiol supplementation with N-acetyl-L-cysteine or dithiothreitol showing that the inhibitory effect of SFN is dependent on its thiol-modifying activity.	Acetylcysteine	106-125	lymphocyte antigen 96	Homo sapiens	59-62
19879309-5	2010	N-acetylcysteine (NAC) and GaE prevented both the MeHg-induced cytotoxic effects on leukocytes according to MTT and AB assays and the effects on the ADA activity.	Acetylcysteine	0-16	adenosine deaminase	Homo sapiens	149-152
19879309-5	2010	N-acetylcysteine (NAC) and GaE prevented both the MeHg-induced cytotoxic effects on leukocytes according to MTT and AB assays and the effects on the ADA activity.	Acetylcysteine	18-21	adenosine deaminase	Homo sapiens	149-152
19885844-7	2010	AGEs-activated EGFR and ERK1/2 were attenuated by an anti-oxidant (NAC) and an EGFR inhibitor (Iressa).	Acetylcysteine	67-70	epidermal growth factor receptor	Rattus norvegicus	15-19
11511177-2	2001	We investigated the first step in the degradation of CA-SG to the mercapturic acid conjugate, clofibryl-S-acyl-N-acetylcysteine (CA-SNAC), which is catalyzed by gamma-glutamyltranspeptidase (gamma-GT).	Acetylcysteine	66-82	gamma-glutamyltransferase 1	Rattus norvegicus	161-189
19722195-6	2010	Furthermore, the PERK-ATF4 pathway, which also induces the expression of CHOP, was activated in NAC-treated cells.	Acetylcysteine	96-99	activating transcription factor 4	Homo sapiens	22-26
20360623-0	2010	N-acetylcysteine inhibits IL-8 and MMP-9 release and ICAM-1 expression by bronchoalveolar cells from interstitial lung disease patients.	Acetylcysteine	0-16	matrix metallopeptidase 9	Homo sapiens	35-40
20360623-0	2010	N-acetylcysteine inhibits IL-8 and MMP-9 release and ICAM-1 expression by bronchoalveolar cells from interstitial lung disease patients.	Acetylcysteine	0-16	intercellular adhesion molecule 1	Homo sapiens	53-59
20360623-7	2010	NAC exerted a dose-dependent inhibitory effect on IL-8 and MMP-9 release and ICAM- expression by BAL macrophages and lymphocytes from patients with IPF and sarcoidosis.	Acetylcysteine	0-3	matrix metallopeptidase 9	Homo sapiens	59-64
23648861-1	2013	We have previously reported that N-acetylcysteine (NAC) not only delayed apoptosis but also enhanced the production of recombinant erythropoietin (EPO) in Chinese hamster ovary (CHO) cell culture.	Acetylcysteine	33-49	erythropoietin	Cricetulus griseus	131-145
23648861-1	2013	We have previously reported that N-acetylcysteine (NAC) not only delayed apoptosis but also enhanced the production of recombinant erythropoietin (EPO) in Chinese hamster ovary (CHO) cell culture.	Acetylcysteine	33-49	erythropoietin	Cricetulus griseus	147-150
23648861-1	2013	We have previously reported that N-acetylcysteine (NAC) not only delayed apoptosis but also enhanced the production of recombinant erythropoietin (EPO) in Chinese hamster ovary (CHO) cell culture.	Acetylcysteine	51-54	erythropoietin	Cricetulus griseus	131-145
23648861-1	2013	We have previously reported that N-acetylcysteine (NAC) not only delayed apoptosis but also enhanced the production of recombinant erythropoietin (EPO) in Chinese hamster ovary (CHO) cell culture.	Acetylcysteine	51-54	erythropoietin	Cricetulus griseus	147-150
23518073-7	2013	Pretreatment with the anti-oxidant N-acetylcysteine (NAC) inhibited B4-mediated effects, including cytotoxicity, ROS production, mitochondrial membrane depolarization increase in intracellular Ca2+, cytochrome c release, PARP cleavage, and AIF translocation.	Acetylcysteine	35-51	apoptosis inducing factor mitochondria associated 1	Homo sapiens	240-243
23518073-7	2013	Pretreatment with the anti-oxidant N-acetylcysteine (NAC) inhibited B4-mediated effects, including cytotoxicity, ROS production, mitochondrial membrane depolarization increase in intracellular Ca2+, cytochrome c release, PARP cleavage, and AIF translocation.	Acetylcysteine	53-56	apoptosis inducing factor mitochondria associated 1	Homo sapiens	240-243
19755521-6	2009	Apocynin, an NAD(P)H oxidase inhibitor, and N-acetyl cysteine (NAC), an ROS scavenger, both inhibited EGFR transactivation induced by U-II.	Acetylcysteine	44-61	epidermal growth factor receptor	Rattus norvegicus	102-106
19755521-6	2009	Apocynin, an NAD(P)H oxidase inhibitor, and N-acetyl cysteine (NAC), an ROS scavenger, both inhibited EGFR transactivation induced by U-II.	Acetylcysteine	63-66	epidermal growth factor receptor	Rattus norvegicus	102-106
23434081-8	2013	The levels of inflammatory cytokines (TNF-alpha, IL-1beta, IL-6, and IL-10) in piglet plasma of the NAC group (mixed feeding concentration of 1200 mg/kg) were significantly lower at 3h after LPS stimulation (P&lt;0.05).	Acetylcysteine	100-103	interleukin 10	Homo sapiens	69-74
11511177-2	2001	We investigated the first step in the degradation of CA-SG to the mercapturic acid conjugate, clofibryl-S-acyl-N-acetylcysteine (CA-SNAC), which is catalyzed by gamma-glutamyltranspeptidase (gamma-GT).	Acetylcysteine	66-82	gamma-glutamyltransferase 1	Rattus norvegicus	191-199
23407882-7	2013	Both NAC and DPI suppressed indoxyl sulfate-induced expression of NF-kappaB p65 and CREB.	Acetylcysteine	5-8	cAMP responsive element binding protein 1	Homo sapiens	84-88
11511177-13	2001	These in vitro and in vivo experiments indicate that gamma-GT mediated degradation of clofibryl-S-acyl-glutathione leads primarily to the formation and excretion of clofibryl-N-acyl-cysteine products rather than the S-acyl-NAC conjugate.	Acetylcysteine	223-226	gamma-glutamyltransferase 1	Rattus norvegicus	53-61
23353715-10	2013	Interestingly, NAC almost completely prevented the Cd-induced elevation of C/EBP homologous protein (CHOP) and phosphorylation of c-Jun N-terminal kinase (JNK), two components of the ER stress-mediated apoptotic pathway.	Acetylcysteine	15-18	mitogen-activated protein kinase 8	Mus musculus	130-153
11488539-9	2001	N-acetyl-cysteine, an antioxidant, also prevented A beta-induced cell death.	Acetylcysteine	0-17	amyloid beta (A4) precursor protein	Mus musculus	50-56
23353715-10	2013	Interestingly, NAC almost completely prevented the Cd-induced elevation of C/EBP homologous protein (CHOP) and phosphorylation of c-Jun N-terminal kinase (JNK), two components of the ER stress-mediated apoptotic pathway.	Acetylcysteine	15-18	mitogen-activated protein kinase 8	Mus musculus	155-158
19747897-6	2009	Further, this required cellular production of ROS; treatment with either N-acetyl-Cysteine (anti-oxidant) or Rotenone (inhibitor of mitochondrial respiration) inhibited nuclear accumulation of TPPII.	Acetylcysteine	73-90	tripeptidyl peptidase 2	Homo sapiens	193-198
19615393-11	2009	NAC co-treatment restored follicle growth and expression of Ccnd2 and Cdk4.	Acetylcysteine	0-3	cyclin D2	Mus musculus	60-65
23254439-10	2013	Z-VAD and N-acetyl cysteine (NAC; a well-known antioxidant) attenuated apoptotic cell death and GSH depletion in H(2)O(2)-treated CPAECs.	Acetylcysteine	10-27	X-linked Kx blood group	Homo sapiens	29-32
19269634-6	2009	NAD(P)H oxidase inhibitor apocynin and ROS scavenger N-acetylcysteine (NAC) inhibited the EGFR transactivation induced by U-II.	Acetylcysteine	53-69	epidermal growth factor receptor	Rattus norvegicus	90-94
11385283-9	2001	Inhibitors of NF-kappa B activation such as N-acetylcysteine or N-tosyl-L-phenylalanine chloromethyl ketone can suppress Fc epsilon RI-induced TNF-alpha and MCP-1 release.	Acetylcysteine	44-60	C-C motif chemokine ligand 2	Homo sapiens	157-162
19269634-6	2009	NAD(P)H oxidase inhibitor apocynin and ROS scavenger N-acetylcysteine (NAC) inhibited the EGFR transactivation induced by U-II.	Acetylcysteine	71-74	epidermal growth factor receptor	Rattus norvegicus	90-94
23159886-7	2013	Similarly, MB and/or PQ-mediated histopathological symptoms and changes in the catalytic activities/expressions of CYP1A2, CYP2E1, iNOS, TNF-alpha, and IL-1beta were alleviated by NAC and SIL.	Acetylcysteine	180-183	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	115-121
11237717-5	2001	Homocysteine, an atherogenic substance believed to exert its effects through oxidative stress, enhanced endothelial LOX-1 gene expression, which was suppressed by N-acetylcysteine.	Acetylcysteine	163-179	oxidized low density lipoprotein receptor 1	Rattus norvegicus	116-121
23811559-1	2013	This study aimed to show if two different sulphur containing drugs sulbutiamine and acetylcysteine (NAC) could attenuate the effects of two different insults being serum deprivation and glutamate/buthionine sulfoximine (GB)-induced death to transformed retinal ganglion cell line (RGC-5) in culture.	Acetylcysteine	84-98	NLR family, pyrin domain containing 1A	Mus musculus	100-103
23853776-0	2013	Antioxidant N-acetylcysteine attenuates the reduction of Brg1 protein expression in the myocardium of type 1 diabetic rats.	Acetylcysteine	12-28	SWI/SNF related, matrix associated, actin dependent regulator of chromatin, subfamily a, member 4	Rattus norvegicus	57-61
23853776-3	2013	We hypothesize that cardiac Brg1 expression is reduced in diabetes which can be restored by antioxidant treatment with N-acetylcysteine (NAC).	Acetylcysteine	119-135	SWI/SNF related, matrix associated, actin dependent regulator of chromatin, subfamily a, member 4	Rattus norvegicus	28-32
23853776-3	2013	We hypothesize that cardiac Brg1 expression is reduced in diabetes which can be restored by antioxidant treatment with N-acetylcysteine (NAC).	Acetylcysteine	137-140	SWI/SNF related, matrix associated, actin dependent regulator of chromatin, subfamily a, member 4	Rattus norvegicus	28-32
23853776-7	2013	NAC normalized tissue and plasma levels of 15-F2t-isoprostane, significantly increased cardiac Brg1, HO-1 and p-STAT3 protein expression levels and reduced TNF-alpha and IL-6, resulting in improved cardiac function.	Acetylcysteine	0-3	SWI/SNF related, matrix associated, actin dependent regulator of chromatin, subfamily a, member 4	Rattus norvegicus	95-99
23853776-7	2013	NAC normalized tissue and plasma levels of 15-F2t-isoprostane, significantly increased cardiac Brg1, HO-1 and p-STAT3 protein expression levels and reduced TNF-alpha and IL-6, resulting in improved cardiac function.	Acetylcysteine	0-3	heme oxygenase 1	Rattus norvegicus	101-111
23853776-8	2013	In conclusion, myocardial Brg1 is reduced in diabetes and enhancement of cardiac Brg1 expression may represent a novel mechanism whereby NAC confers cardioprotection.	Acetylcysteine	137-140	SWI/SNF related, matrix associated, actin dependent regulator of chromatin, subfamily a, member 4	Rattus norvegicus	26-30
19693275-7	2009	Indeed, curcumin caused nuclear translocation of AIF, which could be blocked by the antioxidant N-acetyl cysteine.	Acetylcysteine	96-113	apoptosis inducing factor mitochondria associated 1	Homo sapiens	49-52
19601628-5	2009	The antioxidant N-acetyl-l-cysteine (NAC) significantly reduced ROS production and EGCG-induced apoptosis, suggesting that ROS plays a key role in EGCG-induced apoptosis in hepatocarcinoma SMMC7721 cells.	Acetylcysteine	16-35	X-linked Kx blood group	Homo sapiens	37-40
19034653-8	2009	However, NAC significantly decreased colonic MPO activity, ROS, TNF-alpha and IL-1 beta levels and increased PON1 activity and GSH concentration.	Acetylcysteine	9-12	myeloperoxidase	Mus musculus	45-48
22824136-5	2013	In rat primary hippocampal cultures, we found that N-acetylcysteine (NAC) prevented PILO-mediated thiol oxidation, apoptosis, cell death and NR2B subunit over-expression.	Acetylcysteine	51-67	glutamate ionotropic receptor NMDA type subunit 2B	Rattus norvegicus	141-145
11171043-9	2001	H(2)O(2) also activated the CdRE-binding activity, and pretreatment with N-acetyl-L-cysteine, which replenishes the intracellular levels of GSH, suppressed, in TS-treated cells, both the CdRE-binding activity and the increased HO-1 expression.	Acetylcysteine	73-92	heme oxygenase 1	Homo sapiens	227-231
22824136-5	2013	In rat primary hippocampal cultures, we found that N-acetylcysteine (NAC) prevented PILO-mediated thiol oxidation, apoptosis, cell death and NR2B subunit over-expression.	Acetylcysteine	69-72	glutamate ionotropic receptor NMDA type subunit 2B	Rattus norvegicus	141-145
23536773-1	2013	BACKGROUND: The aim of this study was to investigate the molecular mechanisms involved in the production of Th1 cytokines, namely IL-12 and IL-27, when the intra-macrophage redox state was altered by different chemical entities such as GSH-C4, which is reduced glutathione carrying an aliphatic chain, or I-152, a pro-drug of N-acetyl-cysteine (NAC) and beta-mercaptoethylamine.	Acetylcysteine	326-343	interleukin 27	Mus musculus	140-145
23536773-1	2013	BACKGROUND: The aim of this study was to investigate the molecular mechanisms involved in the production of Th1 cytokines, namely IL-12 and IL-27, when the intra-macrophage redox state was altered by different chemical entities such as GSH-C4, which is reduced glutathione carrying an aliphatic chain, or I-152, a pro-drug of N-acetyl-cysteine (NAC) and beta-mercaptoethylamine.	Acetylcysteine	345-348	interleukin 27	Mus musculus	140-145
24120238-4	2013	ROS scavengers N-acetylcysteine (NAC) and dithiothreitol (DTT) abolish not only collagen, thrombin, and A23187 induced ROS production, but also GPIbalpha ectodomain shedding.	Acetylcysteine	15-31	glycoprotein Ib platelet subunit alpha	Homo sapiens	144-153
24120238-4	2013	ROS scavengers N-acetylcysteine (NAC) and dithiothreitol (DTT) abolish not only collagen, thrombin, and A23187 induced ROS production, but also GPIbalpha ectodomain shedding.	Acetylcysteine	33-36	glycoprotein Ib platelet subunit alpha	Homo sapiens	144-153
24120238-5	2013	Interestingly, a recognized calpain activator, dibucaine, induces both ROS production and GPIbalpha shedding, which are also obviously reduced by NAC and DTT.	Acetylcysteine	146-149	glycoprotein Ib platelet subunit alpha	Homo sapiens	90-99
22824115-0	2012	N-acetylcysteine (NAC) diminishes the severity of PCB 126-induced fatty liver in male rodents.	Acetylcysteine	0-16	pyruvate carboxylase	Rattus norvegicus	50-53
22824115-0	2012	N-acetylcysteine (NAC) diminishes the severity of PCB 126-induced fatty liver in male rodents.	Acetylcysteine	18-21	pyruvate carboxylase	Rattus norvegicus	50-53
19671765-6	2009	We were further able to show that N-acetyl-L-cysteine, a thiol-containing free radical scavenger, partially protects MM cells from HYD1-induced death.	Acetylcysteine	34-53	msh homeobox 1	Homo sapiens	131-135
19671765-7	2009	Additionally, N-acetyl-L-cysteine blocked HYD1-induced as well as basal levels of autophagy, suggesting that ROS can potentially trigger both cell death and cell survival pathways.	Acetylcysteine	14-33	msh homeobox 1	Homo sapiens	42-46
19541933-7	2009	High-dose antioxidant treatment with N-acetylcysteine improved airspace caliber and attenuated oxidative stress and apoptosis in neonatal and adult TSK mice.	Acetylcysteine	37-53	fibrillin 1	Mus musculus	148-151
22824115-8	2012	Dietary NAC resulted in a reduction in hepatocellular lipid in both PCB groups.	Acetylcysteine	8-11	pyruvate carboxylase	Rattus norvegicus	68-71
19211687-7	2009	In experiments designed to unravel the mechanisms underlying BSA-induced ER stress, BSA stimulated the production of cellular reactive oxygen species (ROS), and antioxidants such as ascorbic acid or N-acetylcysteine (NAC) blocked BSA-induced increases in GRP78 activation, eIF2alpha phosphorylation, SGLT expression, and alpha-MG uptake.	Acetylcysteine	199-215	eukaryotic translation initiation factor 2A	Homo sapiens	273-282
11162875-6	2000	The results proved that the use of methanol and N-acetylcysteine increased the activities of Cu,Zn-superoxide dismutase, glutathione peroxidase and glutathione reductase by about 15,15 and 41%, respectively, in comparison to the group of rats receiving methanol alone.	Acetylcysteine	48-64	glutathione-disulfide reductase	Rattus norvegicus	148-169
19211687-7	2009	In experiments designed to unravel the mechanisms underlying BSA-induced ER stress, BSA stimulated the production of cellular reactive oxygen species (ROS), and antioxidants such as ascorbic acid or N-acetylcysteine (NAC) blocked BSA-induced increases in GRP78 activation, eIF2alpha phosphorylation, SGLT expression, and alpha-MG uptake.	Acetylcysteine	217-220	eukaryotic translation initiation factor 2A	Homo sapiens	273-282
19427509-2	2009	In the present study, we examined the role of N-acetyl-L-cysteine (NAC), a clinically proven safe agent, for it"s ability to protect against gamma-ray-induced DNA strand breaks and/or DNA deletions in yeast and mammals.	Acetylcysteine	46-65	X-linked Kx blood group	Homo sapiens	67-70
23089480-6	2012	N-acetyl-L-cysteine (L-NAC), a ROS scavenger, alleviated oxidative stress and inhibited the apoptosis induced by bortezomib.	Acetylcysteine	0-19	X-linked Kx blood group	Homo sapiens	23-26
24977134-11	2013	The magnitude of GFR improvement after N-acetylcysteine administration was less pronounced in the group treated with high-flux biocompatible membranes: +0.17 +- 0.56 mL/min/1.73 m(2) in treatment group and +0.65 +- 0.53 mL/min/1.73 m(2) in control group (P &lt; 0.05).	Acetylcysteine	39-55	Rap guanine nucleotide exchange factor 5	Homo sapiens	17-20
23010594-1	2012	Aminoacylase 3 (AA3) mediates deacetylation of N-acetyl aromatic amino acids and mercapturic acids.	Acetylcysteine	81-98	aminoacylase 3	Homo sapiens	0-14
19428783-6	2009	The results revealed that NAC clearly inhibited JNK3 activation during the early intoxication, whereas ketamine preferably attenuated JNK3 activation during the latter intoxication.	Acetylcysteine	26-29	mitogen-activated protein kinase 10	Mus musculus	48-52
11115065-8	2000	The addition of the antioxidant agents ascorbic acid and N-acetyl-cysteine both lead to dose-dependent inhibition of DA-mediated HO-1 induction.	Acetylcysteine	57-74	heme oxygenase 1	Homo sapiens	129-133
19428783-9	2009	NAC and ketamine exerted a preventive effect against MPTP-induced loss of tyrosine hydroxylase-positive neurons and suppressed the nuclear translocation of JNK3, suggesting that NAC and ketamine can prevent MPTP-induced dopaminergic neuronal death by suppressing JNK3 activation.	Acetylcysteine	0-3	mitogen-activated protein kinase 10	Mus musculus	156-160
19428783-9	2009	NAC and ketamine exerted a preventive effect against MPTP-induced loss of tyrosine hydroxylase-positive neurons and suppressed the nuclear translocation of JNK3, suggesting that NAC and ketamine can prevent MPTP-induced dopaminergic neuronal death by suppressing JNK3 activation.	Acetylcysteine	0-3	mitogen-activated protein kinase 10	Mus musculus	263-267
19428783-9	2009	NAC and ketamine exerted a preventive effect against MPTP-induced loss of tyrosine hydroxylase-positive neurons and suppressed the nuclear translocation of JNK3, suggesting that NAC and ketamine can prevent MPTP-induced dopaminergic neuronal death by suppressing JNK3 activation.	Acetylcysteine	178-181	mitogen-activated protein kinase 10	Mus musculus	156-160
19428783-9	2009	NAC and ketamine exerted a preventive effect against MPTP-induced loss of tyrosine hydroxylase-positive neurons and suppressed the nuclear translocation of JNK3, suggesting that NAC and ketamine can prevent MPTP-induced dopaminergic neuronal death by suppressing JNK3 activation.	Acetylcysteine	178-181	mitogen-activated protein kinase 10	Mus musculus	263-267
23010594-1	2012	Aminoacylase 3 (AA3) mediates deacetylation of N-acetyl aromatic amino acids and mercapturic acids.	Acetylcysteine	81-98	aminoacylase 3	Homo sapiens	16-19
22917563-7	2012	Finally, the antioxidant N-acetyl cysteine antagonized 6-OHDA-induced activation of AMPK, p38 and autophagy.	Acetylcysteine	25-42	protein kinase AMP-activated non-catalytic subunit beta 1	Homo sapiens	84-88
22700867-8	2012	Moreover, the antioxidant, N-acetyl-L-cysteine (NAC), significantly reduced HIF-1alpha, ERK-1,2 phosphorylation, and CCL2 protein levels that were synergistically increased by the combination of PDGF and NiNPs.	Acetylcysteine	27-46	hypoxia inducible factor 1 subunit alpha	Rattus norvegicus	76-86
22700867-8	2012	Moreover, the antioxidant, N-acetyl-L-cysteine (NAC), significantly reduced HIF-1alpha, ERK-1,2 phosphorylation, and CCL2 protein levels that were synergistically increased by the combination of PDGF and NiNPs.	Acetylcysteine	48-51	hypoxia inducible factor 1 subunit alpha	Rattus norvegicus	76-86
11124598-9	2000	In contrast, NAC increased TNF-alpha and IL-10 mRNAs (p &lt; 0.05).	Acetylcysteine	13-16	interleukin 10	Rattus norvegicus	41-46
22353463-3	2012	We have recently shown that treatment with a combination of antioxidants containing alpha-tocopherol, N-acetyl-cysteine and alpha-lipoic acid reversed oxidative damage and energetic failure, together with the axonal degeneration and locomotor impairment displayed by Abcd1 null mice, the animal model of X-ALD.	Acetylcysteine	102-119	ATP-binding cassette, sub-family D (ALD), member 1	Mus musculus	267-272
19168506-3	2009	NAC, which blocked the production of intracellular ROS, also decreased dual oxidases, thyroperoxidase, pendrin, and thyroglobulin protein and/or gene expression.	Acetylcysteine	0-3	thyroid peroxidase	Homo sapiens	86-101
19168506-3	2009	NAC, which blocked the production of intracellular ROS, also decreased dual oxidases, thyroperoxidase, pendrin, and thyroglobulin protein and/or gene expression.	Acetylcysteine	0-3	solute carrier family 26 member 4	Homo sapiens	103-110
10965357-5	2000	We found that 24 h of NAC pre-treatment can shift cellular death from necrotic to apoptotic and determine an early expression of FasL in a 3DO cell line treated with H(2)O(2).	Acetylcysteine	22-25	Fas ligand	Homo sapiens	129-133
19262475-12	2009	NAC administration increased eNOS mRNA expression and activity.	Acetylcysteine	0-3	nitric oxide synthase 3	Rattus norvegicus	29-33
18840412-6	2008	Pretreatment with antioxidant N-acetyl-l-cysteine (NAC) prevented glibenclamide-induced JNK activation, apoptosis and cellular viability decline.	Acetylcysteine	30-49	X-linked Kx blood group	Homo sapiens	51-54
22766540-0	2012	Effects of N-acetylcysteine on matrix metalloproteinase-9 secretion and cell migration of human corneal epithelial cells.	Acetylcysteine	11-27	matrix metallopeptidase 9	Homo sapiens	31-57
22766540-7	2012	RESULTS: Twenty mM NAC inhibited the secretion of MMP-9 significantly.	Acetylcysteine	19-22	matrix metallopeptidase 9	Homo sapiens	50-55
22766540-9	2012	CONCLUSIONS: This study shows that NAC reduces MMP-9 production by HCE cells and inhibits cell migration in vitro.	Acetylcysteine	35-38	matrix metallopeptidase 9	Homo sapiens	47-52
22555846-4	2012	The IS-induced expression of p53 and p21 was suppressed by N-acetylcysteine, an antioxidant.	Acetylcysteine	59-75	KRAS proto-oncogene, GTPase	Rattus norvegicus	37-40
22231145-9	2012	RESULTS: IL-1beta-induced cPLA2 expression was mediated through NOX activation/ROS production, which was attenuated by N-acetylcysteine (NAC; a scavenger of ROS), the inhibitors of NOX (diphenyleneiodonium chloride and apocynin), MEK-1/2 (U0126), and JNK-1/2 (SP600125), transfection with the respective siRNAs, and the overexpression of HO-1 in RASFs.	Acetylcysteine	119-135	mitogen-activated protein kinase 8	Mus musculus	251-258
22231145-9	2012	RESULTS: IL-1beta-induced cPLA2 expression was mediated through NOX activation/ROS production, which was attenuated by N-acetylcysteine (NAC; a scavenger of ROS), the inhibitors of NOX (diphenyleneiodonium chloride and apocynin), MEK-1/2 (U0126), and JNK-1/2 (SP600125), transfection with the respective siRNAs, and the overexpression of HO-1 in RASFs.	Acetylcysteine	137-140	mitogen-activated protein kinase 8	Mus musculus	251-258
10923013-10	2000	RESULTS: At the early time point, both NAC and LipNAC protected the lung with the effects in significantly reducing the increases in transpulmonary albumin flux, neutrophil influx and myeloperoxidase in the lungs of shock/LPS rats.	Acetylcysteine	39-42	myeloperoxidase	Rattus norvegicus	184-199
22537850-14	2012	c-Fos expression and AP-1 binding to oligonucleotide were reduced by the treatment with NAC.	Acetylcysteine	88-91	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	0-5
19120016-16	2008	The effects of traditional antioxidant N-acetyl-L-cysteine (NAC) on tumor growth and tumor cell phenotype were similar to the effects of SkQ1 but more than 1,000,000 times higher doses of NAC than those of SkQ1 were required.	Acetylcysteine	39-58	X-linked Kx blood group	Homo sapiens	60-63
22467308-5	2012	ANG II-mediated VF was suppressed with KN-93 (Ca(2+)/calmodulin-dependent kinase inhibitor) and the reducing agent N-acetylcysteine.	Acetylcysteine	115-131	angiogenin	Rattus norvegicus	0-3
22227002-5	2012	In addition, social isolation-induced increase in calpain activity and p25/p35 ratio concomitant with decrease in membrane-associated p35 and p35/Cdk5 activity was normalized by NAC.	Acetylcysteine	178-181	cyclin-dependent kinase 5	Mus musculus	146-150
18762247-6	2008	Both glutathione (GSH) and N-acetylcysteine (NAC) pretreatment resulted in the complete inhibition of curcumin-induced ROS generation, AIF release from mitochondria, and caspase activation.	Acetylcysteine	27-43	apoptosis-inducing factor, mitochondrion-associated 1	Mus musculus	135-138
18762247-6	2008	Both glutathione (GSH) and N-acetylcysteine (NAC) pretreatment resulted in the complete inhibition of curcumin-induced ROS generation, AIF release from mitochondria, and caspase activation.	Acetylcysteine	45-48	apoptosis-inducing factor, mitochondrion-associated 1	Mus musculus	135-138
10826917-4	2000	LADH inactivation by MPO/H2O2/NaCl and by NaOCl was similarly prevented by thiol compounds such as GSH, L-cysteine, N-acetylcysteine, penicillamine and N-(2-mercaptopropionyl-glycine) in agreement with the role of HOCI in LADH inactivation by MPO/H2O2/NaCl.	Acetylcysteine	116-132	myeloperoxidase	Sus scrofa	21-24
18941206-9	2008	NAC blocked the activation of JNK and down-regulation of ERK, but both z-VAD-fmk (N-benzyloxycarbonyl-Val-Ala-Asp-fluoromethylketone) and ZB4 did not inhibit JNK activation of B7-H1 stimulation.	Acetylcysteine	0-3	mitogen-activated protein kinase 8	Mus musculus	30-33
18941206-9	2008	NAC blocked the activation of JNK and down-regulation of ERK, but both z-VAD-fmk (N-benzyloxycarbonyl-Val-Ala-Asp-fluoromethylketone) and ZB4 did not inhibit JNK activation of B7-H1 stimulation.	Acetylcysteine	0-3	mitogen-activated protein kinase 8	Mus musculus	158-161
22085843-9	2012	Furthermore, Cu(2+)/PDTC complex was capable of increasing the phosphorylations of ERK1/2 and JNK, and its upstream kinase MEK1/2 and MKK4, which could be reversed by NAC.	Acetylcysteine	167-170	mitogen activated protein kinase kinase 4	Rattus norvegicus	134-138
22165969-3	2012	The present study evaluated whether administration of the antioxidants N-acetyl-L-cysteine (NAC) and vitamin C or ascorbic acid (AsA) during pregnancy can protect strain H Swiss mice exposed to CS after birth.	Acetylcysteine	71-90	X-linked Kx blood group	Homo sapiens	92-95
18590811-5	2008	Bacterial lipopolysaccharide (LPS) stimulated the expression of CD11b in mouse BV-2 microglial cells and primary microglia, the effect that was blocked by antioxidants such as N-acetylcysteine (NAC) and pyrrolidine dithiocarbamate (PDTC).	Acetylcysteine	176-192	integrin subunit alpha M	Homo sapiens	64-69
10842199-8	2000	The addition of either ALA or NAC into cultures of PBMC isolated from cancer patients significantly increased the percentage of cells expressing CD25 as well as those expressing CD95.	Acetylcysteine	30-33	Fas cell surface death receptor	Homo sapiens	178-182
18590811-5	2008	Bacterial lipopolysaccharide (LPS) stimulated the expression of CD11b in mouse BV-2 microglial cells and primary microglia, the effect that was blocked by antioxidants such as N-acetylcysteine (NAC) and pyrrolidine dithiocarbamate (PDTC).	Acetylcysteine	194-197	integrin subunit alpha M	Homo sapiens	64-69
18657320-6	2008	The NAC-induced DNA-binding activity of NF-kappaB and phosphorylation of p65 were sensitive to a phosphatidylinositol (PI) 3-kinase inhibitor, partially sensitive to an IkappaB kinase (IKK) inhibitor, but not sensitive to a Bruton"s tyrosine kinase (Btk) inhibitor.	Acetylcysteine	4-7	Bruton tyrosine kinase	Homo sapiens	224-248
21928347-8	2012	Furthermore, these effects were regulated by redox conditions since antioxidant N-acetylcysteine abolished the HO-1/HMGB1/caspase-3 axis.	Acetylcysteine	80-96	caspase 3	Mus musculus	122-131
10811998-2	2000	The effects of the N-acetylcysteine conjugate of phenethyl isothiocyanate (PEITC-NAC) on tumor cell growth were analyzed in human prostate cancer cell lines LNCaP, androgen-dependent, and DU-145, androgen-independent.	Acetylcysteine	19-35	synuclein alpha	Homo sapiens	81-84
22055850-6	2012	Other mice received treatment with the clinical antidote N-acetylcysteine (APAP+NAC).	Acetylcysteine	57-73	NLR family, pyrin domain containing 1A	Mus musculus	80-83
19241570-3	2008	PPO activity increased with storage time and was inhibited by the individual use of N-acetylcysteine and glutathione.	Acetylcysteine	84-100	polyphenol oxidase, chloroplastic	Malus domestica	0-3
10925209-5	2000	The thiol antioxidant, N-acetylcysteine (NAC) abolished the synergism between IL-1beta or IL-6 and 1,25(OH)(2)D(3), but had only a small protective effect when the cytokines acted alone.	Acetylcysteine	23-39	synuclein alpha	Homo sapiens	41-44
10788478-8	2000	A series of antioxidant agents did not prevent the elevation in heme oxygenase activity by hypoxia; however, the precursor of glutathione synthesis and thiol donor, N-acetylcysteine, completely abolished HO-1 induction.	Acetylcysteine	165-181	heme oxygenase 1	Homo sapiens	204-208
18606001-13	2008	Further, also IRFI 016 and N-acetylcysteine were able to significantly reduce caspase-3 activation induced by homocysteine treatment.	Acetylcysteine	27-43	caspase 3	Mus musculus	78-87
10766859-8	2000	N-Acetylcysteine did inhibit the phosphorylation of the calcium sensitive tyrosine kinases PYK2 and Src, effects that also occurred using nitric oxide.	Acetylcysteine	0-16	protein tyrosine kinase 2 beta	Homo sapiens	91-95
10692565-6	2000	AP-1 and NF-kappaB activation were blocked by the thiol antioxidant N-acetylcysteine and by nordihydroguaiaretic acid, an antioxidant and lipooxygenase inhibitor and an inhibitor of the epoxygenase activity of CYP1A1, and did not take place in c35, c37, or in Ah nuclear translator-deficient c4 cells.	Acetylcysteine	68-84	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	210-216
18410509-4	2008	The increase in p21(ras) levels was largely attenuated by the reducing agent, N-acetylcysteine, which was proven to reduce ROS formation in astrocytes subjected to serum deprivation.	Acetylcysteine	78-94	cyclin-dependent kinase inhibitor 1A (P21)	Mus musculus	16-19
10851302-9	2000	Both pyruvate and NAC are capable of detoxifying H(2)O(2) to maintain cell viability and Hsp90 integrity.	Acetylcysteine	18-21	heat shock protein 90 alpha family class A member 1	Homo sapiens	89-94
18450357-7	2008	JNK activation by 15d-PGJ2 was blocked by antioxidants N-acetylcysteine (NAC) and GSH.	Acetylcysteine	55-71	mitogen-activated protein kinase 8	Mus musculus	0-3
18450357-7	2008	JNK activation by 15d-PGJ2 was blocked by antioxidants N-acetylcysteine (NAC) and GSH.	Acetylcysteine	73-76	mitogen-activated protein kinase 8	Mus musculus	0-3
10720473-6	2000	N-Acetylcysteine, a potent antioxidant, also suppressed the GA-induced MCP-1 expression.	Acetylcysteine	0-16	C-C motif chemokine ligand 2	Homo sapiens	71-76
18303122-6	2008	MCP-1 secretion from hypertrophied cells was significantly decreased by treatment with antioxidant N-acetyl-cysteine, JNK inhibitors SP600125 and JIP-1 peptide, and IkappaB phosphorylation inhibitors BAY 11-7085 and BMS-345541 (P &lt; 0.01).	Acetylcysteine	99-116	chemokine (C-C motif) ligand 2	Mus musculus	0-5
10706725-3	2000	Following stimulation with TNF-alpha, pyrrolidine dithiocarbamate (PDTC), N-acetylcysteine, and dexamethasone prevented I kappa B kinase-induced I kappa B-alpha, but not I kappa B-beta or I kappa B-epsilon phosphorylation and degradation.	Acetylcysteine	74-90	inhibitor of nuclear factor kappa B kinase subunit epsilon	Homo sapiens	188-205
18295335-2	2008	The extracellular domain of the human complement receptor 2 (CR2/CD21) is released by proteolytic cleavage as a soluble protein through a variety of stimuli including the thiol antioxidants N-acetylcysteine (NAC) and glutathione (GSH), and the oxidant pervanadate (PV).	Acetylcysteine	190-206	complement receptor 2	Mus musculus	65-69
18295335-2	2008	The extracellular domain of the human complement receptor 2 (CR2/CD21) is released by proteolytic cleavage as a soluble protein through a variety of stimuli including the thiol antioxidants N-acetylcysteine (NAC) and glutathione (GSH), and the oxidant pervanadate (PV).	Acetylcysteine	208-211	complement receptor 2	Mus musculus	65-69
18295335-7	2008	These findings further indicate that GSH and NAC utilize different pathways than PV to activate CD21-shedding.	Acetylcysteine	45-48	complement receptor 2	Mus musculus	96-100
18068290-0	2008	Comparison of S-adenosyl-L-methionine (SAMe) and N-acetylcysteine (NAC) protective effects on hepatic damage when administered after acetaminophen overdose.	Acetylcysteine	49-65	NLR family, pyrin domain containing 1A	Mus musculus	67-70
10669634-8	2000	However, simultaneous blockade of the ERK1/2 and ROS pathways by using PD098059 combined with diphenylene iodonium or N-acetylcysteine potently enhanced the ability of MAPK kinase inhibitors to abrogate MCP-1 mRNA expression (100+/-2% inhibition).	Acetylcysteine	118-134	C-C motif chemokine ligand 2	Homo sapiens	203-208
10634825-6	2000	The combined incubation with reduced glutathione diethyl ester or N-acetylcysteine, antioxidants, suppressed the upregulation of uPA and uPAR mRNA and the increase in plasminogen activator activity by lysoPC.	Acetylcysteine	66-82	plasminogen activator, urokinase receptor	Homo sapiens	137-141
18034189-8	2008	The antioxidant N-acetyl-L-cysteine substantially inhibited conformational changes of Bax, loss of mitochondrial membrane potential, nuclear relocation of mitochondrial factors, and apoptosis induction in 4-OOH-CY-treated T cells.	Acetylcysteine	16-35	BCL2-associated X protein	Mus musculus	86-89
10470760-16	1999	In addition, ip administration of N-acetylcysteine (40 mg/kg, 1 and 6 hrs after zymosan) was effective in preventing the development of lung and intestine injury and neutrophil infiltration, as determined by myeloperoxidase evaluation.	Acetylcysteine	34-50	myeloperoxidase	Rattus norvegicus	208-223
18314480-10	2008	N-acetyl-l-cysteine additionally reversed the salvicine-induced activation of ERK and p38 MAPK, thereby maintaining functional beta(1) integrin activity and restoring cell adhesion and spreading.	Acetylcysteine	0-19	integrin subunit beta 1	Homo sapiens	127-143
10428064-3	1999	Pretreatment of cells with exogenous GSH or NAC resulted in inhibition of both neutral sphingomyelinase (SMase) activation and ceramide formation during hypoxia.	Acetylcysteine	44-47	sphingomyelin phosphodiesterase 2	Rattus norvegicus	79-103
17200984-1	2008	In recent years, N-acetyl-L-cysteine (NAC) has been widely investigated as a potentially useful protective and antioxidative agent to be applied in many pathological states.	Acetylcysteine	17-36	X-linked Kx blood group	Homo sapiens	38-41
10428497-2	1999	A 6 h incubation of H35 cells with the dimeric (diamagnetic) form of dinitrosyl iron complex with glutathione or N-acetyl-L-cysteine activated synthesis of various heat shock proteins, heat shock protein 28, 32, 60, 70, 90 and 100.	Acetylcysteine	113-132	heat shock protein family A (Hsp70) member 1B	Rattus norvegicus	185-230
18483565-4	2008	In this work, we investigated the effect of NAC administration on cortical expressions of nuclear factor kappa B (NF-kappaB) and inflammatory proteins such as interleukin-1beta (IL-1beta), tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6), and intercellular adhesion molecule-1 (ICAM-1) after TBI.	Acetylcysteine	44-47	intercellular adhesion molecule 1	Rattus norvegicus	256-289
18483565-4	2008	In this work, we investigated the effect of NAC administration on cortical expressions of nuclear factor kappa B (NF-kappaB) and inflammatory proteins such as interleukin-1beta (IL-1beta), tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6), and intercellular adhesion molecule-1 (ICAM-1) after TBI.	Acetylcysteine	44-47	intercellular adhesion molecule 1	Rattus norvegicus	291-297
18483565-6	2008	In animals given NAC post-TBI, NF-kappaB, IL-1beta, TNF-alpha, and ICAM-1 were decreased in comparison to vehicle-treated animals.	Acetylcysteine	17-20	intercellular adhesion molecule 1	Rattus norvegicus	67-73
10330231-10	1999	Finally, the oxidant scavenger N-acetylcysteine inhibited HO-1 induction by cytokines.	Acetylcysteine	31-47	heme oxygenase 1	Homo sapiens	58-62
17913704-10	2007	In vivo NAC treatment proved to be a unique tool to selectively neutralize TNFR1-mediated effects of TNFalpha while releasing TNFR2 pathways.	Acetylcysteine	8-11	TNF receptor superfamily member 1A	Rattus norvegicus	75-80
17916643-9	2007	On the other hand, preincubation with potent antioxidants, such as butylated hydroxytoluene, Trolox, and N-acetylcysteine, prevented iron-ascorbate-generating PON2 reduction in parallel with MDA suppression.	Acetylcysteine	105-121	paraoxonase 2	Homo sapiens	159-163
9890986-10	1999	This and the findings that (i) HNE strongly induced intracellular peroxide production, (ii) HNE-induced JNK activation was inhibited by pretreatment of the cells with a thiol antioxidant, N-acetylcysteine, and (iii) H2O2 significantly activated JNK support the hypothesis that pro-oxidants play a crucial role in the HNE-induced activation of stress signaling pathways.	Acetylcysteine	188-204	mitogen-activated protein kinase 8	Rattus norvegicus	104-107
17727829-6	2007	N-Acetyl-l-cysteine (NAC) pretreatment resulted in the increase in glutathione concentration, reduction of intracellular ROS, complete inhibition of DNA fragmentation, mitochondrial membrane potential (MMP) collapse, Fas externalization and caspase-8 activation.	Acetylcysteine	0-19	X-linked Kx blood group	Homo sapiens	21-24
17760507-6	2007	Thiol-protectant, N-acetylcysteine, significantly attenuated the NCX-4016-induced loss of cell viability, suggesting the role of alteration of thiol-redox status therein.	Acetylcysteine	18-34	T cell leukemia homeobox 2	Homo sapiens	65-68
18032928-8	2007	Furthermore, pretreatment of K562/A02 cells with NAC eliminated P-gp downregulation, JNK phosphorylation and c-Jun activation induced by salvicine.	Acetylcysteine	49-52	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	109-114
17479278-2	2007	Because of a potential involvement of N-acetylation in the detoxication of reactive trichloroethylene metabolite(s) to N-acetyl-cysteine derivatives, polymorphisms of the NAT2 gene may also be relevant.	Acetylcysteine	119-136	N-acetyltransferase 2	Homo sapiens	171-175
17964299-5	2007	Supplementation of various reducing reagents, including N-acetylcysteine, DTT and glutathione, reverses the inhibitory effect of BSO on PEPCK mRNA level.	Acetylcysteine	56-72	phosphoenolpyruvate carboxykinase 1	Rattus norvegicus	136-141
17846503-7	2007	Pretreatment of cells with N-acetylcysteine (NAC) reduced ROS generation and cell growth inhibition, and pretreatment with NAC or a caspase 8 inhibitor (Z-IETD-FMK) inhibited the acacetin-induced loss of mitochondrial membrane potential and release of cytochrome c and AIF.	Acetylcysteine	27-43	apoptosis inducing factor mitochondria associated 1	Homo sapiens	269-272
17846503-7	2007	Pretreatment of cells with N-acetylcysteine (NAC) reduced ROS generation and cell growth inhibition, and pretreatment with NAC or a caspase 8 inhibitor (Z-IETD-FMK) inhibited the acacetin-induced loss of mitochondrial membrane potential and release of cytochrome c and AIF.	Acetylcysteine	45-48	apoptosis inducing factor mitochondria associated 1	Homo sapiens	269-272
17846503-7	2007	Pretreatment of cells with N-acetylcysteine (NAC) reduced ROS generation and cell growth inhibition, and pretreatment with NAC or a caspase 8 inhibitor (Z-IETD-FMK) inhibited the acacetin-induced loss of mitochondrial membrane potential and release of cytochrome c and AIF.	Acetylcysteine	123-126	apoptosis inducing factor mitochondria associated 1	Homo sapiens	269-272
17526490-6	2007	Pretreatment with the antioxidant N-acetylcysteine (NAC) and expression of MT1 in the Ikkbeta(-)(/)(-) cells prevented JNK activation; moreover, NAC pretreatment, MT1 expression, MKK4 ablation, and JNK inhibition all protected cells from death induced by arsenic.	Acetylcysteine	34-50	mitogen-activated protein kinase 8	Mus musculus	119-122
17526490-6	2007	Pretreatment with the antioxidant N-acetylcysteine (NAC) and expression of MT1 in the Ikkbeta(-)(/)(-) cells prevented JNK activation; moreover, NAC pretreatment, MT1 expression, MKK4 ablation, and JNK inhibition all protected cells from death induced by arsenic.	Acetylcysteine	34-50	mitogen-activated protein kinase 8	Mus musculus	198-201
17526490-6	2007	Pretreatment with the antioxidant N-acetylcysteine (NAC) and expression of MT1 in the Ikkbeta(-)(/)(-) cells prevented JNK activation; moreover, NAC pretreatment, MT1 expression, MKK4 ablation, and JNK inhibition all protected cells from death induced by arsenic.	Acetylcysteine	52-55	mitogen-activated protein kinase 8	Mus musculus	119-122
17526490-6	2007	Pretreatment with the antioxidant N-acetylcysteine (NAC) and expression of MT1 in the Ikkbeta(-)(/)(-) cells prevented JNK activation; moreover, NAC pretreatment, MT1 expression, MKK4 ablation, and JNK inhibition all protected cells from death induced by arsenic.	Acetylcysteine	145-148	mitogen-activated protein kinase 8	Mus musculus	198-201
17616699-0	2007	Superoxide signaling mediates N-acetyl-L-cysteine-induced G1 arrest: regulatory role of cyclin D1 and manganese superoxide dismutase.	Acetylcysteine	30-49	cyclin D1	Mus musculus	88-97
17616699-2	2007	We investigated the hypothesis that NAC-induced reactive oxygen species (ROS) signaling perturbs cellular proliferation by regulating the cell cycle regulatory protein cyclin D1 and the ROS scavenging enzyme Mn-superoxide dismutase (MnSOD).	Acetylcysteine	36-39	cyclin D1	Mus musculus	168-177
17616699-3	2007	When cultured in media containing NAC, mouse fibroblasts showed G(1) arrest with decreased cyclin D1 protein levels.	Acetylcysteine	34-37	cyclin D1	Mus musculus	91-100
17429056-0	2007	Accelerated urinary excretion of methylmercury following administration of its antidote N-acetylcysteine requires Mrp2/Abcc2, the apical multidrug resistance-associated protein.	Acetylcysteine	88-104	ATP binding cassette subfamily C member 2	Rattus norvegicus	114-118
17429056-0	2007	Accelerated urinary excretion of methylmercury following administration of its antidote N-acetylcysteine requires Mrp2/Abcc2, the apical multidrug resistance-associated protein.	Acetylcysteine	88-104	ATP binding cassette subfamily C member 2	Rattus norvegicus	119-124
17429056-2	2007	MeHg readily binds to NAC to form the MeHg-NAC complex, and recent studies indicate that this complex is an excellent substrate for the basolateral organic anion transporter (Oat)-1, Oat1/Slc22a6, thus potentially explaining the uptake from blood into the renal tubular cells.	Acetylcysteine	22-25	solute carrier family 22 member 6	Rattus norvegicus	183-187
17429056-2	2007	MeHg readily binds to NAC to form the MeHg-NAC complex, and recent studies indicate that this complex is an excellent substrate for the basolateral organic anion transporter (Oat)-1, Oat1/Slc22a6, thus potentially explaining the uptake from blood into the renal tubular cells.	Acetylcysteine	22-25	solute carrier family 22 member 6	Rattus norvegicus	188-195
17429056-2	2007	MeHg readily binds to NAC to form the MeHg-NAC complex, and recent studies indicate that this complex is an excellent substrate for the basolateral organic anion transporter (Oat)-1, Oat1/Slc22a6, thus potentially explaining the uptake from blood into the renal tubular cells.	Acetylcysteine	43-46	solute carrier family 22 member 6	Rattus norvegicus	148-181
17429056-2	2007	MeHg readily binds to NAC to form the MeHg-NAC complex, and recent studies indicate that this complex is an excellent substrate for the basolateral organic anion transporter (Oat)-1, Oat1/Slc22a6, thus potentially explaining the uptake from blood into the renal tubular cells.	Acetylcysteine	43-46	solute carrier family 22 member 6	Rattus norvegicus	183-187
17429056-2	2007	MeHg readily binds to NAC to form the MeHg-NAC complex, and recent studies indicate that this complex is an excellent substrate for the basolateral organic anion transporter (Oat)-1, Oat1/Slc22a6, thus potentially explaining the uptake from blood into the renal tubular cells.	Acetylcysteine	43-46	solute carrier family 22 member 6	Rattus norvegicus	188-195
17429056-3	2007	The present study tested the hypothesis that intracellular MeHg is subsequently transported across the apical membrane of the cells into the tubular fluid as a MeHg-NAC complex using the multidrug resistance-associated protein-2 (Mrp2/Abcc2).	Acetylcysteine	165-168	ATP binding cassette subfamily C member 2	Rattus norvegicus	235-240
17429056-5	2007	In contrast with the normal Wistar rats, NAC was much less effective at stimulating urinary MeHg excretion in the Mrp2-deficient (TR-) Wistar rats.	Acetylcysteine	41-44	ATP binding cassette subfamily C member 2	Rattus norvegicus	114-118
17429056-9	2007	These results indicate that Mrp2 is involved in urinary MeHg excretion after NAC administration and suggest that the transported molecule is most likely the MeHg-NAC complex.	Acetylcysteine	77-80	ATP binding cassette subfamily C member 2	Rattus norvegicus	28-32
17429056-9	2007	These results indicate that Mrp2 is involved in urinary MeHg excretion after NAC administration and suggest that the transported molecule is most likely the MeHg-NAC complex.	Acetylcysteine	162-165	ATP binding cassette subfamily C member 2	Rattus norvegicus	28-32
17171638-7	2007	Curcumin increased the expression of the phosphorylated forms of PTK, PDK1, and PKC-delta, which was attenuated by either GSH or NAC and potentiated by BSO.	Acetylcysteine	129-132	pyruvate dehydrogenase kinase 1	Homo sapiens	70-74
17510393-4	2007	Introduction of oncogenic H- or N-Ras caused elevated intracellular ROS, accumulation of 8-oxo-2"-deoxyguanosine, and increased number of chromosome breaks in mitotic cells, which were prevented by antioxidant N-acetyl-L-cysteine.	Acetylcysteine	210-229	NRAS proto-oncogene, GTPase	Homo sapiens	32-37
17454561-7	2007	Induction of Hsp70 protein by these metals was inhibited by addition of N-acetylcysteine.	Acetylcysteine	72-88	heat shock protein family A (Hsp70) member 4	Homo sapiens	13-18
17321519-5	2007	N-acetylcysteine (but not melatonin) also increased the endothelial NOS protein expression.	Acetylcysteine	0-16	nitric oxide synthase 3	Rattus norvegicus	56-71
17287397-5	2007	The oye2Delta phenotype can be completely suppressed by removing the potential for formation of the actin C285-C374 disulfide bond, the likely substrate of the Oye2p enzyme or by treating the cells with the clinically important reductant N-acetylcysteine.	Acetylcysteine	238-254	NADPH dehydrogenase	Saccharomyces cerevisiae S288C	160-165
17084062-11	2007	Furthermore the increased zinc-mediated toxicity due to hydrocortisone was abolished in the alveolar epithelial cell lines by the NADC/NAC treatment.	Acetylcysteine	130-134	X-linked Kx blood group	Homo sapiens	135-138
17331847-4	2007	After 10 days of NAC treatment, the cytotoxic activity of the LAK cells did not significantly differ from LAK activity generated from spleen cells obtained from untreated controls.	Acetylcysteine	17-20	alpha kinase 1	Homo sapiens	62-65
17250813-10	2007	CONCLUSIONS: The results suggest that PKCbeta(2) overexpression represents a mechanism causing hyperglycemia-mediated myocardial hypertrophy, which can be prevented by the antioxidant N-acetylcysteine.	Acetylcysteine	184-200	protein kinase C, beta	Rattus norvegicus	38-45
17441349-1	2007	OBJECTIVE: To test the effect of N-acetylcysteine (NAC) on the mice with infection associated preterm labor.	Acetylcysteine	33-49	NLR family, pyrin domain containing 1A	Mus musculus	51-54
17223684-3	2007	Recently, MYST enzymes were reported to employ a ping-pong route of catalysis via an acetyl-cysteine intermediate.	Acetylcysteine	85-100	lysine acetyltransferase 5	Homo sapiens	10-14
17223684-6	2007	Previously, Cys-304 of Esa1 was the proposed nucleophile that forms an acetyl-cysteine intermediate.	Acetylcysteine	71-86	lysine acetyltransferase 5	Homo sapiens	23-27
17012540-0	2007	Specificity of aminoacylase III-mediated deacetylation of mercapturic acids.	Acetylcysteine	58-75	aspartoacylase (aminoacylase) 3	Mus musculus	15-31
17012540-6	2007	In the present study we characterized the kinetics of the recently cloned mouse aminoacylase III (AAIII) toward a wide spectrum of halogenated mercapturic acids and N-acetylated amino acids.	Acetylcysteine	143-160	aspartoacylase (aminoacylase) 3	Mus musculus	80-96
17237267-11	2007	Administration of the free radical scavenger l-N-acetylcysteine blocked LAQ824 + CRA-mediated apoptosis in HMV-I cells, suggesting a primary role for reactive oxygen species generation in LAQ824 + CRA-associated lethality.	Acetylcysteine	45-63	LUC7 like 3 pre-mRNA splicing factor	Homo sapiens	81-84
17237267-11	2007	Administration of the free radical scavenger l-N-acetylcysteine blocked LAQ824 + CRA-mediated apoptosis in HMV-I cells, suggesting a primary role for reactive oxygen species generation in LAQ824 + CRA-associated lethality.	Acetylcysteine	45-63	LUC7 like 3 pre-mRNA splicing factor	Homo sapiens	197-200
17108112-7	2006	Addition of NAC to the culture medium prolonged the life span of cells treated with 4-OHT and prevented the up-regulation of Foxo3a protein levels caused by PKB activation.	Acetylcysteine	12-15	forkhead box O3	Mus musculus	125-131
17023264-9	2006	Supporting this notion, cotreatment with NAC inhibited the TNF-alpha-induced rise in MSK1 and MSK2 kinase activity, while siRNA knock-down experiments showed that MSK2 is the predominant isoform involved in TNF-alpha-induced ET-1 upregulation.	Acetylcysteine	41-44	ribosomal protein S6 kinase A4	Homo sapiens	94-98
16860347-11	2006	Post-treatment with NAC diminished the decrease in MAP, increased the HR, and decreased the markers of organ injury (BUN, Cre, LDH, CPK, GOT, GPT) and inflammatory biomarkers (TNF-alpha, IL-6, IL-10) after LPS.	Acetylcysteine	20-23	glutamic--pyruvic transaminase	Rattus norvegicus	142-145
17015178-6	2006	Our results reveal that NAC and GSH employ protein S-thiolation to inhibit organomercurial activation of pro-MMP-9.	Acetylcysteine	24-27	matrix metallopeptidase 9	Homo sapiens	109-114
17015178-7	2006	Gelatinase activity assays showed that GSH and NAC significantly inhibited MMP-9 but not MMP-2 function, implying isoform structural specificity.	Acetylcysteine	47-50	matrix metallopeptidase 9	Homo sapiens	75-80
16989920-4	2006	The powder formulation with NAC gave significant nasal absorption of SCT in both animal models, with absolute bioavailabilities of 30.0% in rats and 24.9% in dogs.	Acetylcysteine	28-31	secretin	Rattus norvegicus	69-72
16886168-5	2006	N-Acetylcysteine treatment delayed and reduced the down-regulation of CD45 expression induced by AP and prevented acinar cells from producing TNF-alpha.	Acetylcysteine	0-16	protein tyrosine phosphatase receptor type C	Homo sapiens	70-74
17072061-0	2006	Influence of N-acetylcysteine on ICAM-1 expression and IL-8 release from endothelial and epithelial cells.	Acetylcysteine	13-29	intercellular adhesion molecule 1	Homo sapiens	33-39
17072061-4	2006	In this study we evaluated the influence of N-acetylcysteine (NAC) (0.01 mM-30 mM) on the cytokine-induced (TNF-alpha/IL-1 beta) expression of the ICAM-1 adhesion molecule and on IL-8 release in endothelial (ECV-304) and bronchial epithelial (H292) cell lines.	Acetylcysteine	44-60	intercellular adhesion molecule 1	Homo sapiens	147-153
17072061-4	2006	In this study we evaluated the influence of N-acetylcysteine (NAC) (0.01 mM-30 mM) on the cytokine-induced (TNF-alpha/IL-1 beta) expression of the ICAM-1 adhesion molecule and on IL-8 release in endothelial (ECV-304) and bronchial epithelial (H292) cell lines.	Acetylcysteine	62-65	intercellular adhesion molecule 1	Homo sapiens	147-153
17072061-6	2006	NAC inhibited the TNF-alpha/IL-1 beta-stimulated ICAM-1 expression and IL-8 release from both cell lines in a concentration dependent manner.	Acetylcysteine	0-3	intercellular adhesion molecule 1	Homo sapiens	49-55
17072061-8	2006	We conclude that NAC is an effective inhibitor of TNF-alpha/IL-1 beta- stimulated ICAM-1 and IL-8 release in endothelial and epithelial cells.	Acetylcysteine	17-20	intercellular adhesion molecule 1	Homo sapiens	82-88
16859669-0	2006	Antioxidant N-acetylcysteine restores myocardial Mn-SOD activity and attenuates myocardial dysfunction in diabetic rats.	Acetylcysteine	12-28	superoxide dismutase 2	Rattus norvegicus	49-55
16859669-3	2006	We hypothesised that chronic treatment with N-acetylcysteine, an antioxidant and glutathione (GSH) precursor, would normalize hyperglycemia induced inactivation of Mn-SOD and attenuate myocardial dysfunction.	Acetylcysteine	44-60	superoxide dismutase 2	Rattus norvegicus	164-170
16760673-6	2006	The induction of both ATM activation and H2AX phosphorylation by MXT was prevented to a large extent by N-acetyl-L-cysteine (NAC), a scavenger of reactive oxygen species (ROS).	Acetylcysteine	104-123	X-linked Kx blood group	Homo sapiens	125-128
16556443-10	2006	Correspondingly, oral administration with either N-acetylcysteine or ascorbic acid significantly attenuated LPS-induced downregulation of intestinal pregnane X receptor and retinoid X receptor alphalpha.	Acetylcysteine	49-65	nuclear receptor subfamily 1, group I, member 2	Mus musculus	149-168
16249273-8	2006	NAC and DPI also inhibited phosphorylation of 4E-BP1 on Thr46 and association of eIF4E with eIF4G, steps that are important in the initiation phase of mRNA translation.	Acetylcysteine	0-3	eukaryotic translation initiation factor 4 gamma 1	Homo sapiens	92-97
16628006-3	2006	We recently reported that this constitutive H2AX phosphorylation (CHP) is markedly reduced by the antioxidant N-acetyl-L-cysteine (NAC), and postulated that it reflects the oxidative DNA damage ("endogenous DSBs") induced by reactive oxygen species (ROS) generated by metabolic activity during progression through the cell cycle.	Acetylcysteine	110-129	X-linked Kx blood group	Homo sapiens	131-134
16391241-5	2006	NADPH oxidase inhibitor diphenyleneiodonium chloride (DPI), ROS scavenger N-acetyl cysteine (NAC), and p47phox small interfering RNA knockdown all inhibited the EGFR transactivation induced by ET-1.	Acetylcysteine	74-91	epidermal growth factor receptor	Rattus norvegicus	161-165
16251475-8	2006	Pretreatment with an ERK1/2 blocker (PD-98059), staurosporine, folate, or NAC modulated Hcy-induced MMP-9 activation as measured using zymography.	Acetylcysteine	74-77	matrix metallopeptidase 9	Homo sapiens	100-105
16411658-7	2006	P4501B1 induction was blocked in AKR1A1 transfectants by the AKR1A1 inhibitor (sulfonylnitromethane), the o-quinone scavenger (N-acetyl-l-cysteine), or the cytosolic AhR antagonist (diflubenzuron).	Acetylcysteine	127-146	aldo-keto reductase family 1 member A1	Homo sapiens	33-39
16424790-8	2006	However, there were some significant differences among Captopril (30 mg/kg or 45 mg/kg), enalapril (20 mg/kg), and N-acetylcysteine particular in the activity of PON1 and ACE.	Acetylcysteine	115-131	paraoxonase 1	Rattus norvegicus	162-166
22089811-8	2012	Preincubation with two other drugs also abolished hypotonicity-induced insulin release and reduced basal insulin output: 1) N-acetyl-L-cysteine (NAC), a glutathione precursor that serves as general antioxidant and 2) betulinic acid a compound that almost totally abolished NOX4 expression.	Acetylcysteine	145-148	NADPH oxidase 4	Rattus norvegicus	273-277
22033125-11	2012	The antioxidant N-acetylcysteine (NAC) protected cells from TEGDMA-induced cell death, and inhibited the activation of ERK1/2, p38 and JNK by TEGDMA.	Acetylcysteine	16-32	mitogen-activated protein kinase 8	Mus musculus	135-138
22033125-11	2012	The antioxidant N-acetylcysteine (NAC) protected cells from TEGDMA-induced cell death, and inhibited the activation of ERK1/2, p38 and JNK by TEGDMA.	Acetylcysteine	34-37	mitogen-activated protein kinase 8	Mus musculus	135-138
21806545-13	2012	The gel shift and promoter activity assay showed that Ang II increased AP-1 (activator protein-1)-binding activity and leptin promoter activity, while SP600125, NAC and atorvastatin inhibited the AP-1-binding activity and leptin promoter activity induced by Ang II.	Acetylcysteine	161-164	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	196-200
22511847-7	2012	RESULTS: Compared with the BSA controls, the RGC-5 cells incubated with AGE-BSA showed a dose- and time-dependent increase in VEGF-A mRNA and VEGF-A protein secretion in the supernatant, with the highest levels achieved at 24 h. AGE-BSA stimulated a significant release of HMGB1 in the supernatant and a significant increase of intracellular ROS production at 3 h. NAC blocked HMGB1 production in a dose-dependent manner.	Acetylcysteine	365-368	vascular endothelial growth factor A	Mus musculus	126-132
23094067-14	2012	NAC also inhibited the overexpression of p-STAT3 and VEGF in CNV and in RPE cells.	Acetylcysteine	0-3	vascular endothelial growth factor A	Mus musculus	53-57
22701695-9	2012	The free radical scavenger N-acetyl-cysteine (NAC) was able to completely suppress cell death induced by jacaranone as it blocked Akt downregulation, p38 MAPK activation as well as upregulation of proapoptotic Bax.	Acetylcysteine	27-44	BCL2-associated X protein	Mus musculus	210-213
22701695-9	2012	The free radical scavenger N-acetyl-cysteine (NAC) was able to completely suppress cell death induced by jacaranone as it blocked Akt downregulation, p38 MAPK activation as well as upregulation of proapoptotic Bax.	Acetylcysteine	46-49	BCL2-associated X protein	Mus musculus	210-213
23006535-0	2012	N-acetylcysteine downregulation of lysyl oxidase activity alleviating bleomycin-induced pulmonary fibrosis in rats.	Acetylcysteine	0-16	lysyl oxidase	Rattus norvegicus	35-48
21723934-9	2011	The known antioxidant N-acetyl-l-cysteine, a known antioxidant, ameliorated global DNA hypomethylation and the decreased DNMT 1 and 3a expression observed during arsenic exposure.	Acetylcysteine	22-41	DNA methyltransferase 1	Gallus gallus	121-134
21453200-7	2011	INNOVATION: Treating Abcd1(-) mice with the antioxidants N-acetylcysteine and alpha-lipoic acid (LA) prevents protein oxidation; preserves NADH, NADPH, ATP, and GSH levels; and normalizes pyruvate kinase activity, which implies that oxidative stress provoked by VLCFA results in bioenergetic dysfunction, at a presymptomatic stage.	Acetylcysteine	57-73	ATP-binding cassette, sub-family D (ALD), member 1	Mus musculus	21-26
21740309-5	2011	VEGF increases IQGAP1-Cys-OH formation, which is prevented by N-acetyl cysteine or dimedone, which inhibits VEGF-induced EC migration and capillary network formation.	Acetylcysteine	62-79	vascular endothelial growth factor A	Mus musculus	0-4
21740309-5	2011	VEGF increases IQGAP1-Cys-OH formation, which is prevented by N-acetyl cysteine or dimedone, which inhibits VEGF-induced EC migration and capillary network formation.	Acetylcysteine	62-79	vascular endothelial growth factor A	Mus musculus	108-112
21642840-6	2011	Treatment with N-acetyl-L-cysteine, a thiol-containing antioxidant completely blocked combined treatment-induced Bax translocation as well as DR5 upregulation.	Acetylcysteine	15-34	BCL2-associated X protein	Mus musculus	113-116
21547497-11	2011	Induction of ICER was stimulated by oxidative stress, whereas antioxidant treatment with N-acetylcysteine or HDL prevented the rise of ICER elicited by oxidised LDL and restored beta cell functions.	Acetylcysteine	89-105	cAMP responsive element modulator	Homo sapiens	135-139
21494874-12	2011	Pretreatment of cells with ROS scavenger N-acetylcysteine completely blocked insulin-induced UCP-2 expression (p &lt; 0.01, one-way ANOVA) and significantly suppressed VEGF expression (p &lt; 0.01, one-way ANOVA).	Acetylcysteine	41-57	vascular endothelial growth factor A	Bos taurus	168-172
21630435-2	2011	By modifying PDMS using short- and long-chain mono-functional polyethylene glycol (PEG604 and PEG5K, respectively) and N-acetyl-L-cysteine via adsorption and covalent binding (NAC and NAC/EDC/NHS, respectively), we increased surface wettability.	Acetylcysteine	119-138	X-linked Kx blood group	Homo sapiens	176-179
21630435-2	2011	By modifying PDMS using short- and long-chain mono-functional polyethylene glycol (PEG604 and PEG5K, respectively) and N-acetyl-L-cysteine via adsorption and covalent binding (NAC and NAC/EDC/NHS, respectively), we increased surface wettability.	Acetylcysteine	119-138	X-linked Kx blood group	Homo sapiens	184-187
23554696-7	2011	Interestingly, EGF could induce a significant production of ROS, and N-acetyl-L-cysteine, a scavenger of ROS which abolished the EGF-induced ROS generation, cell migration, as well as activation of PI3K/Akt and PAK, but not Rac1.	Acetylcysteine	69-88	Rac family small GTPase 1	Homo sapiens	224-228
21640077-6	2011	The increases in Pin1 expression and in AP-1 reporter activity in response to UVA were abolished by N-acetylcysteine (NAC) treatment.	Acetylcysteine	100-116	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	40-44
21640077-6	2011	The increases in Pin1 expression and in AP-1 reporter activity in response to UVA were abolished by N-acetylcysteine (NAC) treatment.	Acetylcysteine	118-121	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	40-44
21335520-10	2011	Inhibition of viral-mediated RIG-I induction by CSE was prevented by the antioxidants N-acetyl-cysteine and glutathione.	Acetylcysteine	86-103	DExD/H-box helicase 58	Homo sapiens	29-34
20354828-6	2011	In contrast, combination of simvastatin and imatinib induced a significant cell death in the subpopulation, which is dependent on the induced ROS by simvastatin as the effect was blocked by ROS scavenger N-acetyl-L: -cysteine (NAC).	Acetylcysteine	204-225	X-linked Kx blood group	Homo sapiens	227-230
21347335-5	2011	Additionally, when ROS production was blocked by N-acetyl-L-cysteine (NAC), HCC cells were protected against Lexa and CHX combination treatment-induced apoptosis.	Acetylcysteine	49-68	X-linked Kx blood group	Homo sapiens	70-73
21268080-8	2011	Furthermore, CSE-induced p300 and c-Jun complex formation was inhibited by pretreatment with diphenyleneiodonium chloride, apocynin, N-acetyl-L-cysteine or SP600125.	Acetylcysteine	133-152	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	34-39
21192843-5	2011	The rapid ApoG2-induced cell death was partially reversed by the antioxidant N-acetyl-L-cysteine (NAC), but the ApoG2-induced reduction of mitochondrial membrane potential (MMP) was not reversed by NAC.	Acetylcysteine	77-96	X-linked Kx blood group	Homo sapiens	98-101
21643558-4	2011	GO-203 treatment resulted in the complete downregulation of Bcr-Abl expression and induced cell cycle arrest by a ROS-mediated mechanism that was blocked by the antioxidant N-acetylcysteine.	Acetylcysteine	173-189	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	60-67
21873804-11	2011	Moreover, we found that NAC down-regulated the expression of VCAM-1, MMP2 and MMP9, accompanied by inhibition of NF-kappaB activation and reduced expression of RAGE.	Acetylcysteine	24-27	matrix metallopeptidase 2	Mus musculus	69-73
21873804-12	2011	CONCLUSION: In the present study, we show novel data to suggest that NAC promotes atherosclerotic plaque stabilization through suppression of RAGE, MMPs and NF-kappaB in apoE(-/-) mice.	Acetylcysteine	69-72	matrix metallopeptidase 2	Mus musculus	148-152
21172010-8	2010	The antioxidants, N-acetylcysteine and glutathione, but not vitamin C or tiron, inhibited perifosine-induced elevation of p-c-Jun, DR4 and DR5.	Acetylcysteine	18-34	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	124-129
20639439-8	2010	This Ca2(+)- and MLC20 phosphorylation-independent contraction was mimicked by hydrogen peroxide and inhibited by N-acetyl cysteine.	Acetylcysteine	114-131	carbonic anhydrase 2	Homo sapiens	5-12
20728534-7	2010	The antioxidants N-acetyl-l-cysteine and Tiron, as well as the FAS inhibitor cerulenin, reversed the effects of CBR1 knockdown.	Acetylcysteine	17-36	carbonyl reductase 1	Mus musculus	112-116
16430375-0	2006	Early, transient increase in complexin I and complexin II in the cerebral cortex following traumatic brain injury is attenuated by N-acetylcysteine.	Acetylcysteine	131-147	complexin 1	Rattus norvegicus	29-40
16319332-2	2005	As an indirect antioxidant NAC was shown to induce superoxide dismutase (SOD) activity in immune cells from endotoxaemic mice.	Acetylcysteine	27-30	superoxide dismutase 2	Rattus norvegicus	73-76
16319332-3	2005	The aim of this study was to assess whether NAC acts as an indirect antioxidant by inducing manganese (Mn)-SOD activity in the diaphragms of endotoxaemic rats, while preventing muscle dysfunction.	Acetylcysteine	44-47	superoxide dismutase 2	Rattus norvegicus	107-110
16319332-9	2005	Pre-treatment with 3 mmol.kg-1 NAC clearly increased muscle Mn-SOD protein content and activity in both LPS- and saline-injected animals, while reducing protein carbonylation and nitration, and partially preventing the LPS-induced respiratory muscle dysfunction.	Acetylcysteine	31-34	superoxide dismutase 2	Rattus norvegicus	60-66
16388726-0	2005	Significant changes of peripheral perfusion and plasma adrenomedullin levels in N-acetylcysteine long term treatment of patients with sclerodermic Raynauds phenomenon.	Acetylcysteine	80-96	adrenomedullin	Homo sapiens	55-69
16109311-4	2005	Interestingly, both IL-1beta and TNF-alpha markedly inhibited the expression of MOG, CNPase, and PLP but not MBP, the effect that was blocked by antioxidants such as N-acetylcysteine (NAC) and pyrrolidine dithiocarbamate (PDTC).	Acetylcysteine	166-182	proteolipid protein 1	Homo sapiens	97-100
16166335-1	2005	We previously showed that dietary treatment with the N-acetylcysteine conjugate of phenethyl isothiocyanate (PEITC-NAC) inhibited benzo(a)pyrene-induced lung tumorigenesis in A/J mice, and that tumor inhibition was associated with induction of activator protein-1 (AP-1) activity and stimulation of apoptosis in the lungs of mice.	Acetylcysteine	53-69	NLR family, pyrin domain containing 1A	Mus musculus	115-118
20932751-5	2010	Pretreatment with the antioxidant N-acetyl-L-cysteine (NAC) markedly inhibited the CWJ-081-induced JNK activation and apoptosis.	Acetylcysteine	34-53	X-linked Kx blood group	Homo sapiens	55-58
20446771-8	2010	The same effect was achieved by the nontargeted antioxidant Trolox at higher concentration, but the thiol antioxidant N-acetylcysteine (NAC) inhibited MMP activity and was not able to induce myofibroblast differentiation.	Acetylcysteine	118-134	matrix metallopeptidase 9	Homo sapiens	151-154
20446771-8	2010	The same effect was achieved by the nontargeted antioxidant Trolox at higher concentration, but the thiol antioxidant N-acetylcysteine (NAC) inhibited MMP activity and was not able to induce myofibroblast differentiation.	Acetylcysteine	136-139	matrix metallopeptidase 9	Homo sapiens	151-154
9890986-10	1999	This and the findings that (i) HNE strongly induced intracellular peroxide production, (ii) HNE-induced JNK activation was inhibited by pretreatment of the cells with a thiol antioxidant, N-acetylcysteine, and (iii) H2O2 significantly activated JNK support the hypothesis that pro-oxidants play a crucial role in the HNE-induced activation of stress signaling pathways.	Acetylcysteine	188-204	mitogen-activated protein kinase 8	Rattus norvegicus	245-248
16115031-5	2005	AngII-induced MCP-1 protein expression in mProx at 6 h was largely blocked by ROS (N-acetylcysteine; 82 +/- 14%), Ras (N-acetyl-S-trans,trans-farnesyl-L-cysteine; 82 +/- 13%), and nuclear factor-kappaB (NF-kappaB) (parthenolide; 89 +/- 7.9%) inhibitors.	Acetylcysteine	83-99	chemokine (C-C motif) ligand 2	Mus musculus	14-19
9823769-5	1998	In addition, it appeared that oxygen radicals functioned as activating molecules during cellular interaction and production of MIP-1alpha, as the addition of the antioxidant N-acetylcysteine (NAC) prevented MIP-1alpha secretion.	Acetylcysteine	174-190	chemokine (C-C motif) ligand 3	Mus musculus	127-137
16061151-8	2005	Exercise stress caused a significant increase in plasma CORT concentrations in EX + SAL + Imm and EX + NAC + Imm groups compared to NonEX mice.	Acetylcysteine	103-106	cortistatin	Mus musculus	56-60
20503249-5	2010	The SAA cytotoxicity was blocked by co-incubation with catalase, whereas the SBA cytotoxicity and its subsequent growth arrest were abolished by N-acetyl-L-cysteine (NAC), but was not affected by PI3K phosphorylation inhibitor LY294002, or catalase, suggesting two separated oxidative stress pathways were mediated by these two ascorbates.	Acetylcysteine	145-164	X-linked Kx blood group	Homo sapiens	166-169
20824644-5	2010	Apoptotic markers Fas, FasL, and caspase-8, up-regulated following repeated hCG exposure, were significantly down-regulated following NAC co-incubation.	Acetylcysteine	134-137	caspase 8	Rattus norvegicus	33-42
9823769-5	1998	In addition, it appeared that oxygen radicals functioned as activating molecules during cellular interaction and production of MIP-1alpha, as the addition of the antioxidant N-acetylcysteine (NAC) prevented MIP-1alpha secretion.	Acetylcysteine	174-190	chemokine (C-C motif) ligand 3	Mus musculus	207-217
20835244-7	2010	Administration of the anti-oxidant, N-acetyl-cysteine, to Prdm16-deficient mice partially rescued defects in neural stem/progenitor cell function and neural development.	Acetylcysteine	36-53	PR domain containing 16	Mus musculus	58-64
9823769-5	1998	In addition, it appeared that oxygen radicals functioned as activating molecules during cellular interaction and production of MIP-1alpha, as the addition of the antioxidant N-acetylcysteine (NAC) prevented MIP-1alpha secretion.	Acetylcysteine	192-195	chemokine (C-C motif) ligand 3	Mus musculus	127-137
20815772-4	2010	The effects of ROS on both BRAK and IL-8 expression were attenuated by pre-treatment with N-acetyl-L-cysteine (NAC), epidermal growth factor receptor (EGFR), and mitogen-activated protein kinase (MAPK) inhibitors.	Acetylcysteine	90-109	X-linked Kx blood group	Homo sapiens	111-114
9823769-5	1998	In addition, it appeared that oxygen radicals functioned as activating molecules during cellular interaction and production of MIP-1alpha, as the addition of the antioxidant N-acetylcysteine (NAC) prevented MIP-1alpha secretion.	Acetylcysteine	192-195	chemokine (C-C motif) ligand 3	Mus musculus	207-217
20632440-14	2010	Peak JNK activation occurred at 12 h post-treatment and this activation persisted for up to 24 h. The expression of phosphorylated JNK and c-Jun protein after 12 h with BrMC-treated cells was inhibited by N-acetylcysteine and SP600125 pre-treatment, but GW9662 had no effect.	Acetylcysteine	205-221	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	139-144
9832211-5	1998	Furthermore, N-acetylcysteine, an antioxidant, prevented the auto-oxidized dopamine-induced JNK/SAPK activation and DNA fragmentation.	Acetylcysteine	13-29	mitogen-activated protein kinase 8	Rattus norvegicus	92-100
20525893-12	2010	N-acetylcysteine abolished STAT-1 phosphorylation, suggesting that STAT-1 activation may be dependent on NiSO(4)-induced alteration of the redox status of the cell.	Acetylcysteine	0-16	signal transducer and activator of transcription 1	Homo sapiens	27-33
20525893-12	2010	N-acetylcysteine abolished STAT-1 phosphorylation, suggesting that STAT-1 activation may be dependent on NiSO(4)-induced alteration of the redox status of the cell.	Acetylcysteine	0-16	signal transducer and activator of transcription 1	Homo sapiens	67-73
15976188-10	2005	Furthermore, LPS-induced downregulation of PXR and cyp3a11 mRNA expression and ERND activity was prevented by maternal pretreatment with N-acetylcysteine (NAC).	Acetylcysteine	137-153	nuclear receptor subfamily 1, group I, member 2	Mus musculus	43-46
15976188-10	2005	Furthermore, LPS-induced downregulation of PXR and cyp3a11 mRNA expression and ERND activity was prevented by maternal pretreatment with N-acetylcysteine (NAC).	Acetylcysteine	137-153	cytochrome P450, family 3, subfamily a, polypeptide 11	Mus musculus	51-58
15976188-10	2005	Furthermore, LPS-induced downregulation of PXR and cyp3a11 mRNA expression and ERND activity was prevented by maternal pretreatment with N-acetylcysteine (NAC).	Acetylcysteine	155-158	nuclear receptor subfamily 1, group I, member 2	Mus musculus	43-46
15976188-10	2005	Furthermore, LPS-induced downregulation of PXR and cyp3a11 mRNA expression and ERND activity was prevented by maternal pretreatment with N-acetylcysteine (NAC).	Acetylcysteine	155-158	cytochrome P450, family 3, subfamily a, polypeptide 11	Mus musculus	51-58
15817678-4	2005	Application of N-acetylcysteine (NAC) or blocking the activity of Nox, a protein leading to the formation of ROS, with diphenylene iodonium (DPI) inhibits the responses of BMM cells to RANKL, including ROS production, activation of c-Jun N-terminal kinase (JNK), p38 mitogen-activated protein (MAP) kinase, and extracellular signal-regulated kinase (ERK), and osteoclast differentiation.	Acetylcysteine	15-31	TNF superfamily member 11	Homo sapiens	185-190
15817678-4	2005	Application of N-acetylcysteine (NAC) or blocking the activity of Nox, a protein leading to the formation of ROS, with diphenylene iodonium (DPI) inhibits the responses of BMM cells to RANKL, including ROS production, activation of c-Jun N-terminal kinase (JNK), p38 mitogen-activated protein (MAP) kinase, and extracellular signal-regulated kinase (ERK), and osteoclast differentiation.	Acetylcysteine	33-36	TNF superfamily member 11	Homo sapiens	185-190
15869837-12	2005	Furthermore, LPS-induced downregulation of PXR, cyp3a11 and mdr1a mRNA in mouse placenta was prevented by N-acetylcysteine (NAC).	Acetylcysteine	106-122	nuclear receptor subfamily 1, group I, member 2	Mus musculus	43-46
15869837-12	2005	Furthermore, LPS-induced downregulation of PXR, cyp3a11 and mdr1a mRNA in mouse placenta was prevented by N-acetylcysteine (NAC).	Acetylcysteine	106-122	cytochrome P450, family 3, subfamily a, polypeptide 11	Mus musculus	48-55
15869837-12	2005	Furthermore, LPS-induced downregulation of PXR, cyp3a11 and mdr1a mRNA in mouse placenta was prevented by N-acetylcysteine (NAC).	Acetylcysteine	124-127	nuclear receptor subfamily 1, group I, member 2	Mus musculus	43-46
15869837-12	2005	Furthermore, LPS-induced downregulation of PXR, cyp3a11 and mdr1a mRNA in mouse placenta was prevented by N-acetylcysteine (NAC).	Acetylcysteine	124-127	cytochrome P450, family 3, subfamily a, polypeptide 11	Mus musculus	48-55
20204677-6	2010	Our results shows that TGF-beta1 stimulation of uPA and MMP-9 expression involve NOXs-dependent ROS and NFkappaB, activation, demonstrated by using DPI, NOXs inhibitor, ROS scavenger N-acetylcysteine and SN50, an NFkb inhibitor.	Acetylcysteine	183-199	matrix metallopeptidase 9	Homo sapiens	56-61
20571742-9	2010	High glucose-induced periostin protein expression was decreased significantly when pretreated with CLT or N-acetylcysteine (NAC), a ROS scavenger.	Acetylcysteine	106-122	periostin	Rattus norvegicus	21-30
20571742-9	2010	High glucose-induced periostin protein expression was decreased significantly when pretreated with CLT or N-acetylcysteine (NAC), a ROS scavenger.	Acetylcysteine	124-127	periostin	Rattus norvegicus	21-30
9795082-5	1998	Carnosine did not significantly enhance the reactivity of Co(2+) toward H(2)O(2), whereas cysteine (Cys) and N-acetylcysteine (NAC) suppressed free radical generation.	Acetylcysteine	109-125	synuclein alpha	Homo sapiens	127-130
20224971-3	2010	The modulation of intracellular reactive oxygen species levels by D: , L: -buthionine-(S, R) sulfoximide (BSO), and N: -acetyl-L: -cysteine (NAC) caused inducer- and time-dependent or stage-specific effects on HL-60 cell growth inhibition, differentiation and subsequent apoptosis.	Acetylcysteine	116-139	X-linked Kx blood group	Homo sapiens	141-144
16134056-8	2005	The apoptotic induction and the ROS generation (statistically correlated to apoptosis) were most pronounced in the Jurkat and EL4 T cell lines, and were partially inhibited by the antioxidant N-acetyl L-cysteine (NAC).	Acetylcysteine	192-211	X-linked Kx blood group	Homo sapiens	213-216
9715438-9	1998	These results suggest that the protective effect of DADS is due to its inhibition of biotransformation of APAP to the reactive metabolite N-acetyl-p-benzoquinone imine (NAPQI) by CYP 1A1/1A2 enzymes and that NAC provides protection by increasing cellular cysteine level and GSH synthesis, thus facilitating detoxification of NAPQI by glutathione conjugation.	Acetylcysteine	208-211	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	179-186
15892579-5	2005	Reaction mixtures containing equimolar N-acetyl cysteine (NAC) and N-acetyl lysine (NAL) provided a major NADPH- and CYP4B1-dependent product.	Acetylcysteine	39-56	cytochrome P450 4B1	Oryctolagus cuniculus	117-123
15892579-5	2005	Reaction mixtures containing equimolar N-acetyl cysteine (NAC) and N-acetyl lysine (NAL) provided a major NADPH- and CYP4B1-dependent product.	Acetylcysteine	58-61	cytochrome P450 4B1	Oryctolagus cuniculus	117-123
15892579-7	2005	Purified native rabbit lung CYP4B1 and purified recombinant rabbit CYP4B1 produced the trapped NAC/NAL-IPO pyrrole adduct at rates of 600-700 nmol/nmol P450/30 min.	Acetylcysteine	95-98	cytochrome P450 4B1	Oryctolagus cuniculus	28-34
20426871-3	2010	In a series of experiments, Kopke has shown that the compound N-acetyl-L-cysteine (L-NAC) can protect the hearing of chinchillas from the effects of a single exposure to noise.	Acetylcysteine	62-81	NLR family, pyrin domain containing 1A	Mus musculus	85-88
9707512-6	1998	IL-8 and MIP-2 secretion induced either by the metals or H2O2 were inhibited by antioxidants such as tetramethyl-thiourea and N-acetyl-cysteine.	Acetylcysteine	126-143	C-X-C motif chemokine ligand 2	Homo sapiens	9-14
20100472-6	2010	NAC also decreased the caspase-3 activity of MG132.	Acetylcysteine	0-3	caspase 3	Mus musculus	23-32
20389059-7	2010	Inhibitors of NF-kappaB (ammonium pyrrolidinedithiocarbamate and isohelenin) and an antioxidant (N-acetyl-L-cysteine) suppressed the indoxyl sulfate-induced expression of ICAM-1 and MCP-1 in HUVEC.	Acetylcysteine	97-116	intercellular adhesion molecule 1	Homo sapiens	171-177
15892579-7	2005	Purified native rabbit lung CYP4B1 and purified recombinant rabbit CYP4B1 produced the trapped NAC/NAL-IPO pyrrole adduct at rates of 600-700 nmol/nmol P450/30 min.	Acetylcysteine	95-98	cytochrome P450 4B1	Oryctolagus cuniculus	67-73
20054154-7	2010	Co-administration of N-Acetylcysteine (NAC) exerted a strong protective effect against CdCl(2) induced barrier damage and stress related genes, while other antioxidants only attenuated CdCl(2) induced HSP70 and HMOX-1 and showed no protective effect on the barrier collapse.	Acetylcysteine	39-42	heat shock protein family A (Hsp70) member 4	Homo sapiens	201-206
15819723-0	2005	N-acetyl-cysteine enhances growth in BCR-ABL-transformed cells.	Acetylcysteine	0-17	BCR activator of RhoGEF and GTPase	Rattus norvegicus	37-40
20054154-9	2010	The protective effect of NAC against CdCl(2) induced MT1X, HSP70 and HMOX-1 genes, demonstrates an anti-oxidant effect of NAC in addition to Cd chelation.	Acetylcysteine	25-28	heat shock protein family A (Hsp70) member 4	Homo sapiens	59-64
9622162-5	1998	This upregulation of HO-1 was completely blocked by the antioxidant N-acetylcysteine (NAC, 20 mmol/L).	Acetylcysteine	68-84	heme oxygenase 1	Homo sapiens	21-25
20054154-9	2010	The protective effect of NAC against CdCl(2) induced MT1X, HSP70 and HMOX-1 genes, demonstrates an anti-oxidant effect of NAC in addition to Cd chelation.	Acetylcysteine	122-125	heat shock protein family A (Hsp70) member 4	Homo sapiens	59-64
20056085-1	2010	AIM: To explore the effect of N-acetylcysteine(NAC)on the interleukin(IL)18-induced expression of tumor necrosis factor (TNF) alpha and interleukin(IL) 6 in mouse vascular smooth muscle cells(VSMC).	Acetylcysteine	30-46	NLR family, pyrin domain containing 1A	Mus musculus	47-50
15819723-5	2005	NAC rendered Rat1/BCR-ABL cells resistance to a Ras inhibitor manumycin in soft agar colony formation.	Acetylcysteine	0-3	BCR activator of RhoGEF and GTPase	Rattus norvegicus	18-21
15819723-6	2005	In the absence of Hsp90 inhibitors, NAC stimulated the activation of MAP kinase in BCR-ABL-transformed but not in the parental Rat1 cells.	Acetylcysteine	36-39	BCR activator of RhoGEF and GTPase	Rattus norvegicus	83-86
15811836-14	2005	The involvement of ROSs was strengthened by the fact that interventions with N-acetylcysteine prevented ufCB-induced generation of ROSs and VEGF in vitro.	Acetylcysteine	77-93	vascular endothelial growth factor A	Mus musculus	140-144
20065493-1	2009	The goal of our study was to determine a contribution of nNOS to the increase of brain NO synthase activity induced by chronic N-acetylcysteine (NAC) treatment.	Acetylcysteine	127-143	nitric oxide synthase 1	Rattus norvegicus	57-61
20065493-1	2009	The goal of our study was to determine a contribution of nNOS to the increase of brain NO synthase activity induced by chronic N-acetylcysteine (NAC) treatment.	Acetylcysteine	145-148	nitric oxide synthase 1	Rattus norvegicus	57-61
20065493-10	2009	Thus, nNOS is responsible not only for strain differences but also for NAC-induced increase of total NOS activity in the brain.	Acetylcysteine	71-74	nitric oxide synthase 1	Rattus norvegicus	6-10
9622162-5	1998	This upregulation of HO-1 was completely blocked by the antioxidant N-acetylcysteine (NAC, 20 mmol/L).	Acetylcysteine	86-89	heme oxygenase 1	Homo sapiens	21-25
19393328-3	2009	OBJECTIVES: The aim of this study was to evaluate whether the antioxidant N-acetyl-l-cysteine (NAC) can affect TGF-beta(1)-mediated tissue remodeling in fibroblasts or modulate the production of fibronectin and vascular endothelial growth factor (VEGF) which are believed to be important mediators of tissue repair and remodeling.	Acetylcysteine	74-93	X-linked Kx blood group	Homo sapiens	95-98
9622162-6	1998	In contrast, steady laminar shear (5 dyne/cm2) induced NADH oxidase activity and NAC-sensitive HO-1 mRNA expression only at 1 and 5 hours, a transient response that returned toward baseline at 24 hours.	Acetylcysteine	81-84	heme oxygenase 1	Homo sapiens	95-99
15851851-4	2005	Dietary supplementation with N-acetyl cysteine (1 g/kg diet), a cell-permeant antioxidant and GSH precursor, alleviated oxidative damage and cognitive decline, and restored glutathione synthase and GSH levels in ApoE-deficient mice deprived of folate to those of normal mice maintained in the presence of folate.	Acetylcysteine	29-46	glutathione synthetase	Mus musculus	173-193
9545524-8	1998	Augmentation of glutathione levels by pretreatment of cells with N-acetyl-L-cysteine attenuated the effect of PGA2 on IGF-I and Waf1 gene expression.	Acetylcysteine	65-84	insulin-like growth factor 1	Rattus norvegicus	118-123
10651168-1	1998	We investigated the effects of the sulfhydryl-donor, N-acetylcysteine (NAC), on nitroglycerin (NTG)-induced relaxation of the vascular smooth muscle.	Acetylcysteine	53-69	synuclein alpha	Homo sapiens	71-74
15629104-4	2005	Consistent with the suppression, NAC inhibited NGF-induced activation of TrkA, formation of receptor complexes comprising TrkA, Shc, Grb2, and Sos, and activation of phospholipase Cgamma and phosphatidylinositol 3-kinase.	Acetylcysteine	33-36	neurotrophic receptor tyrosine kinase 1	Rattus norvegicus	73-77
15629104-4	2005	Consistent with the suppression, NAC inhibited NGF-induced activation of TrkA, formation of receptor complexes comprising TrkA, Shc, Grb2, and Sos, and activation of phospholipase Cgamma and phosphatidylinositol 3-kinase.	Acetylcysteine	33-36	neurotrophic receptor tyrosine kinase 1	Rattus norvegicus	122-126
15629104-4	2005	Consistent with the suppression, NAC inhibited NGF-induced activation of TrkA, formation of receptor complexes comprising TrkA, Shc, Grb2, and Sos, and activation of phospholipase Cgamma and phosphatidylinositol 3-kinase.	Acetylcysteine	33-36	growth factor receptor bound protein 2	Rattus norvegicus	133-137
19684307-2	2009	Functionally, GGT plays important roles in glutathione homeostasis and mercapturic acid metabolism.	Acetylcysteine	71-87	inactive glutathione hydrolase 2	Homo sapiens	14-17
19897918-6	2009	Indeed, excretion of mercapturic acid (acetylcysteine conjugates derived metabolically from the conjugate of each aldehyde with GSH) into the urine increased significantly in MRP2-deficient EHBRs fed DHA.	Acetylcysteine	21-37	ATP binding cassette subfamily C member 2	Rattus norvegicus	175-179
19897918-6	2009	Indeed, excretion of mercapturic acid (acetylcysteine conjugates derived metabolically from the conjugate of each aldehyde with GSH) into the urine increased significantly in MRP2-deficient EHBRs fed DHA.	Acetylcysteine	39-53	ATP binding cassette subfamily C member 2	Rattus norvegicus	175-179
15368090-5	2005	N-Acetyl-L-cysteine (NAC) reduced the cytotoxicity and induction of heme oxygenase-1 (HO-1) mRNA in PAO3+-exposed cells, while NAC affected neither the cytotoxicity nor the HO-1 mRNA level in PAA5+-exposed cells.	Acetylcysteine	0-19	heme oxygenase 1	Rattus norvegicus	68-84
15368090-5	2005	N-Acetyl-L-cysteine (NAC) reduced the cytotoxicity and induction of heme oxygenase-1 (HO-1) mRNA in PAO3+-exposed cells, while NAC affected neither the cytotoxicity nor the HO-1 mRNA level in PAA5+-exposed cells.	Acetylcysteine	0-19	heme oxygenase 1	Rattus norvegicus	86-90
20137606-9	2009	However, NAC significantly decreased the BDNF and increased the TrkB mRNA and protein expression in rat hippocampal neuron after MG induction.	Acetylcysteine	9-12	brain-derived neurotrophic factor	Rattus norvegicus	41-45
9870716-3	1998	Moreover, calphostin C alone induced expression of AR mRNA in a light-dependent manner, and this effect was abrogated by pretreatment with N-acetylcysteine.	Acetylcysteine	139-155	amphiregulin	Rattus norvegicus	51-53
19586904-8	2009	Treating the cells with the broad NOS inhibitor N(G)-methyl-l-arginine, the free radical scavenger N-acetyl-l-cysteine, or the NOS substrate l-arginine partially inhibits UV-induced eIF2alpha phosphorylation.	Acetylcysteine	99-118	eukaryotic translation initiation factor 2A	Homo sapiens	182-191
15368090-5	2005	N-Acetyl-L-cysteine (NAC) reduced the cytotoxicity and induction of heme oxygenase-1 (HO-1) mRNA in PAO3+-exposed cells, while NAC affected neither the cytotoxicity nor the HO-1 mRNA level in PAA5+-exposed cells.	Acetylcysteine	21-24	heme oxygenase 1	Rattus norvegicus	68-84
15368090-5	2005	N-Acetyl-L-cysteine (NAC) reduced the cytotoxicity and induction of heme oxygenase-1 (HO-1) mRNA in PAO3+-exposed cells, while NAC affected neither the cytotoxicity nor the HO-1 mRNA level in PAA5+-exposed cells.	Acetylcysteine	21-24	heme oxygenase 1	Rattus norvegicus	86-90
15368090-5	2005	N-Acetyl-L-cysteine (NAC) reduced the cytotoxicity and induction of heme oxygenase-1 (HO-1) mRNA in PAO3+-exposed cells, while NAC affected neither the cytotoxicity nor the HO-1 mRNA level in PAA5+-exposed cells.	Acetylcysteine	21-24	heme oxygenase 1	Rattus norvegicus	173-177
9358747-0	1997	N-acetyl cysteine blocks mesangial VCAM-1 and NF-kappa B expression in vivo.	Acetylcysteine	0-17	vascular cell adhesion molecule 1	Mus musculus	35-41
16399403-4	2005	GGT also initiates the metabolism of glutathione S-conjugates to mercapturic acids by transferring the gamma-glutamyl moiety to an acceptor amino acid and releasing cysteinylglycine.	Acetylcysteine	65-82	inactive glutathione hydrolase 2	Homo sapiens	0-3
15378659-8	2004	Reactive oxygen species (ROS) scavengers (N-acetyl-cysteine [NAC] and trolox) reduced thrombin-induced CIS expression, and inhibitors of COX and LO reduced ROS produced by thrombin.	Acetylcysteine	42-59	cytokine inducible SH2-containing protein	Rattus norvegicus	103-106
15378659-8	2004	Reactive oxygen species (ROS) scavengers (N-acetyl-cysteine [NAC] and trolox) reduced thrombin-induced CIS expression, and inhibitors of COX and LO reduced ROS produced by thrombin.	Acetylcysteine	61-64	cytokine inducible SH2-containing protein	Rattus norvegicus	103-106
15382121-5	2004	DCA activated the ERK1/2 pathway in HuH7 human hepatoma cells that was blocked by the incubation of cells with an ERBB1 inhibitor, NAC, TX, CsA, or BKA.	Acetylcysteine	131-134	MIR7-3 host gene	Homo sapiens	36-40
19839867-7	2009	The DNA damage and cell death incurred by LBP and BA8C were significantly prevented by N-acetylcysteine (NAC) but not by alpha -tocopherol + ascorbic acid (T + AA).	Acetylcysteine	87-103	lipopolysaccharide binding protein	Homo sapiens	42-45
19839867-7	2009	The DNA damage and cell death incurred by LBP and BA8C were significantly prevented by N-acetylcysteine (NAC) but not by alpha -tocopherol + ascorbic acid (T + AA).	Acetylcysteine	105-108	lipopolysaccharide binding protein	Homo sapiens	42-45
19553346-7	2009	The abilities of NO and antioxidants to inhibit AGE/RAGE-induced hypertrophic growth were verified by the observation that SNAP, SNP, NAC, and taurine inhibited fibronectin, p21(Waf1/Cip1), and RAGE expression.	Acetylcysteine	134-137	long intergenic non-protein coding RNA 914	Homo sapiens	52-56
19468286-3	2009	The reducing agent, N-acetylcysteine (NAC), effectively inhibited the sustained activation of JNK, release of Endo G, and cell death in Jurkat cells treated by AD5-10.	Acetylcysteine	20-36	endonuclease G	Homo sapiens	110-116
19468286-3	2009	The reducing agent, N-acetylcysteine (NAC), effectively inhibited the sustained activation of JNK, release of Endo G, and cell death in Jurkat cells treated by AD5-10.	Acetylcysteine	38-41	endonuclease G	Homo sapiens	110-116
19461054-5	2009	It is noteworthy that we observed that DHMEQ stimulated reactive oxygen species (ROS) production in a dose-dependent manner and that pretreatment of the cells with the antioxidant N-acetyl-L-cysteine (NAC) significantly reduced DHMEQ-induced ROS generation.	Acetylcysteine	180-199	X-linked Kx blood group	Homo sapiens	201-204
9358747-3	1997	Single intraperitoneal administration of N-acetyl cysteine completely suppressed LPS-induced VCAM-1 expression on the GMC surface.	Acetylcysteine	41-58	vascular cell adhesion molecule 1	Mus musculus	93-99
19544430-7	2009	Treatment of these cells with the antioxidant N-acetyl-L-cysteine (NAC) or with a p38 MAPK inhibitor restores normal proliferation and reduced expression of p21(cip1) and p27(kip1) in the Atm(-/-) NSCs.	Acetylcysteine	46-65	cyclin-dependent kinase inhibitor 1A (P21)	Mus musculus	157-160
19544430-7	2009	Treatment of these cells with the antioxidant N-acetyl-L-cysteine (NAC) or with a p38 MAPK inhibitor restores normal proliferation and reduced expression of p21(cip1) and p27(kip1) in the Atm(-/-) NSCs.	Acetylcysteine	46-65	cyclin-dependent kinase inhibitor 1A (P21)	Mus musculus	161-165
15604726-7	2004	Treatment of protoplasts with the antioxidant N -acetyl- -cysteine (NAC) during induction of Bax expression strongly suppressed Bax-mediated ROS production and the cell death phenotype.	Acetylcysteine	46-66	BCL2-associated X protein	Mus musculus	93-96
15604726-7	2004	Treatment of protoplasts with the antioxidant N -acetyl- -cysteine (NAC) during induction of Bax expression strongly suppressed Bax-mediated ROS production and the cell death phenotype.	Acetylcysteine	46-66	BCL2-associated X protein	Mus musculus	128-131
15604726-7	2004	Treatment of protoplasts with the antioxidant N -acetyl- -cysteine (NAC) during induction of Bax expression strongly suppressed Bax-mediated ROS production and the cell death phenotype.	Acetylcysteine	68-71	BCL2-associated X protein	Mus musculus	93-96
19544430-7	2009	Treatment of these cells with the antioxidant N-acetyl-L-cysteine (NAC) or with a p38 MAPK inhibitor restores normal proliferation and reduced expression of p21(cip1) and p27(kip1) in the Atm(-/-) NSCs.	Acetylcysteine	46-65	cyclin-dependent kinase inhibitor 1B	Mus musculus	171-174
19544430-7	2009	Treatment of these cells with the antioxidant N-acetyl-L-cysteine (NAC) or with a p38 MAPK inhibitor restores normal proliferation and reduced expression of p21(cip1) and p27(kip1) in the Atm(-/-) NSCs.	Acetylcysteine	46-65	cyclin-dependent kinase inhibitor 1B	Mus musculus	175-179
15604726-7	2004	Treatment of protoplasts with the antioxidant N -acetyl- -cysteine (NAC) during induction of Bax expression strongly suppressed Bax-mediated ROS production and the cell death phenotype.	Acetylcysteine	68-71	BCL2-associated X protein	Mus musculus	128-131
19544430-7	2009	Treatment of these cells with the antioxidant N-acetyl-L-cysteine (NAC) or with a p38 MAPK inhibitor restores normal proliferation and reduced expression of p21(cip1) and p27(kip1) in the Atm(-/-) NSCs.	Acetylcysteine	67-70	cyclin-dependent kinase inhibitor 1A (P21)	Mus musculus	157-160
9409271-8	1997	Oxidative stress appeared to be involved in this effect, as the antioxidant N-acetylcysteine diminished TF mRNA accumulation in stimulated monocytes.	Acetylcysteine	76-92	coagulation factor III, tissue factor	Homo sapiens	104-106
19544430-7	2009	Treatment of these cells with the antioxidant N-acetyl-L-cysteine (NAC) or with a p38 MAPK inhibitor restores normal proliferation and reduced expression of p21(cip1) and p27(kip1) in the Atm(-/-) NSCs.	Acetylcysteine	67-70	cyclin-dependent kinase inhibitor 1A (P21)	Mus musculus	161-165
19544430-7	2009	Treatment of these cells with the antioxidant N-acetyl-L-cysteine (NAC) or with a p38 MAPK inhibitor restores normal proliferation and reduced expression of p21(cip1) and p27(kip1) in the Atm(-/-) NSCs.	Acetylcysteine	67-70	cyclin-dependent kinase inhibitor 1B	Mus musculus	171-174
19544430-7	2009	Treatment of these cells with the antioxidant N-acetyl-L-cysteine (NAC) or with a p38 MAPK inhibitor restores normal proliferation and reduced expression of p21(cip1) and p27(kip1) in the Atm(-/-) NSCs.	Acetylcysteine	67-70	cyclin-dependent kinase inhibitor 1B	Mus musculus	175-179
15208668-12	2004	Inhibitor (PD980590, SB203580) and ROS scavenger (NAC) studies revealed that the upstream signalings for the transcription factors AP-1 and NF-kappaB were MAPK and ROS, respectively.	Acetylcysteine	50-53	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	131-135
15361285-8	2004	Anti-oxidants, catalase and N-acetyl-cysteine significantly decreased the release of WPB by 34% and 79% in control cells, and further decreased by 63.6% and 46.7% in rac-N17 transferred cells compared with non-infected cells.	Acetylcysteine	28-45	Rac family small GTPase 1	Homo sapiens	166-169
19503098-3	2009	The use of the LOX inhibitor nordihydroguaiaretic acid (NDGA) and of the anti-oxidant N-acetylcysteine (NAC) demonstrated that ROS are important in maintaining the ALK kinase active.	Acetylcysteine	86-102	ALK receptor tyrosine kinase	Homo sapiens	164-167
9316488-7	1997	NAC decreased GSH levels (1.4-fold) and gamma-GT activity (1.8-fold) in the air-exposed type II cells.	Acetylcysteine	0-3	gamma-glutamyltransferase 1	Rattus norvegicus	40-48
19503098-3	2009	The use of the LOX inhibitor nordihydroguaiaretic acid (NDGA) and of the anti-oxidant N-acetylcysteine (NAC) demonstrated that ROS are important in maintaining the ALK kinase active.	Acetylcysteine	104-107	ALK receptor tyrosine kinase	Homo sapiens	164-167
15276427-10	2004	N-acetyl-l-cysteine (NAC) reduced cellular arsenic content in DMA(V)-exposed cells and also decreased the cytotoxicity of DMA(V), whereas it changed neither cellular arsenic content nor the viability in MMA(V)-exposed cells.	Acetylcysteine	0-19	X-linked Kx blood group	Homo sapiens	21-24
15234189-8	2004	MK-801, a non-competitive N-methyl-D-aspartate (NMDA) receptor antagonist, and ROS scavenger N-acetylcysteine obviously blocked ROS generation and attenuated the changes of both expression and activity of P-gp induced by glutamate in RBMECs.	Acetylcysteine	93-109	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	205-209
19362172-1	2009	Aminoacylase 3 (AA3) deacetylates N-acetyl-aromatic amino acids and mercapturic acids including N-acetyl-1,2-dichlorovinyl-L-cysteine (Ac-DCVC), a metabolite of a xenobiotic trichloroethylene.	Acetylcysteine	68-85	aspartoacylase (aminoacylase) 3	Mus musculus	0-14
9316488-8	1997	In the 60% O2-exposed group, no effects of NAC were seen (except for a decrease in gamma-GT mRNA expression), but, in the 85% O2-exposed group, NAC gave rise to higher GSH (2.6-fold) and higher gamma-GT activity (2.9-fold) in the ELF and lower GSH (6.9-fold) and higher gamma-GT activity (3.6-fold) in the type II cells.	Acetylcysteine	144-147	gamma-glutamyltransferase 1	Rattus norvegicus	83-91
19362172-1	2009	Aminoacylase 3 (AA3) deacetylates N-acetyl-aromatic amino acids and mercapturic acids including N-acetyl-1,2-dichlorovinyl-L-cysteine (Ac-DCVC), a metabolite of a xenobiotic trichloroethylene.	Acetylcysteine	68-85	aspartoacylase (aminoacylase) 3	Mus musculus	16-19
19117669-3	2009	Post-irradiation treatment with N-acetyl-L-cysteine (NAC) inhibited cytochrome c release from mitochondria but did not affect expression levels of Bcl-2, Bcl-X(L) and Bax, suggesting that late production of ROS triggered cytochrome c release.	Acetylcysteine	32-51	X-linked Kx blood group	Homo sapiens	53-56
9316488-8	1997	In the 60% O2-exposed group, no effects of NAC were seen (except for a decrease in gamma-GT mRNA expression), but, in the 85% O2-exposed group, NAC gave rise to higher GSH (2.6-fold) and higher gamma-GT activity (2.9-fold) in the ELF and lower GSH (6.9-fold) and higher gamma-GT activity (3.6-fold) in the type II cells.	Acetylcysteine	144-147	gamma-glutamyltransferase 1	Rattus norvegicus	194-202
15183191-12	2004	Finally, LPS-induced downregulation of PXR and CYP3A11 mRNA was prevented in mice pretreated with either N-acetylcysteine or ascorbic acid.	Acetylcysteine	105-121	nuclear receptor subfamily 1, group I, member 2	Mus musculus	39-42
15183191-12	2004	Finally, LPS-induced downregulation of PXR and CYP3A11 mRNA was prevented in mice pretreated with either N-acetylcysteine or ascorbic acid.	Acetylcysteine	105-121	cytochrome P450, family 3, subfamily a, polypeptide 11	Mus musculus	47-54
9316488-8	1997	In the 60% O2-exposed group, no effects of NAC were seen (except for a decrease in gamma-GT mRNA expression), but, in the 85% O2-exposed group, NAC gave rise to higher GSH (2.6-fold) and higher gamma-GT activity (2.9-fold) in the ELF and lower GSH (6.9-fold) and higher gamma-GT activity (3.6-fold) in the type II cells.	Acetylcysteine	144-147	gamma-glutamyltransferase 1	Rattus norvegicus	194-202
19280714-3	2009	CSE induced cPLA2 protein and mRNA expression, and ROS generation was attenuated by pretreatment with a reactive oxygen species (ROS) scavenger (N-acetylcysteine), or inhibitors of NADPH oxidase (diphenyleneiodonium chloride, apocynin) and transfection with p47phox siRNA, suggesting that CSE-induced cPLA2 expression was mediated through NADPH oxidase activation and ROS production in HTSMCs.	Acetylcysteine	145-161	neutrophil cytosolic factor 1	Homo sapiens	258-265
9277499-0	1997	Distinct mechanisms for N-acetylcysteine inhibition of cytokine-induced E-selectin and VCAM-1 expression.	Acetylcysteine	24-40	selectin E	Homo sapiens	72-82
19280714-3	2009	CSE induced cPLA2 protein and mRNA expression, and ROS generation was attenuated by pretreatment with a reactive oxygen species (ROS) scavenger (N-acetylcysteine), or inhibitors of NADPH oxidase (diphenyleneiodonium chloride, apocynin) and transfection with p47phox siRNA, suggesting that CSE-induced cPLA2 expression was mediated through NADPH oxidase activation and ROS production in HTSMCs.	Acetylcysteine	145-161	phospholipase A2 group IVA	Homo sapiens	301-306
19153832-0	2009	N-acetyl cysteine enhances imatinib-induced apoptosis of Bcr-Abl+ cells by endothelial nitric oxide synthase-mediated production of nitric oxide.	Acetylcysteine	0-17	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	57-64
19153832-4	2009	MATERIALS AND METHODS: Effects of imatinib and NAC either alone or in combination were assessed on Bcr-Abl(+) cells to measure apoptosis.	Acetylcysteine	47-50	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	99-106
19153832-6	2009	We report that imatinib-induced apoptosis of imatinib-resistant and imatinib-sensitive Bcr-Abl(+) CML cell lines and primary cells from CML patients is significantly enhanced by co-treatment with NAC compared to imatinib treatment alone.	Acetylcysteine	196-199	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	87-94
19153832-12	2009	CONCLUSION: NAC enhances imatinib-induced apoptosis of Bcr-Abl(+) cells by endothelial nitric oxide synthase-mediated production of nitric oxide.	Acetylcysteine	12-15	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	55-62
15182952-4	2004	In an animal model study, NAC and OTC showed a preventive effect against MPTP-induced loss of tyrosine hydroxylase-positive neurons, and suppressed the nuclear translocation of c-jun N-terminal kinase (JNK), suggesting that NAC and OTC can prevent MPTP-induced apoptosis by suppressing JNK activation.	Acetylcysteine	26-29	mitogen-activated protein kinase 8	Mus musculus	177-200
15182952-4	2004	In an animal model study, NAC and OTC showed a preventive effect against MPTP-induced loss of tyrosine hydroxylase-positive neurons, and suppressed the nuclear translocation of c-jun N-terminal kinase (JNK), suggesting that NAC and OTC can prevent MPTP-induced apoptosis by suppressing JNK activation.	Acetylcysteine	26-29	mitogen-activated protein kinase 8	Mus musculus	202-205
15182952-4	2004	In an animal model study, NAC and OTC showed a preventive effect against MPTP-induced loss of tyrosine hydroxylase-positive neurons, and suppressed the nuclear translocation of c-jun N-terminal kinase (JNK), suggesting that NAC and OTC can prevent MPTP-induced apoptosis by suppressing JNK activation.	Acetylcysteine	26-29	mitogen-activated protein kinase 8	Mus musculus	286-289
15182952-4	2004	In an animal model study, NAC and OTC showed a preventive effect against MPTP-induced loss of tyrosine hydroxylase-positive neurons, and suppressed the nuclear translocation of c-jun N-terminal kinase (JNK), suggesting that NAC and OTC can prevent MPTP-induced apoptosis by suppressing JNK activation.	Acetylcysteine	224-227	mitogen-activated protein kinase 8	Mus musculus	177-200
15182952-4	2004	In an animal model study, NAC and OTC showed a preventive effect against MPTP-induced loss of tyrosine hydroxylase-positive neurons, and suppressed the nuclear translocation of c-jun N-terminal kinase (JNK), suggesting that NAC and OTC can prevent MPTP-induced apoptosis by suppressing JNK activation.	Acetylcysteine	224-227	mitogen-activated protein kinase 8	Mus musculus	202-205
15182952-4	2004	In an animal model study, NAC and OTC showed a preventive effect against MPTP-induced loss of tyrosine hydroxylase-positive neurons, and suppressed the nuclear translocation of c-jun N-terminal kinase (JNK), suggesting that NAC and OTC can prevent MPTP-induced apoptosis by suppressing JNK activation.	Acetylcysteine	224-227	mitogen-activated protein kinase 8	Mus musculus	286-289
9013204-15	1997	A combination of both L-methionine and N-acetylcysteine or nicotinamide (at the low dose of 12.5 mg/kg IP each) resulted also in complete protection from acetaminophen-induced release of GOT and GPT.	Acetylcysteine	39-55	glutamic pyruvic transaminase, soluble	Mus musculus	195-198
19308849-7	2009	However, NAC (200 mg/kg) ip and GSH (600 mg/kg), administered orally prior to R-SO (300 mg/kg) ip, showed significant protection against liver toxicity as measured by SDH activity.	Acetylcysteine	9-12	sorbitol dehydrogenase	Mus musculus	167-170
9001590-0	1996	Effects of 4-hydroxynonenal and N-acetyl-L-cysteine on Myc-induced apoptosis.	Acetylcysteine	32-51	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	55-58
18768868-7	2008	The antioxidant N-acetylcysteine and inhibitors of p38 MAPK or serine/threonine kinase CK2 blocked PMA-dependent HO-1 gene activation.	Acetylcysteine	16-32	heme oxygenase 1	Rattus norvegicus	113-117
18512759-0	2008	N-acetylcysteine prevents beta-amyloid toxicity by a stimulatory effect on p35/cyclin-dependent kinase 5 activity in cultured cortical neurons.	Acetylcysteine	0-16	cyclin dependent kinase 5 regulatory subunit 1	Homo sapiens	75-78
18512759-5	2008	The neuroprotective effect of NAC was significantly attenuated by Cdk5 inhibitors or in neurons transfected with Cdk5 or p35 small interfering RNA (siRNA).	Acetylcysteine	30-33	cyclin dependent kinase 5 regulatory subunit 1	Homo sapiens	121-124
14656720-11	2004	The data suggest that in kidney proximal tubules, aminoacylase III plays an important role in deacetylating mercapturic acids.	Acetylcysteine	108-125	aspartoacylase (aminoacylase) 3	Mus musculus	50-66
14656720-12	2004	The predominant cytoplasmic localization of aminoacylase III may explain the greater sensitivity of the proximal straight tubule to the nephrotoxicity of mercapturic acids.	Acetylcysteine	154-171	aspartoacylase (aminoacylase) 3	Mus musculus	44-60
15093278-10	2004	For instance, in vitro SCE induction by styrene and by epoxide metabolites of 1,3-butadiene is modified by GSTM1 and GSTT1 genotypes--which also influence the excretion of specific mercapturic acids in humans exposed to butadiene and styrene.	Acetylcysteine	181-198	glutathione S-transferase theta 1	Homo sapiens	117-122
18512759-7	2008	A beta(25-35) caused a significant decrease in the level of p35, with a concomitant increase in p25, which was completely prevented by NAC.	Acetylcysteine	135-138	cyclin dependent kinase 5 regulatory subunit 1	Homo sapiens	60-63
18512759-7	2008	A beta(25-35) caused a significant decrease in the level of p35, with a concomitant increase in p25, which was completely prevented by NAC.	Acetylcysteine	135-138	cyclin dependent kinase 5 regulatory subunit 1	Homo sapiens	96-99
18512759-9	2008	In addition, NAC increased Cdk5/p35 kinase activity but reduced Cdk5 kinase activity.	Acetylcysteine	13-16	cyclin dependent kinase 5 regulatory subunit 1	Homo sapiens	32-35
18512759-13	2008	These results suggest that NAC-mediated neuroprotection against A beta toxicity is likely mediated by the p35/Cdk5-ERKs-Bcl-2 signal pathway.	Acetylcysteine	27-30	cyclin dependent kinase 5 regulatory subunit 1	Homo sapiens	106-109
14872485-10	2004	NF-kappaB inhibitors N-acetyl-L-cysteine and Bay 11-7085 and PI 3-kinase inhibitor LY294002 inhibited the enhancing effects of IL-18, but MAPK p38 inhibitor SB203580, ERK inhibitor PD98059, and JNK inhibitor SP600125 did not.	Acetylcysteine	21-40	interleukin 18	Homo sapiens	127-132
9006111-4	1996	Asbestos-induced gene expression was inhibited by millimolar levels of N-acetylcysteine (NAC), supporting a linkage between: (i) induced oxidant stress that was sufficient to promote morphological transformation; (ii) induction of proliferin expression.	Acetylcysteine	71-87	prolactin family 2, subfamily c, member 2	Mus musculus	231-241
14680076-0	2003	Oral N-acetylcysteine reduces bleomycin-induced lung damage and mucin Muc5ac expression in rats.	Acetylcysteine	5-21	mucin 5AC, oligomeric mucus/gel-forming	Rattus norvegicus	70-76
18790751-5	2008	We show that xanthohumol strongly inhibited Bcr-Abl expression at both mRNA and protein levels and show that xanthohumol caused elevation of intracellular reactive oxygen species and that the antioxidant N-acetylcysteine blunted xanthohumol-induced events.	Acetylcysteine	204-220	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	44-51
14556662-6	2003	N-Acetyl-L-cysteine (NAC) completely inhibited EA-induced cell death, but 3(2)-t-butyl-4-hydroxyanisole or pyrrolidinedithiocarbamate ammonium salt did not.	Acetylcysteine	0-19	X-linked Kx blood group	Homo sapiens	21-24
9006111-4	1996	Asbestos-induced gene expression was inhibited by millimolar levels of N-acetylcysteine (NAC), supporting a linkage between: (i) induced oxidant stress that was sufficient to promote morphological transformation; (ii) induction of proliferin expression.	Acetylcysteine	89-92	prolactin family 2, subfamily c, member 2	Mus musculus	231-241
9006111-7	1996	Latex beads and activated charcoal were effective at higher particle densities, implying that ubiquitous particle-induced surface membrane effects can lead to an NAC-reversible step necessary for proliferin induction.	Acetylcysteine	162-165	prolactin family 2, subfamily c, member 2	Mus musculus	196-206
8896414-4	1996	Both PDTC and NAC inhibited, in a dose-dependent manner, the synthesis of IL-6, IL-8, and GM-CSF induced by tumor necrosis factor (TNF)-alpha or bacterial lipopolysaccharides (LPS) in human umbilical vein endothelial cells (HUVEC).	Acetylcysteine	14-17	colony stimulating factor 2	Homo sapiens	90-96
14513055-5	2003	Bortezomib/HA14-1 treatment triggered an increase in reactive oxygen species (ROS), which, along with apoptosis, was blocked by the free radical scavenger N-acetyl-L-cysteine (L-NAC).	Acetylcysteine	155-174	X-linked Kx blood group	Homo sapiens	178-181
18234541-12	2008	The addition of NAC, curcumin, PD98059, and staurosporine markedly inhibited the arecoline-induced HSP70 expression (p&lt;0.05).	Acetylcysteine	16-19	heat shock protein family A (Hsp70) member 4	Homo sapiens	99-104
18234541-15	2008	In addition, arecoline-induced HSP70 expression was downregulated by NAC, curcumin, PD98059, and staurosporine.	Acetylcysteine	69-72	heat shock protein family A (Hsp70) member 4	Homo sapiens	31-36
8662787-7	1996	Furthermore, we show that the induction of AP-1 and NF-kappaB activities and GST Ya gene expression by BHA and TBHQ is due to a pro-oxidant activity, since this induction was inhibited by thiol compounds N-acetyl cysteine and GSH.	Acetylcysteine	204-221	glutathione S-transferase kappa 1	Homo sapiens	77-80
18438937-7	2008	Both the antioxidant N-acetyl-L-cysteine and the broad-spectrum metalloproteases inhibitor TAPI0 were able partially to inhibit shedding of RAGE, suggesting involvement of metalloproteases in cleavage to produce soluble RAGE.	Acetylcysteine	21-40	advanced glycosylation end-product specific receptor	Homo sapiens	140-144
18438937-7	2008	Both the antioxidant N-acetyl-L-cysteine and the broad-spectrum metalloproteases inhibitor TAPI0 were able partially to inhibit shedding of RAGE, suggesting involvement of metalloproteases in cleavage to produce soluble RAGE.	Acetylcysteine	21-40	advanced glycosylation end-product specific receptor	Homo sapiens	220-224
12949729-7	2003	Taurolithocholate-3-sulfate-induced EGF-R phosphorylation was sensitive to N-acetylcysteine (NAC) and genistein, whereas CD95/EGF-R association was inhibited by NAC, JNK, or protein kinase C inhibition but not by AG1478.	Acetylcysteine	75-91	epidermal growth factor receptor	Rattus norvegicus	36-41
12949729-7	2003	Taurolithocholate-3-sulfate-induced EGF-R phosphorylation was sensitive to N-acetylcysteine (NAC) and genistein, whereas CD95/EGF-R association was inhibited by NAC, JNK, or protein kinase C inhibition but not by AG1478.	Acetylcysteine	93-96	epidermal growth factor receptor	Rattus norvegicus	36-41
12949729-7	2003	Taurolithocholate-3-sulfate-induced EGF-R phosphorylation was sensitive to N-acetylcysteine (NAC) and genistein, whereas CD95/EGF-R association was inhibited by NAC, JNK, or protein kinase C inhibition but not by AG1478.	Acetylcysteine	161-164	epidermal growth factor receptor	Rattus norvegicus	126-131
8662787-8	1996	Similarly, induction of AP-1 and GST Ya gene expression by PDTC was inhibited by N-acetyl cysteine and GSH.	Acetylcysteine	81-98	glutathione S-transferase kappa 1	Homo sapiens	33-36
8669050-3	1996	In this study the effect von N-acetylcysteine (NAC) on the release of interleukin-1 alpha and beta (IL-1), interleukin-2 (IL-2), interferon-gamma (IFN-gamma) and tumornecrosisfactor-alpha (TNF-alpha) was assessed in an in vitro assay.	Acetylcysteine	47-50	interleukin 1 alpha	Homo sapiens	70-89
18456002-5	2008	By comparing the effects of MsrA and the small-molecule antioxidants N-acetylcysteine and vitamin E, we provide evidence that MsrA protects against PD-related stresses primarily via methionine sulfoxide repair rather than by scavenging reactive oxygen species.	Acetylcysteine	69-85	methionine sulfoxide reductase A	Homo sapiens	126-130
12810678-13	2003	Finally, the cytotoxicity and radiosensitizing effects of 2DG were more pronounced in v-Fos-transformed versus nontransformed immortalized rat cells, and this radiosensitization was also inhibited by treatment with NAC.	Acetylcysteine	215-218	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	88-91
7592595-5	1995	N-Acetylcysteine (NAC) and glutathione, as well as superoxide dismutase and catalase, inhibited both the increase in endogenous MT-1 mRNA and the activation of reporter gene activity by heme-hemopexin, CoPP-hemopexin, and phorbol 12-myristate 13-acetate.	Acetylcysteine	0-16	hemopexin	Mus musculus	191-200
18535259-5	2008	The induction of GCLM and NQO1 was attenuated by reduction of electrophilic groups with sodium borohydrate, as well as treatment with thiol antioxidant N-acetylcysteine, suggesting that the thiol reactivity of oxPAPC is largely mediating its effect on Nrf2-responsive genes.	Acetylcysteine	152-168	NAD(P)H dehydrogenase, quinone 1	Mus musculus	26-30
12832530-6	2003	Consequently, cotreatment with a caspase inhibitor (zVAD-fmk) or with an antioxidant (N-acetylcysteine) not only deterred 6-OHDA-induced loss of TH-positive neurons but also abolished the appearance of activated caspase-3 in TH-positive neurons.	Acetylcysteine	86-102	caspase 3	Mus musculus	212-221
7592595-5	1995	N-Acetylcysteine (NAC) and glutathione, as well as superoxide dismutase and catalase, inhibited both the increase in endogenous MT-1 mRNA and the activation of reporter gene activity by heme-hemopexin, CoPP-hemopexin, and phorbol 12-myristate 13-acetate.	Acetylcysteine	0-16	hemopexin	Mus musculus	207-216
18490076-7	2008	Conversely, hepatic NOx production, anti-oxidants, and protein expression of MnSOD were increased in NAC-treated BDL rat livers.	Acetylcysteine	101-104	superoxide dismutase 2	Rattus norvegicus	77-82
7592595-5	1995	N-Acetylcysteine (NAC) and glutathione, as well as superoxide dismutase and catalase, inhibited both the increase in endogenous MT-1 mRNA and the activation of reporter gene activity by heme-hemopexin, CoPP-hemopexin, and phorbol 12-myristate 13-acetate.	Acetylcysteine	18-21	hemopexin	Mus musculus	191-200
7592595-5	1995	N-Acetylcysteine (NAC) and glutathione, as well as superoxide dismutase and catalase, inhibited both the increase in endogenous MT-1 mRNA and the activation of reporter gene activity by heme-hemopexin, CoPP-hemopexin, and phorbol 12-myristate 13-acetate.	Acetylcysteine	18-21	hemopexin	Mus musculus	207-216
12763371-7	2003	HO-1 induction and hepatic damage were increased by BSO and only HO-1 induction was attenuated by the antioxidant N-acetylcysteine.	Acetylcysteine	114-130	heme oxygenase 1	Rattus norvegicus	0-4
7638759-7	1995	RESULTS: Exposure of the macrophage to the antioxidants vitamin E and NAC inhibited TNF production, accumulation of TNF messenger RNA, procoagulant activity expression, and prostaglandin E2 production.	Acetylcysteine	70-73	tumor necrosis factor	Oryctolagus cuniculus	84-87
12763371-7	2003	HO-1 induction and hepatic damage were increased by BSO and only HO-1 induction was attenuated by the antioxidant N-acetylcysteine.	Acetylcysteine	114-130	heme oxygenase 1	Rattus norvegicus	65-69
12857601-8	2003	The release of IL-8 from SAA-stimulated neutrophils is strongly suppressed by the addition of N-acetyl-l-cysteine, alpha-mercaptoethanol, glutathione, and dexamethasone.	Acetylcysteine	94-113	serum amyloid A1 cluster	Homo sapiens	25-28
18368580-1	2008	CONCLUSION: L-N-Acetylcysteine (L-NAC) significantly reduced reactive oxygen species (ROS) generation and cochlear cell apoptosis after irradiation.	Acetylcysteine	12-30	NLR family, pyrin domain containing 1A	Mus musculus	34-37
18304734-0	2008	Inhibition of brain creatine kinase activity after renal ischemia is attenuated by N-acetylcysteine and deferoxamine administration.	Acetylcysteine	83-99	creatine kinase B	Rattus norvegicus	14-35
18441387-8	2008	Infarct-sparing effect of PAF was abolished by N-acetyl-L-cysteine and 5-hydroxydecanoate.	Acetylcysteine	47-66	PCNA clamp associated factor	Rattus norvegicus	26-29
12712633-8	2003	On the other hand, N-acetylcysteine prevented cisplatin-induced apoptosis as well as c-myc induction but not p53 induction.	Acetylcysteine	19-35	MYC proto-oncogene, bHLH transcription factor	Sus scrofa	85-90
7638759-7	1995	RESULTS: Exposure of the macrophage to the antioxidants vitamin E and NAC inhibited TNF production, accumulation of TNF messenger RNA, procoagulant activity expression, and prostaglandin E2 production.	Acetylcysteine	70-73	tumor necrosis factor	Oryctolagus cuniculus	116-119
17728093-9	2008	Pretreatment with N-acetyl cysteine (NAC), a GSH precursor, prevented enzymatic changes in CAT, Se-dependent GSH-Px, GR, SOD1 activities, and significantly decreased SOD2 activity following exposure to thiram.	Acetylcysteine	18-35	catalase	Cricetulus griseus	91-94
17728093-9	2008	Pretreatment with N-acetyl cysteine (NAC), a GSH precursor, prevented enzymatic changes in CAT, Se-dependent GSH-Px, GR, SOD1 activities, and significantly decreased SOD2 activity following exposure to thiram.	Acetylcysteine	18-35	superoxide dismutase [Mn], mitochondrial	Cricetulus griseus	166-170
7737603-3	1995	Consistent with its response to other oxidant chemicals, induction of proliferin by ammonium metavanadate was inhibited almost completely by the antioxidant N-acetylcysteine (8 mM).	Acetylcysteine	157-173	prolactin family 2, subfamily c, member 2	Mus musculus	70-80
17728093-9	2008	Pretreatment with N-acetyl cysteine (NAC), a GSH precursor, prevented enzymatic changes in CAT, Se-dependent GSH-Px, GR, SOD1 activities, and significantly decreased SOD2 activity following exposure to thiram.	Acetylcysteine	37-40	catalase	Cricetulus griseus	91-94
17728093-9	2008	Pretreatment with N-acetyl cysteine (NAC), a GSH precursor, prevented enzymatic changes in CAT, Se-dependent GSH-Px, GR, SOD1 activities, and significantly decreased SOD2 activity following exposure to thiram.	Acetylcysteine	37-40	superoxide dismutase [Mn], mitochondrial	Cricetulus griseus	166-170
19099954-7	2008	The mRNA and protein expression of p16INK4a and p21WAF1 were also significantly higher in the group of 5-day + NAC and 10-day + NAC compared with 5-day, 10-day, respectively (P &lt; 0.05 or P &lt; 0.01).	Acetylcysteine	111-114	cyclin-dependent kinase inhibitor 2A	Rattus norvegicus	35-43
19099954-7	2008	The mRNA and protein expression of p16INK4a and p21WAF1 were also significantly higher in the group of 5-day + NAC and 10-day + NAC compared with 5-day, 10-day, respectively (P &lt; 0.05 or P &lt; 0.01).	Acetylcysteine	128-131	cyclin-dependent kinase inhibitor 2A	Rattus norvegicus	35-43
19099954-10	2008	CONCLUSION: NAC could promote aging through upregulating the expression of p16INK4a and p21WAF1 and inhibiting Rb phosphorylation in neonatal SD rat cardiomyocytes.	Acetylcysteine	12-15	cyclin-dependent kinase inhibitor 2A	Rattus norvegicus	75-83
12629154-6	2003	N-acetyl L-cysteine significantly inhibited the translocation of AIF induced by UVB.	Acetylcysteine	0-19	apoptosis inducing factor mitochondria associated 1	Homo sapiens	65-68
12590163-5	2003	Our results show that AGEs induce lipid peroxidation in a neuronal cell line in a dose-dependant manner, and that blocking the specific AGE-receptor RAGE, as well as using different antioxidants (alpha-lipoic acid, N-acetylcysteine, 17 beta-estradiol or aminoguanidine) can reduce the AGE-mediated formation of lipid peroxidation products.	Acetylcysteine	215-231	advanced glycosylation end-product specific receptor	Homo sapiens	149-153
7889134-15	1994	CONCLUSION: These data indicate that N-AC administration in endotoxic shock is well tolerated, may increase oxygen availability to the tissues, and is associated with an attenuation of TNF release.	Acetylcysteine	37-41	tumor necrosis factor	Canis lupus familiaris	185-188
12368297-4	2002	This strain-induced PYK2 and Src phosphorylation was inhibited by pretreating ECs with an antioxidant N-acetylcysteine.	Acetylcysteine	102-118	protein tyrosine kinase 2 beta	Bos taurus	20-24
12480817-5	2002	Antioxidants, including N-acetylcysteine (NAC), various NAD(P)H oxidase inhibitors, and N17Rac1 significantly attenuate not only VEGF-induced KDR tyrosine phosphorylation but also proliferation and migration of ECs.	Acetylcysteine	24-40	vascular endothelial growth factor A	Mus musculus	129-133
17916640-8	2008	Preincubation of fetal liver HSCs with N-acetylcysteine, a glutathione (GSH) precursor, caused an increase in cellular GSH concentrations, restored mitochondrial redox status, and ameliorated the toxicity of BDE 47.	Acetylcysteine	39-55	homeobox D13	Homo sapiens	208-211
18096486-7	2007	NAC also resulted in significantly fewer macrophages, lymphocytes and neutrophils as well as IL-1 beta, keratinocyte cytokine (KC), monocyte chemoattractant protein (MCP)-1 and IL-6 levels in BAL taken after reperfusion.	Acetylcysteine	0-3	chemokine (C-C motif) ligand 2	Mus musculus	132-172
17959032-9	2007	Furthermore, NAC pretreatment significantly alleviated GalN/LPS-induced hepatic apoptosis, measured by the inhibition of hepatic caspase-3 activity and attenuation of DNA laddering.	Acetylcysteine	13-16	caspase 3	Mus musculus	129-138
12480817-5	2002	Antioxidants, including N-acetylcysteine (NAC), various NAD(P)H oxidase inhibitors, and N17Rac1 significantly attenuate not only VEGF-induced KDR tyrosine phosphorylation but also proliferation and migration of ECs.	Acetylcysteine	42-45	vascular endothelial growth factor A	Mus musculus	129-133
12480817-8	2002	Sponge implant assays demonstrate that VEGF-, but not S1P-, induced angiogenesis is significantly reduced in wild-type mice treated with NAC and in gp91(phox-/-) mice, suggesting that ROS derived from gp91(phox)-containing NAD(P)H oxidase play an important role in angiogenesis in vivo.	Acetylcysteine	137-140	vascular endothelial growth factor A	Mus musculus	39-43
7954424-3	1994	GGT catalyzes the initial step in the metabolism of glutathione-conjugated drugs to mercapturic acids, some of which are severely nephrotoxic.	Acetylcysteine	84-101	gamma-glutamyltransferase 1	Rattus norvegicus	0-3
12426206-5	2002	The activation of PYK2 and phosphorylation of Cas induced by flow were inhibited by pretreatment with the antioxidant N-acetylcysteine.	Acetylcysteine	118-134	protein tyrosine kinase 2 beta	Bos taurus	18-22
17761673-6	2007	Using an antibody that specifically recognizes sulfinylated and sulfonylated Prxs, it is demonstrated that primary rat cortical nerve cells exposed to Abeta display a time-dependent increase in cysteine oxidation of the catalytic site of Prxs that can be blocked by the addition of the thiol-antioxidant N-acetylcysteine.	Acetylcysteine	304-320	amyloid beta precursor protein	Rattus norvegicus	151-156
17596533-10	2007	It is concluded that both NAC and taurine significantly attenuated HG-induced activation of the Raf-1/MAPK and the JAK2-STAT1/STAT3 signaling pathways and hypertrophic growth in renal tubular epithelial cells.	Acetylcysteine	26-29	signal transducer and activator of transcription 1	Homo sapiens	120-125
17868448-9	2007	MAdCAM-1 expression was also reduced by N-acetylcysteine and by two NO donors (SperNO, DETANO) suggesting that hepatic endothelial MAdCAM-1 is oxidant and NO regulated.	Acetylcysteine	40-56	mucosal vascular addressin cell adhesion molecule 1	Mus musculus	0-8
17868448-9	2007	MAdCAM-1 expression was also reduced by N-acetylcysteine and by two NO donors (SperNO, DETANO) suggesting that hepatic endothelial MAdCAM-1 is oxidant and NO regulated.	Acetylcysteine	40-56	mucosal vascular addressin cell adhesion molecule 1	Mus musculus	131-139
12353212-2	2002	The aim of the present work was to study if exogenous administration of one lipid peroxide, the isoprostane 8-iso-PGF(2alpha), is teratogenic per se in rat embryos in vitro, and if such teratological effects may be diminished by supplementation of an antioxidative agent, i.e., N-acetylcysteine or superoxide dismutase, to the culture medium.	Acetylcysteine	278-294	placental growth factor	Rattus norvegicus	114-117
12353212-5	2002	Adding N-acetylcysteine or superoxide dismutase to the culture medium with isoprostane normalized almost all morphological and biochemical parameters, including the elevated tissue concentration of 8-iso-PGF(2alpha).	Acetylcysteine	7-23	placental growth factor	Rattus norvegicus	204-207
17707397-6	2007	Attenuation of oxidative stress, downregulation of the pro-inflammatory cytokine tumor necrosis factor-alpha (TNF-alpha) and its TNF-R1 receptor were significant after 1-month NAC treatment.	Acetylcysteine	176-179	TNF receptor superfamily member 1A	Rattus norvegicus	129-135
8207209-0	1994	Use of N-acetyl cysteine to increase intracellular glutathione during the induction of antitumor responses by IL-2.	Acetylcysteine	7-24	interleukin 2	Mus musculus	110-114
17707397-8	2007	NAC treatment in post-MI rats is a way to disrupt the vicious sTNF-alpha/TNF-R1/N-SMase cycle.	Acetylcysteine	0-3	TNF receptor superfamily member 1A	Rattus norvegicus	73-79
17696279-7	2007	NAC in combination with vanadate appeared to increase the efficacy of c-fos/c-jun inhibition, while decreasing toxicity.	Acetylcysteine	0-3	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	70-75
12393931-6	2002	Anti-AGE-R1,2,3 and -RAGE IgG each inhibited cell-associated (125) I-dAGE by approximately 30-55%; GSH/GPx were effectively blocked by N-acetyl-cysteine (NAC, 800 uM, p &lt; 0.01) and aminoguanidine-HCl (AG, 100 uM, p &lt; 0.01).	Acetylcysteine	135-152	long intergenic non-protein coding RNA 914	Homo sapiens	21-25
12393931-6	2002	Anti-AGE-R1,2,3 and -RAGE IgG each inhibited cell-associated (125) I-dAGE by approximately 30-55%; GSH/GPx were effectively blocked by N-acetyl-cysteine (NAC, 800 uM, p &lt; 0.01) and aminoguanidine-HCl (AG, 100 uM, p &lt; 0.01).	Acetylcysteine	154-157	long intergenic non-protein coding RNA 914	Homo sapiens	21-25
12027535-10	2002	On the other hand, NAC was capable of counteracting the LPS-induced inhibition of TGF-beta2 expression.	Acetylcysteine	19-22	transforming growth factor beta 2	Homo sapiens	82-91
8207209-3	1994	N-Acetyl cysteine (NAc-cys) was used to increase intracellular glutathione levels during lymphokine-activated killer (LAK) cell activation by IL-2.	Acetylcysteine	0-17	interleukin 2	Mus musculus	142-146
12061835-7	2002	IL-12 dimer formation appears to be reduced by NAC also in vivo, because pretreatment with NAC (1 g/kg, orally), before LPS injection in mice, inhibited peak IL-12 p75 serum levels without affecting those of p40.	Acetylcysteine	91-94	interleukin 12b	Mus musculus	208-211
8145281-8	1994	This interorgan model of mercapturic acid synthesis is based largely on the interorgan distribution of the enzymes involved in their formation, and in particular of the enzyme gamma-glutamyltransferase.	Acetylcysteine	25-41	gamma-glutamyltransferase 1	Rattus norvegicus	176-201
11828388-6	2002	RESULTS: Pretreatment of cells with NAC prior to Ad infection enhanced beta-Gal activity by two-fold due to an increase in viral DNA, which was related to increased CAR expression.	Acetylcysteine	36-39	CXADR Ig-like cell adhesion molecule	Homo sapiens	165-168
17545941-4	2007	Mice subjected to HS and resuscitated with Ringer"s ethyl pyruvate solution (REPS) or N-acetylcysteine (NAC), two scavengers of ROS, demonstrated decreased levels of phosphorylated JNK.	Acetylcysteine	86-102	mitogen-activated protein kinase 8	Mus musculus	181-184
17545941-4	2007	Mice subjected to HS and resuscitated with Ringer"s ethyl pyruvate solution (REPS) or N-acetylcysteine (NAC), two scavengers of ROS, demonstrated decreased levels of phosphorylated JNK.	Acetylcysteine	104-107	mitogen-activated protein kinase 8	Mus musculus	181-184
17376491-11	2007	In contrast, we found that addition of N-acetylcysteine or vitamin C enhanced transcription of MCP-1 by B[a]P. In conclusion, our studies revealed potent vascular pro-inflammatory effects of B[a]P, as evidenced by AhR-mediated induction of MCP-1.	Acetylcysteine	39-55	chemokine (C-C motif) ligand 2	Mus musculus	95-100
11704541-4	2001	Increased expression of MMP-9 and NF-kappa B activation induced by TNF-alpha were inhibited by pyrrolidine dithiocarbamate and N-acetyl-L-cysteine but were not inhibited by curcumin.	Acetylcysteine	127-146	matrix metallopeptidase 9	Homo sapiens	24-29
17376491-11	2007	In contrast, we found that addition of N-acetylcysteine or vitamin C enhanced transcription of MCP-1 by B[a]P. In conclusion, our studies revealed potent vascular pro-inflammatory effects of B[a]P, as evidenced by AhR-mediated induction of MCP-1.	Acetylcysteine	39-55	chemokine (C-C motif) ligand 2	Mus musculus	240-245
8361551-1	1993	The effect of N-acetyl-L-cysteine on the cytotoxicity of tumor necrosis factor-alpha was investigated in cultured bovine pulmonary artery endothelial cells and L929 mouse tumor cells.	Acetylcysteine	14-33	tumor necrosis factor	Bos taurus	57-84
17616699-9	2007	These results show that an O(2)(*-) signaling pathway regulates NAC-induced G(1) arrest by decreasing cyclin D1 protein levels and increasing MnSOD activity.	Acetylcysteine	64-67	cyclin D1	Mus musculus	102-111
11532081-11	2001	HG conditioned cells were also treated with the antioxidants L-N-acetylcysteine (L-NAC) or diphenyliodonium (DPI) prior to harvest.	Acetylcysteine	61-79	X-linked Kx blood group	Homo sapiens	83-86
17468103-1	2007	In murine embryonic fibroblasts, N-acetyl-L-cysteine (NAC), a GSH generating agent, enhances hypoxic apoptosis by blocking the NFkappaB survival pathway (Qanungo, S., Wang, M., and Nieminen, A. L. (2004) J. Biol.	Acetylcysteine	33-52	X-linked Kx blood group	Homo sapiens	54-57
1452401-1	1992	In this study we evaluated the effects of N-acetyl-cysteine and indomethacin in restoring IL-2 producing ability in vitro of splenocytes from mice infected with Trypanosoma equiperdum.	Acetylcysteine	42-59	interleukin 2	Mus musculus	90-94
17615545-9	2007	Early NAC-treated retinas had significantly reduced LHP compared to PBS-control at p18 (p&lt;0.012).	Acetylcysteine	6-9	cyclin-dependent kinase inhibitor 2C	Rattus norvegicus	83-86
11344087-6	2001	The degree of staining for the ICAM-1, P-selectin, nitrotyrosine, and PARS was reduced by NAC.	Acetylcysteine	90-93	intercellular adhesion molecule 1	Rattus norvegicus	31-37
1452401-5	1992	In fact, the IL-2-producing ability of lymphocytes from infected mice could be efficiently restored by in vitro exposure to N-acetyl-cysteine or indomethacin.	Acetylcysteine	124-141	interleukin 2	Mus musculus	13-17
11341511-6	2001	At 28 days, bound thrombin activity and platelet adhesion 1 h after a repeated balloon injury decreased in animals receiving NAC, HEP and NAC+HEP bv 54%, 63% and 64% for thrombin activity (p &lt;0.05 vs CONTROLS), and by 56%, 66% and 75% respectively for 111Indium-platelet deposition (p &lt;0.05 vs CONTROLS).	Acetylcysteine	125-128	prothrombin	Oryctolagus cuniculus	18-26
17526765-3	2007	The role of reactive oxygen species (ROS) as mediators in the expression of ICAM-1 and CD11b/CD18 was examined by using N-acetylcysteine (NAC) as an antioxidant treatment.	Acetylcysteine	120-136	intercellular adhesion molecule 1	Homo sapiens	76-82
17526765-3	2007	The role of reactive oxygen species (ROS) as mediators in the expression of ICAM-1 and CD11b/CD18 was examined by using N-acetylcysteine (NAC) as an antioxidant treatment.	Acetylcysteine	120-136	integrin subunit alpha M	Homo sapiens	87-92
11341511-6	2001	At 28 days, bound thrombin activity and platelet adhesion 1 h after a repeated balloon injury decreased in animals receiving NAC, HEP and NAC+HEP bv 54%, 63% and 64% for thrombin activity (p &lt;0.05 vs CONTROLS), and by 56%, 66% and 75% respectively for 111Indium-platelet deposition (p &lt;0.05 vs CONTROLS).	Acetylcysteine	125-128	prothrombin	Oryctolagus cuniculus	170-178
11341511-6	2001	At 28 days, bound thrombin activity and platelet adhesion 1 h after a repeated balloon injury decreased in animals receiving NAC, HEP and NAC+HEP bv 54%, 63% and 64% for thrombin activity (p &lt;0.05 vs CONTROLS), and by 56%, 66% and 75% respectively for 111Indium-platelet deposition (p &lt;0.05 vs CONTROLS).	Acetylcysteine	138-141	prothrombin	Oryctolagus cuniculus	18-26
17526765-3	2007	The role of reactive oxygen species (ROS) as mediators in the expression of ICAM-1 and CD11b/CD18 was examined by using N-acetylcysteine (NAC) as an antioxidant treatment.	Acetylcysteine	138-141	intercellular adhesion molecule 1	Homo sapiens	76-82
1309791-2	1992	The reactivity of several thiols, including glutathione, dihydrolipoic acid, cysteine, N-acetyl cysteine, and ergothioneine, as well as several disulfides, toward different redox states of myoglobin, mainly met-myoglobin (HX-FeIII) and ferrylmyoglobin (HX-FeIV=O), was evaluated by optical spectral analysis, product formation, and thiyl free radical generation.	Acetylcysteine	87-104	myoglobin	Homo sapiens	189-198
17526765-6	2007	Since NAC treatment reduced neutrophil infiltration in the pancreas, we conclude that CD11b/CD18 over-expression is required for leukocyte recruitment; however, other adhesion molecules in addition to ICAM-1 seem to contribute to leukocyte homing during BPDO-induced AP.	Acetylcysteine	6-9	integrin subunit alpha M	Homo sapiens	86-91
17526765-6	2007	Since NAC treatment reduced neutrophil infiltration in the pancreas, we conclude that CD11b/CD18 over-expression is required for leukocyte recruitment; however, other adhesion molecules in addition to ICAM-1 seem to contribute to leukocyte homing during BPDO-induced AP.	Acetylcysteine	6-9	intercellular adhesion molecule 1	Homo sapiens	201-207
17456219-3	2007	OBJECTIVE: The aim of this work was to study the effects of the clinically used antioxidant N-acetyl-L-cysteine (NAC) on the functional responses of human-isolated eosinophils.	Acetylcysteine	92-111	X-linked Kx blood group	Homo sapiens	113-116
11341511-6	2001	At 28 days, bound thrombin activity and platelet adhesion 1 h after a repeated balloon injury decreased in animals receiving NAC, HEP and NAC+HEP bv 54%, 63% and 64% for thrombin activity (p &lt;0.05 vs CONTROLS), and by 56%, 66% and 75% respectively for 111Indium-platelet deposition (p &lt;0.05 vs CONTROLS).	Acetylcysteine	138-141	prothrombin	Oryctolagus cuniculus	170-178
11273999-8	2001	Treatment with 2 different antioxidants, Trolox or N:-acetylcysteine, only partially rescued the H(mox-1)(+/)(-) hearts from ischemia/reperfusion injury.	Acetylcysteine	51-68	mesenchyme homeobox 1	Mus musculus	99-104
2059159-0	1991	Genetic deficiency of human class mu glutathione S-transferase isoenzymes in relation to the urinary excretion of the mercapturic acids of Z- and E-1,3-dichloropropene.	Acetylcysteine	118-135	glutathione S-transferase kappa 1	Homo sapiens	37-62
11171565-6	2001	Likewise, the NF-kappaB inhibitors pyrrolidine dithiocarbamate and N-acetyl-L-cysteine inhibited CCK stimulation of NF-kappaB and intracellular trypsinogen activation.	Acetylcysteine	67-86	cholecystokinin	Rattus norvegicus	97-100
17135302-9	2007	In addition, IL-1beta could induce the production of reactive oxygen species (ROS), and N-acetyl-L-cysteine, a scavenger of ROS, reversed the decreased level of ABCA1 induced by IL-1beta.	Acetylcysteine	88-107	ATP binding cassette subfamily A member 1	Homo sapiens	161-166
11298119-1	2001	The thiol antioxidant N-acetyl- L-cysteine (NAC), known as a precursor of glutathione (GSH), is used in AIDS treatment trials, as a chemoprotectant in cancer chemotherapy and in treatment of chronic bronchitis.	Acetylcysteine	22-42	X-linked Kx blood group	Homo sapiens	44-47
33772418-6	2021	While NAC treatment improved TAC and IL-10 values, it decreased MDA and TNF-alpha levels in the liver of rats exposed to Cd (P < 0.001).	Acetylcysteine	6-9	interleukin 10	Rattus norvegicus	37-42
33772418-7	2021	NAC decreased Bax/Bcl2 in the liver of G4 and G5 groups (P < 0.001).	Acetylcysteine	0-3	BCL2 associated X, apoptosis regulator	Rattus norvegicus	14-17
16930891-2	2007	N-acetyl-L-cysteine (L-NAC) has been shown to be protective against noise exposure, a condition that leads to increased oxidative stress.	Acetylcysteine	0-19	NLR family, pyrin domain containing 1A	Mus musculus	23-26
11299737-0	2001	Inhibitory effect of N-acetylcysteine on invasion and MMP-9 production of T24 human bladder cancer cells.	Acetylcysteine	21-37	matrix metallopeptidase 9	Homo sapiens	54-59
33772418-9	2021	NAC increased Fxr, LXRalpha, and Sirt1 expression (P < 0.01) and decreased Cd concentrations in both serum and tissue samples in G4 and G5 groups.	Acetylcysteine	0-3	nuclear receptor subfamily 1, group H, member 4	Rattus norvegicus	14-17
11156586-7	2001	Human pulmonary vascular endothelial cells that had been preincubated with NAC were stimulated with TNF-alpha and then the activation of p38 MAP kinase and MKK3/MKK6 in the cells and IL-8 concentrations in the culture supernatants were determined.	Acetylcysteine	75-78	mitogen-activated protein kinase kinase 3	Homo sapiens	156-160
17270171-0	2007	Effect of N-acetylcysteine on plasma adiponectin and renal adiponectin receptors in streptozotocin-induced diabetic rats.	Acetylcysteine	10-26	adiponectin, C1Q and collagen domain containing	Rattus norvegicus	59-70
17253623-7	2007	Protection by NAC was associated with the following factors: (1) reduced isoprostane activation and nitrotyrosine formation; (2) increased levels of the antioxidants glutathione, thioredoxin-2, and (3) inhibition of caspase-3, calpain, and caspase-1 activation.	Acetylcysteine	14-17	thioredoxin 2	Rattus norvegicus	179-192
17253623-7	2007	Protection by NAC was associated with the following factors: (1) reduced isoprostane activation and nitrotyrosine formation; (2) increased levels of the antioxidants glutathione, thioredoxin-2, and (3) inhibition of caspase-3, calpain, and caspase-1 activation.	Acetylcysteine	14-17	caspase 1	Rattus norvegicus	240-249
11156586-11	2001	NAC attenuated TNF-alpha-induced activation of p38 MAP kinase and MKK3/MKK6.	Acetylcysteine	0-3	mitogen-activated protein kinase kinase 3	Homo sapiens	66-70
11112413-5	2000	Furthermore, pretreatment of C6 cells with N-acetyl-l-cysteine (NAC), an antioxidant, nullified the inhibitory effect of iNOS on HIF-1 binding.	Acetylcysteine	43-62	X-linked Kx blood group	Homo sapiens	64-67
11428623-9	2000	The NAC treatment yielded LDH, ALB and TP values that, although elevated, were not significantly different from the control.	Acetylcysteine	4-7	albumin	Rattus norvegicus	31-34
33772418-10	2021	Our results suggested that NAC protects liver tissue against Cd toxicity by elevating antioxidant capacity, mitigating oxidative stress, inflammation, apoptosis and up-regulation of FXR, LXR, and SIRT1 genes.	Acetylcysteine	27-30	nuclear receptor subfamily 1, group H, member 4	Rattus norvegicus	182-185
32890923-10	2020	In addition, NAC pretreatment promoted the phagocytic activity of Cd-exposed chicken peritoneal macrophages, and significantly inhibited expression of pro-inflammatory factors (IL-1beta, IL-6 and TNF-alpha) in both Cd-exposed macrophages and Cd-treated cells in response to LPS stimuli.	Acetylcysteine	13-16	interleukin 1, beta	Gallus gallus	177-185
17329835-7	2007	The effect of the antioxidant N-acetyl-L-cysteine (NAC) on HO-1 expression was also tested.	Acetylcysteine	30-49	heme oxygenase 1	Rattus norvegicus	59-63
34944997-4	2021	Since the mercapturic acid pathway enzyme RALBP1 (also known as RLIP76 or Rlip) that limits cellular accumulation of 4-HNE also mediates dox resistance, the combination of Omega-6 PUFAs and Rlip depletion could synergistically improve the efficacy of dox.	Acetylcysteine	10-26	ralA binding protein 1	Homo sapiens	42-48
17329835-7	2007	The effect of the antioxidant N-acetyl-L-cysteine (NAC) on HO-1 expression was also tested.	Acetylcysteine	51-54	heme oxygenase 1	Rattus norvegicus	59-63
17329835-12	2007	NAC attenuated the HO-1 expression in a dose-dependent manner.	Acetylcysteine	0-3	heme oxygenase 1	Rattus norvegicus	19-23
17329835-14	2007	We showed that NAC inhibited HO-1 upregulation.	Acetylcysteine	15-18	heme oxygenase 1	Rattus norvegicus	29-33
16990448-3	2006	Recent studies suggested that N-acetylcysteine enhances the extracellular degradation of PDGF-beta receptor by cathepsin B, thus suggesting that the absence of PDGF-beta receptors in quiescent cells is due to an active process of elimination and not to a lack of expression.	Acetylcysteine	30-46	cathepsin B	Mus musculus	111-122
16990553-6	2006	NAC treatment prevented H2O2-induced PTP inhibition, and reduced H2O2- and ligand-induced PDGF beta-receptor phosphorylation, PDGF-induced proliferation, and chemotaxis of VSMCs.	Acetylcysteine	0-3	platelet derived growth factor subunit B	Rattus norvegicus	90-99
10748142-5	2000	Both PDGF-BB- and AngII-induced phosphorylation of the Shc.PDGFbeta-R complex was inhibited by antioxidants such as N-acetylcysteine and Tiron, but not by calcium chelation.	Acetylcysteine	116-132	SHC adaptor protein 1	Homo sapiens	55-58
10843427-5	2000	RESULTS: The results showed that 1) NAC attenuated TNF-alpha-induced p38MAP kinase activation and RANTES production 2) SB 203580 as the specific inhibitor of p38 MAP kinase activity attenuated TNF-alpha-induced RANTES production 3) BSO facilitated TNF-alpha-induced p38 MAP kinase activation and RANTES production 4) SB 203580 attenuated BSO-mediated facilitation of TNF-alpha-induced RANTES production.	Acetylcysteine	36-39	C-C motif chemokine ligand 5	Homo sapiens	98-104
10843427-5	2000	RESULTS: The results showed that 1) NAC attenuated TNF-alpha-induced p38MAP kinase activation and RANTES production 2) SB 203580 as the specific inhibitor of p38 MAP kinase activity attenuated TNF-alpha-induced RANTES production 3) BSO facilitated TNF-alpha-induced p38 MAP kinase activation and RANTES production 4) SB 203580 attenuated BSO-mediated facilitation of TNF-alpha-induced RANTES production.	Acetylcysteine	36-39	C-C motif chemokine ligand 5	Homo sapiens	211-217
10843427-5	2000	RESULTS: The results showed that 1) NAC attenuated TNF-alpha-induced p38MAP kinase activation and RANTES production 2) SB 203580 as the specific inhibitor of p38 MAP kinase activity attenuated TNF-alpha-induced RANTES production 3) BSO facilitated TNF-alpha-induced p38 MAP kinase activation and RANTES production 4) SB 203580 attenuated BSO-mediated facilitation of TNF-alpha-induced RANTES production.	Acetylcysteine	36-39	C-C motif chemokine ligand 5	Homo sapiens	211-217
10843427-5	2000	RESULTS: The results showed that 1) NAC attenuated TNF-alpha-induced p38MAP kinase activation and RANTES production 2) SB 203580 as the specific inhibitor of p38 MAP kinase activity attenuated TNF-alpha-induced RANTES production 3) BSO facilitated TNF-alpha-induced p38 MAP kinase activation and RANTES production 4) SB 203580 attenuated BSO-mediated facilitation of TNF-alpha-induced RANTES production.	Acetylcysteine	36-39	C-C motif chemokine ligand 5	Homo sapiens	211-217
10771087-4	2000	By the effect of NAC and DFO, significant increases were detected in the levels of mRNA of catalase, manganese superoxide dismutase and glutathione peroxidase.	Acetylcysteine	17-20	superoxide dismutase 2	Rattus norvegicus	101-131
16563723-7	2006	PEITC and NAC-PEITC treatment caused dose-dependent decreases in MMP-2/MMP-9 and MT1-MMP mRNA levels, as determined by reverse transcription polymerase chain reaction.	Acetylcysteine	10-13	matrix metallopeptidase 9	Homo sapiens	71-76
34944997-4	2021	Since the mercapturic acid pathway enzyme RALBP1 (also known as RLIP76 or Rlip) that limits cellular accumulation of 4-HNE also mediates dox resistance, the combination of Omega-6 PUFAs and Rlip depletion could synergistically improve the efficacy of dox.	Acetylcysteine	10-26	ralA binding protein 1	Homo sapiens	64-70
17030433-0	2006	Antioxidant N-acetylcysteine inhibits the activation of JNK3 mediated by the GluR6-PSD95-MLK3 signaling module during cerebral ischemia in rat hippocampus.	Acetylcysteine	12-28	mitogen activated protein kinase 10	Rattus norvegicus	56-60
17030433-7	2006	To further investigate the possible mechanism of JNK3 activation, antioxidant N-acetylcysteine (NAC) was given to the rats 20 min prior to ischemia.	Acetylcysteine	78-94	mitogen activated protein kinase 10	Rattus norvegicus	49-53
34619980-9	2021	NAC treatment reduced TGF-beta signaling, p-Smad2 and collagen levels, and mesenchymal transition from Isolectin-B4 and CD45-positive cells in LDLR mice.	Acetylcysteine	0-3	transforming growth factor alpha	Mus musculus	22-30
17030433-7	2006	To further investigate the possible mechanism of JNK3 activation, antioxidant N-acetylcysteine (NAC) was given to the rats 20 min prior to ischemia.	Acetylcysteine	96-99	mitogen activated protein kinase 10	Rattus norvegicus	49-53
17030433-8	2006	Results indicate that NAC distinctly inhibited the association of PSD95 with GluR6 and MLK3, the autophosphorylation of MLK3, the combination of MLK3 with JNK3 and JNK3 activation.	Acetylcysteine	22-25	mitogen activated protein kinase 10	Rattus norvegicus	155-159
17030433-8	2006	Results indicate that NAC distinctly inhibited the association of PSD95 with GluR6 and MLK3, the autophosphorylation of MLK3, the combination of MLK3 with JNK3 and JNK3 activation.	Acetylcysteine	22-25	mitogen activated protein kinase 10	Rattus norvegicus	164-168
10809266-5	2000	INTERVENTIONS: Generation of 16% to 18% of methemoglobin in red blood cells by NO and subsequent addition of MB, riboflavin, or NAC.	Acetylcysteine	128-131	hemoglobin subunit gamma 2	Homo sapiens	43-56
10775566-5	2000	In addition, the induction c-fos mRNA levels by bradykinin was completely abolished by N-acetyl-L-cysteine and alpha-lipoic acid.	Acetylcysteine	87-106	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	27-32
10527705-6	1999	Infusion of NAc twice daily for 4 days following transplantation further altered chemokine mRNA expression (increased MCP-1 and RANTES; decreased CINC); led to more enhanced type 2 cytokine production relative to control animals; and further increased xenograft survival.	Acetylcysteine	12-15	C-C motif chemokine ligand 5	Homo sapiens	128-134
17108135-7	2006	Conversely, treatment of Hsp27 siRNA-transfected cells with N-acetylcysteine, an antioxidant and GSH precursor, reversed their sensitivity to 17-AAG.	Acetylcysteine	60-76	N-methylpurine DNA glycosylase	Homo sapiens	145-148
34619980-9	2021	NAC treatment reduced TGF-beta signaling, p-Smad2 and collagen levels, and mesenchymal transition from Isolectin-B4 and CD45-positive cells in LDLR mice.	Acetylcysteine	0-3	protein tyrosine phosphatase, receptor type, C	Mus musculus	120-124
10508828-7	1999	Finally, although concomitant ingestion of N-acetylcysteine had no effect (p &gt; 0.05) on MMP production, it increased (p &gt; 0.05) lung glutathione levels, blocked (p &lt; 0.05) MMP-9 and MMP-2 activation, and decreased (p &lt; 0.05) levels of the 7S fragment of type IV collagen.	Acetylcysteine	43-59	matrix metallopeptidase 9	Rattus norvegicus	181-186
34468764-11	2021	Eliminating ROS by N-acetyl-l-cysteine abrogated Cd-induced PP2A-JNK pathway disruption and concurrently reinforced MgIG-conferred protective effects, which could be further slightly strengthened by PP2A overexpression.	Acetylcysteine	19-38	protein phosphatase 2 phosphatase activator	Homo sapiens	60-64
10224123-1	1999	In this study, we show that N-acetylcysteine (NAC), a precursor of glutathione and an intracellular free radical scavenger, almost completely prevented hepatocyte growth factor (HGF)-suppressed growth of Sarcoma 180 and Meth A cells, and HGF-induced apoptosis, assessed by DNA fragmentation, and increase in caspase-3 activity, in Sarcoma 180 cells.	Acetylcysteine	28-44	hepatocyte growth factor	Mus musculus	152-176
10224123-1	1999	In this study, we show that N-acetylcysteine (NAC), a precursor of glutathione and an intracellular free radical scavenger, almost completely prevented hepatocyte growth factor (HGF)-suppressed growth of Sarcoma 180 and Meth A cells, and HGF-induced apoptosis, assessed by DNA fragmentation, and increase in caspase-3 activity, in Sarcoma 180 cells.	Acetylcysteine	28-44	hepatocyte growth factor	Mus musculus	178-181
16916625-11	2006	This hypothesis was tested by treating Ku86(-/-) mice with the well known free radical scavenger, thiol antioxidant N-acetyl-cysteine (NAC), during embryonic development.	Acetylcysteine	116-133	X-ray repair complementing defective repair in Chinese hamster cells 5	Mus musculus	39-43
16916625-11	2006	This hypothesis was tested by treating Ku86(-/-) mice with the well known free radical scavenger, thiol antioxidant N-acetyl-cysteine (NAC), during embryonic development.	Acetylcysteine	135-138	X-ray repair complementing defective repair in Chinese hamster cells 5	Mus musculus	39-43
16916625-12	2006	We found that a significantly higher percentage, 7.7% of NAC treated Ku86(-/-) offspring versus 1.5% untreated Ku86(-/-) mice were alive at 1 month of age.	Acetylcysteine	57-60	X-ray repair complementing defective repair in Chinese hamster cells 5	Mus musculus	69-73
10224123-1	1999	In this study, we show that N-acetylcysteine (NAC), a precursor of glutathione and an intracellular free radical scavenger, almost completely prevented hepatocyte growth factor (HGF)-suppressed growth of Sarcoma 180 and Meth A cells, and HGF-induced apoptosis, assessed by DNA fragmentation, and increase in caspase-3 activity, in Sarcoma 180 cells.	Acetylcysteine	28-44	hepatocyte growth factor	Mus musculus	238-241
10224123-1	1999	In this study, we show that N-acetylcysteine (NAC), a precursor of glutathione and an intracellular free radical scavenger, almost completely prevented hepatocyte growth factor (HGF)-suppressed growth of Sarcoma 180 and Meth A cells, and HGF-induced apoptosis, assessed by DNA fragmentation, and increase in caspase-3 activity, in Sarcoma 180 cells.	Acetylcysteine	28-44	caspase 3	Mus musculus	308-317
16765414-10	2006	The increase in HO-1 expression was diminished by N-acetyl-l-cysteine (NAC) treatment of each CB nanoparticles before exposure although the difference between the effects of NAC-treated and untreated 14nm CB did not achieve significant.	Acetylcysteine	50-69	heme oxygenase 1	Rattus norvegicus	16-20
10224123-1	1999	In this study, we show that N-acetylcysteine (NAC), a precursor of glutathione and an intracellular free radical scavenger, almost completely prevented hepatocyte growth factor (HGF)-suppressed growth of Sarcoma 180 and Meth A cells, and HGF-induced apoptosis, assessed by DNA fragmentation, and increase in caspase-3 activity, in Sarcoma 180 cells.	Acetylcysteine	46-49	hepatocyte growth factor	Mus musculus	152-176
16765414-10	2006	The increase in HO-1 expression was diminished by N-acetyl-l-cysteine (NAC) treatment of each CB nanoparticles before exposure although the difference between the effects of NAC-treated and untreated 14nm CB did not achieve significant.	Acetylcysteine	71-74	heme oxygenase 1	Rattus norvegicus	16-20
10224123-1	1999	In this study, we show that N-acetylcysteine (NAC), a precursor of glutathione and an intracellular free radical scavenger, almost completely prevented hepatocyte growth factor (HGF)-suppressed growth of Sarcoma 180 and Meth A cells, and HGF-induced apoptosis, assessed by DNA fragmentation, and increase in caspase-3 activity, in Sarcoma 180 cells.	Acetylcysteine	46-49	hepatocyte growth factor	Mus musculus	178-181
16765414-10	2006	The increase in HO-1 expression was diminished by N-acetyl-l-cysteine (NAC) treatment of each CB nanoparticles before exposure although the difference between the effects of NAC-treated and untreated 14nm CB did not achieve significant.	Acetylcysteine	174-177	heme oxygenase 1	Rattus norvegicus	16-20
10224123-1	1999	In this study, we show that N-acetylcysteine (NAC), a precursor of glutathione and an intracellular free radical scavenger, almost completely prevented hepatocyte growth factor (HGF)-suppressed growth of Sarcoma 180 and Meth A cells, and HGF-induced apoptosis, assessed by DNA fragmentation, and increase in caspase-3 activity, in Sarcoma 180 cells.	Acetylcysteine	46-49	hepatocyte growth factor	Mus musculus	238-241
34794237-10	2021	TGF-beta-induced upregulation of KCa2.3, KCa3.1, collagen, and alpha-smooth muscle actin and downregulation of catalase were reversed by modafinil, polyethylene glycol catalase, N-acetylcysteine, siRNA against KCa2.3 or KCa3.1, and Epac inhibitors.	Acetylcysteine	178-194	potassium calcium-activated channel subfamily N member 3	Homo sapiens	33-39
10224123-1	1999	In this study, we show that N-acetylcysteine (NAC), a precursor of glutathione and an intracellular free radical scavenger, almost completely prevented hepatocyte growth factor (HGF)-suppressed growth of Sarcoma 180 and Meth A cells, and HGF-induced apoptosis, assessed by DNA fragmentation, and increase in caspase-3 activity, in Sarcoma 180 cells.	Acetylcysteine	46-49	caspase 3	Mus musculus	308-317
10224123-2	1999	The reduced form of glutathione also prevented HGF-suppressed growth of the cells as effective as NAC.	Acetylcysteine	98-101	hepatocyte growth factor	Mus musculus	47-50
10224123-5	1999	NAC completely prevented both HGF-induced morphological changes and the enhancement of ROS generation in the cells.	Acetylcysteine	0-3	hepatocyte growth factor	Mus musculus	30-33
16896059-9	2006	Pretreatment with 20mM N-acetylcysteine prevented mitochondrial dysfunction, the nuclear translocation of endonuclease G and AIF, and the nuclear DNA fragmentation.	Acetylcysteine	23-39	apoptosis-inducing factor, mitochondrion-associated 1	Mus musculus	125-128
34850077-8	2021	Finally, we demonstrated that NAC selectively normalized uterine leukemia inhibitory factor, osteopontin/secreted phosphoprotein 1, progesterone receptor, and homeobox A11 mRNA expression and placental estrogen related receptor beta and trophoblast specific protein alpha mRNA expression.	Acetylcysteine	30-33	progesterone receptor	Rattus norvegicus	132-153
16978029-5	2006	In this study, we developed a method for quantitation of a mercapturic acid, N-acetyl-S-(9,10-dihydro-9-hydroxy-10-phenanthryl)-l-cysteine (PheO-NAC, 12), the end product of the reaction of phenanthrene-9,10-epoxide (11) with glutathione.	Acetylcysteine	59-75	X-linked Kx blood group	Homo sapiens	145-148
17034719-1	2006	OBJECTIVE: To explore the effect of N-acetyl L-cysteine (NAC) on expressions of matrix metalloproteinases-2, 9 (MMP-2, MMP-9) in lung fibroblasts of SiO(2) exposed rats.	Acetylcysteine	36-55	matrix metallopeptidase 9	Rattus norvegicus	119-124
17034719-1	2006	OBJECTIVE: To explore the effect of N-acetyl L-cysteine (NAC) on expressions of matrix metalloproteinases-2, 9 (MMP-2, MMP-9) in lung fibroblasts of SiO(2) exposed rats.	Acetylcysteine	57-60	matrix metallopeptidase 9	Rattus norvegicus	119-124
10331420-7	1999	VEGF-induced NF-kappaB activation was inhibited by TLCK and NAC, but not by PD 98059.	Acetylcysteine	60-63	vascular endothelial growth factor A	Bos taurus	0-4
17034719-11	2006	CONCLUSION: NAC inhibits the expressions of MMP-2, MMP-9 in lung fibroblasts.	Acetylcysteine	12-15	matrix metallopeptidase 9	Rattus norvegicus	51-56
34884437-8	2021	In U937 cells, the weak cytotoxicity of NAC is probably caused by lower expression of NOX2, SOD1, SOD3, and by the absence of MOP expression.	Acetylcysteine	40-43	opioid receptor mu 1	Homo sapiens	126-129
16859669-11	2006	N-acetylcysteine attenuation of diabetic myocardial dysfunction could be attributed to the restoration of myocardial Mn-SOD activity.	Acetylcysteine	0-16	superoxide dismutase 2	Rattus norvegicus	117-123
34420083-7	2021	Delayed NAC treatment had no effect on APAP-induced liver injury at 24 h but reduced the decline of plasma ALT activities and prevented the shrinkage of the areas of necrosis at 48 h. This effect correlated with down-regulation of key activators of mitochondrial biogenesis (AMPK, PGC-1alpha, Nrf1/2, TFAM) and reduced expression of Tom 20 (mitochondrial mass) and PCNA (cell proliferation).	Acetylcysteine	8-11	glutamic pyruvic transaminase, soluble	Mus musculus	107-110
10217408-6	1999	The activation of STATs by oxidized LDL was almost completely inhibited by the lipophilic antioxidant vitamin E, and partially antagonized by the hydrophilic thiol-containing compound N-acetylcysteine, suggesting that the oxidative stress induced by oxidized LDL is involved in the observed phenomenon.	Acetylcysteine	184-200	signal transducer and activator of transcription 1	Homo sapiens	18-23
34703822-10	2021	NAC suppressed TNF-alpha- or poly (I:C)-induced expression of MCP-1 and CX3CL1.	Acetylcysteine	0-3	C-C motif chemokine ligand 2	Rattus norvegicus	62-67
34680443-5	2021	Furthermore, IS and UT mix induced the production of intracellular reactive oxygen species, and caspase-1 activity and IL-1beta secretion were reduced in the presence of antioxidant N-acetylcysteine.	Acetylcysteine	182-198	interleukin 1 alpha	Homo sapiens	119-127
10190554-9	1999	Conversely, antioxidants (1 mM ascorbate, 10 mM mannitol, 2% dimethyl sulphoxide, 10 mM N-acetylcysteine) markedly suppressed intrinsic mdr1b mRNA and P-glycoprotein overexpression.	Acetylcysteine	88-104	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	136-141
10190554-9	1999	Conversely, antioxidants (1 mM ascorbate, 10 mM mannitol, 2% dimethyl sulphoxide, 10 mM N-acetylcysteine) markedly suppressed intrinsic mdr1b mRNA and P-glycoprotein overexpression.	Acetylcysteine	88-104	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	151-165
16497787-9	2006	Pretreatment with the glutathione precursor N-acetyl-l-cysteine (NAC) prevented DNA-strand breakage and apoptosis.	Acetylcysteine	44-63	X-linked Kx blood group	Homo sapiens	65-68
16565438-0	2006	Allyl isothiocyanate and its N-acetylcysteine conjugate suppress metastasis via inhibition of invasion, migration, and matrix metalloproteinase-2/-9 activities in SK-Hep 1 human hepatoma cells.	Acetylcysteine	29-45	DNL-type zinc finger	Homo sapiens	166-171
16565438-4	2006	Our results demonstrate that AITC and NAC-AITC suppress SK-Hep 1 cell proliferation in a dose-dependent manner; by 25% and 30% for 10 microM AITC and 10 microM NAC-AITC, respectively.	Acetylcysteine	38-41	DNL-type zinc finger	Homo sapiens	59-64
15982852-6	2006	Moreover, NAC treatment reduced the expression levels of c-Myc, Cyclin D2, and Cyclin E, and induced expression of p27, thus inhibiting the G1 to S phase transition of cells cultured with IL-3.	Acetylcysteine	10-13	cyclin D2	Mus musculus	64-73
15982852-6	2006	Moreover, NAC treatment reduced the expression levels of c-Myc, Cyclin D2, and Cyclin E, and induced expression of p27, thus inhibiting the G1 to S phase transition of cells cultured with IL-3.	Acetylcysteine	10-13	proliferating cell nuclear antigen	Mus musculus	64-70
15982852-6	2006	Moreover, NAC treatment reduced the expression levels of c-Myc, Cyclin D2, and Cyclin E, and induced expression of p27, thus inhibiting the G1 to S phase transition of cells cultured with IL-3.	Acetylcysteine	10-13	cyclin-dependent kinase inhibitor 1B	Mus musculus	115-118
34572286-8	2021	In addition, the supplementation of ROS scavenger N-acetylcysteine and the maintenance of intracellular levels of amino acids via sulfasalazine (xCT inhibitor) or dimethyl-alpha-ketoglutarate decreased the levels of mitochondrial ROS and protected cells from death.	Acetylcysteine	50-66	solute carrier family 7 member 11	Homo sapiens	145-148
16456238-11	2006	That both NAC and apocynin reduced ROS activities and abolished Ang II-mediated increase in p22phox and gp91phox activity further suggest that such redox cycling occurs via both NADPH oxidase-dependent and -independent pathways.	Acetylcysteine	10-13	cytochrome b-245 beta chain	Homo sapiens	104-112
15964899-6	2005	Whereas N-acetylcysteine (an antioxidant) effectively reversed the SE-induced increase in ROS and depletion of glutathione, it also suppressed SE-induced nuclear translocation of either AIF or EndoG and prevented the enhanced DNA fragmentation that would have resulted from this.	Acetylcysteine	8-24	apoptosis inducing factor mitochondria associated 1	Homo sapiens	186-189
15964899-6	2005	Whereas N-acetylcysteine (an antioxidant) effectively reversed the SE-induced increase in ROS and depletion of glutathione, it also suppressed SE-induced nuclear translocation of either AIF or EndoG and prevented the enhanced DNA fragmentation that would have resulted from this.	Acetylcysteine	8-24	endonuclease G	Homo sapiens	193-198
10435037-10	1999	The induction of mRNA levels and the promoter activities of c-fos gene by Et-1 or H2O2 were abolished by pretreating cardiomyocytes with catalase or NAC.	Acetylcysteine	149-152	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	60-65
10193576-0	1999	N-acetylcysteine increases the biosynthesis of recombinant EPO in apoptotic Chinese hamster ovary cells.	Acetylcysteine	0-16	erythropoietin	Cricetulus griseus	59-62
10193576-5	1999	Strikingly, the NAC treatment enhanced the production of recombinant EPO two-fold compared with that of the culture without NAC supplementation.	Acetylcysteine	16-19	erythropoietin	Cricetulus griseus	69-72
10193576-5	1999	Strikingly, the NAC treatment enhanced the production of recombinant EPO two-fold compared with that of the culture without NAC supplementation.	Acetylcysteine	124-127	erythropoietin	Cricetulus griseus	69-72
35550579-8	2022	The probe of related mechanism in CSE-induced HE4 increase in HBE was conducted by administrating N-acetylcysteine (NAC).	Acetylcysteine	98-114	WAP four-disulfide core domain 2	Homo sapiens	46-49
10193576-6	1999	These results showed that NaBu treatment supplemented with NAC not only inhibits apoptosis, but also exerts a synergistic effect on the biosynthesis of recombinant EPO.	Acetylcysteine	59-62	erythropoietin	Cricetulus griseus	164-167
10193578-8	1999	L-cysteine, N-acetylcysteine, penicillamine, N-(2-mercaptopropionylglycine), Captopril and taurine protected LADH against MPO systems and NaOCl.	Acetylcysteine	12-28	myeloperoxidase	Equus caballus	122-125
9927194-9	1999	Pretreatment with the antioxidants N-acetyl-L-cysteine (NAC), ascorbic acid or vitamin E, blocked H2O2- or doxorubicin-induced JNKI activity, but had no effect on JNKI activation by MBAs, excluding a role for oxidative stress.	Acetylcysteine	35-54	X-linked Kx blood group	Homo sapiens	56-59
9862355-5	1998	Blocking ROI production by preincubation with the antioxidant N-acetyl-L-cysteine inhibits JNK activation, NF-kappaB-driven luciferase activity, and IL-6 secretion following CD40 ligation, suggesting a role for ROI in CD40-mediated signaling events.	Acetylcysteine	62-81	mitogen-activated protein kinase 8	Mus musculus	91-94
15978632-3	2005	We showed that arsenic trioxide-induced Hsp70 expression was caused by activation of ROS and prevented by the antioxidant N-Acetyl-Cysteine (NAC).	Acetylcysteine	122-139	heat shock protein family A (Hsp70) member 4	Homo sapiens	40-45
15978632-3	2005	We showed that arsenic trioxide-induced Hsp70 expression was caused by activation of ROS and prevented by the antioxidant N-Acetyl-Cysteine (NAC).	Acetylcysteine	141-144	heat shock protein family A (Hsp70) member 4	Homo sapiens	40-45
16151024-7	2005	Pretreatment of rat VSMCs with the NOX inhibitor diphenylene iodonium or the antioxidants N-acetylcysteine or ebselen significantly inhibited Ang II-induced cAbl phosphorylation.	Acetylcysteine	90-106	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	157-161
35550579-8	2022	The probe of related mechanism in CSE-induced HE4 increase in HBE was conducted by administrating N-acetylcysteine (NAC).	Acetylcysteine	116-119	WAP four-disulfide core domain 2	Homo sapiens	46-49
35417750-6	2022	In the P. bovis group, treatment with N-acetyl-l-cysteine (NAC) significantly decreased protein expression in NF-kappaB and the NLRP3 inflammasome pathway, as well as IL-1beta, IL-6 and IL-18, whereas protein expression in the Nrf2 pathway was significantly changed.	Acetylcysteine	38-57	NLR family, pyrin domain containing 3	Mus musculus	128-133
9739453-6	1998	Glutathione and N-acetylcysteine also reactivated H2O2-treated SHP-1.	Acetylcysteine	16-32	protein tyrosine phosphatase non-receptor type 6	Homo sapiens	63-68
9718198-9	1998	An antioxidant, N-acetyl-L-cysteine, significantly attenuated the TNF-alpha-dependent increase in these mRNAs, and simultaneously reduced the activation of NF-kappaB by TNF-alpha, indicating that NF-kappaB mediates the TNF-alpha-dependent expression of IL-6 and ICAM-1 in ROS17/2.8 cells.	Acetylcysteine	16-35	intercellular adhesion molecule 1	Rattus norvegicus	262-268
35417750-6	2022	In the P. bovis group, treatment with N-acetyl-l-cysteine (NAC) significantly decreased protein expression in NF-kappaB and the NLRP3 inflammasome pathway, as well as IL-1beta, IL-6 and IL-18, whereas protein expression in the Nrf2 pathway was significantly changed.	Acetylcysteine	59-62	NLR family, pyrin domain containing 3	Mus musculus	128-133
15921899-7	2005	However, NAC+TAU treatment provided partial protection from glutathione oxidation in the liver of diabetic rats; moreover, the antioxidant treatment reduced the hepatic overexpression of heme oxygenase 1 (HO-1) mRNA which was detected in the diabetic rats.	Acetylcysteine	9-12	heme oxygenase 1	Rattus norvegicus	187-203
15921899-7	2005	However, NAC+TAU treatment provided partial protection from glutathione oxidation in the liver of diabetic rats; moreover, the antioxidant treatment reduced the hepatic overexpression of heme oxygenase 1 (HO-1) mRNA which was detected in the diabetic rats.	Acetylcysteine	9-12	heme oxygenase 1	Rattus norvegicus	205-209
35473933-9	2022	In addition, we showed that necrotic TECs-induced activation of TLR2/caspase-5/Panx1 axis could be decreased in macrophages when TECs was protected by N-acetylcysteine (NAC).	Acetylcysteine	151-167	caspase 5	Homo sapiens	69-78
15869713-1	2005	We report that N-acetyl-L-cysteine (NAC) treatment blocked induction of TNF-alpha, IL-1beta, IFN-gamma and iNOS in the CNS and attenuated clinical disease in the myelin basic protein induced model of experimental allergic encephalomyelitis (EAE) in Lewis rats.	Acetylcysteine	15-34	myelin basic protein	Rattus norvegicus	162-182
9529157-11	1998	Experiments performed in the presence of the antioxidant N-acetylcysteine demonstrated that the expression of vascular cell adhesion molecule-1 could be almost totally abolished, whereas that of intercellular adhesion molecule-1 was typically reduced by approximately 70%.	Acetylcysteine	57-73	intercellular adhesion molecule 1	Homo sapiens	195-228
15869713-1	2005	We report that N-acetyl-L-cysteine (NAC) treatment blocked induction of TNF-alpha, IL-1beta, IFN-gamma and iNOS in the CNS and attenuated clinical disease in the myelin basic protein induced model of experimental allergic encephalomyelitis (EAE) in Lewis rats.	Acetylcysteine	36-39	myelin basic protein	Rattus norvegicus	162-182
35473933-9	2022	In addition, we showed that necrotic TECs-induced activation of TLR2/caspase-5/Panx1 axis could be decreased in macrophages when TECs was protected by N-acetylcysteine (NAC).	Acetylcysteine	169-172	caspase 5	Homo sapiens	69-78
15845704-4	2005	We investigated the effect of NAC on the expression of CD11b and CD62L in endotoxin-stimulated human whole blood.	Acetylcysteine	30-33	integrin subunit alpha M	Homo sapiens	55-60
35293662-8	2022	Inhibition of ROS using N-acetyl-l-cysteine (NAC) inhibited chromium-induced activation of ATF6 and upregulation of PLK4.	Acetylcysteine	24-43	activating transcription factor 6	Homo sapiens	91-95
15845704-5	2005	NAC (&gt;10 mM) significantly inhibited the lipopolysaccharide (LPS)-induced upregulation of CD11b in a concentration-dependent manner.	Acetylcysteine	0-3	integrin subunit alpha M	Homo sapiens	93-98
15845704-7	2005	We also analyzed the effect of NAC on interleukin-8 (IL-8)-induced expression of CD11b in human whole blood.	Acetylcysteine	31-34	integrin subunit alpha M	Homo sapiens	81-86
15845704-8	2005	IL-8 (10 ng/mL) significantly upregulated the expression of CD11b, and the IL-8-induced upregulation was significantly attenuated by NAC (&gt;10 mM) in a dose-dependent manner.	Acetylcysteine	133-136	integrin subunit alpha M	Homo sapiens	60-65
9530210-6	1998	Inclusion of 20 mM N-acetyl-L-cysteine in the medium during hypoxia reduced the increase in HSP 32 mRNA and protein expression by 25.50% compared with hypoxia alone.	Acetylcysteine	19-38	heme oxygenase 1	Rattus norvegicus	92-98
15845704-9	2005	We conclude that NAC attenuates the increased expression of CD11b in either LPS or IL-8-stimulated human whole blood.	Acetylcysteine	17-20	integrin subunit alpha M	Homo sapiens	60-65
35293662-8	2022	Inhibition of ROS using N-acetyl-l-cysteine (NAC) inhibited chromium-induced activation of ATF6 and upregulation of PLK4.	Acetylcysteine	45-48	activating transcription factor 6	Homo sapiens	91-95
35065167-9	2022	Further studies revealed that beneficial effects of NAC is through targeting the mitochondrial autophagy via regulating the GSK-3beta/Drp1mediated mitochondrial fission and inhibiting the expression of beclin-1 and conversion of LC3, as well as activating the p-Akt pro-survival pathway.	Acetylcysteine	52-55	collapsin response mediator protein 1	Rattus norvegicus	134-138
35065167-10	2022	CONCLUSION: Our results suggest that NAC exerts neuroprotective effects to inhibit the altered mitochondrial changes and cell death in I/R injury via regulation of p-GSK-3beta mediated Drp-1 translocation to the mitochondria.	Acetylcysteine	37-40	collapsin response mediator protein 1	Rattus norvegicus	185-190
15867362-7	2005	N-acetyl-L-cysteine (NAC), but not caspase inhibitors, blocked FTI-induced DSBs, suggesting that the DSBs were caused by ROS and did not result from apoptosis.	Acetylcysteine	0-19	X-linked Kx blood group	Homo sapiens	21-24
9437207-8	1997	Pretreatment of ECs with an antioxidant, N-acetyl-cysteine (NAC) or catalase, inhibited this shear-induced or oxidant-induced ICAM-1 expression.	Acetylcysteine	41-58	intercellular adhesion molecule 1	Homo sapiens	126-132
9437207-8	1997	Pretreatment of ECs with an antioxidant, N-acetyl-cysteine (NAC) or catalase, inhibited this shear-induced or oxidant-induced ICAM-1 expression.	Acetylcysteine	60-63	intercellular adhesion molecule 1	Homo sapiens	126-132
9437207-11	1997	Flow cytometric analysis and monocytic adhesion assay confirmed the inhibitory effect of NAC and catalase on the shear-induced ICAM-1 expression on ECs.	Acetylcysteine	89-92	intercellular adhesion molecule 1	Homo sapiens	127-133
15670787-3	2005	Both Cd-induced JNK and c-Jun phosphorylation and apoptosis were inhibited dramatically by N-acetyl-L-cysteine, a free radical scavenger.	Acetylcysteine	91-110	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	24-29
35278063-8	2022	RESULTS: By adding NAC into CIK cell culture, the percentage of CD3+CD56+ cells along with the expression of Th1 cytokines and cytolytic granules increased significantly, resulting in an improvement of cytotoxicity against the cancer cell lines CL6 and K562.	Acetylcysteine	19-22	neural cell adhesion molecule 1	Homo sapiens	68-72
15802865-5	2005	The post-irradiation treatment of the cells with N-acetyl-L-cysteine (NAC) abolished the up-regulation of the expression of Fas and DR5 on the plasma membrane.	Acetylcysteine	49-68	X-linked Kx blood group	Homo sapiens	70-73
15986094-8	2005	Lack of gENaC completely blocked salt absorption and caused dramatic reversal of skin potentials associated with pilocarpine-induced sweat secretion from significantly negative in normal subjects (-13 +/- 7.0 mV) to significantly positive (+22 +/- 11.0 mV) in PHA-1 patients.	Acetylcysteine	8-13	sodium channel epithelial 1 subunit gamma	Homo sapiens	260-265
9043100-0	1997	Suppression of UVB-induced c-fos and c-jun expression in human keratinocytes by N-acetylcysteine.	Acetylcysteine	80-96	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	27-32
9043100-0	1997	Suppression of UVB-induced c-fos and c-jun expression in human keratinocytes by N-acetylcysteine.	Acetylcysteine	80-96	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	37-42
9043100-4	1997	Preincubation with 1 and 3 mM NAC suppressed c-jun and c-fos induction by UVB in a dose-dependent fashion.	Acetylcysteine	30-33	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	45-50
9043100-4	1997	Preincubation with 1 and 3 mM NAC suppressed c-jun and c-fos induction by UVB in a dose-dependent fashion.	Acetylcysteine	30-33	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	55-60
9043100-5	1997	These applied concentrations of NAC were not toxic to the keratinocytes, as determined by Trypan Blue exclusion assay and completely suppressed c-jun and c-fos induction by the chemical cadmium chloride (oxidative stress).	Acetylcysteine	32-35	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	144-149
9043100-5	1997	These applied concentrations of NAC were not toxic to the keratinocytes, as determined by Trypan Blue exclusion assay and completely suppressed c-jun and c-fos induction by the chemical cadmium chloride (oxidative stress).	Acetylcysteine	32-35	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	154-159
8955147-5	1996	NAC suppressed NGF-induced c-fos gene expression and AP-1 activation.	Acetylcysteine	0-3	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	27-32
35008006-6	2022	Suppressing ROS with N-acetylcysteine (NAC) or interfering with NOX2 by small interfering RNA weakened the promoting effect of CTRP9 on the NLRP3 inflammasome.	Acetylcysteine	39-42	NLR family, pyrin domain containing 3	Mus musculus	140-145
8670763-5	1996	Furthermore, 10.54 ng/ml of TGF-beta1 and 2.98 ng/ml of TGF-beta2 were detected in tears treated with the mucolytic agent, acetylcysteine.	Acetylcysteine	123-137	transforming growth factor beta 2	Homo sapiens	56-65
15744360-5	2004	All these patients were administered acetylcysteine (NAC) 600 mg/day orally during 20 days.	Acetylcysteine	37-51	X-linked Kx blood group	Homo sapiens	53-56
35217818-11	2022	In vitro, N-acetylcysteine (NAC) inhibited NLRP3 inflammasome activation and NLRP3 knockdown reduced GSDMD expression, in MOVAS cells treated with TNF-alpha.	Acetylcysteine	10-26	NLR family, pyrin domain containing 3	Mus musculus	43-48
8607802-4	1996	Indeed the antioxidant N-acetyl-cysteine (NAC) completely prevents the MnSOD mRNA up-regulation observed after DDC administration.	Acetylcysteine	23-40	superoxide dismutase 2	Rattus norvegicus	71-76
8607802-4	1996	Indeed the antioxidant N-acetyl-cysteine (NAC) completely prevents the MnSOD mRNA up-regulation observed after DDC administration.	Acetylcysteine	42-45	superoxide dismutase 2	Rattus norvegicus	71-76
35217818-11	2022	In vitro, N-acetylcysteine (NAC) inhibited NLRP3 inflammasome activation and NLRP3 knockdown reduced GSDMD expression, in MOVAS cells treated with TNF-alpha.	Acetylcysteine	28-31	NLR family, pyrin domain containing 3	Mus musculus	43-48
8607802-6	1996	Both NAC and DESF significantly down-regulate MnSOD gene expression also in normal untreated rat liver.	Acetylcysteine	5-8	superoxide dismutase 2	Rattus norvegicus	46-51
8607802-7	1996	While the observed inhibitory effect of NAC in MnSOD mRNA up-regulation can be ascribed mainly to its antioxidant property, iron chelation could act with an antioxidant effect and/or affecting some iron-dependent factor(s) possibly involved in MnSOD gene regulation.	Acetylcysteine	40-43	superoxide dismutase 2	Rattus norvegicus	47-52
15336321-8	2004	The protective effect of N-acetyl-l-cysteine suggests both a direct action of reactive oxygen species on the protein and a more delayed action on the transcriptional regulation of UGT1A6.	Acetylcysteine	25-44	UDP glucuronosyltransferase family 1 member A6	Rattus norvegicus	180-186
35217818-11	2022	In vitro, N-acetylcysteine (NAC) inhibited NLRP3 inflammasome activation and NLRP3 knockdown reduced GSDMD expression, in MOVAS cells treated with TNF-alpha.	Acetylcysteine	28-31	NLR family, pyrin domain containing 3	Mus musculus	77-82
15175554-3	2004	In the present study, by using the antioxidant N-acetylcysteine (NAC), we investigated in human umbilical vein endothelial cells (HUVECs) the roles of oxidative stress in PDGF-B expression induced by tumor necrosis factor alpha (TNFalpha) and its underlying mechanisms.	Acetylcysteine	47-63	platelet derived growth factor subunit B	Homo sapiens	171-177
15175554-4	2004	Exposure of HUVECs to TNFalpha (200 U/ml) for 24 hours caused significant increases of both the PDGF-B expression and its promoter/enhancer activity, which were abolished by NAC (20 mmol/L).	Acetylcysteine	174-177	platelet derived growth factor subunit B	Homo sapiens	96-102
8607802-7	1996	While the observed inhibitory effect of NAC in MnSOD mRNA up-regulation can be ascribed mainly to its antioxidant property, iron chelation could act with an antioxidant effect and/or affecting some iron-dependent factor(s) possibly involved in MnSOD gene regulation.	Acetylcysteine	40-43	superoxide dismutase 2	Rattus norvegicus	244-249
35035661-8	2022	Notably, when LPS/ATP-stimulated RAW264.7 macrophages were treated with CoQ0, Mito-TEMPO (a mitochondrial ROS inhibitor), or N-acetylcysteine (NAC, a ROS inhibitor), there was a significant reduction of LPS/ATP-stimulated NLRP3 inflammasome activation and IL1beta expression.	Acetylcysteine	125-141	NLR family, pyrin domain containing 3	Mus musculus	222-227
7491977-2	1995	NAC, DTT, and 2-ME each activated the transcription factor NF-kappa B and increased steady-state levels of MnSOD mRNA and enzyme activity in these cells.	Acetylcysteine	0-3	superoxide dismutase 2	Rattus norvegicus	107-112
7491977-3	1995	In addition, NAC, DTT, and 2-ME increased chloramphenicol acetyltransferase (CAT) activity in cells transfected with a construct containing the CAT gene under the control of the rat MnSOD promoter.	Acetylcysteine	13-16	superoxide dismutase 2	Rattus norvegicus	182-187
15033544-17	2004	Anti-TNF-alpha and NAC partially inhibited AP-1 activation.	Acetylcysteine	19-22	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	43-47
14701705-7	2004	In addition, AR secretion was inhibited by the antioxidant N-acetyl cysteine, but not by a neutralizing anti-EGFR, suggesting an EGFR transactivation via oxidative stress.	Acetylcysteine	59-76	amphiregulin	Homo sapiens	13-15
7724734-2	1995	In these cell types, the radiation- and H2O2-mediated increase in c-jun mRNA levels could be prevented by pretreatment of the cells with N-acetylcysteine, an antioxidant, or H7, an inhibitor of protein kinase C and protein kinase A, but not by HA1004, a specific inhibitor of protein kinase A and G. These results suggest a role for protein kinase C and reactive oxygen intermediates in the induction of c-jun gene expression in both normal and tumor cells.	Acetylcysteine	137-153	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	66-71
7724734-2	1995	In these cell types, the radiation- and H2O2-mediated increase in c-jun mRNA levels could be prevented by pretreatment of the cells with N-acetylcysteine, an antioxidant, or H7, an inhibitor of protein kinase C and protein kinase A, but not by HA1004, a specific inhibitor of protein kinase A and G. These results suggest a role for protein kinase C and reactive oxygen intermediates in the induction of c-jun gene expression in both normal and tumor cells.	Acetylcysteine	137-153	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	404-409
35035661-8	2022	Notably, when LPS/ATP-stimulated RAW264.7 macrophages were treated with CoQ0, Mito-TEMPO (a mitochondrial ROS inhibitor), or N-acetylcysteine (NAC, a ROS inhibitor), there was a significant reduction of LPS/ATP-stimulated NLRP3 inflammasome activation and IL1beta expression.	Acetylcysteine	125-141	interleukin 1 alpha	Mus musculus	256-263
14747374-7	2004	The activation of STATs was inhibited by N-acetyl-L-cysteine, a precursor of glutathione and a reactive oxygen species (ROS) scavenger, and fluorescence-activated cell sorter analysis showed upregulation of intracellular ROS after albumin overloading, suggesting that albumin per se could generate ROS in proximal tubular cells.	Acetylcysteine	41-60	signal transducer and activator of transcription 1	Mus musculus	18-23
35035661-8	2022	Notably, when LPS/ATP-stimulated RAW264.7 macrophages were treated with CoQ0, Mito-TEMPO (a mitochondrial ROS inhibitor), or N-acetylcysteine (NAC, a ROS inhibitor), there was a significant reduction of LPS/ATP-stimulated NLRP3 inflammasome activation and IL1beta expression.	Acetylcysteine	143-146	NLR family, pyrin domain containing 3	Mus musculus	222-227
35035661-8	2022	Notably, when LPS/ATP-stimulated RAW264.7 macrophages were treated with CoQ0, Mito-TEMPO (a mitochondrial ROS inhibitor), or N-acetylcysteine (NAC, a ROS inhibitor), there was a significant reduction of LPS/ATP-stimulated NLRP3 inflammasome activation and IL1beta expression.	Acetylcysteine	143-146	interleukin 1 alpha	Mus musculus	256-263
7796876-6	1995	These results show that the induction of xanthine oxidase is not deleterious in this model of sepsis and suggest that N-acetyl-L-cysteine works as a direct antioxidant and scavenger of free radicals generated from other sources.	Acetylcysteine	118-137	xanthine dehydrogenase	Mus musculus	41-57
35035668-10	2022	We also noted that administration of MG increased cellular oxidative stress as measured by reactive oxygen species (ROS) generation, enhanced AGE accumulation, and receptor for advanced glycation end-product (RAGE) expression in the cultured HBMECs, which were partially reversed by GLO1, AG, or NAC.	Acetylcysteine	296-299	glyoxalase I	Homo sapiens	283-287
7798616-5	1994	We found that N-acetyl-L-cysteine treatment reduced ICAM-1 mRNA levels when keratinocytes were stimulated with either IFN-gamma or TNF-alpha; however, pyrrolidine dithiocarbamate and alpha-tocopherol had no effect on either IFN-gamma- or TNF-alpha-induced ICAM-1 mRNA levels.	Acetylcysteine	14-33	intercellular adhesion molecule 1	Homo sapiens	52-58
7798616-5	1994	We found that N-acetyl-L-cysteine treatment reduced ICAM-1 mRNA levels when keratinocytes were stimulated with either IFN-gamma or TNF-alpha; however, pyrrolidine dithiocarbamate and alpha-tocopherol had no effect on either IFN-gamma- or TNF-alpha-induced ICAM-1 mRNA levels.	Acetylcysteine	14-33	intercellular adhesion molecule 1	Homo sapiens	256-262
15673194-6	2004	Manganese (Mn)-TBAP, a mitochondria-specific SOD mimetic agent and NAC/GSH (N-acetyl cysteine/ reduced glutathione) reduced the YHT-induced cytotoxicity and decreased the number of the YHT-induced apoptotic cells.	Acetylcysteine	76-93	X-linked Kx blood group	Homo sapiens	67-70
14734137-8	2004	N-acetylcysteine (NAC) was able to decrease IL-17-induced 8-isoprostane production, with a maximum decrease of 59.3 +/- 9% (p &lt; 0.001, n = 12) with 10 mmol/liter of N-acetylcysteine, which also decreased IL-17-induced IL-8 production in a concentration-dependent manner (with maximum inhibition of 86.3% when combined with NAC 10 mmol/liter as compared with IL-17 alone).	Acetylcysteine	0-16	interleukin 17A	Homo sapiens	44-49
6132449-0	1983	N-acetylcysteine prevents the doxorubicin-induced decrease of cyclic GMP.	Acetylcysteine	0-16	5'-nucleotidase, cytosolic II	Homo sapiens	69-72
14734137-8	2004	N-acetylcysteine (NAC) was able to decrease IL-17-induced 8-isoprostane production, with a maximum decrease of 59.3 +/- 9% (p &lt; 0.001, n = 12) with 10 mmol/liter of N-acetylcysteine, which also decreased IL-17-induced IL-8 production in a concentration-dependent manner (with maximum inhibition of 86.3% when combined with NAC 10 mmol/liter as compared with IL-17 alone).	Acetylcysteine	0-16	interleukin 17A	Homo sapiens	207-212
14734137-8	2004	N-acetylcysteine (NAC) was able to decrease IL-17-induced 8-isoprostane production, with a maximum decrease of 59.3 +/- 9% (p &lt; 0.001, n = 12) with 10 mmol/liter of N-acetylcysteine, which also decreased IL-17-induced IL-8 production in a concentration-dependent manner (with maximum inhibition of 86.3% when combined with NAC 10 mmol/liter as compared with IL-17 alone).	Acetylcysteine	0-16	interleukin 17A	Homo sapiens	207-212
14734137-8	2004	N-acetylcysteine (NAC) was able to decrease IL-17-induced 8-isoprostane production, with a maximum decrease of 59.3 +/- 9% (p &lt; 0.001, n = 12) with 10 mmol/liter of N-acetylcysteine, which also decreased IL-17-induced IL-8 production in a concentration-dependent manner (with maximum inhibition of 86.3% when combined with NAC 10 mmol/liter as compared with IL-17 alone).	Acetylcysteine	18-21	interleukin 17A	Homo sapiens	44-49
14734137-8	2004	N-acetylcysteine (NAC) was able to decrease IL-17-induced 8-isoprostane production, with a maximum decrease of 59.3 +/- 9% (p &lt; 0.001, n = 12) with 10 mmol/liter of N-acetylcysteine, which also decreased IL-17-induced IL-8 production in a concentration-dependent manner (with maximum inhibition of 86.3% when combined with NAC 10 mmol/liter as compared with IL-17 alone).	Acetylcysteine	18-21	interleukin 17A	Homo sapiens	207-212
14734137-8	2004	N-acetylcysteine (NAC) was able to decrease IL-17-induced 8-isoprostane production, with a maximum decrease of 59.3 +/- 9% (p &lt; 0.001, n = 12) with 10 mmol/liter of N-acetylcysteine, which also decreased IL-17-induced IL-8 production in a concentration-dependent manner (with maximum inhibition of 86.3% when combined with NAC 10 mmol/liter as compared with IL-17 alone).	Acetylcysteine	18-21	interleukin 17A	Homo sapiens	207-212
14710110-0	2003	Mechanisms of matrix metalloproteinase-9 and matrix metalloproteinase-2 inhibition by N-acetylcysteine in the human term decidua and fetal membranes.	Acetylcysteine	86-102	matrix metallopeptidase 9	Homo sapiens	14-40
14588145-11	2003	Also, NAC prevented H(2)O(2)- and diamide-induced p38 MAPK, but not ERK activation.	Acetylcysteine	6-9	mitogen-activated protein kinase 14	Bos taurus	50-53
14575811-5	2003	Moreover, MKK7 activation was markedly reduced by pretreatment of the free radical scavenging thiol antioxidant N-acetylcysteine (NAC).	Acetylcysteine	112-128	mitogen activated protein kinase kinase 7	Rattus norvegicus	10-14
14575811-5	2003	Moreover, MKK7 activation was markedly reduced by pretreatment of the free radical scavenging thiol antioxidant N-acetylcysteine (NAC).	Acetylcysteine	130-133	mitogen activated protein kinase kinase 7	Rattus norvegicus	10-14
14607909-8	2003	We also found that NAC increased two IL-4 relevant transcription factors (AP-1) and NFATc.	Acetylcysteine	19-22	nuclear factor of activated T cells 1	Homo sapiens	84-89
19003216-0	2003	Blockade of endogenous reactive oxygen species by N-acetyl-L-cysteine suppresses the invasive activity of rat hepatoma cells by modulating the expression of hepatocyte growth factor gene.	Acetylcysteine	50-69	hepatocyte growth factor	Rattus norvegicus	157-181
19003216-4	2003	NAC also decreased the content of HGF mRNA and the secretion of HGF at these concentrations, leading to suppression of their invasion.	Acetylcysteine	0-3	hepatocyte growth factor	Rattus norvegicus	34-37
19003216-4	2003	NAC also decreased the content of HGF mRNA and the secretion of HGF at these concentrations, leading to suppression of their invasion.	Acetylcysteine	0-3	hepatocyte growth factor	Rattus norvegicus	64-67
19003216-5	2003	In the present study, blockade of endogenous ROS by NAC proved to efficiently suppress the invasive activity of hepatoma cells by down-regulating HGF gene expression, suggesting the importance of endogenous ROS in cellular signaling of tumor cell invasion.	Acetylcysteine	52-55	hepatocyte growth factor	Rattus norvegicus	146-149
14536032-5	2003	The copper-mediated modification of NF-L was significantly inhibited by thiol antioxidants, Nacetylcysteine, glutathione, and thiourea.	Acetylcysteine	92-107	neurofilament light chain	Homo sapiens	36-40
12941301-6	2003	Interestingly, NAC pretreatment protected cells from H(2)O(2)-induced PP1 inactivation and, consequently, it abolished increased H(2)O(2)-induced eIF2 alpha phosphorylation and protein synthesis inhibition.	Acetylcysteine	15-18	eukaryotic translation initiation factor 2A	Rattus norvegicus	146-156
12857675-9	2003	Moreover, PKC-delta activity was inhibited in HF adipocytes either by glucose deprivation or by treatment with the antioxidant N-acetyl-l-cysteine.	Acetylcysteine	127-146	protein kinase C, delta	Mus musculus	10-19
12847270-8	2003	Consistent with the inhibitory effect of reactive oxygen species on STAT1 signaling, STAT1 inhibition by 15dPGJ(2) was abrogated by N-acetylcysteine, glutathione, superoxide dismutase, and catalase.	Acetylcysteine	132-148	signal transducer and activator of transcription 1	Homo sapiens	85-90
12799770-7	2003	N-acetyl- l-cysteine (NAC) reduced both the cytotoxicity of inorganic arsenic and the HO-1 mRNA level, and buthionine sulfoximine enhanced cytotoxicity of inorganic arsenic.	Acetylcysteine	0-20	heme oxygenase 1	Rattus norvegicus	86-90
12799770-7	2003	N-acetyl- l-cysteine (NAC) reduced both the cytotoxicity of inorganic arsenic and the HO-1 mRNA level, and buthionine sulfoximine enhanced cytotoxicity of inorganic arsenic.	Acetylcysteine	22-25	heme oxygenase 1	Rattus norvegicus	86-90
12566084-6	2003	Activation of dCK by UV-C was mimicked by H(2)O(2), markedly counteracted by N-acetylcysteine, a general antioxidant, and completely abolished by the growth factor receptor inhibitor suramin.	Acetylcysteine	77-93	Calcium/calmodulin-dependent protein kinase II	Drosophila melanogaster	14-17
14518593-5	2003	Telmisartan, a newly developed Ang II type 1 receptor antagonist, or an antioxidant N-acetylcysteine significantly inhibited PDGF-B gene induction in Ang II-exposed pericytes.	Acetylcysteine	84-100	ANG	Bos taurus	150-153
12194971-13	2002	N-Acetylcysteine almost completely abolished AS-mediated induction of HO-1, whereas a glutathione synthesis inhibitor (buthionine sulfoximine) significantly decreased heme oxygenase activation by AS, indicating that sulfydryl groups are crucial targets in the regulation of HO-1 expression by NO(-).	Acetylcysteine	0-16	heme oxygenase 1	Rattus norvegicus	70-74
12011048-4	2002	Mechanical suppression of vitamin D(3)-up-regulated protein-1 gene expression was blocked by N-acetylcysteine.	Acetylcysteine	93-109	thioredoxin interacting protein	Rattus norvegicus	26-61
12091442-10	2002	CONCLUSIONS: Retinal redox status is altered by intense light and is normalized partially by the effect of NAC on TRX and GSH tissue levels.	Acetylcysteine	107-110	thioredoxin 1	Mus musculus	114-117
12126787-7	2002	The AGE-induced increases in VEGF expression and PKC activation were inhibited by the pan-specific PKC inhibitor, calphostin C, and by the antioxidant drug and compounds, gliclazide, N-acetylcysteine, and vitamin E.	Acetylcysteine	183-199	vascular endothelial growth factor A	Bos taurus	29-33
12124425-8	2002	The increase in IRP1 activity was mediated by oxidative-stress as it was largely abolished by N-acetyl-L-cysteine.	Acetylcysteine	94-113	aconitase 1	Mus musculus	16-20
11884408-7	2002	We found that ROS production by V12-H-Ras expression was mediated by the Ras/phosphatidylinositol 3-kinase (PI3K)/Rac1/NADPH oxidase-dependent pathway and that pretreatment of V12-H-Ras-transformed cells with an antioxidant (N-acetylcysteine) and an NADPH oxidase inhibitor (diphenyleneiodonium) decreased DNA repair capacity.	Acetylcysteine	225-241	Harvey rat sarcoma virus oncogene	Mus musculus	36-41
12076523-4	2002	VP-16 has been shown to stimulate the Ca2+-dependent MPT induction similarly to prooxidants and to promote apoptosis by oxidative stress mechanisms, which is prevented by glutathione (GSH) and N-acetylcysteine (NAC).	Acetylcysteine	193-209	host cell factor C1	Homo sapiens	0-5
12076523-4	2002	VP-16 has been shown to stimulate the Ca2+-dependent MPT induction similarly to prooxidants and to promote apoptosis by oxidative stress mechanisms, which is prevented by glutathione (GSH) and N-acetylcysteine (NAC).	Acetylcysteine	211-214	host cell factor C1	Homo sapiens	0-5
12076523-8	2002	The inhibition of the VP-16-induced MPT by antioxidants agrees with the prevention of etoposide-induced apoptosis by GSH and NAC and suggests the generation of oxidant species as a potential mechanism underlying the MPT that may trigger the release of mitochondrial apoptogenic factors responsible for apoptotic cascade activation.	Acetylcysteine	125-128	host cell factor C1	Homo sapiens	22-27
11858945-6	2002	In addition, we demonstrated that the chemical antioxidant, N-acetylcysteine attenuated Raf-1 activation induced by S1P, suggesting that H(2)O(2) may be required for the signalling pathway leading to Raf-1 activation.	Acetylcysteine	60-76	v-raf-leukemia viral oncogene 1	Mus musculus	88-93
11858945-6	2002	In addition, we demonstrated that the chemical antioxidant, N-acetylcysteine attenuated Raf-1 activation induced by S1P, suggesting that H(2)O(2) may be required for the signalling pathway leading to Raf-1 activation.	Acetylcysteine	60-76	v-raf-leukemia viral oncogene 1	Mus musculus	200-205
11834240-5	2002	N-acetyl-L-cysteine, a free radical scavenger, completely inhibited the stimulation of adrenomedullin secretion by hydrogen peroxide, and this agent reduced the stimulation of adrenomedullin secretion by hypoxia.	Acetylcysteine	0-19	adrenomedullin	Rattus norvegicus	87-101
12404881-2	2002	N-Acetylcysteine (CAS 616-91-1, NAC), a known mucolytic drug, possesses also antioxidant properties, but it undergoes a rapid and extensive first-pass metabolism resulting in low tissue availability.	Acetylcysteine	0-16	X-linked Kx blood group	Homo sapiens	32-35
11709424-7	2001	In addition, both NAC treatment and MnSOD overexpression significantly inhibited IL-1 beta-stimulated MMP-9 induction (P &lt; 0.05).	Acetylcysteine	18-21	matrix metallopeptidase 9	Homo sapiens	102-107
11571584-6	2001	The Ad.CFTR-dependent increase of ICAM-1 mRNA was abolished by inhibitors of NF-kB, such as N-acetyl-L-cysteine, pyrrolidine dithiocarbamate, parthenolide and the synthetic peptide SN50.	Acetylcysteine	92-111	intercellular adhesion molecule 1	Homo sapiens	34-40
11502879-6	2001	The glutathione precursor, N-acetylcysteine also partially protected T47D/H3 cells from the lethal effect of doxorubicin, whereas L-buthionine-(S,R)-sulfoximine, an inhibitor of glutathione biosynthesis, sensitized both GPx-1--deficient and -proficient cells.	Acetylcysteine	27-43	glutathione peroxidase 1	Homo sapiens	220-225
11544433-0	2001	N-acetylcysteine attenuates the increase in alpha-glutathione S-transferase and circulating ICAM-1 and VCAM-1 after reperfusion in humans undergoing liver transplantation.	Acetylcysteine	0-16	intercellular adhesion molecule 1	Homo sapiens	92-98
11544433-10	2001	CONCLUSIONS: NAC attenuated the increase in alpha-glutathione S-transferase and circulating ICAM-1 and VCAM-1 after reperfusion of the donor liver, indicating possible cytoprotective effects of NAC.	Acetylcysteine	13-16	intercellular adhesion molecule 1	Homo sapiens	92-98
11488598-4	2001	Pretreatment of cells with N-acetylcysteine, a scavenger of reactive oxygen species (ROS), conferred resistance to the induction of the membrane depolarization, cytochrome c release, and caspase-3 activation by SA-liposomes.	Acetylcysteine	27-43	caspase 3	Mus musculus	187-196
11498285-6	2001	The Ras-induced increase in NF-kappaB DNA binding could be inhibited by treatment with the antioxidants N-acetyl-L-cysteine and glutathione monoester, suggesting that intracellular oxidant levels can mediate MMP-9 transcription.	Acetylcysteine	104-123	matrix metallopeptidase 9	Rattus norvegicus	208-213
11768769-7	2001	Free radical scavengers N-acetyl-L-cysteine (NAC), or glutathione (GSH), inhibited ERK2 activation and, to a much lesser extent, JNK1 activation by BHA/tBHQ, implicating the role of oxidative stress.	Acetylcysteine	24-43	X-linked Kx blood group	Homo sapiens	45-48
11375353-5	2001	Signal transduction from RAGE to NF-kappaB involved the generation of reactive oxygen species, since reporter gene expression was blocked with the antioxidant N-acetyl-L-cysteine.	Acetylcysteine	159-178	advanced glycosylation end-product specific receptor	Homo sapiens	25-29
11020383-8	2001	Consistent with the idea that ROS may participate in mdr1b regulation, antioxidant N-acetylcysteine inhibited the induction of mdr1b by 2-AAF.	Acetylcysteine	83-99	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	53-58
11020383-8	2001	Consistent with the idea that ROS may participate in mdr1b regulation, antioxidant N-acetylcysteine inhibited the induction of mdr1b by 2-AAF.	Acetylcysteine	83-99	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	127-132
11167962-3	2001	It has previously been shown that tumour necrosis factor (TNF)-MA activates p38 mitogen-activated protein (MAP) kinase to produce cytokine, including RANTES, that N-acetylcysteine (NAC) attenuates cytokine production by human bronchial epithelial cells (BECs), and that sensitivity to TNFalpha is inversely correlated with cellular redox state.	Acetylcysteine	163-179	C-C motif chemokine ligand 5	Homo sapiens	150-156
11167962-3	2001	It has previously been shown that tumour necrosis factor (TNF)-MA activates p38 mitogen-activated protein (MAP) kinase to produce cytokine, including RANTES, that N-acetylcysteine (NAC) attenuates cytokine production by human bronchial epithelial cells (BECs), and that sensitivity to TNFalpha is inversely correlated with cellular redox state.	Acetylcysteine	181-184	C-C motif chemokine ligand 5	Homo sapiens	150-156
10964049-7	2000	Furthermore, we observed that pre-incubation of cells with either N-acetyl-cysteine [a glutathione (GSH) precursor] or L-buthionine-S,R-sulfoximine (a specific inhibitor of GSH biosynthesis) had a minimal effect on arecoline-induced c-jun expression.	Acetylcysteine	66-83	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	233-238
10989603-4	2000	When cells were cultured at lower oxygen tension in the presence of an antioxidant N-acetyl-L-cysteine (NAC) or under physiologically hypoxic (5% O2) conditions, the elevation of the oxidative level by UV-irradiation was significantly reduced.	Acetylcysteine	83-102	X-linked Kx blood group	Homo sapiens	104-107
10963726-10	2000	NAC treatment markedly reduced the intensity and degree of P-selectin and ICAM-1 in tissue section from SAO-shocked rats.	Acetylcysteine	0-3	intercellular adhesion molecule 1	Rattus norvegicus	74-80
10833515-8	2000	Treatment of the BCR/ABL-expressing cell line MO7/p210 with the reducing agents pyrrolidine dithiocarbamate or N-acetylcysteine reduced the accumulation of ROS and also decreased tyrosine phosphorylation of cellular proteins.	Acetylcysteine	111-127	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	17-24
10953313-3	2000	The CGA radical was scavenged by 100-300-fold lower concentrations of sodium ascorbate or N-acetyl-l-cysteine (NAC), whereas the ascorbate radical was not completely scavenged by CGA.	Acetylcysteine	90-109	X-linked Kx blood group	Homo sapiens	111-114
10924861-11	2000	Furthermore, the involvement of the oxidative stress in the UVA-induced effect on STAT1 activity is suggested by the protective action of the antioxidants alpha-tocopherol and N-acetylcysteine on both the activation phase (UVA doses lower than 1.5 J/cm(2)) and the inhibitory phase.	Acetylcysteine	176-192	signal transducer and activator of transcription 1	Homo sapiens	82-87
10667587-2	2000	Here, we present evidence indicating that subsequent reduction of surface protein disulfides with N-acetyl-L-cysteine (NAC) further augments the immunogenic potential of PCL-modified tumor cells both in vitro and in vivo.	Acetylcysteine	98-117	X-linked Kx blood group	Homo sapiens	119-122
10619832-7	2000	NAC inhibited DEP-induced p38 MAP kinase activation and IL-8 and RANTES production.	Acetylcysteine	0-3	C-C motif chemokine ligand 5	Homo sapiens	65-71
26368632-9	2000	Crocidolite asbestos caused a dose-dependent depletion of GSH in RPM cells, and the presence of NAC ameliorated the expression of EGF-R protein by crocidolite.	Acetylcysteine	96-99	epidermal growth factor receptor	Rattus norvegicus	130-135
10649673-5	2000	If there is doubt about the dose or time of ingestion, one should err on the side of treatment with acetylcysteine, because it is both effective and safe.	Acetylcysteine	100-114	solute carrier family 7 member 1	Homo sapiens	66-69
11124650-8	2000	NAC also enhanced LPS-induced IL-10 secretion, while AMB did not.	Acetylcysteine	0-3	interleukin 10	Homo sapiens	30-35
11124650-10	2000	CONCLUSIONS: The results suggest that NAC enhances inflammatory and immune responses and prevents excessive responses reciprocally, through keeping local balance of IL-12 and IL-10 production in alveolar macrophages at inflammatory sites of bacterial pneumonia.	Acetylcysteine	38-41	interleukin 10	Homo sapiens	175-180
10573084-9	1999	We noticed significant decrease in CD80, CD25, and CD8+ cells after NAC therapy.	Acetylcysteine	68-71	CD8a molecule	Homo sapiens	35-38
10526120-2	1999	Recent experiments showed that the thiolic antioxidant N-acetylcysteine (NAC) can protect against age-related impairment in COX activity in mice hepatic mitochondria.	Acetylcysteine	55-71	cytochrome c oxidase subunit 4I1	Mus musculus	124-127
10526120-2	1999	Recent experiments showed that the thiolic antioxidant N-acetylcysteine (NAC) can protect against age-related impairment in COX activity in mice hepatic mitochondria.	Acetylcysteine	73-76	cytochrome c oxidase subunit 4I1	Mus musculus	124-127
10526120-3	1999	The present paper shows that NAC enhances COX activity in vitro in synaptic mitochondria isolated from young and old mice.	Acetylcysteine	29-32	cytochrome c oxidase subunit 4I1	Mus musculus	42-45
10526120-4	1999	The optimum NAC concentration for maximum COX activity was 5 mM in young and 10 mM in old synaptic preparations.	Acetylcysteine	12-15	cytochrome c oxidase subunit 4I1	Mus musculus	42-45
10397638-9	1999	In addition, 6-OHDA induced ROS-mediated c-Jun N-terminal kinase (JNK) activation that was attenuated in the presence of N-acetylcysteine or MnTBAP but not catalase or Z-VAD-fmk.	Acetylcysteine	121-137	mitogen-activated protein kinase 8	Mus musculus	41-64
10397638-9	1999	In addition, 6-OHDA induced ROS-mediated c-Jun N-terminal kinase (JNK) activation that was attenuated in the presence of N-acetylcysteine or MnTBAP but not catalase or Z-VAD-fmk.	Acetylcysteine	121-137	mitogen-activated protein kinase 8	Mus musculus	66-69
10391097-8	1999	Moreover, TdT-mediated dUTP-biotin nick-end labeling (TUNEL) assay showed that CDDP-induced apoptosis (31.1+/-3.8%) was significantly inhibited by pretreatment with NAC in KU1 cells (11.2+/-2.6%).	Acetylcysteine	165-168	DNA nucleotidylexotransferase	Homo sapiens	10-13
10051543-6	1999	However, both PKC activation and oxidant generation were necessary for ICAM-1 mRNA expression because the pretreatment of HPAE cells with either calphostin C or N-acetylcysteine inhibited the TNF-alpha-induced activation of NF-kappaB and prevented the activation of ICAM-1 promoter.	Acetylcysteine	161-177	intercellular adhesion molecule 1	Homo sapiens	71-77
10051543-6	1999	However, both PKC activation and oxidant generation were necessary for ICAM-1 mRNA expression because the pretreatment of HPAE cells with either calphostin C or N-acetylcysteine inhibited the TNF-alpha-induced activation of NF-kappaB and prevented the activation of ICAM-1 promoter.	Acetylcysteine	161-177	intercellular adhesion molecule 1	Homo sapiens	266-272
9843726-8	1998	Activation of STATs by platelet-derived growth factor (PDGF) is significantly inhibited by N-acetyl-L-cysteine and diphenylene iodonium, indicating that ROS production contributes to STAT activation in response to PDGF.	Acetylcysteine	91-110	signal transducer and activator of transcription 1	Homo sapiens	14-19
9824639-3	1998	In both cases, AIF production is inhibited by the antioxidant N-Acetylcysteine, indicating that similar or identical signalling pathways are utilized.	Acetylcysteine	62-78	apoptosis inducing factor mitochondria associated 1	Homo sapiens	15-18
9765355-7	1998	One mM NAC also suppressed Cd-induced increase of c-Fos protein although NAC alone did not change the protein content.	Acetylcysteine	7-10	protein c-Fos	Sus scrofa	50-55
9765355-9	1998	Thus, NAC-induced protection appeared to be independent of glutathione level or the transcriptional activation of genes including c-fos.	Acetylcysteine	6-9	protein c-Fos	Sus scrofa	130-135
9699515-1	1998	We have examined the effects of three structurally distinct antioxidants (N-acetylcysteine [NAC], Trolox C [a water-soluble vitamin E derivative], and nordihydroguaiaretic acid [NGA]) on the expression of the c-fos gene over a 2-hour period.	Acetylcysteine	74-90	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	209-214
9699515-6	1998	NAC induction of c-fos is unaffected by PMA pretreatment, while Trolox C superinduced c-fos following PMA pretreatment.	Acetylcysteine	0-3	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	17-22
12671299-5	1998	Pretreatment with free radical scavengers N-acetyl-L-cysteine (NAC), glutathione (GSH), or vitamin E, inhibited ERK2 activation and, to a much lesser extent, JNK 1 activation by BHA and tBHQ, implicating the role of oxidative stress.	Acetylcysteine	42-61	X-linked Kx blood group	Homo sapiens	63-66
9571990-9	1998	NAC prevented activation of mitogen-activated protein (MAP) kinases p42MAPK and p44MAPK and inhibited expression of cyclin D1, but had no effect on the levels of proliferating cell nuclear antigen.	Acetylcysteine	0-3	cyclin D1	Mus musculus	116-125
9654239-9	1998	The GSTT1 polymorphism could also influence the urinary excretion of SO-specific mercapturic acids.	Acetylcysteine	81-98	glutathione S-transferase theta 1	Homo sapiens	4-9
9299415-4	1997	Furthermore, Lfcin-B-induced apoptosis in THP-1 cells was completely abolished by addition of antioxidants such as N-acetyl-L-cysteine (NAC) and glutathione (GSH), but not by various cytokines and mitogen which can activate monocytic cells.	Acetylcysteine	115-134	X-linked Kx blood group	Homo sapiens	136-139
9242544-1	1997	Because of its anticarcinogenic and antimutagenic properties, N-acetyl-L-cysteine (NAC) has been proposed for cancer treatment.	Acetylcysteine	62-81	X-linked Kx blood group	Homo sapiens	83-86
9099368-9	1997	The M2 mercapturic acid had a better correlation (r = 0.56) with respect to M1-R and M1-S.	Acetylcysteine	7-23	cholinergic receptor muscarinic 1	Homo sapiens	76-80
9197915-1	1997	A new approach to reduce the level of reactive oxygen species (ROS) in human semen by using N-acetyl-L-cysteine (NAC) was evaluated.	Acetylcysteine	92-111	X-linked Kx blood group	Homo sapiens	113-116
9003061-8	1997	N-Acetylcysteine reduced (50%) the accumulation of HO-1 mRNA in astroglial cells after PrP 106-126 (25 microM) given for 5 days.	Acetylcysteine	0-16	heme oxygenase 1	Rattus norvegicus	51-55
9000534-2	1997	In T cells, N-acetyl-L-cysteine (NAC) inhibits the induction of NF-kappaB and transcription of HIV-1.	Acetylcysteine	12-31	X-linked Kx blood group	Homo sapiens	33-36
8921438-5	1996	N-acetylcysteine inhibited this effect, indicating that reactive oxygen intermediates are required for RANTES production.	Acetylcysteine	0-16	C-C motif chemokine ligand 5	Homo sapiens	103-109
8863052-10	1996	Four series of randomized, controlled and double-blind experiments were carried out and consistently showed a lower increase in SDH in NAC-treated animals in each series.	Acetylcysteine	135-138	succinate dehydrogenase complex iron sulfur subunit B	Homo sapiens	128-131
9173679-12	1996	NAC treatment led to a recovery in the liver of total CYP content (+35 %), CYP3A content (total recovery), and the rates of Ery (+59%) and CyA (+87%) metabolism, whereas inconsistent results were obtained with NMMA.	Acetylcysteine	0-3	cytochrome P450, family 3, subfamily a, polypeptide 11	Mus musculus	75-80
9173679-13	1996	These results suggest that NAC, but probably not NMMA, partially protects hepatic CYP3A from Toxoplasma-mediated suppression in mouse.	Acetylcysteine	27-30	cytochrome P450, family 3, subfamily a, polypeptide 11	Mus musculus	82-87
8733110-5	1996	N-acetyl cysteine (NAC) induces c-fos transcription in both early and late passage cells, while nordihydroguaiaretic acid (NGA) induced c-fos transcription in early passage cells but fails to stimulate it in late passage cells.	Acetylcysteine	0-17	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	32-37
8733110-5	1996	N-acetyl cysteine (NAC) induces c-fos transcription in both early and late passage cells, while nordihydroguaiaretic acid (NGA) induced c-fos transcription in early passage cells but fails to stimulate it in late passage cells.	Acetylcysteine	19-22	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	32-37
8825185-13	1996	Pretreatment with N-acetylcysteine did not affect c-fos or c-jun mRNA levels and diminished CCI4-stimulated c-fos and c-jun gene expression by 44 and 55%, respectively, relative to the immediate-early gene mRNA levels monitored in the hepatic tissue of CCI4-treated animals.	Acetylcysteine	18-34	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	108-113
7673190-5	1995	The observation that in quiescent myoblasts Ang-II increase of AP1 binding and induction of DNA synthesis and, in differentiated myotubes, Ang-II stimulation of protein synthesis are abolished by the cysteine-derivative and glutathione precursor N-acetyl-L-cysteine strongly suggests a role for reactive oxygen intermediates in the intracellular transduction of Ang-II signals for immediate early gene induction, cell proliferation, and hypertrophic responses.	Acetylcysteine	246-265	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	63-66
7642556-2	1995	The H2O2-induced increase in ICAM-1 mRNA was inhibited by actinomycin D, by the antioxidant N-acetylcysteine, and by 3-amino-benzamide (which blocks oxidant-induced AP-1 activity), but not by pyrrolidine dithiocarbamate (which blocks oxidant-induced NF-kappa B activity).	Acetylcysteine	92-108	intercellular adhesion molecule 1	Homo sapiens	29-35
7548745-5	1995	We also observed the formation of 5-(N-acetyl-L-cystein-S-yl)-alpha-MeDA (5-[NAC]-alpha-MeDA) in all brain regions, indicating that the brain has the ability to synthesize mercapturic acids.	Acetylcysteine	172-189	nascent polypeptide associated complex subunit alpha	Rattus norvegicus	77-87
7767940-10	1995	Compounds containing a free sulfhydryl group (cysteine, N-acetylcysteine, GSH or 3,4-dichlorobenzenethiol) decreased the amount of covalent binding to various degrees, suggesting the involvement of the sulfhydryl group in adduct formation with TNT following bioactivation.	Acetylcysteine	56-72	troponin T3, fast skeletal type	Rattus norvegicus	244-247
7743507-0	1995	Induction of c-fos and c-jun proto-oncogene expression by asbestos is ameliorated by N-acetyl-L-cysteine in mesothelial cells.	Acetylcysteine	85-104	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-18
7743507-7	1995	Here we report that addition of N-acetyl-L-cysteine decreases asbestos-mediated induction of c-fos and c-jun mRNA levels in a dose-dependent fashion.	Acetylcysteine	32-51	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	93-98
7705924-3	1995	As assessed by zymographic analysis, NAC completely inhibited the gelatinolytic activity of type-IV collagenases in the cells tested (gelatinases A and B).	Acetylcysteine	37-40	matrix metallopeptidase 2	Mus musculus	134-153
7841193-6	1995	N-Acetylcysteine inhibited IL1-induced interleukin-2 in EL4, however, demonstrating that N-acetylcysteine was biologically active.	Acetylcysteine	0-16	epilepsy 4	Mus musculus	56-59
7841193-6	1995	N-Acetylcysteine inhibited IL1-induced interleukin-2 in EL4, however, demonstrating that N-acetylcysteine was biologically active.	Acetylcysteine	89-105	epilepsy 4	Mus musculus	56-59
7798616-3	1994	Expression of ICAM-1 was induced on keratinocytes by treatment with 300 microM H2O2 for 1 h. The antioxidant N-acetyl-L-cysteine strongly inhibited H2O2-induced ICAM-1 expression, whereas the antioxidants pyrrolidine dithiocarbamate and alpha-tocopherol were less inhibitory.	Acetylcysteine	109-128	intercellular adhesion molecule 1	Homo sapiens	14-20
7798616-3	1994	Expression of ICAM-1 was induced on keratinocytes by treatment with 300 microM H2O2 for 1 h. The antioxidant N-acetyl-L-cysteine strongly inhibited H2O2-induced ICAM-1 expression, whereas the antioxidants pyrrolidine dithiocarbamate and alpha-tocopherol were less inhibitory.	Acetylcysteine	109-128	intercellular adhesion molecule 1	Homo sapiens	161-167
7798616-4	1994	N-acetyl-L-cysteine also suppressed keratinocyte surface expression of ICAM-1 induced by the cytokines interferon-gamma (IFN-gamma) or tumor necrosis factor-alpha (TNF-alpha), whereas pyrrolidine dithiocarbamate and alpha-tocopherol suppressed IFN-gamma-induced surface expression but not TNF-alpha-induced expression.	Acetylcysteine	0-19	intercellular adhesion molecule 1	Homo sapiens	71-77
8194136-3	1994	We confirmed that N-acetyl-L-cysteine (NAC), a cysteine prodrug which maintains intracellular GSH levels during oxidative stress, inhibits in the chronically infected U1 cells, the stimulation of HIV replication induced by phorbol 12-myristate 13-acetate (PMA), interleukin-6 (IL-6) or granulocyte-macrophage colony stimulating factor (GM-CSF).	Acetylcysteine	18-37	X-linked Kx blood group	Homo sapiens	39-42
1639069-3	1992	While an inhibitor of protein kinase C could not block gene induction by MHBst, the antioxidants N-acetyl-L-cysteine (NAC) and pyrrolidine dithiocarbamate (PDTC) could potently suppress transactivation at mM and microM concentrations, respectively.	Acetylcysteine	97-116	X-linked Kx blood group	Homo sapiens	118-121
2112750-1	1990	We show that the stimulation of human immunodeficiency virus (HIV) brought about by tumor necrosis factor alpha and phorbol 12-myristate 13-acetate can be inhibited by adding N-acetyl-L-cysteine (NAC).	Acetylcysteine	175-194	X-linked Kx blood group	Homo sapiens	196-199
33775218-11	2021	BM-MNCs combination with NAC or ALA exerted significant antioxidant, anti-inflammatory and anti-cytogenetical aberrations effect compared to each of them alone.HighlightsCCl4 elevated ALT, AST, TNF-alpha, IL-6 and MDACCl4 reduced ALB, IL-10, SOD, CAT, GPx and TACCCl4 increased the number of DNA breaks in liverNAC, ALA and BM-MNCs reduced ALT, AST, while, increase albumin, CAT, TAC, GPx, SODNAC, ALA and BM-MNCs decreased in MDA, IL-6 and TNF-alpha and increased IL-10.	Acetylcysteine	25-28	albumin	Rattus norvegicus	230-233
33771976-7	2021	Increased reactive oxygen species (ROS) levels and the expression of HIF-1alpha and Nrf2 decreased under the hypoxic condition following incubation with N-acetylcysteine, a ROS scavenger, which was associated with a decrease in CXCR4 expression.	Acetylcysteine	153-169	C-X-C motif chemokine receptor 4	Homo sapiens	228-233
33763172-7	2021	On the contrary, overexpression of BECN1 or treating cells with the antioxidant N-acetylcysteine (NAC) could restore the survival of hTERT knockdown cells.	Acetylcysteine	80-96	beclin 1	Homo sapiens	35-40
33763172-7	2021	On the contrary, overexpression of BECN1 or treating cells with the antioxidant N-acetylcysteine (NAC) could restore the survival of hTERT knockdown cells.	Acetylcysteine	98-101	beclin 1	Homo sapiens	35-40
19409485-8	2009	Furthermore, when cells were pretreated with scavengers of hydrogen peroxide such as N-acetylcysteine, or overexpression of Nrf2, or Keap1 knockdown by siRNA, Tat-induced HIV-1 LTR transactivation was suppressed, whereas buthionine sulfoximine or Nrf2 knockdown by siRNA potentiated Tat-induced HIV-1 LTR transactivation.	Acetylcysteine	85-101	Tat	Human immunodeficiency virus 1	159-162
34182114-11	2022	Combining colchicine with N-acetylcysteine instead of fenofibrate (MD: 5.00, 95% CI: 1.45-8.54) led to a more robust reduction in KLF4 expression.	Acetylcysteine	26-42	Krueppel-like factor 4	Oryctolagus cuniculus	130-134
34951044-2	2021	High dose acetylcysteine (NAC) has been proposed in patients taking large paracetamol overdoses based on reports of hepatotoxicity despite early initiation of NAC treatment with the commonly used 300 mg/kg intravenous acetylcysteine regimen.	Acetylcysteine	10-24	X-linked Kx blood group	Homo sapiens	26-29
34951044-2	2021	High dose acetylcysteine (NAC) has been proposed in patients taking large paracetamol overdoses based on reports of hepatotoxicity despite early initiation of NAC treatment with the commonly used 300 mg/kg intravenous acetylcysteine regimen.	Acetylcysteine	218-232	X-linked Kx blood group	Homo sapiens	159-162
34948425-11	2021	NAC administration to dams or offspring demonstrated lower brain NF-kappaB p65, nNOS, TNF-alpha and IL-6 protein levels compared to hypoxia alone.	Acetylcysteine	0-3	nitric oxide synthase 1	Rattus norvegicus	80-84
34924003-8	2021	Exogenous supplementation of NAC or GSH reduced the expression of NRF2 and GCLC, suggesting the NRF2/GCLC-related antioxidant production pathway might be desensitized.	Acetylcysteine	29-32	glutamate-cysteine ligase, catalytic subunit	Mus musculus	75-79
34924003-8	2021	Exogenous supplementation of NAC or GSH reduced the expression of NRF2 and GCLC, suggesting the NRF2/GCLC-related antioxidant production pathway might be desensitized.	Acetylcysteine	29-32	glutamate-cysteine ligase, catalytic subunit	Mus musculus	101-105
34899969-0	2021	N-Acetylcysteine (NAC) Inhibits Synthesis of IL-18 in Macrophage by Suppressing NLRP3 Expression to Reduce the Production of IFN-gamma from NK Cells.	Acetylcysteine	0-16	interleukin 18	Homo sapiens	45-50
34899969-0	2021	N-Acetylcysteine (NAC) Inhibits Synthesis of IL-18 in Macrophage by Suppressing NLRP3 Expression to Reduce the Production of IFN-gamma from NK Cells.	Acetylcysteine	18-21	interleukin 18	Homo sapiens	45-50
34899969-3	2021	This study was designed to evaluate the specific mechanism of NAC regulating IL-18.	Acetylcysteine	62-65	interleukin 18	Homo sapiens	77-82
34711021-7	2021	Compared to rats that treated to continuous dose of Cd, NAC supplementation enhanced the expression of Nrf2 by 1.67-fold (p<0.001) and reduced the expression of NLRP3 and Caspase 1 genes by 1.39-fold (p<0.001) and 1.58-fold (p<0.001), respectively.	Acetylcysteine	56-59	caspase 1	Rattus norvegicus	171-180
34711021-9	2021	NAC protects liver tissue against Cd-induced oxidative injuries via enhancement of Nrf2 expression and reduction of NLRP3 and caspase 1 genes.	Acetylcysteine	0-3	caspase 1	Rattus norvegicus	126-135
34387802-8	2021	Treatment with the antioxidant N-acetyl cysteine decreased the number of TUNEL-stained cells in high glucose and improved the alpha-actinin 2 striated pattern.	Acetylcysteine	31-48	actinin alpha 2	Mus musculus	126-141
34884437-4	2021	In HL-60 cells, NAC activated NOX2 to produce superoxide (O2 -).	Acetylcysteine	16-19	cytochrome b-245 beta chain	Homo sapiens	30-34
34672197-5	2021	We not only monitor the gradual activation of Casp-3 in the kidney of mice upon AKI progression but also can report on the progressive recovery of kidney functions in AKI mice following N-acetyl-l-cysteine (NAC) therapy via real-time fluorescence imaging by 1-DPA2.	Acetylcysteine	186-205	caspase 3	Mus musculus	46-52
34672197-5	2021	We not only monitor the gradual activation of Casp-3 in the kidney of mice upon AKI progression but also can report on the progressive recovery of kidney functions in AKI mice following N-acetyl-l-cysteine (NAC) therapy via real-time fluorescence imaging by 1-DPA2.	Acetylcysteine	207-210	caspase 3	Mus musculus	46-52
34739934-9	2021	Concurrently, the results indicated that NAC attenuated NiCl2-induced apoptosis, as evidenced by reduction of apoptotic cells and cleaved-caspase-3/- 8/- 9 together with cleaved-PARP protein levels.	Acetylcysteine	41-44	poly (ADP-ribose) polymerase family, member 1	Mus musculus	178-182
34390848-3	2021	Herein, we introduced a controllable ROS-scavenging nanoplatform by encasing N-acetylcysteine (NAC, (a well-known ROS scavenger) into tailor-made ROS-cleavable amphiphilic polymer nanoparticles (PEG-ss-PCL NPs) as an intracellular delivery carrier.	Acetylcysteine	77-93	X-linked Kx blood group	Homo sapiens	95-98
34080015-0	2021	Timely N-Acetyl-Cysteine and Environmental Enrichment Rescue Oxidative Stress-Induced Parvalbumin Interneuron Impairments via MMP9/RAGE Pathway: A Translational Approach for Early Intervention in Psychosis.	Acetylcysteine	7-24	matrix metallopeptidase 9	Homo sapiens	126-130
34080015-0	2021	Timely N-Acetyl-Cysteine and Environmental Enrichment Rescue Oxidative Stress-Induced Parvalbumin Interneuron Impairments via MMP9/RAGE Pathway: A Translational Approach for Early Intervention in Psychosis.	Acetylcysteine	7-24	advanced glycosylation end-product specific receptor	Homo sapiens	131-135
34664816-10	2021	However, non-significant variations in the IL-1beta and IL-17 levels suggest an alternative way of NAC effectiveness without influencing the measured cytokines.	Acetylcysteine	99-102	interleukin 17A	Homo sapiens	56-61
34146985-6	2021	Cell cycle was arrested in G1 phase by BDE-47; (2) Elevated intracellular ROS, LDH levels and necrosis were found, which was alleviated by pretreatment with ROS scavenger N-acetylcysteine (NAC); (3) AhR plays an essential role in ligand-regulated transcription factor activation by exogenous environmental compounds.	Acetylcysteine	171-187	homeobox D13	Homo sapiens	39-42
34146985-6	2021	Cell cycle was arrested in G1 phase by BDE-47; (2) Elevated intracellular ROS, LDH levels and necrosis were found, which was alleviated by pretreatment with ROS scavenger N-acetylcysteine (NAC); (3) AhR plays an essential role in ligand-regulated transcription factor activation by exogenous environmental compounds.	Acetylcysteine	189-192	homeobox D13	Homo sapiens	39-42
34763128-7	2021	Inhibiting Nrf2 activation either by reducing ROS levels by N-acetylcysteine or by knocking down of Nrf2 by small interfering RNA attenuated both Notch signaling activation and EMT development.	Acetylcysteine	60-76	notch receptor 4	Homo sapiens	146-151
34346218-5	2021	The results from the TC uptake assay using N-acetylcysteine suggested that the inhibitory effect of TF2A and TF2B was attributed to the oxidization of their benzotropolone rings and their covalent bonding with ASBT"s cysteine.	Acetylcysteine	43-59	solute carrier family 10 member 2	Homo sapiens	210-214
34445365-0	2021	Single Dose of N-Acetylcysteine in Local Anesthesia Increases Expression of HIF1alpha, MAPK1, TGFbeta1 and Growth Factors in Rat Wound Healing.	Acetylcysteine	15-31	hypoxia inducible factor 1 subunit alpha	Rattus norvegicus	76-85
34439496-10	2021	Dnmt3b inhibitor 5"-azacytosine, antioxidant N-acetylcysteine, or Oxr1 recombinant protein attenuated loss in miR-29a and FoxO3 to mitigate oxidative stress, senescence, and mineralization matrix underproduction.	Acetylcysteine	45-61	forkhead box O3	Mus musculus	122-127
34303734-8	2021	Subsequent incubation with N-Acetyl-L-cysteine (NAC, 1 mM) reestablished GSH content and reverted concomitantly the alteration in Mrp2 localization and function induced by TBH.	Acetylcysteine	27-46	ATP binding cassette subfamily C member 2	Rattus norvegicus	130-134
34349610-10	2021	Antioxidant N-acetyl cysteine (NAC) and ML171, a specific NADPH oxidase 1 inhibitor, suppressed cerulein/resistin-induced ROS production, NF-kappaB activation, and IL-6 expression.	Acetylcysteine	31-34	NADPH oxidase 1	Rattus norvegicus	58-73
34185060-9	2021	The decreased levels of ATP7A and Atox1 proteins were restored by the antioxidant N-acetylcysteine and the lysosomal inhibitor bafilomycin A1.	Acetylcysteine	82-98	ATPase copper transporting alpha	Homo sapiens	24-29
34185060-9	2021	The decreased levels of ATP7A and Atox1 proteins were restored by the antioxidant N-acetylcysteine and the lysosomal inhibitor bafilomycin A1.	Acetylcysteine	82-98	antioxidant 1 copper chaperone	Homo sapiens	34-39
34206987-10	2021	NAC and DFMO suppressed NO and interleukin 10 (IL-10) production by splenocytes, while DFMO increased the levels of IL-12.	Acetylcysteine	0-3	interleukin 10	Homo sapiens	31-45
34206987-10	2021	NAC and DFMO suppressed NO and interleukin 10 (IL-10) production by splenocytes, while DFMO increased the levels of IL-12.	Acetylcysteine	0-3	interleukin 10	Homo sapiens	47-52
35507947-8	2022	In addition, the expression of Gdf9, Lif, Bax, and Bcl2 genes were increased and Amh was decreased in groups cultured in the presence of NAC compared to groups cultured without NAC.	Acetylcysteine	137-140	BCL2-associated X protein	Mus musculus	42-45
35507947-8	2022	In addition, the expression of Gdf9, Lif, Bax, and Bcl2 genes were increased and Amh was decreased in groups cultured in the presence of NAC compared to groups cultured without NAC.	Acetylcysteine	177-180	BCL2-associated X protein	Mus musculus	42-45
35181322-10	2022	Interestingly, ser36 phosphorylation mutant transfection and pretreatment with antioxidant N-acetylcysteine results indicate that vitamin C induced Rac1 activation, ROS production and apoptosis is p66Shc ser36 phosphorylation dependent.	Acetylcysteine	91-107	Rac family small GTPase 1	Homo sapiens	148-152
35470759-9	2022	Antioxidative N-acetylcysteine (NAC) inhibited VSMC proliferation and migration induced by PDGF-BB or plin5 knockdown.	Acetylcysteine	14-30	perilipin 5	Mus musculus	102-107
35470759-9	2022	Antioxidative N-acetylcysteine (NAC) inhibited VSMC proliferation and migration induced by PDGF-BB or plin5 knockdown.	Acetylcysteine	32-35	perilipin 5	Mus musculus	102-107
35372029-5	2022	Pre-treatment with the anti-oxidant, N-acetylcysteine (NAC), reversed the ONC201-induced oxidative stress response, and prevented ONC201-reduced VEGF and cell invasion by regulating epithelial-mesenchymal transition protein expression.	Acetylcysteine	37-53	vascular endothelial growth factor A	Mus musculus	145-149
35372029-5	2022	Pre-treatment with the anti-oxidant, N-acetylcysteine (NAC), reversed the ONC201-induced oxidative stress response, and prevented ONC201-reduced VEGF and cell invasion by regulating epithelial-mesenchymal transition protein expression.	Acetylcysteine	55-58	vascular endothelial growth factor A	Mus musculus	145-149
35249163-0	2022	DMBT1 is upregulated in cystic fibrosis, affects ciliary motility, and is reduced by acetylcysteine.	Acetylcysteine	85-99	deleted in malignant brain tumors 1	Homo sapiens	0-5
35249163-14	2022	Application of ACC, leading to reduced DMBT1 concentrations, could be a potential therapeutic option for CF patients.	Acetylcysteine	15-18	deleted in malignant brain tumors 1	Homo sapiens	39-44
35169555-10	2022	Apoptotic features such as chromatin condensation, nuclear fragmentation, and caspase 3 activation were observed 1 h after the NAC treatment.	Acetylcysteine	127-130	caspase 3	Mus musculus	78-87
35296207-7	2022	I/R-induced upregulation of STAT3 phosphorylation and ZIP2 expression was reversed by the ROS scavenger N-acetylcysteine (NAC) and the NOX inhibitor diphenyleneiodonium (DPI).	Acetylcysteine	104-120	solute carrier family 39 (zinc transporter), member 2	Mus musculus	54-58
35296207-7	2022	I/R-induced upregulation of STAT3 phosphorylation and ZIP2 expression was reversed by the ROS scavenger N-acetylcysteine (NAC) and the NOX inhibitor diphenyleneiodonium (DPI).	Acetylcysteine	122-125	solute carrier family 39 (zinc transporter), member 2	Mus musculus	54-58
35296207-9	2022	Both NAC and DPI prevented upregulation of STAT3 phosphorylation and ZIP2 expression induced by overexpression of p67phox, whereas the STAT3 inhibitor stattic abrogated upregulation ZIP2 expression, indicating that the increase of p67phox at reperfusion is an upstream signaling event responsible for ZIP2 upregulation via STAT3.	Acetylcysteine	5-8	solute carrier family 39 (zinc transporter), member 2	Mus musculus	69-73
35296207-9	2022	Both NAC and DPI prevented upregulation of STAT3 phosphorylation and ZIP2 expression induced by overexpression of p67phox, whereas the STAT3 inhibitor stattic abrogated upregulation ZIP2 expression, indicating that the increase of p67phox at reperfusion is an upstream signaling event responsible for ZIP2 upregulation via STAT3.	Acetylcysteine	5-8	neutrophil cytosolic factor 2	Mus musculus	114-121
35296207-9	2022	Both NAC and DPI prevented upregulation of STAT3 phosphorylation and ZIP2 expression induced by overexpression of p67phox, whereas the STAT3 inhibitor stattic abrogated upregulation ZIP2 expression, indicating that the increase of p67phox at reperfusion is an upstream signaling event responsible for ZIP2 upregulation via STAT3.	Acetylcysteine	5-8	neutrophil cytosolic factor 2	Mus musculus	231-238
35296207-9	2022	Both NAC and DPI prevented upregulation of STAT3 phosphorylation and ZIP2 expression induced by overexpression of p67phox, whereas the STAT3 inhibitor stattic abrogated upregulation ZIP2 expression, indicating that the increase of p67phox at reperfusion is an upstream signaling event responsible for ZIP2 upregulation via STAT3.	Acetylcysteine	5-8	solute carrier family 39 (zinc transporter), member 2	Mus musculus	301-305
7835407-0	1994	The redox active components H2O2 and N-acetyl-L-cysteine regulate expression of c-jun and c-fos in lens systems.	Acetylcysteine	37-56	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	80-85
7835407-0	1994	The redox active components H2O2 and N-acetyl-L-cysteine regulate expression of c-jun and c-fos in lens systems.	Acetylcysteine	37-56	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	90-95
7835407-7	1994	The antioxidant N-acetyl-cysteine (NAC) has a dual effect on the induction of c-jun and c-fos.	Acetylcysteine	16-33	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	78-83
7835407-7	1994	The antioxidant N-acetyl-cysteine (NAC) has a dual effect on the induction of c-jun and c-fos.	Acetylcysteine	16-33	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	88-93
7835407-7	1994	The antioxidant N-acetyl-cysteine (NAC) has a dual effect on the induction of c-jun and c-fos.	Acetylcysteine	35-38	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	78-83
7835407-7	1994	The antioxidant N-acetyl-cysteine (NAC) has a dual effect on the induction of c-jun and c-fos.	Acetylcysteine	35-38	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	88-93
7912865-11	1994	Pretreatment with N-acetyl-L-cysteine can completely block the increase in ICAM-1 mRNA levels.	Acetylcysteine	18-37	intercellular adhesion molecule 1	Homo sapiens	75-81
8123651-3	1994	In the presence of the antioxidants N-acetyl-L-cysteine (NAC, 10 mumol/L) or vitamin E (100 mumol/L), basal and bradykinin-stimulated formation of 6-keto-PGF1 alpha was potentiated by 20 micrograms protein/mL of LDL.	Acetylcysteine	36-55	kininogen 1	Bos taurus	112-122
8123651-3	1994	In the presence of the antioxidants N-acetyl-L-cysteine (NAC, 10 mumol/L) or vitamin E (100 mumol/L), basal and bradykinin-stimulated formation of 6-keto-PGF1 alpha was potentiated by 20 micrograms protein/mL of LDL.	Acetylcysteine	57-60	kininogen 1	Bos taurus	112-122
1343225-5	1992	In this study, N-acetylcysteine (NAC) 1800 mg/day was used for 3 reasons: (i) its -SH groups directly scavenge H2O2; (ii) ferrochelatase can be activated by sulfhydryl groups; (iii) NAC was reported to upregulate the glutathione redox system, which is a major endogenous anti-oxidant system.	Acetylcysteine	15-31	ferrochelatase	Homo sapiens	122-136
1343225-5	1992	In this study, N-acetylcysteine (NAC) 1800 mg/day was used for 3 reasons: (i) its -SH groups directly scavenge H2O2; (ii) ferrochelatase can be activated by sulfhydryl groups; (iii) NAC was reported to upregulate the glutathione redox system, which is a major endogenous anti-oxidant system.	Acetylcysteine	33-36	ferrochelatase	Homo sapiens	122-136
2251674-3	1990	Compounds that form GSH conjugates are processed by gamma-glutamyl transpeptidase (gamma-GT) and dipeptidases to cysteine S-conjugates, which are usually excreted in urine as their corresponding mercapturic acids (S-substituted N-acetyl-L-cysteine conjugates).	Acetylcysteine	195-212	inactive glutathione hydrolase 2	Homo sapiens	52-81
2251674-3	1990	Compounds that form GSH conjugates are processed by gamma-glutamyl transpeptidase (gamma-GT) and dipeptidases to cysteine S-conjugates, which are usually excreted in urine as their corresponding mercapturic acids (S-substituted N-acetyl-L-cysteine conjugates).	Acetylcysteine	195-212	inactive glutathione hydrolase 2	Homo sapiens	83-91
2251674-3	1990	Compounds that form GSH conjugates are processed by gamma-glutamyl transpeptidase (gamma-GT) and dipeptidases to cysteine S-conjugates, which are usually excreted in urine as their corresponding mercapturic acids (S-substituted N-acetyl-L-cysteine conjugates).	Acetylcysteine	228-247	inactive glutathione hydrolase 2	Homo sapiens	52-81
2251674-3	1990	Compounds that form GSH conjugates are processed by gamma-glutamyl transpeptidase (gamma-GT) and dipeptidases to cysteine S-conjugates, which are usually excreted in urine as their corresponding mercapturic acids (S-substituted N-acetyl-L-cysteine conjugates).	Acetylcysteine	228-247	inactive glutathione hydrolase 2	Homo sapiens	83-91
34801870-10	2022	We also found that either TSH or NAC enhanced PKA, Akt, mTORC, AMPK, Sirtuins, PGC1alpha, NRF-2, mitofusin-2, TFAM and catalase in the N-TSHR-mAb stressed cells.	Acetylcysteine	33-36	mitofusin 2	Rattus norvegicus	97-108
34948343-6	2021	Klotho protein inhibited NAC-induced apoptosis and restored cellular tissue damage, suggesting that klotho protein may be an effective antioxidant for the cryopreservation of ovarian tissue.	Acetylcysteine	25-28	klotho	Mus musculus	0-6
34948343-6	2021	Klotho protein inhibited NAC-induced apoptosis and restored cellular tissue damage, suggesting that klotho protein may be an effective antioxidant for the cryopreservation of ovarian tissue.	Acetylcysteine	25-28	klotho	Mus musculus	100-106
34553295-8	2021	MR dramatically sensitized TNBC cells to TXNRD1 silencing and the TXNRD inhibitor auranofin, as determined by crystal violet staining and caspase activity; these effects were suppressed by the antioxidant N-acetylcysteine.	Acetylcysteine	205-221	thioredoxin reductase 1	Mus musculus	41-47
34776955-5	2021	This was confirmed by which the JNK inhibitor SP600125 partially rescued CRC cells from chaetocin induced apoptosis and the ROS scavenger N-acetyl-L-cysteine (NAC) reversed both the chaetocin induced apoptosis and the JNK/c-Jun pathway activation.	Acetylcysteine	138-157	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	222-227
34776955-5	2021	This was confirmed by which the JNK inhibitor SP600125 partially rescued CRC cells from chaetocin induced apoptosis and the ROS scavenger N-acetyl-L-cysteine (NAC) reversed both the chaetocin induced apoptosis and the JNK/c-Jun pathway activation.	Acetylcysteine	159-162	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	222-227
34080015-6	2021	We show that a sequential combination of NAC+EE applied after an early-life oxidative insult recovers integrity and function of PVI network in adult Gclm KO, via the inhibition of MMP9/RAGE.	Acetylcysteine	41-44	matrix metallopeptidase 9	Homo sapiens	180-184
34080015-6	2021	We show that a sequential combination of NAC+EE applied after an early-life oxidative insult recovers integrity and function of PVI network in adult Gclm KO, via the inhibition of MMP9/RAGE.	Acetylcysteine	41-44	advanced glycosylation end-product specific receptor	Homo sapiens	185-189
34080015-8	2021	The sequential combination of NAC+EE reverses long-lasting effects of an early oxidative insult on PVI/perineuronal net (PNN) through the inhibition of MMP9/RAGE mechanism.	Acetylcysteine	30-33	matrix metallopeptidase 9	Homo sapiens	152-156
34080015-8	2021	The sequential combination of NAC+EE reverses long-lasting effects of an early oxidative insult on PVI/perineuronal net (PNN) through the inhibition of MMP9/RAGE mechanism.	Acetylcysteine	30-33	advanced glycosylation end-product specific receptor	Homo sapiens	157-161
34755672-5	2021	The effects of chrysin, LPS, and their combination on the mRNA expressions of iNOS and COX-2 were detected using RT-PCR; Western blotting was performed to examine the changes in cellular expressions of p-AKT, p-PRAS40, p-mTOR, mTOR, p-P70S6k, p-S6RP and S6RP following the treatments with LPS, N-Acetyl-L-cysteine, and chrysin, alone or in combinations.	Acetylcysteine	294-313	AKT1 substrate 1 (proline-rich)	Mus musculus	211-217
34755672-5	2021	The effects of chrysin, LPS, and their combination on the mRNA expressions of iNOS and COX-2 were detected using RT-PCR; Western blotting was performed to examine the changes in cellular expressions of p-AKT, p-PRAS40, p-mTOR, mTOR, p-P70S6k, p-S6RP and S6RP following the treatments with LPS, N-Acetyl-L-cysteine, and chrysin, alone or in combinations.	Acetylcysteine	294-313	ribosomal protein S6 kinase, polypeptide 1	Mus musculus	235-241
34482039-12	2021	CONCLUSIONS: Reversible alteration of mRNA levels by removing morphine from culture medium, and effect of NAC in co-treatment of morphine plus NAC, emphasize the role of reactive oxygen species in down-regulation of the expression of hTERT and TERF2 by morphine.	Acetylcysteine	106-109	telomeric repeat binding factor 2	Homo sapiens	244-249
34098069-5	2021	Elevated ROS and NLRP3, caspase-1, IL-1beta and IL-18 were detected, which was attenuated by N-acetylcysteine.	Acetylcysteine	93-109	interleukin 18	Homo sapiens	48-53
34540868-11	2021	N-acetylcysteine (NAC) suppressed acrolein-associated Rock1 upregulation in TR-MUL5 cells.	Acetylcysteine	0-16	Rho-associated coiled-coil containing protein kinase 1	Rattus norvegicus	54-59
34540868-11	2021	N-acetylcysteine (NAC) suppressed acrolein-associated Rock1 upregulation in TR-MUL5 cells.	Acetylcysteine	18-21	Rho-associated coiled-coil containing protein kinase 1	Rattus norvegicus	54-59
34479474-0	2021	The antioxidant N-acetylcysteine promotes immune response and inhibits epithelial-mesenchymal transition to alleviate pulmonary fibrosis in chronic obstructive pulmonary disease by suppressing the VWF/p38 MAPK axis.	Acetylcysteine	16-32	von Willebrand factor	Rattus norvegicus	197-200
34479474-8	2021	NAC inhibited p38 MAPK phosphorylation by reducing the VWF expression.	Acetylcysteine	0-3	von Willebrand factor	Rattus norvegicus	55-58
34479474-9	2021	NAC could inhibit cell migration and invasion, elevate E-cadherin expression, the ratio of CD3+, CD4+, CD8+ and CD4+/CD8+T lymphocytes, and levels of IgG, IgA, and IgM, and reduce N-cadherin expression and levels of IL-6 and TNF-alpha in CSE cells and serum of COPD rats.	Acetylcysteine	0-3	Cd4 molecule	Rattus norvegicus	97-100
34479474-9	2021	NAC could inhibit cell migration and invasion, elevate E-cadherin expression, the ratio of CD3+, CD4+, CD8+ and CD4+/CD8+T lymphocytes, and levels of IgG, IgA, and IgM, and reduce N-cadherin expression and levels of IL-6 and TNF-alpha in CSE cells and serum of COPD rats.	Acetylcysteine	0-3	Cd4 molecule	Rattus norvegicus	112-115
34479474-10	2021	NAC promoted immune response and suppressed epithelial-mesenchymal transformation (EMT) to relieve COPD-induced pulmonary fibrosis in vitro and in vivo by inhibiting the VWF/p38 MAPK axis.	Acetylcysteine	0-3	von Willebrand factor	Rattus norvegicus	170-173
34479474-11	2021	CONCLUSIONS: Collectively, NAC could ameliorate COPD-induced pulmonary fibrosis by promoting immune response and inhibiting EMT process via the VWF/p38 MAPK axis, therefore providing us with a potential therapeutic target for treating COPD.	Acetylcysteine	27-30	von Willebrand factor	Rattus norvegicus	144-147
34753839-9	2021	NAC incorporated at a concentration of 2.5 mM showed higher mineralization and considerably increased gene expression levels of runt-related transcription factor 2 (RUNX2), COL1A1, DSPP, and DMP-1.	Acetylcysteine	0-3	collagen type I alpha 1 chain	Homo sapiens	173-179
34303734-8	2021	Subsequent incubation with N-Acetyl-L-cysteine (NAC, 1 mM) reestablished GSH content and reverted concomitantly the alteration in Mrp2 localization and function induced by TBH.	Acetylcysteine	48-51	ATP binding cassette subfamily C member 2	Rattus norvegicus	130-134
34358621-7	2021	In vitro analysis, after H9c2 cells were pretreated with or without PCr (0.5 mM) or NAC (0.5 mM) or 5Z-7-oxozeaenol (5z-7-Ox, 1 muM) for 1 h, subsequently treated with DOX (1 muM ) for 24 h. The results revealed that inhibition of TAK1 further deteriorated apoptotic and necroptotic cell death induced by DOX in H9c2 cells, but didn"t affect oxidative stress.	Acetylcysteine	84-87	mitogen activated protein kinase kinase kinase 7	Rattus norvegicus	231-235
34358621-9	2021	Consistent with the results in vivo, PCr or NAC significantly inhibited the decrease of TAK1 expression induced by DOX.	Acetylcysteine	44-47	mitogen activated protein kinase kinase kinase 7	Rattus norvegicus	88-92
34236028-0	2021	(N-acetylcysteine inhibits the proliferation of hydrogen peroxide treated fibroblast-like synoviocytes in rats with adjuvant arthritis (AA) via blocking Nrf2/Keap1 pathway).	Acetylcysteine	1-17	Kelch-like ECH-associated protein 1	Rattus norvegicus	158-163
34236028-8	2021	The effects of NAC (final concentration 0, 3, 10, 30 mumol/L) on Nrf2 and Keap1 protein expressions in AA-FLS treated with H2O2 at low concentration were detected by Western blotting.	Acetylcysteine	15-18	Kelch-like ECH-associated protein 1	Rattus norvegicus	74-79
34250770-11	2021	NAC treatments decreased the expression of MMP2 and MMP9 in rats exposed to single or continuous Cd.	Acetylcysteine	0-3	matrix metallopeptidase 9	Rattus norvegicus	52-56
34064109-4	2021	Inhibition of apigenin-induced reactive oxygen species (ROS) generation by a ROS scavenger N-acetyl-L-cysteine blocked the lipid raft membrane localization and activation of ASM and formation of ceramide-enriched lipid raft membranes, returned PI3K-Akt-GTP-Rac1-modulated CDK1-cyclin B1 activity, and subsequently restored the BCL-2/BCL-xL-regulated ER-mitochondrial bioenergetic activity.	Acetylcysteine	91-110	Rac family small GTPase 1	Homo sapiens	257-261
35621139-4	2022	Low-density lipoprotein (LDL) receptor knockout mice were pretreated with 1 mg/ml NAC in drinking water for 1 week and continued to receive NAC, high-fat diet and intranasal instillation of PM for 1 week or 6 months.	Acetylcysteine	82-85	low density lipoprotein receptor	Mus musculus	0-38
35633910-8	2022	N-acetyl-L-cysteine was used to remove ROS, and the expression of Sirt1 was inhibited by nicotinamide.	Acetylcysteine	0-19	sirtuin 1	Homo sapiens	66-71
35635082-7	2022	N-acetyl cysteine (NAC), which is an inhibitor of ROS, was used to confirm whether AF exerted its effects on KLE cells through ROS/AMPK/mTOR signaling.	Acetylcysteine	0-17	protein kinase AMP-activated non-catalytic subunit beta 1	Homo sapiens	131-135
35635082-10	2022	NAC reversed the effects of AF on biological behaviors of KLE cells by inactivating ROS/AMPK/mTOR signaling.	Acetylcysteine	0-3	protein kinase AMP-activated non-catalytic subunit beta 1	Homo sapiens	88-92
35420738-0	2022	Diverse Impact of N-Acetylcysteine or Alpha-Lipoic Acid Supplementation during High-Fat Diet Regime on Matrix Metalloproteinase-2 and Matrix Metalloproteinase-9 in Visceral and Subcutaneous Adipose Tissue.	Acetylcysteine	18-34	matrix metallopeptidase 9	Rattus norvegicus	134-160
35420738-8	2022	Moreover, NAC and ALA have a divergent impact on MMP2 and MMP9 expression in different adipose tissue localization.	Acetylcysteine	10-13	matrix metallopeptidase 9	Rattus norvegicus	58-62
35319066-6	2022	Second, we have established that in experimental conditions in which the sulfhydryl arylation by menadione or plumbagin is prevented by the thiol reducing agent N-acetyl-L-cysteine, the inhibition of Sirtuin 7 catalytic activity is also prevented.	Acetylcysteine	161-180	sirtuin 7	Homo sapiens	200-209
35422087-6	2022	Notably, blocking ROS production with the one-carbon donor formate and the ROS scavenger N-acetyl-cysteine (NAC) effectively rescued SHMT2 deficiency-induced cell apoptosis via the intrinsic signaling pathway.	Acetylcysteine	89-106	serine hydroxymethyltransferase 2	Homo sapiens	133-138
35422087-6	2022	Notably, blocking ROS production with the one-carbon donor formate and the ROS scavenger N-acetyl-cysteine (NAC) effectively rescued SHMT2 deficiency-induced cell apoptosis via the intrinsic signaling pathway.	Acetylcysteine	108-111	serine hydroxymethyltransferase 2	Homo sapiens	133-138
35368869-5	2022	Antioxidant N-acetyl cysteine reduced both MD- and AA+MD-induced autophagy, as well as changes in AMPK/mTORC1/ULK1 activity and cell death triggered by the drug combination.	Acetylcysteine	12-29	protein kinase AMP-activated non-catalytic subunit beta 1	Homo sapiens	98-102
35023144-9	2022	After HSP70 stimulation, the expression of ROS, NLRP3, Caspase-1, and interleukin-18 (IL-18) increased significantly and could be reduced by ROS inhibitor NAC.	Acetylcysteine	155-158	heat shock protein family A (Hsp70) member 4	Homo sapiens	6-11
35023144-9	2022	After HSP70 stimulation, the expression of ROS, NLRP3, Caspase-1, and interleukin-18 (IL-18) increased significantly and could be reduced by ROS inhibitor NAC.	Acetylcysteine	155-158	interleukin 18	Homo sapiens	70-84
35023144-9	2022	After HSP70 stimulation, the expression of ROS, NLRP3, Caspase-1, and interleukin-18 (IL-18) increased significantly and could be reduced by ROS inhibitor NAC.	Acetylcysteine	155-158	interleukin 18	Homo sapiens	86-91
35023144-11	2022	In beagle models that received TmLRP, HSP70, NLRP3, Caspase-1, IL-1beta, and IL-18 were highly expressed in the wound tissue or urine, and could also be reduced by NAC pretreatment.	Acetylcysteine	164-167	heat shock protein family A (Hsp70) member 4	Homo sapiens	38-43
35023144-11	2022	In beagle models that received TmLRP, HSP70, NLRP3, Caspase-1, IL-1beta, and IL-18 were highly expressed in the wound tissue or urine, and could also be reduced by NAC pretreatment.	Acetylcysteine	164-167	interleukin 18	Homo sapiens	77-82
35280167-7	2022	Furthermore, NAC normalized the altered GSH levels displayed by these animals in the hippocampus and nucleus accumbens, and it partially rescued the altered expression of post-synaptic terminal network genes found in VPA-exposed rats, such as NR2a, MGLUR5, GLUR1, and GLUR2 in nucleus accumbens, and CAMK2, NR1, and GLUR2 in cerebellum.	Acetylcysteine	13-16	glutamate metabotropic receptor 5	Rattus norvegicus	249-255
35216241-0	2022	N-Acetylcysteine and Aripiprazole Improve Social Behavior and Cognition and Modulate Brain BDNF Levels in a Rat Model of Schizophrenia.	Acetylcysteine	0-16	brain-derived neurotrophic factor	Rattus norvegicus	91-95
35216241-5	2022	Both doses of NAC and 0.3 mg/kg of ARI increased the expression of BDNF mRNA in the PFC, while all doses of these drugs and their combinations enhanced the levels of BDNF protein in this brain structure.	Acetylcysteine	14-17	brain-derived neurotrophic factor	Rattus norvegicus	67-71
35216241-5	2022	Both doses of NAC and 0.3 mg/kg of ARI increased the expression of BDNF mRNA in the PFC, while all doses of these drugs and their combinations enhanced the levels of BDNF protein in this brain structure.	Acetylcysteine	14-17	brain-derived neurotrophic factor	Rattus norvegicus	166-170
35216241-7	2022	These data show that in the rat BSO-induced neurodevelopmental model of schizophrenia, ARI and NAC differently modulated BDNF levels in the PFC and HIP.	Acetylcysteine	95-98	brain-derived neurotrophic factor	Rattus norvegicus	121-125
35123263-5	2022	Consistently, in vitro binding of RBD and ACE2, spike-mediated cell-cell fusion, and pseudotyped viral infection of VeroE6/TMPRSS2 cells were inhibited by the thiol-reactive compounds N-acetylcysteine (NAC) and a reduced form of glutathione (GSH).	Acetylcysteine	184-200	transmembrane protease serine 2	Chlorocebus sabaeus	123-130
35123263-5	2022	Consistently, in vitro binding of RBD and ACE2, spike-mediated cell-cell fusion, and pseudotyped viral infection of VeroE6/TMPRSS2 cells were inhibited by the thiol-reactive compounds N-acetylcysteine (NAC) and a reduced form of glutathione (GSH).	Acetylcysteine	202-205	transmembrane protease serine 2	Chlorocebus sabaeus	123-130
33724537-10	2021	NAC treatment significantly increased the antioxidant state, testicular function beside structural germ cell and seminiferous tubules histology accompanied by upsurge of steroidogenic mRNA expressions (P450scc and 3beta-HSD) and downregulated the pro-inflammatory cytokines mRNA expression (TNF-alpha, IL-1beta).	Acetylcysteine	0-3	cytochrome P450, family 11, subfamily a, polypeptide 1	Rattus norvegicus	202-219
33503268-13	2021	Regarding mitochondrial dynamics, the use of NAC alone promoted significant Mfn-2/Drp-1 expression (P<0.05).	Acetylcysteine	45-48	mitofusin 2	Homo sapiens	76-81
33503268-13	2021	Regarding mitochondrial dynamics, the use of NAC alone promoted significant Mfn-2/Drp-1 expression (P<0.05).	Acetylcysteine	45-48	utrophin	Homo sapiens	82-87
32291602-8	2021	Further in vitro studies show that CD21 (20 muM) strongly enhanced the Msr1 mRNA and MSR1 protein levers in RAW264.7 cells and PRX1 internalization in cellular lysosomes, which were significantly reversed by N-acetylcysteine treatment.	Acetylcysteine	208-224	complement receptor 2	Mus musculus	35-39
33642448-1	2021	This study examined the effects of N-acetylcysteine (NAC) on the inflammatory reactions of murine osteoblastic cells cultured on the 4-methacryloxyethyl trimellitate anhydride/methyl methacrylate (4-META/MMA)-based resin.	Acetylcysteine	35-51	NLR family, pyrin domain containing 1A	Mus musculus	53-56
34016350-6	2021	In addition, NAC attenuated the activity of the Nf-kappaB pathway activated by heat stress and decreased the expression of the proinflammatory cytokines IL-6, IL-18, TNF-alpha, IKK, and IFN-gamma.	Acetylcysteine	13-16	interleukin 6	Gallus gallus	153-157
34016350-6	2021	In addition, NAC attenuated the activity of the Nf-kappaB pathway activated by heat stress and decreased the expression of the proinflammatory cytokines IL-6, IL-18, TNF-alpha, IKK, and IFN-gamma.	Acetylcysteine	13-16	interferon gamma	Gallus gallus	186-195
34016350-7	2021	In addition, NAC treatment regulated the expression of HO-1, GSH, SOD2 and PRDX3 by regulating the activity of Nrf2 at different time points to resist oxidative stress caused by heat exposure.	Acetylcysteine	13-16	superoxide dismutase 2, mitochondrial	Gallus gallus	66-70
33749848-7	2021	NAC co-administered with GA3 significantly normalized the kidney and liver function and the antioxidant state, besides normal histological structure of both liver and kidney tissue and downregulated expression of the pro-inflammatory cytokines as well as, fibrogenic gene expression.	Acetylcysteine	0-3	succinyl-CoA:glutarate-CoA transferase	Homo sapiens	25-28
33749848-8	2021	PRACTICAL APPLICATIONS: The current study confirmed that GA3 induced hepto-renal dysfunction that was ameliorated by NAC administration.	Acetylcysteine	117-120	succinyl-CoA:glutarate-CoA transferase	Homo sapiens	57-60
34012594-11	2021	Compared with BVP treatment alone, IGFBP4 expression decreased in A549 cells treated with BVP and the ROS scavenger N-acetylcysteine.	Acetylcysteine	116-132	insulin like growth factor binding protein 4	Homo sapiens	35-41
33720480-8	2021	Additionally, NAC"s effect is not apparent on SiO2 -mediated autophagy through the PI3K/Akt/mTOR signaling pathway, but it can reduce the inflammatory response on NR8383 cells mediated by SiO2-exposed.	Acetylcysteine	14-17	mechanistic target of rapamycin kinase	Rattus norvegicus	92-96
33720480-10	2021	Taken together, our data demonstrated that SiO2 -exposed can induce pulmonary fibrosis along with autophagy both in vivo and in vitro, NAC could alleviate the inflammatory response NR8383 cells by SiO2 -exposed through non PI3K/Akt/mTOR signaling pathway, and the specific mechanism of its action needs further studying.	Acetylcysteine	135-138	mechanistic target of rapamycin kinase	Rattus norvegicus	232-236
33585475-6	2021	Elimination of ROS with N-acetyl-L-cysteine (NAC) could rescued the decidualization inhibition caused by SIRT1 knockdown.	Acetylcysteine	24-43	sirtuin 1	Homo sapiens	105-110
33585475-6	2021	Elimination of ROS with N-acetyl-L-cysteine (NAC) could rescued the decidualization inhibition caused by SIRT1 knockdown.	Acetylcysteine	45-48	sirtuin 1	Homo sapiens	105-110
33441976-6	2021	NAC numerically reduced diarrhea incidence (- 46.2%) and the concentrations of hydrogen peroxide and malondialdehyde, but increased claudin-1 and intestinal fatty-acid binding protein (iFABP) protein abundances and activities of catalase and glutathione peroxidase in the jejunum of beta-CG-challenged piglets.	Acetylcysteine	0-3	claudin 1	Homo sapiens	132-141
33441976-8	2021	Moreover, NAC increased the concentrations of citrulline and D-xylose in the plasma, as well as the expression of genes for aquaporin (AQP) 3, AQP4, peptide transporter 1 (PepT1), sodium/glucose co-transporter-1 (SGLT-1), potassium inwardly-rectifying channel, subfamily J, member 13 (KCNJ13), and solute carrier family 1 member 1 (SLC1A1) in the jejunum, demonstrating that NAC augmented intestinal metabolic activity and absorptive function.	Acetylcysteine	10-13	aquaporin 4	Homo sapiens	143-147
33441976-8	2021	Moreover, NAC increased the concentrations of citrulline and D-xylose in the plasma, as well as the expression of genes for aquaporin (AQP) 3, AQP4, peptide transporter 1 (PepT1), sodium/glucose co-transporter-1 (SGLT-1), potassium inwardly-rectifying channel, subfamily J, member 13 (KCNJ13), and solute carrier family 1 member 1 (SLC1A1) in the jejunum, demonstrating that NAC augmented intestinal metabolic activity and absorptive function.	Acetylcysteine	10-13	potassium inwardly rectifying channel subfamily J member 13	Homo sapiens	222-283
33441976-8	2021	Moreover, NAC increased the concentrations of citrulline and D-xylose in the plasma, as well as the expression of genes for aquaporin (AQP) 3, AQP4, peptide transporter 1 (PepT1), sodium/glucose co-transporter-1 (SGLT-1), potassium inwardly-rectifying channel, subfamily J, member 13 (KCNJ13), and solute carrier family 1 member 1 (SLC1A1) in the jejunum, demonstrating that NAC augmented intestinal metabolic activity and absorptive function.	Acetylcysteine	10-13	potassium inwardly rectifying channel subfamily J member 13	Homo sapiens	285-291
33182097-9	2021	Moreover, the intervention with antioxidants to reduce mitochondrial redox, such as N-acetyl-l-cysteine (NAC) and mitochondria-targeted antioxidant Mito-TEMPO, reduced the S-glutathionylation of Mfn2 involved in the antagonism of CdCl2-induced necroptosis and neurotoxicity in vivo and in vitro.	Acetylcysteine	84-103	mitofusin 2	Homo sapiens	195-199
33361545-10	2020	Furthermore, z-VAD, NAC, and BI-1 effectively blocked the Nox2 inhibitor-induced apoptosis of Raji cells.	Acetylcysteine	20-23	cytochrome b-245 beta chain	Homo sapiens	58-62
33371832-7	2021	Furthermore, NAC decreases TNF-alpha, IL-1beta, IL-6, IL-8, IL-10, and IL-17 serum levels in patients with sepsis, severe burns, acute liver failure, or peritoneal dialysis and may also reduce cytokine storm in COVID-19.	Acetylcysteine	13-16	interleukin 10	Homo sapiens	60-65
33371832-7	2021	Furthermore, NAC decreases TNF-alpha, IL-1beta, IL-6, IL-8, IL-10, and IL-17 serum levels in patients with sepsis, severe burns, acute liver failure, or peritoneal dialysis and may also reduce cytokine storm in COVID-19.	Acetylcysteine	13-16	interleukin 17A	Homo sapiens	71-76
32871518-6	2020	Mechanistically, NAC alleviated radiation-induced oxidative damage through significantly increased glutathione peroxidase activity by 102% alongside with decreasing NADPH oxidase subunits (p22 and NOX4) gene expressions by 48% and 38%, respectively compared to the irradiated untreated group.	Acetylcysteine	17-20	NADPH oxidase 4	Rattus norvegicus	197-201
32871518-10	2020	Taken together, our results suggest that NAC can inhibit radiotherapy-induced POF while preserving ovarian function and structure through upregulating VEGF expression and suppressing NOX4/MAPK/p53 apoptotic signaling.	Acetylcysteine	41-44	NADPH oxidase 4	Rattus norvegicus	183-187
33198515-12	2020	Furthermore, 5 mM N-acetylcysteine caused a decrease in ubiquitinated protein and HSP70 levels; however, 6.79 microM curcumin did not affect 10 mM in acrylamide-treated cells.	Acetylcysteine	18-34	heat shock protein family A (Hsp70) member 4	Homo sapiens	82-87
33198515-13	2020	Our study showed that acrylamide at high concentration inhibits UPS and mTOR, activates autophagy, and increases HSP70 levels in HepG2 cells, and N-acetylcysteine reduces UPS inhibition and HSP70 levels in acrylamide-treated cells.	Acetylcysteine	146-162	heat shock protein family A (Hsp70) member 4	Homo sapiens	190-195
32896808-3	2020	The western blot analysis also showed that NO scavenger N-acetyl cysteine (NAC) could weaken the intracellular HDAC inhibitory ability of compound 7c, supporting the HDAC inhibitory effect of NO generated by 7c.	Acetylcysteine	56-73	histone deacetylase 9	Homo sapiens	111-115
32896808-3	2020	The western blot analysis also showed that NO scavenger N-acetyl cysteine (NAC) could weaken the intracellular HDAC inhibitory ability of compound 7c, supporting the HDAC inhibitory effect of NO generated by 7c.	Acetylcysteine	56-73	histone deacetylase 9	Homo sapiens	166-170
32896808-3	2020	The western blot analysis also showed that NO scavenger N-acetyl cysteine (NAC) could weaken the intracellular HDAC inhibitory ability of compound 7c, supporting the HDAC inhibitory effect of NO generated by 7c.	Acetylcysteine	75-78	histone deacetylase 9	Homo sapiens	111-115
32896808-3	2020	The western blot analysis also showed that NO scavenger N-acetyl cysteine (NAC) could weaken the intracellular HDAC inhibitory ability of compound 7c, supporting the HDAC inhibitory effect of NO generated by 7c.	Acetylcysteine	75-78	histone deacetylase 9	Homo sapiens	166-170
33123307-8	2020	ROS induced by iron overload promote necroptosis via a positive feedback mechanism, as on the one hand N-acetylcysteine attenuates the upregulation of RIPK1 and RIPK3 and phosphorylation of RIPK1, RIPK3, and MLKL and on the other hand Nec-1, siRIPK1, or siRIPK3 reduced ROS generation.	Acetylcysteine	103-119	receptor interacting serine/threonine kinase 3	Homo sapiens	161-166
33123307-8	2020	ROS induced by iron overload promote necroptosis via a positive feedback mechanism, as on the one hand N-acetylcysteine attenuates the upregulation of RIPK1 and RIPK3 and phosphorylation of RIPK1, RIPK3, and MLKL and on the other hand Nec-1, siRIPK1, or siRIPK3 reduced ROS generation.	Acetylcysteine	103-119	receptor interacting serine/threonine kinase 3	Homo sapiens	197-202
32504923-8	2020	NAC has also been shown to inhibit the NLRP3 inflammasome pathway (IL1beta and IL18) in vitro, and decrease plasma TNF-alpha in human clinical trials.	Acetylcysteine	0-3	interleukin 18	Homo sapiens	79-83
32916895-7	2020	In addition, well-known antioxidants, trolox and N-acetyl cysteine, significantly attenuated the BBB permeability increase, disruption of claudin-5 and ZO-1, and FoxO3a activation during hypoxia, suggesting that ROS are important mediators of BBB dysfunction during hypoxia.	Acetylcysteine	49-66	forkhead box O3	Mus musculus	162-168
32334250-10	2020	We further found that N-acetylcysteine, a well-known antioxidant, obviously reversed Cd-downregulated 11beta-HSD2 protein expression by inhibiting p-PERK/p-eIF2alpha signaling in placental trophoblasts.	Acetylcysteine	22-38	eukaryotic translation initiation factor 2A	Homo sapiens	156-165
30587055-7	2020	ROS inhibitor N-acetylcysteine (NAC) significantly reversed Xanthatin-mediated XIAP down-regulation, G2/M phase arrest, apoptosis and autophagosome accumulation.	Acetylcysteine	14-30	X-linked inhibitor of apoptosis	Homo sapiens	79-83
30587055-7	2020	ROS inhibitor N-acetylcysteine (NAC) significantly reversed Xanthatin-mediated XIAP down-regulation, G2/M phase arrest, apoptosis and autophagosome accumulation.	Acetylcysteine	32-35	X-linked inhibitor of apoptosis	Homo sapiens	79-83
32574682-0	2020	Activation of PPARgamma reduces N-acetyl-cysteine -induced hypercorticoidism by down-regulating MC2R expression into adrenal glands.	Acetylcysteine	32-49	melanocortin 2 receptor	Mus musculus	96-100
32782443-9	2020	Results: Results showed that after treatment with NAC, there was significantly better myocardial function and survival duration; protein expression levels of NLRP3, adaptor apoptosis-associated speck-like protein (ASC), Cleaved-Caspase-1 and gasdermin D (GSDMD) in myocardial tissues were significantly decreased; and inflammatory cytokines levels were reduced.	Acetylcysteine	50-53	PYD and CARD domain containing	Rattus norvegicus	173-212
32782443-9	2020	Results: Results showed that after treatment with NAC, there was significantly better myocardial function and survival duration; protein expression levels of NLRP3, adaptor apoptosis-associated speck-like protein (ASC), Cleaved-Caspase-1 and gasdermin D (GSDMD) in myocardial tissues were significantly decreased; and inflammatory cytokines levels were reduced.	Acetylcysteine	50-53	PYD and CARD domain containing	Rattus norvegicus	214-217
32583517-8	2020	Relative to Bmi-1-/- mice, the control and Bmi-1-/- +NAC mice showed significantly lower p16, p21, and p53 levels.	Acetylcysteine	53-56	cyclin-dependent kinase inhibitor 1A (P21)	Mus musculus	94-97
32418119-8	2020	Mechanistically, CXCR4 signaling prevents BM MSC dysfunction by suppressing oxidative stress, as treatment of old or CXCR4 deficient MSC with N-acetyl-L-cysteine (NAC), improved their niche supporting activity, and attenuated the HSPC aging phenotype.	Acetylcysteine	142-161	chemokine (C-X-C motif) receptor 4	Mus musculus	17-22
32418119-8	2020	Mechanistically, CXCR4 signaling prevents BM MSC dysfunction by suppressing oxidative stress, as treatment of old or CXCR4 deficient MSC with N-acetyl-L-cysteine (NAC), improved their niche supporting activity, and attenuated the HSPC aging phenotype.	Acetylcysteine	142-161	chemokine (C-X-C motif) receptor 4	Mus musculus	117-122
32418119-8	2020	Mechanistically, CXCR4 signaling prevents BM MSC dysfunction by suppressing oxidative stress, as treatment of old or CXCR4 deficient MSC with N-acetyl-L-cysteine (NAC), improved their niche supporting activity, and attenuated the HSPC aging phenotype.	Acetylcysteine	163-166	chemokine (C-X-C motif) receptor 4	Mus musculus	17-22
32353430-9	2020	In the meantime, OSS time-dependently decreased p53 expression in EPCs, which was partially abolished by treatment with ROS scavenger N-acetylcysteine (NAC) or protein kinase C zeta (PKCzeta) inhibitor Go6983.	Acetylcysteine	134-150	tumor protein p53	Rattus norvegicus	48-51
32353430-9	2020	In the meantime, OSS time-dependently decreased p53 expression in EPCs, which was partially abolished by treatment with ROS scavenger N-acetylcysteine (NAC) or protein kinase C zeta (PKCzeta) inhibitor Go6983.	Acetylcysteine	152-155	tumor protein p53	Rattus norvegicus	48-51
32635894-10	2020	This was further verified by the loss of JB-induced C-Jun activation and maintenance of cell viability when using the ROS scavenger N-acetyl-L-cysteine (NAC).	Acetylcysteine	153-156	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	52-57
32303987-10	2020	Intraperitoneal injection of N-acetyl-cysteine, a source of cysteine that prevents the oxidation of cysteine residues on MMP-9, significantly relieved high estrogen-induced postoperative hyperalgesia via suppression of MMP-9 and IL-1beta activation in DRGs.	Acetylcysteine	29-46	matrix metallopeptidase 9	Rattus norvegicus	121-126
32303987-10	2020	Intraperitoneal injection of N-acetyl-cysteine, a source of cysteine that prevents the oxidation of cysteine residues on MMP-9, significantly relieved high estrogen-induced postoperative hyperalgesia via suppression of MMP-9 and IL-1beta activation in DRGs.	Acetylcysteine	29-46	matrix metallopeptidase 9	Rattus norvegicus	219-224
32433928-7	2020	Moreover, the levels of CREB, miR-630 expression, and double-strand breaks (DSBs) were attenuated by 5 mM N-acetyl-L-cysteine (NAC) pretreatment, indicating that reactive oxygen species (ROS)-dependent CREB-miR-630 was involved in DSB repair.	Acetylcysteine	106-125	cAMP responsive element binding protein 1	Homo sapiens	24-28
32433928-7	2020	Moreover, the levels of CREB, miR-630 expression, and double-strand breaks (DSBs) were attenuated by 5 mM N-acetyl-L-cysteine (NAC) pretreatment, indicating that reactive oxygen species (ROS)-dependent CREB-miR-630 was involved in DSB repair.	Acetylcysteine	106-125	cAMP responsive element binding protein 1	Homo sapiens	202-206
32433928-7	2020	Moreover, the levels of CREB, miR-630 expression, and double-strand breaks (DSBs) were attenuated by 5 mM N-acetyl-L-cysteine (NAC) pretreatment, indicating that reactive oxygen species (ROS)-dependent CREB-miR-630 was involved in DSB repair.	Acetylcysteine	127-130	cAMP responsive element binding protein 1	Homo sapiens	24-28
32433928-7	2020	Moreover, the levels of CREB, miR-630 expression, and double-strand breaks (DSBs) were attenuated by 5 mM N-acetyl-L-cysteine (NAC) pretreatment, indicating that reactive oxygen species (ROS)-dependent CREB-miR-630 was involved in DSB repair.	Acetylcysteine	127-130	cAMP responsive element binding protein 1	Homo sapiens	202-206
31837856-8	2020	Incidentally, both CH and NAC attenuated the EOM-induced changes in the mRNA expression of genes involved in cardiac development (nkx2.5, sox9b), oxidative stress (nrf2a, nrf2b, gstp1, gstp2, sod2, ho1, cat) and apoptosis (p53, bax).	Acetylcysteine	26-29	NK2 homeobox 5	Danio rerio	130-136
31837856-8	2020	Incidentally, both CH and NAC attenuated the EOM-induced changes in the mRNA expression of genes involved in cardiac development (nkx2.5, sox9b), oxidative stress (nrf2a, nrf2b, gstp1, gstp2, sod2, ho1, cat) and apoptosis (p53, bax).	Acetylcysteine	26-29	SRY-box transcription factor 9b	Danio rerio	138-143
31837856-8	2020	Incidentally, both CH and NAC attenuated the EOM-induced changes in the mRNA expression of genes involved in cardiac development (nkx2.5, sox9b), oxidative stress (nrf2a, nrf2b, gstp1, gstp2, sod2, ho1, cat) and apoptosis (p53, bax).	Acetylcysteine	26-29	glutathione S-transferase pi 1.2	Danio rerio	178-183
32450865-9	2020	Furthermore, NAC treatment also reduced cellular apoptosis and caspase-3 expression.	Acetylcysteine	13-16	caspase 3	Mus musculus	63-72
32395078-6	2020	Pretreating cells with either NAC or DPI significantly enhanced the oncogenic H-Ras-mediated down-regulation of mdr1b expression and markedly prevented doxorubicin-induced cell death.	Acetylcysteine	30-33	Harvey rat sarcoma virus oncogene	Mus musculus	78-83
32313093-8	2020	The addition of NAC and miR-200c inhibitor had an opposite impact on the expression of miR-200c and ZEB1, thus hindered the effects of UTMD on MDA231 cells EMT.	Acetylcysteine	16-19	zinc finger E-box binding homeobox 1	Homo sapiens	100-104
31587481-8	2020	The NAC therapy considerably attenuated the exacerbated effects of BPA, which was associated with increased AMP-activated protein kinase (AMPK), PGC-1alpha, silent information regulator 3 or sirtuin 3 (SIRT3), and mitofusin 2 (MFN2) expressions but decreased Phosphorylated dynamin-related protein 1 (p-DRP1)/Dynamin-related protein 1 (DRP1), PTEN-induced putative kinase (PINK), and PARKIN expressions.	Acetylcysteine	4-7	mitofusin 2	Rattus norvegicus	214-225
31587481-8	2020	The NAC therapy considerably attenuated the exacerbated effects of BPA, which was associated with increased AMP-activated protein kinase (AMPK), PGC-1alpha, silent information regulator 3 or sirtuin 3 (SIRT3), and mitofusin 2 (MFN2) expressions but decreased Phosphorylated dynamin-related protein 1 (p-DRP1)/Dynamin-related protein 1 (DRP1), PTEN-induced putative kinase (PINK), and PARKIN expressions.	Acetylcysteine	4-7	mitofusin 2	Rattus norvegicus	227-231
31587481-8	2020	The NAC therapy considerably attenuated the exacerbated effects of BPA, which was associated with increased AMP-activated protein kinase (AMPK), PGC-1alpha, silent information regulator 3 or sirtuin 3 (SIRT3), and mitofusin 2 (MFN2) expressions but decreased Phosphorylated dynamin-related protein 1 (p-DRP1)/Dynamin-related protein 1 (DRP1), PTEN-induced putative kinase (PINK), and PARKIN expressions.	Acetylcysteine	4-7	dynamin 1-like	Rattus norvegicus	274-299
31587481-8	2020	The NAC therapy considerably attenuated the exacerbated effects of BPA, which was associated with increased AMP-activated protein kinase (AMPK), PGC-1alpha, silent information regulator 3 or sirtuin 3 (SIRT3), and mitofusin 2 (MFN2) expressions but decreased Phosphorylated dynamin-related protein 1 (p-DRP1)/Dynamin-related protein 1 (DRP1), PTEN-induced putative kinase (PINK), and PARKIN expressions.	Acetylcysteine	4-7	dynamin 1-like	Rattus norvegicus	303-307
31587481-8	2020	The NAC therapy considerably attenuated the exacerbated effects of BPA, which was associated with increased AMP-activated protein kinase (AMPK), PGC-1alpha, silent information regulator 3 or sirtuin 3 (SIRT3), and mitofusin 2 (MFN2) expressions but decreased Phosphorylated dynamin-related protein 1 (p-DRP1)/Dynamin-related protein 1 (DRP1), PTEN-induced putative kinase (PINK), and PARKIN expressions.	Acetylcysteine	4-7	dynamin 1-like	Rattus norvegicus	309-334
31587481-8	2020	The NAC therapy considerably attenuated the exacerbated effects of BPA, which was associated with increased AMP-activated protein kinase (AMPK), PGC-1alpha, silent information regulator 3 or sirtuin 3 (SIRT3), and mitofusin 2 (MFN2) expressions but decreased Phosphorylated dynamin-related protein 1 (p-DRP1)/Dynamin-related protein 1 (DRP1), PTEN-induced putative kinase (PINK), and PARKIN expressions.	Acetylcysteine	4-7	dynamin 1-like	Rattus norvegicus	336-340
32440328-9	2020	Indeed, there was decrease in the MMP-9/TIMP ratio in bleomycin-instilled rats, which increased with NAC treatment.	Acetylcysteine	101-104	matrix metallopeptidase 9	Rattus norvegicus	34-39
32411331-9	2020	These increases in caspase-3 protein expression were suppressed by pretreatment with NAC.	Acetylcysteine	85-88	caspase 3	Mus musculus	19-28
32423248-16	2020	More importantly, the reactive oxygen species (ROS) scavenger N-acetyl-L-cysteine (NAC) pretreatment significantly inhibited HS-induced RIPK1/RIPK3-dependent necroptosis formation both in vivo and in vitro, suggesting that preventing necroptosis via scavenging ROS production might alleviate HS-induced small intestinal tissue injury and cell death.Conclusion: This study provides strong evidence that HS causes damage to both the small intestine and intestinal epithelial cells, scavenging ROS production can significantly alleviate such RIPK1/RIPK3-dependent necroptosis, mediating HS-induced intestinal damage both in vitro and in vivo.	Acetylcysteine	62-81	receptor-interacting serine-threonine kinase 3	Mus musculus	142-147
32423248-16	2020	More importantly, the reactive oxygen species (ROS) scavenger N-acetyl-L-cysteine (NAC) pretreatment significantly inhibited HS-induced RIPK1/RIPK3-dependent necroptosis formation both in vivo and in vitro, suggesting that preventing necroptosis via scavenging ROS production might alleviate HS-induced small intestinal tissue injury and cell death.Conclusion: This study provides strong evidence that HS causes damage to both the small intestine and intestinal epithelial cells, scavenging ROS production can significantly alleviate such RIPK1/RIPK3-dependent necroptosis, mediating HS-induced intestinal damage both in vitro and in vivo.	Acetylcysteine	62-81	receptor-interacting serine-threonine kinase 3	Mus musculus	545-550
32423248-16	2020	More importantly, the reactive oxygen species (ROS) scavenger N-acetyl-L-cysteine (NAC) pretreatment significantly inhibited HS-induced RIPK1/RIPK3-dependent necroptosis formation both in vivo and in vitro, suggesting that preventing necroptosis via scavenging ROS production might alleviate HS-induced small intestinal tissue injury and cell death.Conclusion: This study provides strong evidence that HS causes damage to both the small intestine and intestinal epithelial cells, scavenging ROS production can significantly alleviate such RIPK1/RIPK3-dependent necroptosis, mediating HS-induced intestinal damage both in vitro and in vivo.	Acetylcysteine	83-86	receptor-interacting serine-threonine kinase 3	Mus musculus	142-147
32423248-16	2020	More importantly, the reactive oxygen species (ROS) scavenger N-acetyl-L-cysteine (NAC) pretreatment significantly inhibited HS-induced RIPK1/RIPK3-dependent necroptosis formation both in vivo and in vitro, suggesting that preventing necroptosis via scavenging ROS production might alleviate HS-induced small intestinal tissue injury and cell death.Conclusion: This study provides strong evidence that HS causes damage to both the small intestine and intestinal epithelial cells, scavenging ROS production can significantly alleviate such RIPK1/RIPK3-dependent necroptosis, mediating HS-induced intestinal damage both in vitro and in vivo.	Acetylcysteine	83-86	receptor-interacting serine-threonine kinase 3	Mus musculus	545-550
32922469-9	2020	The measurement of p-NGAL levels showed that the patients in the NAC group had significantly greater reduction of p-NGAL by both days 1 and 5 post-transplantation than those in the placebo group.	Acetylcysteine	65-68	lipocalin 2	Homo sapiens	21-25
32922469-9	2020	The measurement of p-NGAL levels showed that the patients in the NAC group had significantly greater reduction of p-NGAL by both days 1 and 5 post-transplantation than those in the placebo group.	Acetylcysteine	65-68	lipocalin 2	Homo sapiens	116-120
31655538-14	2019	Interestingly, NAC elevated MPO and HMGB-1 levels significantly.	Acetylcysteine	15-18	high mobility group box 1	Rattus norvegicus	36-42
30873870-8	2019	Moreover, after pretreatment with N-acetyl-cysteine, Shikonin increased the production of reactive oxygen species that are involved in regulating ER stress-mediated apoptosis and p38-activated autophagy, as evidenced by the reversion of cell viability and apoptosis and a decrease in p-eIF2alpha, CHOP, p-p38, LC3B-II, and Beclin 1 levels.	Acetylcysteine	34-51	eukaryotic translation initiation factor 2A	Homo sapiens	286-295
30873870-8	2019	Moreover, after pretreatment with N-acetyl-cysteine, Shikonin increased the production of reactive oxygen species that are involved in regulating ER stress-mediated apoptosis and p38-activated autophagy, as evidenced by the reversion of cell viability and apoptosis and a decrease in p-eIF2alpha, CHOP, p-p38, LC3B-II, and Beclin 1 levels.	Acetylcysteine	34-51	beclin 1	Homo sapiens	323-331
31880113-5	2019	CMECs with downregulation of spartin expression were firstly treated with anti-oxidant N-acetylcysteine (NAC) or Asp respectively for 48 h, and then were interfered with 30 mmol/L glucose for 24 h afterward.	Acetylcysteine	87-103	spastic paraplegia 20, spartin (Troyer syndrome) homolog (human)	Mus musculus	29-36
31880113-5	2019	CMECs with downregulation of spartin expression were firstly treated with anti-oxidant N-acetylcysteine (NAC) or Asp respectively for 48 h, and then were interfered with 30 mmol/L glucose for 24 h afterward.	Acetylcysteine	105-108	spastic paraplegia 20, spartin (Troyer syndrome) homolog (human)	Mus musculus	29-36
31880113-16	2019	In addition, the antioxidant NAC partly reversed the above changes caused by downregulating spartin.	Acetylcysteine	29-32	spastic paraplegia 20, spartin (Troyer syndrome) homolog (human)	Mus musculus	92-99
31799124-0	2019	N-Acetyl cysteine ameliorates hyperglycemia-induced cardiomyocyte toxicity by improving mitochondrial energetics and enhancing endogenous Coenzyme Q9/10 levels.	Acetylcysteine	0-17	coenzyme Q9	Homo sapiens	138-152
31430466-7	2019	Consistent with these morphologic improvements, placentas from HFD dams treated with NAC had decreased mRNA and immunostaining of IL-1beta and monocyte chemoattractant protein-1, decreased mRNA of inflammatory genes, and increased mRNA of Vegfa.	Acetylcysteine	85-88	chemokine (C-C motif) ligand 2	Mus musculus	143-177
31430466-7	2019	Consistent with these morphologic improvements, placentas from HFD dams treated with NAC had decreased mRNA and immunostaining of IL-1beta and monocyte chemoattractant protein-1, decreased mRNA of inflammatory genes, and increased mRNA of Vegfa.	Acetylcysteine	85-88	vascular endothelial growth factor A	Mus musculus	239-244
30953354-7	2019	The levels of fibrotic proteins in CFs stimulated with high concentrations of the recombinant FGF23 protein were reversed by N-acetylcysteine (NAC, a ROS inhibitor), ship information system 3 (a SMAD3 inhibitor), and Stattic (a STAT3 inhibitor).	Acetylcysteine	125-141	fibroblast growth factor 23	Homo sapiens	94-99
30953354-7	2019	The levels of fibrotic proteins in CFs stimulated with high concentrations of the recombinant FGF23 protein were reversed by N-acetylcysteine (NAC, a ROS inhibitor), ship information system 3 (a SMAD3 inhibitor), and Stattic (a STAT3 inhibitor).	Acetylcysteine	143-146	fibroblast growth factor 23	Homo sapiens	94-99
31797710-5	2019	Urine and blood samples were collected before and at the following time sequence: 2, 6, 12, 24, 48, and 120 h after the contrast administration, for creatinine and NGAL determination.Results: Pretreated with N-acetyl-L-cysteine prior to administration of contrast media (CM) to CKD patients caused a significant increase in urinary but not of plasma neutrophil gelatinase-associated lipocalin (NGAL) and serum creatinine (SCr).	Acetylcysteine	208-227	lipocalin 2	Homo sapiens	164-168
31797710-5	2019	Urine and blood samples were collected before and at the following time sequence: 2, 6, 12, 24, 48, and 120 h after the contrast administration, for creatinine and NGAL determination.Results: Pretreated with N-acetyl-L-cysteine prior to administration of contrast media (CM) to CKD patients caused a significant increase in urinary but not of plasma neutrophil gelatinase-associated lipocalin (NGAL) and serum creatinine (SCr).	Acetylcysteine	208-227	lipocalin 2	Homo sapiens	350-392
31797710-5	2019	Urine and blood samples were collected before and at the following time sequence: 2, 6, 12, 24, 48, and 120 h after the contrast administration, for creatinine and NGAL determination.Results: Pretreated with N-acetyl-L-cysteine prior to administration of contrast media (CM) to CKD patients caused a significant increase in urinary but not of plasma neutrophil gelatinase-associated lipocalin (NGAL) and serum creatinine (SCr).	Acetylcysteine	208-227	lipocalin 2	Homo sapiens	394-398
31319114-10	2019	We also found that Cd triggered the generation of MDA in a xenograft tumour model and that N-acetyl-l-cysteine, a reactive oxygen species (ROS) scavenger, abrogated the effects of Cd on NUPR1-dependent autophagy in vivo.	Acetylcysteine	91-110	nuclear protein 1, transcriptional regulator	Homo sapiens	186-191
31510052-7	2019	Cytochrome c and caspase 3/9 activities were significantly induced in the mouse KECs after a high-dose rmC5a (50 ng/mL) treatment, and this was rescued by pretreatment with the C5a receptor (C5aR) inhibitor (W-54011) and N-acetylcysteine (NAC).	Acetylcysteine	221-237	caspase 3	Mus musculus	17-26
31510052-7	2019	Cytochrome c and caspase 3/9 activities were significantly induced in the mouse KECs after a high-dose rmC5a (50 ng/mL) treatment, and this was rescued by pretreatment with the C5a receptor (C5aR) inhibitor (W-54011) and N-acetylcysteine (NAC).	Acetylcysteine	239-242	caspase 3	Mus musculus	17-26
31583053-10	2019	Antioxidant treatment with NAC could restore RPC-induced cardioprotection in diabetes by improving Cav-3-dependent Akt and STAT3 activation and by facilitating the cross talk between PI3K/Akt and JAK2/STAT3 signaling pathways.	Acetylcysteine	27-30	Janus kinase 2	Rattus norvegicus	196-200
30793306-10	2019	Furthermore, N-acetyl- l-cysteine markedly abrogated VEGF-A-increased ROS production, IRE-1, GRP78/Bip, beclin-1 expression, and LC3-II/LC3-I in the HUVECs.	Acetylcysteine	13-33	vascular endothelial growth factor A	Mus musculus	53-59
31085209-9	2019	Resveratrol and N-acetylcysteine, as reactive oxygen species (ROS) scavengers, attenuated BPDE-mediated mitochondrial damage by increasing SIRT1 activity and expression in GC-2 cells.	Acetylcysteine	16-32	sirtuin 1	Sus scrofa	139-144
31257027-3	2019	Here, we show that long-term supplementation with the antioxidants N-acetylcysteine and vitamin E promotes KRAS-driven lung cancer metastasis.	Acetylcysteine	67-83	KRAS proto-oncogene, GTPase	Homo sapiens	107-111
31172724-8	2019	Claudin-1 was also degraded by GCE, and was restored by PAR2-ant or NAC.	Acetylcysteine	68-71	claudin 1	Mus musculus	0-9
30511398-7	2019	Furthermore, Mad-induced reactive oxygen species (ROS) activated PTEN and inactivated Akt-Erk1/2 contributing to cell death, as N-acetyl- L-cysteine ameliorated the event.	Acetylcysteine	128-148	phosphatase and tensin homolog	Rattus norvegicus	65-69
30421167-6	2019	Indeed, NAC administration improved the cognitive performance, ROS production, neuroinflammation, and caspase activation induced by GA. NAC did not prevent neuronal death, however protected against alterations induced by GA on Iba-1 and GFAP immunoreactivities and AChE activity.	Acetylcysteine	8-11	glial fibrillary acidic protein	Rattus norvegicus	237-241
30421167-6	2019	Indeed, NAC administration improved the cognitive performance, ROS production, neuroinflammation, and caspase activation induced by GA. NAC did not prevent neuronal death, however protected against alterations induced by GA on Iba-1 and GFAP immunoreactivities and AChE activity.	Acetylcysteine	136-139	glial fibrillary acidic protein	Rattus norvegicus	237-241
30834613-7	2019	Treatment of cells with N-acetylcysteine or simvastatin restored Dox-induced depletion of GSH levels that in turn inhibited ABCG4 levels.	Acetylcysteine	24-40	ATP binding cassette subfamily G member 4	Homo sapiens	124-129
31178664-7	2019	Notably, NAC, a ROS scavenger, could attenuate high glucose-induced ROS formation and IL-18 and IL-1beta mRNA and protein expression and block inflammasome activation.	Acetylcysteine	9-12	interleukin 18	Homo sapiens	86-91
31178957-11	2019	During the activation of cardiac fibroblasts, knockdown of Mfn2 also increased the production of reactive oxygen species (ROS), while ROS scavenger N-acetyl-l-cysteine (NAC) could attenuate the effect caused by knockdown of Mfn2.	Acetylcysteine	148-167	mitofusin 2	Rattus norvegicus	224-228
31178957-11	2019	During the activation of cardiac fibroblasts, knockdown of Mfn2 also increased the production of reactive oxygen species (ROS), while ROS scavenger N-acetyl-l-cysteine (NAC) could attenuate the effect caused by knockdown of Mfn2.	Acetylcysteine	169-172	mitofusin 2	Rattus norvegicus	59-63
31178957-11	2019	During the activation of cardiac fibroblasts, knockdown of Mfn2 also increased the production of reactive oxygen species (ROS), while ROS scavenger N-acetyl-l-cysteine (NAC) could attenuate the effect caused by knockdown of Mfn2.	Acetylcysteine	169-172	mitofusin 2	Rattus norvegicus	224-228
30644245-3	2019	The present study investigated the protective effect of N-Acetyl Cysteine (NAC), a potent antioxidant against testicular toxicity of CPF in male mice.	Acetylcysteine	56-73	NLR family, pyrin domain containing 1A	Mus musculus	75-78
30648648-6	2019	Co-treating MA-10 cells with MEHP and the ROS scavenger N-acetyl cysteine (NAC) blocked the activation of HSL, blunted MEHP-induced STAR, and reduced basal progesterone formation.	Acetylcysteine	56-73	lipase, hormone sensitive	Mus musculus	106-109
30648648-6	2019	Co-treating MA-10 cells with MEHP and the ROS scavenger N-acetyl cysteine (NAC) blocked the activation of HSL, blunted MEHP-induced STAR, and reduced basal progesterone formation.	Acetylcysteine	75-78	lipase, hormone sensitive	Mus musculus	106-109
30453236-7	2019	In addition, AA-induced toxicity in BRF41 cells and the expression of glutathione S-transferase pi 1 (gstp1) in zebrafish larvae were reduced by N-acetylcysteine.	Acetylcysteine	145-161	glutathione S-transferase pi 1.2	Danio rerio	70-100
30453236-7	2019	In addition, AA-induced toxicity in BRF41 cells and the expression of glutathione S-transferase pi 1 (gstp1) in zebrafish larvae were reduced by N-acetylcysteine.	Acetylcysteine	145-161	glutathione S-transferase pi 1.2	Danio rerio	102-107
30496017-9	2019	Expressions of Brca2, Xpc, Mlh3, Rad51, Xrcc2, Hus1, Rad9a, Cdkn1a, Gadd45a which are the DNA-repair genes were found to be significantly higher in NAC + ALC + IR group than those in individual treatment of ALC or NAC.	Acetylcysteine	148-151	BRCA2 DNA repair associated	Homo sapiens	15-20
30496017-9	2019	Expressions of Brca2, Xpc, Mlh3, Rad51, Xrcc2, Hus1, Rad9a, Cdkn1a, Gadd45a which are the DNA-repair genes were found to be significantly higher in NAC + ALC + IR group than those in individual treatment of ALC or NAC.	Acetylcysteine	148-151	RAD51 recombinase	Homo sapiens	33-38
30496017-9	2019	Expressions of Brca2, Xpc, Mlh3, Rad51, Xrcc2, Hus1, Rad9a, Cdkn1a, Gadd45a which are the DNA-repair genes were found to be significantly higher in NAC + ALC + IR group than those in individual treatment of ALC or NAC.	Acetylcysteine	214-217	BRCA2 DNA repair associated	Homo sapiens	15-20
30840811-0	2019	N-acetyl-l-cysteine controls osteoclastogenesis through regulating Th17 differentiation and RANKL production in rheumatoid arthritis.	Acetylcysteine	0-19	TNF superfamily member 11	Homo sapiens	92-97
30690042-5	2019	In addition, an in vivo model of prostatectomy was established in beagles by subjecting them to TmLRP, and were either treated with N-acetyl-L-cysteine (NAC) and or placebo.	Acetylcysteine	132-151	X-linked Kx blood group	Homo sapiens	153-156
30447351-0	2019	N-acetylcysteine ameliorates cisplatin-induced renal senescence and renal interstitial fibrosis through sirtuin1 activation and p53 deacetylation.	Acetylcysteine	0-16	sirtuin 1	Homo sapiens	104-112
30447351-10	2019	N-acetylcysteine (NAC), an antioxidant, attenuated premature senescence and decreased renal fibrosis, and its effects were dependent on sirtuin1 (SIRT1) activation and p53 deacetylation.	Acetylcysteine	0-16	sirtuin 1	Homo sapiens	136-144
30447351-10	2019	N-acetylcysteine (NAC), an antioxidant, attenuated premature senescence and decreased renal fibrosis, and its effects were dependent on sirtuin1 (SIRT1) activation and p53 deacetylation.	Acetylcysteine	0-16	sirtuin 1	Homo sapiens	146-151
30447351-10	2019	N-acetylcysteine (NAC), an antioxidant, attenuated premature senescence and decreased renal fibrosis, and its effects were dependent on sirtuin1 (SIRT1) activation and p53 deacetylation.	Acetylcysteine	18-21	sirtuin 1	Homo sapiens	136-144
30447351-10	2019	N-acetylcysteine (NAC), an antioxidant, attenuated premature senescence and decreased renal fibrosis, and its effects were dependent on sirtuin1 (SIRT1) activation and p53 deacetylation.	Acetylcysteine	18-21	sirtuin 1	Homo sapiens	146-151
29923087-9	2019	Moreover, a published report showed treatment of a transaldolase-deficient patient with N-acetylcysteine was associated with a decrease in alpha-fetoprotein levels.	Acetylcysteine	88-104	transaldolase 1	Homo sapiens	51-64
30971653-8	2019	Strikingly, NAC canceled these taxodione-caused inhibition of BCR-ABL, STAT5 and Akt.	Acetylcysteine	12-15	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	62-69
30326393-3	2019	Extracellular GSH is unable to be taken into the majority of human cells, and the GSH prodrug N-acetyl-l-cysteine (NAC) does not exhibit promising clinical effects.	Acetylcysteine	94-113	X-linked Kx blood group	Homo sapiens	115-118
30326393-7	2019	Moreover, both in vivo and in vitro experiments demonstrated that gamma-GC exhibited better therapeutic effects against inflammation compared with N-acetyl-L-cysteine (NAC) and GSH.	Acetylcysteine	147-166	X-linked Kx blood group	Homo sapiens	168-171
29993290-0	2018	Commentary on Modarresi, A. et al (2018) N-acetylcysteine decreases urinary level of neutrophil gelatinase associated lipocalin in deceased-donor renal transplant recipients: a randomized clinical trial.	Acetylcysteine	39-57	lipocalin 2	Homo sapiens	85-127
30107137-9	2018	NAC supplementation also downregulated the expression of inflammatory markers (TNF-alpha, IL-1beta, IL-6) and upregulated the expression of marker genes associated with aging (sirtuin-1) and neurodegeneration (neuron-specific enolase, neuroglobin, synapsin-I, myelin basic protein 2) in old rats.	Acetylcysteine	0-3	synapsin I	Rattus norvegicus	248-258
30290020-7	2018	Additionally, AMN induced c-Jun N-terminal kinase (JNK) protein phosphorylation in B16F0 cells, which was inhibited by the addition of NAC.	Acetylcysteine	135-138	mitogen-activated protein kinase 8	Mus musculus	26-49
30290020-7	2018	Additionally, AMN induced c-Jun N-terminal kinase (JNK) protein phosphorylation in B16F0 cells, which was inhibited by the addition of NAC.	Acetylcysteine	135-138	mitogen-activated protein kinase 8	Mus musculus	51-54
30290020-9	2018	Data of Western blotting showed that increased protein levels of melanogenesis-related enzymes of tyrosinase-related protein-1 (TRP1), TRP2 and TYR were observed in AMN-treated B16F0 cells which were inhibited by the addition of NAC and SP.	Acetylcysteine	229-232	tyrosinase-related protein 1	Mus musculus	98-126
30290020-9	2018	Data of Western blotting showed that increased protein levels of melanogenesis-related enzymes of tyrosinase-related protein-1 (TRP1), TRP2 and TYR were observed in AMN-treated B16F0 cells which were inhibited by the addition of NAC and SP.	Acetylcysteine	229-232	tyrosinase-related protein 1	Mus musculus	128-132
30559650-5	2018	The astroglial response was also explored by co-immunostaining for GFAP and S100b together with p-JNK and it was found to be particularly exacerbated in the MPTP+NAC+HA-1077 group.	Acetylcysteine	162-165	mitogen-activated protein kinase 8	Mus musculus	98-101
30584464-5	2018	When treating PC cells with N-acetyl-L-cysteine (NAC), the intracellular ROS generation is repressed, but the expression of phosphorylation of JNK and c-Jun increased.	Acetylcysteine	28-47	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	151-156
30584464-5	2018	When treating PC cells with N-acetyl-L-cysteine (NAC), the intracellular ROS generation is repressed, but the expression of phosphorylation of JNK and c-Jun increased.	Acetylcysteine	49-52	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	151-156
30351107-1	2018	The important cyclization reaction of antioxidant drug N-acetyl-l-cysteine (NAC) has been monitored in vitro at basic pH with the help of time series Raman spectroscopy.	Acetylcysteine	55-74	X-linked Kx blood group	Homo sapiens	76-79
30035652-0	2018	N-acetylcysteine suppresses colistimethate sodium-induced nephrotoxicity via activation of SOD2, eNOS, and MMP3 protein expressions.	Acetylcysteine	0-16	superoxide dismutase 2	Rattus norvegicus	91-95
30035652-0	2018	N-acetylcysteine suppresses colistimethate sodium-induced nephrotoxicity via activation of SOD2, eNOS, and MMP3 protein expressions.	Acetylcysteine	0-16	nitric oxide synthase 3	Rattus norvegicus	97-101
30035652-0	2018	N-acetylcysteine suppresses colistimethate sodium-induced nephrotoxicity via activation of SOD2, eNOS, and MMP3 protein expressions.	Acetylcysteine	0-16	matrix metallopeptidase 3	Rattus norvegicus	107-111
30035652-10	2018	The expression levels of eNOS, SOD2, and MMP3 decreased significantly in the kidneys of colistin-treated rats; these changes were reversed in the kidneys of NAC co-treated rats.	Acetylcysteine	157-160	nitric oxide synthase 3	Rattus norvegicus	25-29
30035652-10	2018	The expression levels of eNOS, SOD2, and MMP3 decreased significantly in the kidneys of colistin-treated rats; these changes were reversed in the kidneys of NAC co-treated rats.	Acetylcysteine	157-160	superoxide dismutase 2	Rattus norvegicus	31-35
30035652-10	2018	The expression levels of eNOS, SOD2, and MMP3 decreased significantly in the kidneys of colistin-treated rats; these changes were reversed in the kidneys of NAC co-treated rats.	Acetylcysteine	157-160	matrix metallopeptidase 3	Rattus norvegicus	41-45
30035652-11	2018	CONCLUSIONS: N-acetylcysteine prevented colistin-induced nephrotoxicity through activation of expression levels of SOD2, eNOS, and MMP3.	Acetylcysteine	13-29	superoxide dismutase 2	Rattus norvegicus	115-119
30035652-11	2018	CONCLUSIONS: N-acetylcysteine prevented colistin-induced nephrotoxicity through activation of expression levels of SOD2, eNOS, and MMP3.	Acetylcysteine	13-29	nitric oxide synthase 3	Rattus norvegicus	121-125
30035652-11	2018	CONCLUSIONS: N-acetylcysteine prevented colistin-induced nephrotoxicity through activation of expression levels of SOD2, eNOS, and MMP3.	Acetylcysteine	13-29	matrix metallopeptidase 3	Rattus norvegicus	131-135
30037311-9	2018	NAC administration decreased the mRNA levels of both iNOS and NOX4 with a concomitant increase in Gpx1 expression.	Acetylcysteine	0-3	glutathione peroxidase 1	Homo sapiens	98-102
30237126-8	2018	ROS scavenger, N-acetyl-L-cysteine (NAC) impaired RIPK3-mediated necroptosis.	Acetylcysteine	15-34	receptor-interacting serine-threonine kinase 3	Mus musculus	50-55
30237126-8	2018	ROS scavenger, N-acetyl-L-cysteine (NAC) impaired RIPK3-mediated necroptosis.	Acetylcysteine	36-39	receptor-interacting serine-threonine kinase 3	Mus musculus	50-55
29334756-9	2018	We further demonstrated that the general reactive oxygen species inhibitor, Nacetylcysteine (NAC), maintained the regulation of ADAM17 dependent of Trx-1 reductase activity levels; whereas the electron transport chain modulator, rotenone, abolished Trx-1 effect on ADAM17 activity.	Acetylcysteine	76-91	ADAM metallopeptidase domain 17	Homo sapiens	128-134
29334756-9	2018	We further demonstrated that the general reactive oxygen species inhibitor, Nacetylcysteine (NAC), maintained the regulation of ADAM17 dependent of Trx-1 reductase activity levels; whereas the electron transport chain modulator, rotenone, abolished Trx-1 effect on ADAM17 activity.	Acetylcysteine	76-91	ADAM metallopeptidase domain 17	Homo sapiens	265-271
29334756-9	2018	We further demonstrated that the general reactive oxygen species inhibitor, Nacetylcysteine (NAC), maintained the regulation of ADAM17 dependent of Trx-1 reductase activity levels; whereas the electron transport chain modulator, rotenone, abolished Trx-1 effect on ADAM17 activity.	Acetylcysteine	93-96	ADAM metallopeptidase domain 17	Homo sapiens	128-134
29334756-9	2018	We further demonstrated that the general reactive oxygen species inhibitor, Nacetylcysteine (NAC), maintained the regulation of ADAM17 dependent of Trx-1 reductase activity levels; whereas the electron transport chain modulator, rotenone, abolished Trx-1 effect on ADAM17 activity.	Acetylcysteine	93-96	ADAM metallopeptidase domain 17	Homo sapiens	265-271
29655793-9	2018	Pre-treatment of MLE-12 cells with ROS scavenger of N-acetylcysteine (NAC) remarkably decreased lipopolysaccharide (LPS)- and rMuNLRP9-induced production of ROS, and the secretion of inflammatory cytokines or chemokine, as well as the activity of IkappaBalpha/NF-kappaB, ASC/Casapse-1 and Caspase-3/PARP signaling pathways.	Acetylcysteine	52-68	caspase 3	Mus musculus	289-298
29655793-9	2018	Pre-treatment of MLE-12 cells with ROS scavenger of N-acetylcysteine (NAC) remarkably decreased lipopolysaccharide (LPS)- and rMuNLRP9-induced production of ROS, and the secretion of inflammatory cytokines or chemokine, as well as the activity of IkappaBalpha/NF-kappaB, ASC/Casapse-1 and Caspase-3/PARP signaling pathways.	Acetylcysteine	52-68	poly (ADP-ribose) polymerase family, member 1	Mus musculus	299-303
29704590-0	2018	Protective influences of N-acetylcysteine against alcohol abstinence-induced depression by regulating biochemical and GRIN2A, GRIN2B gene expression of NMDA receptor signaling pathway in rats.	Acetylcysteine	25-41	glutamate ionotropic receptor NMDA type subunit 2B	Rattus norvegicus	126-132
29704590-15	2018	The increased expression levels of GRIN2A and GRIN2B following ethanol abstinence were reversed with a higher dose of NAC (100 mg/kg) treatment.	Acetylcysteine	118-121	glutamate ionotropic receptor NMDA type subunit 2B	Rattus norvegicus	46-52
29704590-16	2018	In conclusion, the results of the study reveal that NAC has remarkable protective effects in the alcohol abstinence-induced depression by modulating alcohol markers, serotonin levels and GRIN2A, GRIN2B gene expression of NMDAR signaling pathway in rats.	Acetylcysteine	52-55	glutamate ionotropic receptor NMDA type subunit 2B	Rattus norvegicus	195-201
29890337-7	2018	Pretreatment with the thiol reducing agents, N-acetylcysteine (NAC) or dithiothreitol (DTT), attenuated Nrf2 activation and HO-1 expression.	Acetylcysteine	45-61	heme oxygenase 1	Rattus norvegicus	124-128
29890337-7	2018	Pretreatment with the thiol reducing agents, N-acetylcysteine (NAC) or dithiothreitol (DTT), attenuated Nrf2 activation and HO-1 expression.	Acetylcysteine	63-66	heme oxygenase 1	Rattus norvegicus	124-128
30012208-7	2018	Pretreatment of ARPE-19 cells with NAC or 3-MA under high glucose stress resulted in a marked reduction in the expression levels of PINK1, BNIP3L and LC3-II (p &lt; 0.05).	Acetylcysteine	35-38	PTEN induced kinase 1	Homo sapiens	132-137
29753736-6	2018	Co-treatment with antioxidant agent N-acetyl-l-cysteine (NAC) prevented ROS accumulation and pexophagy by modulating peroxisome protein levels and the association of NBR1, a pexophagy receptor with peroxisomes.	Acetylcysteine	36-55	X-linked Kx blood group	Homo sapiens	57-60
29753736-6	2018	Co-treatment with antioxidant agent N-acetyl-l-cysteine (NAC) prevented ROS accumulation and pexophagy by modulating peroxisome protein levels and the association of NBR1, a pexophagy receptor with peroxisomes.	Acetylcysteine	36-55	NBR1 autophagy cargo receptor	Homo sapiens	166-170
29655131-1	2018	In this work, a new assembled copper ions sensor based on the Mn metal-enhanced fluorescence of N-acetyl-l-cysteine protected CdS quantum dots (NAC-Mn:CdS QDs) was developed.	Acetylcysteine	96-115	X-linked Kx blood group	Homo sapiens	144-147
29736011-10	2018	Protein expression of P-VASP-Ser-239 was decreased (P &lt; 0.05) after BCNI, and showed a trend towards increase by NAC treatment.	Acetylcysteine	116-119	vasodilator-stimulated phosphoprotein	Rattus norvegicus	24-28
30025127-6	2018	Results: The NAC group showed significant decreases in tear secretion, corneal wetting ability, tear MUC5AC concentration, and conjunctival goblet cell numbers as compared with the control group (all P &lt; 0.01).	Acetylcysteine	13-16	mucin 5AC, oligomeric mucus/gel-forming	Rattus norvegicus	101-107
29348462-9	2018	Ectopic expression of GSTP1 or pre-treatment with antioxidant N-acetyl-L-cysteine (NAC) abrogates the ROS elevation and decreases DNA damage, apoptosis, and autophagic cell death prompted by PL/APR-246.	Acetylcysteine	62-81	X-linked Kx blood group	Homo sapiens	83-86
29656300-10	2018	N-acetyl-L-cysteine (NAC) partially attenuated SIX1 siRNA-induced ROS level increases, and autophagy inhibitor 3-MA notably enhanced SIX1 siRNA-induced cell apoptosis.	Acetylcysteine	0-19	X-linked Kx blood group	Homo sapiens	21-24
28965082-8	2018	BS generated reactive oxygen species (ROS), which could be reduced by antioxidant N-acetyl-L-cysteine (NAC) and NADPH oxidase inhibitor DPI.	Acetylcysteine	82-101	X-linked Kx blood group	Homo sapiens	103-106
29353042-12	2018	The expressions of autophagy- and cell cycle arrest-related molecules, as well as mTORC1 were also reversed by N-acetyl-l-cysteine (NAC) in GA-treated cells.	Acetylcysteine	111-130	X-linked Kx blood group	Homo sapiens	132-135
29593571-7	2018	As compared to non-treatment, both NAC and PQQ treatment (1) reversed the increase in the ROS level in two muscle samples; (2) attenuated the reduction in the cross-sectional area (CSA) of denervated mouse muscle or in the diameter of fasted C2C12 myotube; (3) increased the myosin heavy chain (MHC) level and decreased the muscle atrophy F-box (MAFbx) and muscle-specific RING finger-1 (MuRF-1) levels in two muscle samples.	Acetylcysteine	35-38	tripartite motif-containing 63	Mus musculus	357-386
29593571-7	2018	As compared to non-treatment, both NAC and PQQ treatment (1) reversed the increase in the ROS level in two muscle samples; (2) attenuated the reduction in the cross-sectional area (CSA) of denervated mouse muscle or in the diameter of fasted C2C12 myotube; (3) increased the myosin heavy chain (MHC) level and decreased the muscle atrophy F-box (MAFbx) and muscle-specific RING finger-1 (MuRF-1) levels in two muscle samples.	Acetylcysteine	35-38	tripartite motif-containing 63	Mus musculus	388-394
29187367-8	2018	Concurrent administration of the antioxidant N-acetyl-cysteine blocked the effects of high glucose on megalin expression.	Acetylcysteine	45-62	LDL receptor related protein 2	Rattus norvegicus	102-109
29328400-6	2018	Nacetylcysteine, a Nox4 inhibitor, was demonstrated to inhibit ROS generation, suppress VCAM-1 and ICAM-1 protein expression, and decrease oxidative stress and inflammation in HK-2 cells following overexpression of miR-146a.	Acetylcysteine	0-15	intercellular adhesion molecule 1	Homo sapiens	99-105
29474366-6	2018	Moreover, CRIF1 deficiency-induced vascular adhesion molecule-1 (VCAM-1) expression was consistently attenuated by the antioxidant N-acetyl-cysteine and NF-kappaB inhibitor (BAY11).	Acetylcysteine	131-148	growth arrest and DNA-damage-inducible, gamma interacting protein 1	Mus musculus	10-15
29084209-6	2018	Pretreatment with the ROS scavenger N-acetyl-L-cysteine, the ERK1/2 inhibitor UO126, or ERK1/2 siRNA knockdown blocked the H2O2-induced shift of MLK3, while MLK3 inhibition with Cep1347 did not.	Acetylcysteine	36-55	mitogen-activated protein kinase kinase kinase 11	Homo sapiens	145-149
29084209-6	2018	Pretreatment with the ROS scavenger N-acetyl-L-cysteine, the ERK1/2 inhibitor UO126, or ERK1/2 siRNA knockdown blocked the H2O2-induced shift of MLK3, while MLK3 inhibition with Cep1347 did not.	Acetylcysteine	36-55	mitogen-activated protein kinase kinase kinase 11	Homo sapiens	157-161
29472923-9	2018	As IL-18 serum levels increase in patients after APAP overdosing, targeting IL-18 may evolve as novel therapeutic option in those hard-to-treat patients where standard therapy with N-acetylcysteine is unsuccessful.	Acetylcysteine	181-197	interleukin 18	Homo sapiens	76-81
27722780-1	2018	PURPOSE: The objective of the present study was to test the hypothesis that N-acetylcysteine (NAC) may play beneficial roles against intrauterine growth retardation (IUGR)-induced hepatic damage in suckling piglets.	Acetylcysteine	76-92	X-linked Kx blood group	Homo sapiens	94-97
29364969-8	2018	In addition, N-acetyl cysteine (NAC), a scavenger of O2-, inhibitors of growth factor receptors and of c-Src, all inhibited the overexpression of cell cycle proteins cyclin D1 and cdk4 in VSMC from SHR.	Acetylcysteine	13-30	SRC proto-oncogene, non-receptor tyrosine kinase	Rattus norvegicus	103-108
29364969-8	2018	In addition, N-acetyl cysteine (NAC), a scavenger of O2-, inhibitors of growth factor receptors and of c-Src, all inhibited the overexpression of cell cycle proteins cyclin D1 and cdk4 in VSMC from SHR.	Acetylcysteine	32-35	SRC proto-oncogene, non-receptor tyrosine kinase	Rattus norvegicus	103-108
29043702-9	2018	The GDF-9 expression in unfertilized mature oocytes were significantly higher in the NAC group compared to the other groups (P&lt;0.001).	Acetylcysteine	85-88	growth differentiation factor 9	Homo sapiens	4-9
29202574-5	2017	Only NAC plus Aa treatment enhance the expression of other genes related to tissue growth and elasticity like FBN1, ITGA1 and ITGB1.	Acetylcysteine	5-8	integrin subunit beta 1	Homo sapiens	126-131
29107181-7	2017	However, Sb-induced autophagy and the upregulation of p62 were inhibited by treatment with the antioxidant N-acetylcysteine (NAC).	Acetylcysteine	107-123	nucleoporin 62	Homo sapiens	54-57
29107181-7	2017	However, Sb-induced autophagy and the upregulation of p62 were inhibited by treatment with the antioxidant N-acetylcysteine (NAC).	Acetylcysteine	125-128	nucleoporin 62	Homo sapiens	54-57
29154739-10	2017	Pretreatment of cells with NAC attenuated MD-induced COX-2 expression by scavenging intracellular ROS and enhancing intracellular glutathione levels.	Acetylcysteine	27-30	prostaglandin-endoperoxide synthase 2	Bos taurus	53-58
28782507-3	2017	Exposing YD8 cells to Cd reduced the expression levels of catalase and superoxide dismutase 1/2 and induced the expression of HO-1 as well as autophagy and apoptosis, which were reversed by N-acetyl-l-cysteine (NAC).	Acetylcysteine	190-209	X-linked Kx blood group	Homo sapiens	211-214
28904338-1	2017	Stable water-soluble copper sulfide(Cu2S) quantum dots(QDs) with near-infrared emission were synthesized using N-acetyl-L-cysteine(NAC) as a modifier in aqueous solution and nitrogen atmosphere at room temperature.	Acetylcysteine	111-130	X-linked Kx blood group	Homo sapiens	131-134
28244691-8	2017	Both 2-DG and H2 O2 treatment suppressed DCLK1 expression, which was also rescued by NAC.	Acetylcysteine	85-88	doublecortin like kinase 1	Homo sapiens	41-46
28583366-8	2017	Pre-treatment with n-acetyl-l-cysteine (NAC), a ROS scavenger, enhanced PTX-mediated cell cycle arrest, apoptosis and the JNK and ERK MAPK activation, while pre-treatment with SP600125 or PD98509 attenuated PTX-mediated effects in HepG2 cells.	Acetylcysteine	19-38	X-linked Kx blood group	Homo sapiens	40-43
28769771-7	2017	Furthermore, since pretreatment of n-acetyl-l-cysteine (NAC), a powerful antioxidant amino acid, could attenuate the elevated levels of MMP-9, p-p38, p-ERK2 and p-JNK1/2 in 2-CE exposed astrocytes, activation of MAPK signal pathways in 2-CE exposed astrocytes could be mediated partially by reactive oxygen species (ROS), which was most likely generated in the metabolism of 2-CE.	Acetylcysteine	35-54	matrix metallopeptidase 9	Rattus norvegicus	136-141
28769771-7	2017	Furthermore, since pretreatment of n-acetyl-l-cysteine (NAC), a powerful antioxidant amino acid, could attenuate the elevated levels of MMP-9, p-p38, p-ERK2 and p-JNK1/2 in 2-CE exposed astrocytes, activation of MAPK signal pathways in 2-CE exposed astrocytes could be mediated partially by reactive oxygen species (ROS), which was most likely generated in the metabolism of 2-CE.	Acetylcysteine	56-59	matrix metallopeptidase 9	Rattus norvegicus	136-141
28323129-10	2017	However, the impaired steroidogenesis and PGF2alpha-induced JNK-dependent apoptosis were rescued by the addition of the antioxidant N-acetyl-L-cysteine (NAC).	Acetylcysteine	132-151	mitogen-activated protein kinase 8	Mus musculus	60-63
28323129-10	2017	However, the impaired steroidogenesis and PGF2alpha-induced JNK-dependent apoptosis were rescued by the addition of the antioxidant N-acetyl-L-cysteine (NAC).	Acetylcysteine	153-156	mitogen-activated protein kinase 8	Mus musculus	60-63
28672788-9	2017	The suppression of sEH was attenuated by the p38 kinase inhibitor (SB203580) and by treatment with the antioxidant N-acetyl-L-cysteine.	Acetylcysteine	115-134	epoxide hydrolase 2	Rattus norvegicus	19-22
28545464-9	2017	RESULTS: We report for the first time that DEPP induces ROS accumulation and thereby mediates the formation of autophagosomes as inhibition of ROS formation by N-acetyl-cysteine completely blocks autophagy.	Acetylcysteine	160-177	DEPP1 autophagy regulator	Homo sapiens	43-47
28341536-11	2017	Beyond that, the antioxidant N-acetyl cysteine (NAC) could reverse the changes of both cPLA2 and NF-kappaB caused by MGO.	Acetylcysteine	29-46	phospholipase A2 group IVA	Homo sapiens	87-92
28341536-11	2017	Beyond that, the antioxidant N-acetyl cysteine (NAC) could reverse the changes of both cPLA2 and NF-kappaB caused by MGO.	Acetylcysteine	48-51	phospholipase A2 group IVA	Homo sapiens	87-92
27531051-8	2017	OxS being drug-targetable, it represents an interesting therapeutic target for these incurable conditions, and following preclinical correction of the cell or animal model phenotype, the first clinical trials with the antioxidants N-acetylcysteine (SEPN1- and RYR1-related myopathies) or epigallocatechin-gallate (DMD) have been launched recently.	Acetylcysteine	231-247	selenoprotein N	Homo sapiens	249-254
27648632-10	2017	Treatment with NAC and inhibitor of JNK decreased JNK phosphorylation and restored cell proliferation, respectively.	Acetylcysteine	15-18	mitogen-activated protein kinase 8	Mus musculus	36-39
27648632-10	2017	Treatment with NAC and inhibitor of JNK decreased JNK phosphorylation and restored cell proliferation, respectively.	Acetylcysteine	15-18	mitogen-activated protein kinase 8	Mus musculus	50-53
28000869-7	2017	Conversely, N-acetylcysteine inhibited the activation of JNK and p38 MAPK, thus suggesting that the AOPPs-induced activation of JNK/p38 MAPK is reactive oxygen species (ROS)-dependent.	Acetylcysteine	12-28	mitogen-activated protein kinase 8	Mus musculus	57-60
28000869-7	2017	Conversely, N-acetylcysteine inhibited the activation of JNK and p38 MAPK, thus suggesting that the AOPPs-induced activation of JNK/p38 MAPK is reactive oxygen species (ROS)-dependent.	Acetylcysteine	12-28	mitogen-activated protein kinase 8	Mus musculus	128-131
28086830-5	2017	However, both cytotoxicity and caspase-3 activation involved generation of Reactive Oxygen Species (ROS), which could be partially reverted by the lipid antioxidant alpha-tocopherol, but not by the hydrophilic N-acetylcysteine (NAC) indicating crucial differences in the intracellular sites exposed to oxidative stress induced by sigma-2 receptor ligands.	Acetylcysteine	228-231	caspase 3	Mus musculus	31-40
28214842-0	2017	Inhibition of Methylglyoxal-Induced AGEs/RAGE Expression Contributes to Dermal Protection by N-Acetyl-L-Cysteine.	Acetylcysteine	93-112	long intergenic non-protein coding RNA 914	Homo sapiens	41-45
28214842-5	2017	The present study aimed to observe the effects of NAC on MGO-induced inflammatory injury and investigate the roles of AGEs and its receptor (RAGE) in NAC"s dermal protection in human HaCaT keratinocytes.	Acetylcysteine	150-153	long intergenic non-protein coding RNA 914	Homo sapiens	141-145
27709431-6	2017	In addition, endosulfan promoted the increases of ROS, IL-1alpha, and IL-33 levels while antioxidant N-acetyl-L-cysteine (NAC) effectively attenuated the cytotoxicity from endosulfan.	Acetylcysteine	101-120	X-linked Kx blood group	Homo sapiens	122-125
28063010-6	2017	N-acetyl-L-cysteine (NAC), an ROS inhibitor, suppressed chaetocin-induced EBV activation.	Acetylcysteine	0-19	X-linked Kx blood group	Homo sapiens	21-24
28081748-8	2016	Inhibition of ROS generation by NAC resulted in a significant reduction of HVJ-E-induced Erk1/2, JNK, and p38 MAPK activation.	Acetylcysteine	32-35	mitogen-activated protein kinase 8	Mus musculus	97-100
27701797-4	2016	Here we probed the ability of two drugs with opposite effects on system xc-, the inhibitor sulfasalazine and facilitator N-acetylcysteine, to modulate the ability of Ass1-42 to inhibit long-term potentiation (LTP) in the CA1 area of the anaesthetized rat.	Acetylcysteine	121-137	argininosuccinate synthase 1	Rattus norvegicus	166-170
27721085-5	2016	The induction of HSP32 by HBO was significantly reversed by pretreatment neurons with ROS scavenger N-Acetyl-L-cysteine, p38 MAPK inhibitor or Nrf2 gene knockdown, enhanced by MEK1/2 inhibitors or gene knockdown but not by ERK1/2 inhibitor.	Acetylcysteine	100-119	heme oxygenase 1	Rattus norvegicus	17-22
27932980-8	2016	We found that pretreatment with NAC, DPI, or APO also attenuated the TNF-alpha-stimulated IKKalpha/beta and NF-kappaB p65 phosphorylation, NF-kappaB (p65) translocation, and NF-kappaB promoter activity in HPAEpiCs.	Acetylcysteine	32-35	component of inhibitor of nuclear factor kappa B kinase complex	Homo sapiens	90-103
27863474-0	2016	Hypoxic resistance of KRAS mutant tumor cells to 3-Bromopyruvate is counteracted by Prima-1 and reversed by N-acetylcysteine.	Acetylcysteine	108-124	KRAS proto-oncogene, GTPase	Homo sapiens	22-26
27863474-8	2016	Death from joint Prima-1 and 3-BrPA treatment in KRAS mutant A549 and C8161 cells seemed mediated by potentiating oxidative stress, since it was antagonized by the anti-oxidant and glutathione precursor N-acetylcysteine.	Acetylcysteine	203-219	KRAS proto-oncogene, GTPase	Homo sapiens	49-53
27733157-4	2016	We hypothesized that treatment with antioxidant N-acetylcysteine (NAC) could enhance cardiac Cav-3 expression and attenuate caveolae dysfunction and the accompanying eNOS/NO signaling abnormalities in diabetes.	Acetylcysteine	48-64	nitric oxide synthase 3	Rattus norvegicus	166-170
27733157-4	2016	We hypothesized that treatment with antioxidant N-acetylcysteine (NAC) could enhance cardiac Cav-3 expression and attenuate caveolae dysfunction and the accompanying eNOS/NO signaling abnormalities in diabetes.	Acetylcysteine	66-69	nitric oxide synthase 3	Rattus norvegicus	166-170
27733157-9	2016	NAC attenuated the reductions of NO, Cav-3 and phosphorylated eNOS and mitigated the augmentation of O2-, nitrotyrosine and 15-F2t-isoprostane in diabetic myocardium.	Acetylcysteine	0-3	nitric oxide synthase 3	Rattus norvegicus	62-66
27733157-11	2016	Immunoprecipitation analysis revealed that diabetic conditions decreased the association of Cav-3 and eNOS in isolated cardiomyocytes, which was enhanced by treatment with NAC.	Acetylcysteine	172-175	nitric oxide synthase 3	Rattus norvegicus	102-106
27733157-13	2016	NAC treatment attenuated the reductions of Cav-3 expression and eNOS phosphorylation in HG-treated cardiomyocytes or H9C2 cells.	Acetylcysteine	0-3	nitric oxide synthase 3	Rattus norvegicus	64-68
27733157-14	2016	NAC treatment attenuated HG and H/R induced cell injury, which was abolished during concomitant treatment with Cav-3 siRNA or eNOS siRNA.	Acetylcysteine	0-3	nitric oxide synthase 3	Rattus norvegicus	126-130
27733157-16	2016	Antioxidant NAC attenuated myocardial dysfunction and myocardial I/R injury by improving Cav-3/eNOS signaling.	Acetylcysteine	12-15	nitric oxide synthase 3	Rattus norvegicus	95-99
27572503-12	2016	Curcumin and NAC were able to inhibit H2O2-induced ROS production, reduce the migration and invasion, and decrease the expression of MMP-2 and MMP-9 in pancreatic cancer cells.	Acetylcysteine	13-16	matrix metallopeptidase 9	Homo sapiens	143-148
27075430-5	2016	Both the in vitro (0.1 mM) and in vivo application of NAC significantly suppressed the activity of MMP-9/2.	Acetylcysteine	54-57	matrix metallopeptidase 9	Rattus norvegicus	99-104
27106530-8	2016	CuE-triggered protein expression of p-AKT, p-mTOR, Beclin-1, and p-ULK1 was partially reversed by NAC pretreatment.	Acetylcysteine	98-101	beclin 1	Homo sapiens	51-59
27054409-6	2016	O-Monomethyl-O-monosulfonated-6-EC-catechol, its monohydroxy products, and N-acetyl-l-cysteine(NAC)-6-EC-ortho-quinone were discovered as signature metabolites of the ortho-quinone pathway.	Acetylcysteine	75-94	X-linked Kx blood group	Homo sapiens	95-98
27322250-9	2016	Further, pretreatment with antioxidant N-acetylcysteine (NAC) effectively abrogated cypermethrin-induced cell cytotoxicity, G1 cell cycle arrest, DNA damage, PARP activity, and JNK and ERK1/2 activation.	Acetylcysteine	39-55	poly (ADP-ribose) polymerase family, member 1	Mus musculus	158-162
27322250-9	2016	Further, pretreatment with antioxidant N-acetylcysteine (NAC) effectively abrogated cypermethrin-induced cell cytotoxicity, G1 cell cycle arrest, DNA damage, PARP activity, and JNK and ERK1/2 activation.	Acetylcysteine	39-55	mitogen-activated protein kinase 8	Mus musculus	177-180
27322250-9	2016	Further, pretreatment with antioxidant N-acetylcysteine (NAC) effectively abrogated cypermethrin-induced cell cytotoxicity, G1 cell cycle arrest, DNA damage, PARP activity, and JNK and ERK1/2 activation.	Acetylcysteine	57-60	poly (ADP-ribose) polymerase family, member 1	Mus musculus	158-162
27322250-9	2016	Further, pretreatment with antioxidant N-acetylcysteine (NAC) effectively abrogated cypermethrin-induced cell cytotoxicity, G1 cell cycle arrest, DNA damage, PARP activity, and JNK and ERK1/2 activation.	Acetylcysteine	57-60	mitogen-activated protein kinase 8	Mus musculus	177-180
26993523-5	2016	Both CS-induced VEGFR2 expression and tyrosine phosphorylation were abrogated by cotreatment with reactive oxygen species inhibitor, N-acetyl cysteine.	Acetylcysteine	133-150	kinase insert domain receptor	Homo sapiens	16-22
27059143-7	2016	Treatment with N-acetylcysteine as an ROS scavenger reduced augmented HO-1 levels in MsrB3-depleted cells.	Acetylcysteine	15-31	methionine sulfoxide reductase B3	Homo sapiens	85-90
26825874-10	2016	Additionally, both apocynin and NAC completely prevented the decreased MHC, decreased myotube diameter, and increased MuRF-1 induced by TGF-beta.	Acetylcysteine	32-35	tripartite motif-containing 63	Mus musculus	118-124
26846682-11	2016	N-acetylcysteine restored Brg1, Nrf2 and p-STAT3, and IsoPostC-induced protection in H9C2 cells exposed to HG and HR.	Acetylcysteine	0-16	SWI/SNF related, matrix associated, actin dependent regulator of chromatin, subfamily a, member 4	Rattus norvegicus	26-30
26852701-5	2016	Interestingly, co-administration of 17beta-estradiol with N-acetylcysteine (NAC, precursor molecule of glutathione (GSH)) further significantly increased the survival of dopaminergic neurons in the SN (by 85%), with a parallel further decrease of lipid peroxidation to normal levels.	Acetylcysteine	58-74	NLR family, pyrin domain containing 1A	Mus musculus	76-79
26846549-6	2016	Changes in AR in SERCA2a-upregulated mice were significantly less pronounced than those observed in control in seven of nine tested conditions (P&lt; 0.04).N-acetyl-l-cysteine (NAC), rescued alternans in myocytes that were previously exposed to an oxidizing agent (P&lt; 0.001).	Acetylcysteine	156-175	ATPase, Ca++ transporting, cardiac muscle, slow twitch 2	Mus musculus	17-24
26846549-6	2016	Changes in AR in SERCA2a-upregulated mice were significantly less pronounced than those observed in control in seven of nine tested conditions (P&lt; 0.04).N-acetyl-l-cysteine (NAC), rescued alternans in myocytes that were previously exposed to an oxidizing agent (P&lt; 0.001).	Acetylcysteine	177-180	ATPase, Ca++ transporting, cardiac muscle, slow twitch 2	Mus musculus	17-24
26564153-7	2016	On the contrary, BPIQ-induced apoptosis of Y79 cells was attenuated significantly by N-acetyl-L-cysteine (NAC), an ROS scavenger.	Acetylcysteine	85-104	X-linked Kx blood group	Homo sapiens	106-109
27126918-11	2016	AVP-modulated expression of Hmgb1 protein was reduced by the addition of the antioxidant N-acetylcysteine (NAC).	Acetylcysteine	89-105	high mobility group box 1	Rattus norvegicus	28-33
27126918-11	2016	AVP-modulated expression of Hmgb1 protein was reduced by the addition of the antioxidant N-acetylcysteine (NAC).	Acetylcysteine	107-110	high mobility group box 1	Rattus norvegicus	28-33
26896612-8	2016	Compared with that in high glucose group, antioxidant NAC inhibited the expression of integrin alphavbeta3, NAC and the anti-body for blocking integrin alphavbeta3 (clone LM609) down-regulated the expression of LN.	Acetylcysteine	54-57	integrin subunit alpha V	Homo sapiens	86-106
26896612-8	2016	Compared with that in high glucose group, antioxidant NAC inhibited the expression of integrin alphavbeta3, NAC and the anti-body for blocking integrin alphavbeta3 (clone LM609) down-regulated the expression of LN.	Acetylcysteine	54-57	integrin subunit alpha V	Homo sapiens	143-163
26812176-7	2016	The mercapturic acids are extracted from the urinary matrix on a restricted access material (RAM RP 18) and separated on a reversed phase column (Synergi Polar RP C18).	Acetylcysteine	4-21	pre-mRNA processing factor 3	Homo sapiens	97-102
26804764-10	2016	Moreover, The activation of AMPK/mTOR/p70s6k/4EBP1 and JNK signalling pathways induced by NP could be efficiently reversed by pretreatment of N-acetylcysteine or 3-MA.	Acetylcysteine	142-158	mechanistic target of rapamycin kinase	Rattus norvegicus	33-37
27003169-5	2016	Rap, an mTOR inhibitor and NAC, a ROS scavenger, blocked Cd-induced activation of Akt/mTOR signaling and apoptosis of neuronal cells.	Acetylcysteine	27-30	mechanistic target of rapamycin kinase	Rattus norvegicus	86-90
26177712-9	2016	NAC down-regulates the expression and release of ICAM-1 as well as the expression and activation of TACE.	Acetylcysteine	0-3	intercellular adhesion molecule 1	Homo sapiens	49-55
26177712-9	2016	NAC down-regulates the expression and release of ICAM-1 as well as the expression and activation of TACE.	Acetylcysteine	0-3	ADAM metallopeptidase domain 17	Homo sapiens	100-104
26177712-10	2016	However, in TNFalpha stimulated cells NAC treatment reduces only in part ICAM-1 expression and sICAM-1 release.	Acetylcysteine	38-41	intercellular adhesion molecule 1	Homo sapiens	73-79
26111538-6	2016	Coincidently, both superoxide formation and ERK1/2 phosphorylation were observed in Met-5A cells exposed to MWCNTs and were diminished by pretreatment with the reactive oxidative species (ROS) scavenger, N-acetyl-l-(+)-cysteine (NAC).	Acetylcysteine	204-227	X-linked Kx blood group	Homo sapiens	229-232
26671656-2	2016	Whether this process can be modulated by a small molecular weight thiol antioxidant N-acetyl-L-cysteine (NAC) was tested in normal human skin fibroblasts (NHFs) using a uni-directional wound healing assay.	Acetylcysteine	84-103	X-linked Kx blood group	Homo sapiens	105-108
26449932-6	2015	Interestingly, when the HepG2 cells were pre-treated with N-Acetyl-L-Cysteine (NAC) for 1 h, which inhibited ROS generation before being exposed to GRh2, the permeabilization of lysosomal membranes and the levels of Cat B in the cytosol were down-regulated.	Acetylcysteine	58-77	cathepsin B	Homo sapiens	216-221
26449932-6	2015	Interestingly, when the HepG2 cells were pre-treated with N-Acetyl-L-Cysteine (NAC) for 1 h, which inhibited ROS generation before being exposed to GRh2, the permeabilization of lysosomal membranes and the levels of Cat B in the cytosol were down-regulated.	Acetylcysteine	79-82	cathepsin B	Homo sapiens	216-221
25772235-6	2015	Addition of the ROS scavenger N-acetyl cysteine prevented p62 accumulation in PFKFB4-depleted cells, suggesting that the upregulation of p62 and autophagy was a response to oxidative stress caused by PFKFB4 elimination.	Acetylcysteine	30-47	sequestosome 1	Homo sapiens	58-61
25772235-6	2015	Addition of the ROS scavenger N-acetyl cysteine prevented p62 accumulation in PFKFB4-depleted cells, suggesting that the upregulation of p62 and autophagy was a response to oxidative stress caused by PFKFB4 elimination.	Acetylcysteine	30-47	sequestosome 1	Homo sapiens	137-140
26289753-7	2015	Preincubation with the antioxidant N-acetyl-l-cysteine (NAC) resulted in increased DMT1 at the apical membrane before and after addition of iron.	Acetylcysteine	35-54	X-linked Kx blood group	Homo sapiens	56-59
26316066-1	2015	We have designed and synthesised a [Ru(CO)3 Cl2 (NAC)] pro-drug that features an N-acetyl cysteine (NAC) ligand.	Acetylcysteine	49-52	endogenous retrovirus group W member 5	Homo sapiens	44-47
26316066-1	2015	We have designed and synthesised a [Ru(CO)3 Cl2 (NAC)] pro-drug that features an N-acetyl cysteine (NAC) ligand.	Acetylcysteine	81-98	endogenous retrovirus group W member 5	Homo sapiens	44-47
26316066-1	2015	We have designed and synthesised a [Ru(CO)3 Cl2 (NAC)] pro-drug that features an N-acetyl cysteine (NAC) ligand.	Acetylcysteine	100-103	endogenous retrovirus group W member 5	Homo sapiens	44-47
26184052-11	2015	We further show that systemic administration of a single dose of dendrimer-N-acetyl cysteine conjugate (D-NAC) at either sub-acute or delayed time points after injury results in sustained attenuation of the "detrimental" pro-inflammatory response up to 9days after injury, while not impacting the "favorable" anti-inflammatory response.	Acetylcysteine	75-92	NLR family, pyrin domain containing 1A	Mus musculus	106-109
26150435-6	2015	Chemerin increased generation of reactive oxygen species and phosphorylation of mitogen-activated protein kinases, effects that were inhibited by ML171, GKT137831 (Nox inhibitors), and N-acetylcysteine (reactive oxygen species scavenger).	Acetylcysteine	185-201	retinoic acid receptor responder 2	Homo sapiens	0-8
26711827-1	2015	OBJECTIVE: To investigate the possible effect and mechanism of N-Acetyl-L-cysteine (NAC) on fibrillar Abeta(25-35)-induced tau hyperphosphorylation.	Acetylcysteine	63-82	X-linked Kx blood group	Homo sapiens	84-87
26157141-7	2015	In addition, rotenone-induced Cln-1 expression was attenuated by N-acetylcysteine, an antioxidant, and exogenous H2O2 treatment was enough to increase Cln-1 transcription, implying the involvement of ROS.	Acetylcysteine	65-81	claudin 1	Homo sapiens	30-35
25998848-4	2015	We show that LA, but not its reduced form dihydrolipoic acid, potently inhibits the activity of recombinant MGMT by interfering with its catalytic Cys-145 residue, which was partially reversible by N-acetyl cysteine.	Acetylcysteine	198-215	O-6-methylguanine-DNA methyltransferase	Homo sapiens	108-112
26250417-2	2015	Administration of N-acetyl cysteine (NAC) within 8 hours of APAP overdose effectively mitigates APAP-induced hepatotoxicity.	Acetylcysteine	18-35	NLR family, pyrin domain containing 1A	Mus musculus	37-40
25891473-7	2015	Further study showed that PE increased LDH release, induced apoptosis, disrupted mitochondrial membrane potential and elevated intracellular reactive oxygen species (ROS) in HepG2 cells, whereas the antioxidant N-acetyl-l-cysteine (NAC) prevented PE-induced ROS generation.	Acetylcysteine	211-230	X-linked Kx blood group	Homo sapiens	232-235
25241892-4	2015	The addition of N-acetyl cysteine attenuated ROS production and reversed the cytotoxic effects of K-Ras(G12V) in the TKO MEFs.	Acetylcysteine	16-33	KRAS proto-oncogene, GTPase	Homo sapiens	98-102
25834143-9	2015	Furthermore, NAC treatment could inhibit NLRP3 inflammasome formation and caspase-1 activation and suppress the release of IL-1beta and IL-18 from H. pylori-infected THP-1 cells.	Acetylcysteine	13-16	interleukin 18	Homo sapiens	136-141
25817999-8	2015	However, the N-acetylcysteine-sensitive fraction of insulin secretion by WT islets was increased by temperature elevation, and this temperature-dependent enhancement was diminished significantly in TRPM2KO islets.	Acetylcysteine	13-29	transient receptor potential cation channel, subfamily M, member 2	Mus musculus	198-203
25619687-10	2015	ANT inhibition or anti-oxidant strategy (N-acetylcysteine) prevented SR Ca(2+) leak, FKBP12.6 depletion and RyR2 oxidation/S-nitrosylation induced by PC.	Acetylcysteine	41-57	ryanodine receptor 2, cardiac	Mus musculus	108-112
25738249-5	2015	Pemetrexed-induced apoptosis, which was prevented by pretreatment with N-acetyl-cysteine (NAC), was mediated by effects on the mitochondria, including mitochondrial membrane potential transition (MPT) and cytosolic release of cytochrome c, and also involved regulation of SIRT1 expression.	Acetylcysteine	71-88	sirtuin 1	Homo sapiens	272-277
25738249-5	2015	Pemetrexed-induced apoptosis, which was prevented by pretreatment with N-acetyl-cysteine (NAC), was mediated by effects on the mitochondria, including mitochondrial membrane potential transition (MPT) and cytosolic release of cytochrome c, and also involved regulation of SIRT1 expression.	Acetylcysteine	90-93	sirtuin 1	Homo sapiens	272-277
25832424-8	2015	Pretreatment of the cells with the ROS scavenger N-acetyl-L-cysteine, ERK inhibitor PD98059 or NF-kappaB inhibitor PDTC blocked CRP-stimulated RAGE expression, but pretreatment with the NADPH oxidase inhibitor DPI, JNK inhibitor SP600125 or p38 MAPK inhibitor SB203580 did not significantly alter CRP-stimulated RAGE expression.	Acetylcysteine	49-68	advanced glycosylation end-product specific receptor	Homo sapiens	143-147
25732239-0	2015	N-acetylcysteine prevents rotenone-induced Parkinson"s disease in rat: An investigation into the interaction of parkin and Drp1 proteins.	Acetylcysteine	0-16	dynamin 1-like	Rattus norvegicus	123-127
25732239-8	2015	Western blot analysis was also done for parkin and Drp1 (dynamin related protein-1) proteins quantification in SN and ST. Our results indicated that NAC significantly ameliorated the rotenone-induced motor dysfunction and dopamine loss.	Acetylcysteine	149-152	dynamin 1-like	Rattus norvegicus	51-55
25732239-8	2015	Western blot analysis was also done for parkin and Drp1 (dynamin related protein-1) proteins quantification in SN and ST. Our results indicated that NAC significantly ameliorated the rotenone-induced motor dysfunction and dopamine loss.	Acetylcysteine	149-152	dynamin 1-like	Rattus norvegicus	57-82
25732239-9	2015	Furthermore, NAC was able to prevent the rotenone-induced changes in parkin and Drp1 levels in the both studied areas.	Acetylcysteine	13-16	dynamin 1-like	Rattus norvegicus	80-84
25834400-9	2015	Moreover, PLB induced intracellular reactive oxygen species (ROS) generation and this effect was attenuated by l-glutathione (GSH) and n-acetyl-l-cysteine (NAC).	Acetylcysteine	135-154	X-linked Kx blood group	Homo sapiens	156-159
25489974-10	2015	The expression of AA-induced ICAM-1 was significantly reduced when cells were pretreated with either NAC or p38 MAPK inhibitor.	Acetylcysteine	101-104	intercellular adhesion molecule 1	Homo sapiens	29-35
25410913-4	2015	A common technique involves incubation of a new chemical entity with NADPH-supplemented human liver microsomes (HLMs) in the presence of soft nucleophilic trapping agents, such as glutathione (GSH) or N-acetylcysteine (NAC).	Acetylcysteine	219-222	2,4-dienoyl-CoA reductase 1	Homo sapiens	69-74
25451595-8	2015	Additionally, pretreatment with 2.5 mM N-acetylcysteine (NAC; a glutathione (GSH) precursor) dramatically suppressed the increase in lipid peroxidation, cytotoxicity, apoptotic events, calpain and caspase-12 activity, and ER stress-related molecules in CA-exposed cells.	Acetylcysteine	39-55	NLR family, pyrin domain containing 1A	Mus musculus	57-60
26394653-9	2015	In addition, TDT induced the generation of reactive oxygen species (ROS), which was reversed by N-acetylcysteine (NAC).	Acetylcysteine	96-112	DNA nucleotidylexotransferase	Homo sapiens	13-16
26394653-9	2015	In addition, TDT induced the generation of reactive oxygen species (ROS), which was reversed by N-acetylcysteine (NAC).	Acetylcysteine	114-117	DNA nucleotidylexotransferase	Homo sapiens	13-16
26394653-10	2015	NAC also reversed TDT-induced depolarization of Deltapsi, MDC staining, up-regulation of Bax, cleaved-PARP, Beclin-1, LC3-II, and cell viability.	Acetylcysteine	0-3	DNA nucleotidylexotransferase	Homo sapiens	18-21
26394653-10	2015	NAC also reversed TDT-induced depolarization of Deltapsi, MDC staining, up-regulation of Bax, cleaved-PARP, Beclin-1, LC3-II, and cell viability.	Acetylcysteine	0-3	beclin 1	Homo sapiens	108-116
26075245-8	2015	The cytotoxic effect promoted by MRE was prevented by pretreatment of HepG2 cells with N-acetyl-L-cysteine (NAC), suggesting that oxidative stress was pivotal in MRE-mediated cell death.	Acetylcysteine	87-106	X-linked Kx blood group	Homo sapiens	108-111
25327779-8	2015	Moreover, pannexin-1 protein expression and cathepsin B release were strongly attenuated by N-acetylcysteine.	Acetylcysteine	92-108	pannexin 1	Homo sapiens	10-20
25327779-8	2015	Moreover, pannexin-1 protein expression and cathepsin B release were strongly attenuated by N-acetylcysteine.	Acetylcysteine	92-108	cathepsin B	Homo sapiens	44-55
25599738-0	2015	Effect of N-acetyl cysteine and vitamin C on kidney allograft function biomarkers interleukin-18 and neutrophil gelatinase-associated lipocalin.	Acetylcysteine	10-27	interleukin 18	Homo sapiens	82-96
25437876-7	2015	This alteration in the CD4+ T cell populations was mediated in part through ROS, as N-acetyl cysteine (NAC) treatment restored Th17 cell generation.	Acetylcysteine	84-101	CD4 antigen	Mus musculus	23-26
25437876-7	2015	This alteration in the CD4+ T cell populations was mediated in part through ROS, as N-acetyl cysteine (NAC) treatment restored Th17 cell generation.	Acetylcysteine	103-106	CD4 antigen	Mus musculus	23-26
25392528-8	2014	Furthermore, reactive oxygen species scavenger (N-acetyl-l-cysteine) and the ERK inhibitor (FR180204) impaired LPS-induced PARP activation and HMGB1 release.	Acetylcysteine	48-67	poly (ADP-ribose) polymerase family, member 1	Mus musculus	123-127
25041185-5	2014	ROS scavenger N-acetylcysteine reduced expression of HSP70 and HSP32 (haeme oxygenase-1, HO-1).	Acetylcysteine	14-30	heme oxygenase 1	Rattus norvegicus	63-68
25041185-5	2014	ROS scavenger N-acetylcysteine reduced expression of HSP70 and HSP32 (haeme oxygenase-1, HO-1).	Acetylcysteine	14-30	heme oxygenase 1	Rattus norvegicus	70-93
25301941-9	2014	The cytoprotective antioxidant N-acetylcysteine inhibited Dp44mT-induced autophagosome synthesis and p62 accumulation.	Acetylcysteine	31-47	nucleoporin 62	Homo sapiens	101-104
25305669-0	2014	N-acetylcysteine prevents endoplasmic reticulum stress elicited in macrophages by serum albumin drawn from chronic kidney disease rats and selectively affects lipid transporters, ABCA-1 and ABCG-1.	Acetylcysteine	0-16	ATP binding cassette subfamily A member 1	Rattus norvegicus	179-185
25305669-18	2014	ABCA-1 expression was lower (87% and 70%, p &lt; 0.001) in macrophage treated with Sham + NAC and CKD albumin respectively in comparison to Sham albumin; ABCG-1 was higher (4 and 7 times, p &lt; 0.001) in macrophages treated with Sham + NAC and CKD + NAC albumin, respectively in comparison to Sham and CKD albumin.	Acetylcysteine	90-93	ATP binding cassette subfamily A member 1	Rattus norvegicus	0-6
25305669-18	2014	ABCA-1 expression was lower (87% and 70%, p &lt; 0.001) in macrophage treated with Sham + NAC and CKD albumin respectively in comparison to Sham albumin; ABCG-1 was higher (4 and 7 times, p &lt; 0.001) in macrophages treated with Sham + NAC and CKD + NAC albumin, respectively in comparison to Sham and CKD albumin.	Acetylcysteine	237-240	ATP binding cassette subfamily A member 1	Rattus norvegicus	0-6
25305669-18	2014	ABCA-1 expression was lower (87% and 70%, p &lt; 0.001) in macrophage treated with Sham + NAC and CKD albumin respectively in comparison to Sham albumin; ABCG-1 was higher (4 and 7 times, p &lt; 0.001) in macrophages treated with Sham + NAC and CKD + NAC albumin, respectively in comparison to Sham and CKD albumin.	Acetylcysteine	237-240	ATP binding cassette subfamily A member 1	Rattus norvegicus	0-6
25085248-4	2014	TIGAR silencing enhanced epirubicin-induced elevations in ROS levels and apoptosis rates, in a manner that was blocked by ectopic addition of NADPH or N-acetyl cysteine.	Acetylcysteine	151-168	Trp53 induced glycolysis regulatory phosphatase	Mus musculus	0-5
25132466-4	2014	Juvenile and adolescent treatment with the antioxidant N-acetyl cysteine prevented the reduction of prefrontal parvalbumin interneuron activity observed in this model, as well as electrophysiological and behavioral deficits relevant to schizophrenia.	Acetylcysteine	55-72	parvalbumin	Rattus norvegicus	111-122
25257100-11	2014	In addition, NAC plus gemcitabine treatment decreased anti-apoptotic XIAP protein expression compared to gemcitabine alone.	Acetylcysteine	13-16	X-linked inhibitor of apoptosis	Homo sapiens	69-73
24933620-5	2014	Cadmium-induced decrease in phosphorylated Akt1 correlated with increased association of wild-type (WT) Akt1 with PP2A, which was absent in the C296-310S Akt1 mutant and was also abolished by N-acetylcysteine treatment.	Acetylcysteine	192-208	protein phosphatase 2, regulatory subunit A, alpha	Mus musculus	114-118
25438539-10	2014	NAC was also found to suppress the levels of GRP78, PERK and CHOP expression in NaF-treated cells (p&lt;0.01).	Acetylcysteine	0-3	heat shock protein family A (Hsp70) member 5	Rattus norvegicus	45-50
24976129-6	2014	In addition, the N-acetylcysteine inhibited ROS/RNS generation, elevation of antioxidants level, expression of ERK1/2, Akt, tuberin phosphorylation, resulted in deceased 8-OHdG accumulation and upregulation of OGG1 protein expression suggesting no involvement of Akt and ERK1/2MAPK pathways after CEES and LPS challenge.	Acetylcysteine	17-33	8-oxoguanine DNA-glycosylase 1	Mus musculus	210-214
24799199-7	2014	In addition, NAC pretreatment partly ameliorated OTA-induced S-phase arrest by preventing the down-regulation of cyclin A2, cyclin E1 and CDK2 expression in HEK-293 cells.	Acetylcysteine	13-16	cyclin E1	Homo sapiens	124-133
24979751-11	2014	Treatment with N-acetyl cysteine positively regulated the PON 2 expression, thus promoting the antioxidant defense put up by the cells in response to chlorpyrifos.	Acetylcysteine	15-32	paraoxonase 2	Homo sapiens	58-63
24726524-10	2014	NAC attenuated BLM induced oxidative damage, changes in E-cadherin and vimentin expressions and collagen deposition in the sclerotic skin of mice.	Acetylcysteine	0-3	vimentin	Mus musculus	71-79
24614837-8	2014	The glutathione peroxidase-1 activity was also significantly higher in the NAC group seven days after transplantation (3.38(2.19) vs 2.41(1.70) ng/mL, P=0.003).	Acetylcysteine	75-78	glutathione peroxidase 1	Homo sapiens	4-28
24857964-5	2014	Moreover, our findings indicated that the pretreatment of HL 60 cells with N-acetyl-l-cysteine (NAC), a reactive oxygen species (ROS) scavenger, diminished MMP disruption and apoptosis induced by 10AB, suggesting that ROS overproduction plays a crucial rule in the cytotoxic activity of 10AB.	Acetylcysteine	75-94	X-linked Kx blood group	Homo sapiens	96-99
23644946-0	2014	Dietary antioxidants (selenium and N-acetylcysteine) modulate paraoxonase 1 (PON1) in PCB 126-exposed rats.	Acetylcysteine	35-51	paraoxonase 1	Rattus norvegicus	62-75
23644946-0	2014	Dietary antioxidants (selenium and N-acetylcysteine) modulate paraoxonase 1 (PON1) in PCB 126-exposed rats.	Acetylcysteine	35-51	paraoxonase 1	Rattus norvegicus	77-81
23644946-0	2014	Dietary antioxidants (selenium and N-acetylcysteine) modulate paraoxonase 1 (PON1) in PCB 126-exposed rats.	Acetylcysteine	35-51	pyruvate carboxylase	Rattus norvegicus	86-89
24548678-10	2014	N-acetyl-cysteine (1mM NAC) fully prevented the vacuoles and chloropicrin-induced cytotoxicity.	Acetylcysteine	0-17	X-linked Kx blood group	Homo sapiens	23-26
24164541-4	2014	HN2-induced EGFR phosphorylation and IL-6 secretion in NHBECs were inhibited by the antioxidant N-acetyl-L-cysteine (NAC) and by the flavoprotein inhibitor diphenyleneiodonium chloride (DPI).	Acetylcysteine	96-115	X-linked Kx blood group	Homo sapiens	117-120
24681574-14	2014	IL-6 and HSP-70 release was significantly induced by IFN-gamma treatment, which was largely inhibited by NAC.	Acetylcysteine	105-108	heat shock protein family A (Hsp70) member 4	Homo sapiens	9-15
24577230-1	2014	We investigated whether treatment with N-acetylcysteine (NAC) reduces oxidative stress intensity and restores the expression and activities of superoxide dismutase (Sod1, SOD), catalase (Cat, CAT) and glutathione peroxidase (Gpx1, GPx) in lead-exposed workers.	Acetylcysteine	39-55	glutathione peroxidase 1	Homo sapiens	225-229
24577230-1	2014	We investigated whether treatment with N-acetylcysteine (NAC) reduces oxidative stress intensity and restores the expression and activities of superoxide dismutase (Sod1, SOD), catalase (Cat, CAT) and glutathione peroxidase (Gpx1, GPx) in lead-exposed workers.	Acetylcysteine	57-60	glutathione peroxidase 1	Homo sapiens	225-229
24681787-9	2014	NAC or HMGB1 neutralizing antibody also significantly suppressed the release of LDH and the expression of HMGB1.	Acetylcysteine	0-3	high mobility group box 1	Rattus norvegicus	106-111
24385538-4	2014	Importantly, treatment of pfn1-deficient mice with the antioxidant N-acetyl-l-cysteine reversed the ROS level and loss of quiescence of HSCs, suggesting that the metabolism is mechanistically linked to the cell cycle quiescence of stem cells.	Acetylcysteine	67-86	profilin 1	Mus musculus	26-30
24493151-9	2014	NAC (10  mM) inhibited accumulation of PGE2 and IL10 only; NBDI (10  muM) had no significant effect.	Acetylcysteine	0-3	interleukin 10	Homo sapiens	48-52
24258150-8	2014	Msh2 expression in skin tissues of Tg mice was significantly increased by NAC treatment, as was Msh2 promoter demethylation.	Acetylcysteine	74-77	mutS homolog 2	Mus musculus	0-4
24967005-6	2014	All the biological effects of PL in scratched LN229 cells were completely abolished by the antioxidant N-acetyl-L-cysteine (NAC).	Acetylcysteine	103-122	X-linked Kx blood group	Homo sapiens	124-127
23758132-6	2013	Treatment of RA PB T cells with the GSH precursor N-acetyl cysteine increased CD45 phosphatase activity and proliferation, while it decreased Lck kinase phosphorylation, which is regulated by CD45.	Acetylcysteine	50-67	protein tyrosine phosphatase receptor type C	Homo sapiens	78-82
23758132-6	2013	Treatment of RA PB T cells with the GSH precursor N-acetyl cysteine increased CD45 phosphatase activity and proliferation, while it decreased Lck kinase phosphorylation, which is regulated by CD45.	Acetylcysteine	50-67	protein tyrosine phosphatase receptor type C	Homo sapiens	192-196
24349127-9	2013	The combined anti-HCV activity of ART or its analogues with L-N-Acetylcysteine (L-NAC) [a molecule that inhibits ROS generation] was studied.	Acetylcysteine	60-78	X-linked Kx blood group	Homo sapiens	82-85
23896433-8	2013	BBR and N-acetylcysteine inhibited RhoA/ROCK signaling activation in high glucose-exposed GMCs.	Acetylcysteine	8-24	ras homolog family member A	Rattus norvegicus	35-39
24149112-3	2013	Because the AGE-elicited expression of LCN2 was diminished by an antibody against the AGE receptor (RAGE), diphenylene iodonium (DPI), N-acetyl cysteine, LY294002, and SP600125, we suggest that AGEs enhance the expression of LCN2 via a RAGE-NADPH oxidase-reactive oxygen species pathway, leading to the phosphorylation of PI3K-Akt and JNK in HASMCs.	Acetylcysteine	135-152	lipocalin 2	Homo sapiens	39-43
24025361-10	2013	BBMD3 increased the production of reactive oxygen species (ROS) and ROS scavenger, N-acetylcysteine (NAC), could block the phosphorylation of JNK and c-Jun induced by BBMD3.	Acetylcysteine	83-99	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	150-155
24025361-10	2013	BBMD3 increased the production of reactive oxygen species (ROS) and ROS scavenger, N-acetylcysteine (NAC), could block the phosphorylation of JNK and c-Jun induced by BBMD3.	Acetylcysteine	101-104	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	150-155
23589029-4	2013	Indeed, the addition of N-acetyl cysteine to cell cultures abated Pyr2 enV(IV)-induced apoptosis.	Acetylcysteine	24-41	endogenous retrovirus group K member 20	Homo sapiens	71-74
23263277-7	2013	The enhancement of osteoclast differentiation of FKBP5 transfectants was only partially inhibited by N-acetyl L-cysteine.	Acetylcysteine	101-120	FK506 binding protein 5	Mus musculus	49-54
24179013-6	2013	Finally, treatment with the antioxidative compounds N-acetyl cysteine or MP865, but not with placebo, was associated with higher plasma FGF-19 (NAC and MP865 coefficients -0.28 and -0.23, P &lt; 0.05, respectively).	Acetylcysteine	52-69	X-linked Kx blood group	Homo sapiens	144-147
24370292-1	2013	OBJECTIVE: To investigate the relationship between genetic polymorphisms of glutathione S-transferase P1 (GSTP1), glutathione S-transferase M1 (GSTM1), and glutathione S-transferase T1 (GSTT1) and urinary level of mercapturic acids of styrene (PHEMAs) in workers exposed to styrene.	Acetylcysteine	214-231	glutathione S-transferase theta 1	Homo sapiens	156-184
23515941-7	2013	Finally, pretreatment with the antioxidant N-acetyl-L-cysteine (NAC) reduced the OTA-induced DNA DSBs, ATM phosphorylation, and G2 arrest.	Acetylcysteine	43-62	X-linked Kx blood group	Homo sapiens	64-67
23747931-0	2013	N-Acetylcysteine and allopurinol up-regulated the Jak/STAT3 and PI3K/Akt pathways via adiponectin and attenuated myocardial postischemic injury in diabetes.	Acetylcysteine	0-16	adiponectin, C1Q and collagen domain containing	Rattus norvegicus	86-97
23747931-3	2013	We postulated that NAC and ALP attenuated diabetic MI/R injury by up-regulating phosphatidylinositol 3-kinase/Akt (PI3K/Akt) and Janus kinase 2/signal transducer and activator of transcription-3 (JAK2/STAT3) pathways subsequent to adiponectin (APN) activation.	Acetylcysteine	19-22	Janus kinase 2	Rattus norvegicus	196-200
23747931-3	2013	We postulated that NAC and ALP attenuated diabetic MI/R injury by up-regulating phosphatidylinositol 3-kinase/Akt (PI3K/Akt) and Janus kinase 2/signal transducer and activator of transcription-3 (JAK2/STAT3) pathways subsequent to adiponectin (APN) activation.	Acetylcysteine	19-22	adiponectin, C1Q and collagen domain containing	Rattus norvegicus	231-242
23747931-3	2013	We postulated that NAC and ALP attenuated diabetic MI/R injury by up-regulating phosphatidylinositol 3-kinase/Akt (PI3K/Akt) and Janus kinase 2/signal transducer and activator of transcription-3 (JAK2/STAT3) pathways subsequent to adiponectin (APN) activation.	Acetylcysteine	19-22	adiponectin, C1Q and collagen domain containing	Rattus norvegicus	244-247
23747931-6	2013	NAC and ALP decreased MI/R injury in D rats, enhanced phosphorylation of Akt and STAT3, and increased NO and APN.	Acetylcysteine	0-3	adiponectin, C1Q and collagen domain containing	Rattus norvegicus	109-112
23747931-8	2013	The PI3K inhibitor wortmannin and Jak2 inhibitor AG490 abolished the protection of NAC and ALP.	Acetylcysteine	83-86	Janus kinase 2	Rattus norvegicus	34-38
23747931-11	2013	In conclusion, NAC and ALP prevented diabetic MI/R injury through PI3K/Akt and Jak2/STAT3 and cardiac APN may serve as a mediator via AdipoR2 in this process.	Acetylcysteine	15-18	Janus kinase 2	Rattus norvegicus	79-83
23747931-11	2013	In conclusion, NAC and ALP prevented diabetic MI/R injury through PI3K/Akt and Jak2/STAT3 and cardiac APN may serve as a mediator via AdipoR2 in this process.	Acetylcysteine	15-18	adiponectin, C1Q and collagen domain containing	Rattus norvegicus	102-105
23900601-6	2013	Moreover, the combined treatment induced intracellular reactive oxygen species (ROS) and the radical scavenger N-acetyl-L-cysteine (NAC) blocked the intracellular ROS and apoptosis induced by OBP-801 and LY294002.	Acetylcysteine	111-130	X-linked Kx blood group	Homo sapiens	132-135
22989604-9	2013	Reduced superoxide levels and DCF in the exer+NAC group were associated with decreased Akt, AMPK and eNOS phosphorylation.	Acetylcysteine	46-49	nitric oxide synthase 3	Rattus norvegicus	101-105
22989604-10	2013	These results appear to be connected with vascular function because VASP phosphorylation increased in acute exercise and decreased in exer+NAC.	Acetylcysteine	139-142	vasodilator-stimulated phosphoprotein	Rattus norvegicus	68-72
22532030-9	2013	Moreover, NAC prevented LPS-induced increases in abundances of intestinal HSP70 and NF-kappaB p65 proteins and TLR4 mRNA.	Acetylcysteine	10-13	heat shock protein family A (Hsp70) member 4	Homo sapiens	74-79
24005553-6	2013	The levels of monocyte chemoattractant protein-1, interleukin-2, interleukin-6, and mouse gamma interferon in lung tissue after intranasal exposure to SEB were also significantly reduced in mice given a combination of dexamethasone and NAC versus controls.	Acetylcysteine	236-239	chemokine (C-C motif) ligand 2	Mus musculus	14-48
24001404-14	2013	In addition, NAC prevented the AA-induced increase in caspase-3 protein, while stimulating claudin-1 protein expression in the colonic mucosa.	Acetylcysteine	13-16	claudin 1	Homo sapiens	91-100
24001404-15	2013	Moreover, NAC enhanced mRNA levels for epidermal growth factor and amphiregulin in the colonic mucosa.	Acetylcysteine	10-13	amphiregulin	Homo sapiens	67-79
23874823-0	2013	N-acetylcysteine and allopurinol confer synergy in attenuating myocardial ischemia injury via restoring HIF-1alpha/HO-1 signaling in diabetic rats.	Acetylcysteine	0-16	hypoxia inducible factor 1 subunit alpha	Rattus norvegicus	104-114
23874823-0	2013	N-acetylcysteine and allopurinol confer synergy in attenuating myocardial ischemia injury via restoring HIF-1alpha/HO-1 signaling in diabetic rats.	Acetylcysteine	0-16	heme oxygenase 1	Rattus norvegicus	115-119
23874823-6	2013	NAC and ALP given alone and in particular their combination normalized cardiac levels of HO-1 and HIF-1alpha protein expression and prevented the increase in 15-F2t-isoprostane, resulting in significantly attenuated post-ischemic myocardial infarction.	Acetylcysteine	0-3	heme oxygenase 1	Rattus norvegicus	89-93
23874823-6	2013	NAC and ALP given alone and in particular their combination normalized cardiac levels of HO-1 and HIF-1alpha protein expression and prevented the increase in 15-F2t-isoprostane, resulting in significantly attenuated post-ischemic myocardial infarction.	Acetylcysteine	0-3	hypoxia inducible factor 1 subunit alpha	Rattus norvegicus	98-108
23874823-8	2013	However, all the above protective effects of NAC and ALP were cancelled either by inhibition of HO-1 or HIF-1alpha with SnPP-IX and 2ME2 in vivo or by HO-1 or HIF-1alpha gene knock-down in vitro.	Acetylcysteine	45-48	heme oxygenase 1	Rattus norvegicus	96-100
23874823-8	2013	However, all the above protective effects of NAC and ALP were cancelled either by inhibition of HO-1 or HIF-1alpha with SnPP-IX and 2ME2 in vivo or by HO-1 or HIF-1alpha gene knock-down in vitro.	Acetylcysteine	45-48	hypoxia inducible factor 1 subunit alpha	Rattus norvegicus	104-114
23874823-8	2013	However, all the above protective effects of NAC and ALP were cancelled either by inhibition of HO-1 or HIF-1alpha with SnPP-IX and 2ME2 in vivo or by HO-1 or HIF-1alpha gene knock-down in vitro.	Acetylcysteine	45-48	heme oxygenase 1	Rattus norvegicus	151-155
23874823-8	2013	However, all the above protective effects of NAC and ALP were cancelled either by inhibition of HO-1 or HIF-1alpha with SnPP-IX and 2ME2 in vivo or by HO-1 or HIF-1alpha gene knock-down in vitro.	Acetylcysteine	45-48	hypoxia inducible factor 1 subunit alpha	Rattus norvegicus	159-169
23874823-9	2013	CONCLUSION: NAC and ALP confer synergistic cardioprotection in diabetes via restoration of cardiac HIF-1alpha and HO-1 signaling.	Acetylcysteine	12-15	heme oxygenase 1	Rattus norvegicus	114-118
23508966-8	2013	High glucose increased reactive oxygen species generation and RAGE expression levels in tubular cells, both of which were partly suppressed by SGLT2 siRNAs or an antioxidant, N-acetylcysteine.	Acetylcysteine	175-191	long intergenic non-protein coding RNA 914	Homo sapiens	62-66
23803658-7	2013	We also identified the coexpression of CD44 with the EMT marker N-cadherin in sphere cells, and downregulated CD44 expression after the addition of the antioxidant N-acetyl cysteine.	Acetylcysteine	164-181	CD44 molecule (Indian blood group)	Homo sapiens	39-43
23803658-7	2013	We also identified the coexpression of CD44 with the EMT marker N-cadherin in sphere cells, and downregulated CD44 expression after the addition of the antioxidant N-acetyl cysteine.	Acetylcysteine	164-181	CD44 molecule (Indian blood group)	Homo sapiens	110-114
23376588-6	2013	IRP1 upregulation could be fully abolished by co-administration of radical scavenger N-acetyl-l-cysteine and inducible NO synthetase inhibitor Nomega-nitro-l-arginine methyl ester hydrochloride.	Acetylcysteine	85-104	aconitase 1	Mus musculus	0-4
23648861-8	2013	When alpha2,3-ST was expressed in the presence of NAC, reduced sialylation was restored and an even more sialylated EPO was produced.	Acetylcysteine	50-53	erythropoietin	Cricetulus griseus	116-119
23297317-6	2013	The CD41(high) cells sustained intracellular ROS at the initial level for up to 72 h, but CD41(low) cells had reduced ROS by 48 h. The maximum suppressive effect on CD41 expression was observed when N-acetyl cysteine, which is known to act as a ROS scavenger, was administered 48 h after PMA stimulation.	Acetylcysteine	199-216	integrin subunit alpha 2b	Homo sapiens	4-8
23297317-6	2013	The CD41(high) cells sustained intracellular ROS at the initial level for up to 72 h, but CD41(low) cells had reduced ROS by 48 h. The maximum suppressive effect on CD41 expression was observed when N-acetyl cysteine, which is known to act as a ROS scavenger, was administered 48 h after PMA stimulation.	Acetylcysteine	199-216	integrin subunit alpha 2b	Homo sapiens	90-94
23297317-6	2013	The CD41(high) cells sustained intracellular ROS at the initial level for up to 72 h, but CD41(low) cells had reduced ROS by 48 h. The maximum suppressive effect on CD41 expression was observed when N-acetyl cysteine, which is known to act as a ROS scavenger, was administered 48 h after PMA stimulation.	Acetylcysteine	199-216	integrin subunit alpha 2b	Homo sapiens	90-94
23333634-6	2013	While the knockout down of SelW up-regulated Bax and caspase-3 and down-regulated Bcl-2, the induced oxidative injuries were alleviated by treatment with a ROS scavenger, N-acetyl-l-cysteine (NAC).	Acetylcysteine	171-190	selenoprotein W	Gallus gallus	27-31
23333634-6	2013	While the knockout down of SelW up-regulated Bax and caspase-3 and down-regulated Bcl-2, the induced oxidative injuries were alleviated by treatment with a ROS scavenger, N-acetyl-l-cysteine (NAC).	Acetylcysteine	192-195	selenoprotein W	Gallus gallus	27-31
23154184-8	2013	NAC supplementation in MR rats raised tCys and partly or completely reversed MR effects on weight, fat %, Scd1 expression in liver and white adipose tissue, and estimated SCD1 activity.	Acetylcysteine	0-3	stearoyl-CoA desaturase	Rattus norvegicus	106-110
23154184-8	2013	NAC supplementation in MR rats raised tCys and partly or completely reversed MR effects on weight, fat %, Scd1 expression in liver and white adipose tissue, and estimated SCD1 activity.	Acetylcysteine	0-3	stearoyl-CoA desaturase	Rattus norvegicus	171-175
23154184-9	2013	In CF rats, NAC decreased body fat % and lowered SCD1-18 activity index (P&lt;0.001).	Acetylcysteine	12-15	stearoyl-CoA desaturase	Rattus norvegicus	49-53
23292300-8	2013	However, the quenching of ROS generation with antioxidant N-acetyl-L-cysteine conferred significant protection against cordycepin-elicited ROS generation, disruption of the MMP, modulation of Bcl-2 and IAP family proteins, caspase-3 and -9 activation and apoptosis.	Acetylcysteine	58-77	magnesium transporter 1	Homo sapiens	202-205
23449454-6	2013	Statin-induced cytotoxic effects, DNA fragmentation and changes of activation of caspase-3, Akt, Erk and p38 were blocked by antioxidant (N-acetylcysteine) and metabolic products of the HMG-CoA reductase reaction, such as mevalonate, farnesyl pyrophosphate (FPP) and geranylgeranyl pyrophosphate (GGPP).	Acetylcysteine	138-154	caspase 3	Mus musculus	81-90
22944050-5	2013	RESULTS: NAC treatment suppressed cell growth, with concomitantly increased expression of HMG box-containing protein 1 (HBP1), a transcription suppressor, and decreased EGFR/Akt activation, in EGFR-overexpressing HSC-3 oral cancer cells.	Acetylcysteine	9-12	DnaJ heat shock protein family (Hsp40) member B7	Homo sapiens	213-218
22944050-7	2013	Lastly, NAC and AG1478, an EGFR inhibitor, additively suppressed colony formation in HSC-3 cells.	Acetylcysteine	8-11	DnaJ heat shock protein family (Hsp40) member B7	Homo sapiens	85-90
23319318-14	2013	TNF-alpha increased tyrosine phosphorylation of Syk, which was attenuated by NAC and MPA.	Acetylcysteine	77-80	spleen associated tyrosine kinase	Homo sapiens	48-51
23853776-8	2013	In conclusion, myocardial Brg1 is reduced in diabetes and enhancement of cardiac Brg1 expression may represent a novel mechanism whereby NAC confers cardioprotection.	Acetylcysteine	137-140	SWI/SNF related, matrix associated, actin dependent regulator of chromatin, subfamily a, member 4	Rattus norvegicus	81-85
23124098-8	2013	Furthermore, additional experiments indicated that the inhibitory effect of curcumin on LPS-induced MCP-1 expression was significantly attenuated in the presence of N-acetylcysteine (an effective ROS scavenger).	Acetylcysteine	165-181	chemokine (C-C motif) ligand 2	Mus musculus	100-105
23161516-6	2013	Functional studies confirmed that AL-1 induced apoptosis of K562 cells through a ROS-dependent mechanism, and anti-oxidant, N-acetyl-L-cysteine, could completely block AL-1-induced cytotoxicity, implicating that ROS generation played a vital role in AL-1 cytotoxicity.	Acetylcysteine	124-143	ephrin A5	Homo sapiens	168-172
23161516-6	2013	Functional studies confirmed that AL-1 induced apoptosis of K562 cells through a ROS-dependent mechanism, and anti-oxidant, N-acetyl-L-cysteine, could completely block AL-1-induced cytotoxicity, implicating that ROS generation played a vital role in AL-1 cytotoxicity.	Acetylcysteine	124-143	ephrin A5	Homo sapiens	168-172
24112955-4	2013	RESULTS: NAC treatment inhibited fat accumulation and reduced the expression of obesity-related proteins, including monoamine oxidase A, heat shock protein 70 (HSP70), aminoacylase -1 (ACY-1), and transketolase.	Acetylcysteine	9-12	heat shock protein family A (Hsp70) member 4	Homo sapiens	137-158
24112955-4	2013	RESULTS: NAC treatment inhibited fat accumulation and reduced the expression of obesity-related proteins, including monoamine oxidase A, heat shock protein 70 (HSP70), aminoacylase -1 (ACY-1), and transketolase.	Acetylcysteine	9-12	heat shock protein family A (Hsp70) member 4	Homo sapiens	160-165
22854047-6	2012	Modulating the redox-state using decomposing peroxynitrite (FeTPPS, 2.5 microM) or the GSH-precursor [N-acetylcysteine (NAC), 1 mM] caused a positive-shift of the redox-state and prevented VEGF-mediated S-glutathionylation and oxidative inhibition of LMW-PTP.	Acetylcysteine	102-118	acid phosphatase 1	Homo sapiens	251-258
22854047-6	2012	Modulating the redox-state using decomposing peroxynitrite (FeTPPS, 2.5 microM) or the GSH-precursor [N-acetylcysteine (NAC), 1 mM] caused a positive-shift of the redox-state and prevented VEGF-mediated S-glutathionylation and oxidative inhibition of LMW-PTP.	Acetylcysteine	120-123	acid phosphatase 1	Homo sapiens	251-258
22854047-7	2012	NAC and FeTPPS prevented the activation of FAK, its association with LMW-PTP and cell migration.	Acetylcysteine	0-3	acid phosphatase 1	Homo sapiens	69-76
22749861-10	2012	Furthermore, HSA increased ADMA generation by RPTECs in a dose- and time-dependent manner and induced gene expression of PRMT-1 but not DDAHs, which were also suppressed by NAC.	Acetylcysteine	173-176	protein arginine methyltransferase 1	Homo sapiens	121-127
23351387-7	2012	Significant difference in IL-17 level was observed between NAC/ibuprofen combination group and placebo (p = 0.043).	Acetylcysteine	59-62	interleukin 17A	Homo sapiens	26-31
22749809-8	2012	The antioxidant N-acetylcysteine decreased the acute alcohol-induced oxidative stress, the activation of JNK, and the steatosis but not the activation of CYP2E1.	Acetylcysteine	16-32	mitogen-activated protein kinase 8	Mus musculus	105-108
22161819-11	2012	Treatment of the cells with NAC restored the activity of PTP1B, improved the profile of PDGFR phosphorylation, decreased the numbers of tyrosine-phosphorylated proteins and levels of type I collagen, and scavenged ROS in SSc fibroblasts.	Acetylcysteine	28-31	protein tyrosine phosphatase non-receptor type 1	Homo sapiens	57-62
22161819-13	2012	The study also presents a novel molecular mechanism by which NAC may act on ROS and PTP1B to provide therapeutic benefit in SSc.	Acetylcysteine	61-64	protein tyrosine phosphatase non-receptor type 1	Homo sapiens	84-89
22537194-8	2012	We show that an increment of the intracellular reactive oxygen species (ROS) and p53 is required for MTA-induced cytotoxicity by utilizing N-Acetyl-L-Cysteine (NAC) to blockage of ROS and p53-defective H1299 NSCLC cell line.	Acetylcysteine	139-158	X-linked Kx blood group	Homo sapiens	160-163
22781576-10	2012	The average optical density value of Caspase 3 in spiral ganglion in NAC group significantly decreased versus the irradiation group (0.08 +- 0.02 vs 0.10 +- 0.01, P &lt; 0.01).	Acetylcysteine	69-72	caspase-3	Cavia porcellus	37-46
22052190-7	2012	PATZ1 knockdown increased ROS levels, and pretreatment with N-acetylcysteine abolished EC senescence induced by PATZ1 knockdown.	Acetylcysteine	60-76	POZ/BTB and AT hook containing zinc finger 1	Homo sapiens	112-117
21952821-9	2012	VEGF and ICAM-1 expressions were significantly up-regulated in retinal blood vessels from diabetic rats, and such up-regulation was attenuated by N-acetylcysteine treatment.	Acetylcysteine	146-162	intercellular adhesion molecule 1	Rattus norvegicus	9-15
21952821-11	2012	Long-term N-acetylcysteine treatment exerts protective effects on the diabetic retinas, possibly through its down-regulation of the expression of VEGF and ICAM-1, and reduction of reactive oxygen species content in retinal vascular tissues in diabetic rats.	Acetylcysteine	10-26	intercellular adhesion molecule 1	Rattus norvegicus	155-161
22392142-7	2012	On the other hand, N-acetyl-L-cysteine decreased mRNA stability of ICAM-1 and IL-6 in LPS-treated cells and IL-6 and ICAM-1 in TNF-alpha-treated cells.	Acetylcysteine	19-38	intercellular adhesion molecule 1	Homo sapiens	67-73
22392142-7	2012	On the other hand, N-acetyl-L-cysteine decreased mRNA stability of ICAM-1 and IL-6 in LPS-treated cells and IL-6 and ICAM-1 in TNF-alpha-treated cells.	Acetylcysteine	19-38	intercellular adhesion molecule 1	Homo sapiens	117-123
22187484-5	2012	To determine whether human liver microsomes metabolize furan to BDA, a liquid chromatography/tandem mass spectrometry method was developed to detect and quantify BDA by trapping this reactive metabolite with N-acetyl-l-cysteine (NAC) and N-acetyl-l-lysine (NAL).	Acetylcysteine	208-227	X-linked Kx blood group	Homo sapiens	229-232
22353666-3	2012	The aim of this study is to determine the cost effectiveness of using N-acetylcysteine over methionine in the management of acute paracetamol poisoning in Sri Lanka.	Acetylcysteine	70-86	sorcin	Homo sapiens	155-158
21660448-9	2012	Pretreatment with N-acetylcysteine (NAC) inhibited DMF-induced upregulation of DR5, CHOP, GPR78, and ATF4 protein expression and blocked the cotreatment-induced apoptosis.	Acetylcysteine	18-34	G protein-coupled receptor 78	Homo sapiens	90-95
21660448-9	2012	Pretreatment with N-acetylcysteine (NAC) inhibited DMF-induced upregulation of DR5, CHOP, GPR78, and ATF4 protein expression and blocked the cotreatment-induced apoptosis.	Acetylcysteine	18-34	activating transcription factor 4	Homo sapiens	101-105
21660448-9	2012	Pretreatment with N-acetylcysteine (NAC) inhibited DMF-induced upregulation of DR5, CHOP, GPR78, and ATF4 protein expression and blocked the cotreatment-induced apoptosis.	Acetylcysteine	36-39	G protein-coupled receptor 78	Homo sapiens	90-95
21660448-9	2012	Pretreatment with N-acetylcysteine (NAC) inhibited DMF-induced upregulation of DR5, CHOP, GPR78, and ATF4 protein expression and blocked the cotreatment-induced apoptosis.	Acetylcysteine	36-39	activating transcription factor 4	Homo sapiens	101-105
22739240-7	2012	The H(2)O(2)-induced gene repression or activation of SP-A, SP-B, SP-D and ABCA3 was blocked by pretreatment with the antioxidants N-acetyl-L-cysteine (NAC) and catalase.	Acetylcysteine	131-150	surfactant protein D	Homo sapiens	66-70
22044588-8	2012	Furthermore, the activation of Bnip3 and mitophagy due to p53/TIGAR inhibition were reversed with antioxidant N-acetyl-cysteine, indicating that this adaptive response requires ROS signal.	Acetylcysteine	110-127	Trp53 induced glycolysis regulatory phosphatase	Mus musculus	62-67
23006535-5	2012	Then, we focused our studies on NAC modulation of LOX activity.	Acetylcysteine	32-35	lysyl oxidase	Rattus norvegicus	50-53
23006535-7	2012	Interestingly, NAC treatment for 14 days from day 0 reversed LOX activity to normal levels and increased GSH levels in the lung of BLM-dosed rats.	Acetylcysteine	15-18	lysyl oxidase	Rattus norvegicus	61-64
23006535-9	2012	CONCLUSIONS: Our study supports a novel mechanism of NAC alleviating IPF by inhibition of LOX activity via elevation of lung GSH in BLM-induced pulmonary fibrosis.	Acetylcysteine	53-56	lysyl oxidase	Rattus norvegicus	90-93
21790669-7	2011	In ethanol-fed rats, NAC reduced inflammation, converted the steatosis from a predominantly microvesicular to a mainly macrovesicular histological pattern, reduced pro-inflammatory cytokine gene expression, ceramide load, and acid sphingomyelinase activity, and increased expression of IGF-1 receptor and IGF-2 in liver.	Acetylcysteine	21-24	insulin-like growth factor 2	Rattus norvegicus	305-310
21712088-5	2011	Furthermore, the enhanced phosphorylation of EGFR in VSMC from SHR was also restored to control levels by captopril, losartan, PP2, a c-Src inhibitor and N-acetyl-L-cysteine (NAC), superoxide anion (O(2)(-)) scavenger, whereas enhanced ERK1/2 phosphorylation was attenuated by captopril and losartan.	Acetylcysteine	154-173	epidermal growth factor receptor	Rattus norvegicus	45-49
21712088-5	2011	Furthermore, the enhanced phosphorylation of EGFR in VSMC from SHR was also restored to control levels by captopril, losartan, PP2, a c-Src inhibitor and N-acetyl-L-cysteine (NAC), superoxide anion (O(2)(-)) scavenger, whereas enhanced ERK1/2 phosphorylation was attenuated by captopril and losartan.	Acetylcysteine	175-178	epidermal growth factor receptor	Rattus norvegicus	45-49
21712088-6	2011	Furthermore, NAC also restored the enhanced phosphorylation of c-Src in SHR to control levels.	Acetylcysteine	13-16	SRC proto-oncogene, non-receptor tyrosine kinase	Rattus norvegicus	63-68
21683791-12	2011	An anti-oxidant, N-acetyl-L-cysteine blocked the TNF-alpha-induced activation of NF-kappaB, PKCtheta and expression of ICAM-1.	Acetylcysteine	17-36	intercellular adhesion molecule 1	Rattus norvegicus	119-125
21828049-8	2011	The addition of the antioxidant N-acetyl cysteine inhibited PKCdelta, and silencing of PKCdelta inhibited MAPK p38, which was also required.	Acetylcysteine	32-49	protein kinase C, delta	Mus musculus	60-68
21635874-0	2011	N-acetyl-L-cysteine (NAC) inhibit mucin synthesis and pro-inflammatory mediators in alveolar type II epithelial cells infected with influenza virus A and B and with respiratory syncytial virus (RSV).	Acetylcysteine	0-19	X-linked Kx blood group	Homo sapiens	21-24
20407854-5	2011	N-acetyl-L cysteine (NAC) blocked the pro-apoptotic effects of SOD1 knockdown, suggesting the antioxidant effects of SOD1 was essential for the resistance of CD34+ cells to imatinib therapy.	Acetylcysteine	0-19	X-linked Kx blood group	Homo sapiens	21-24
21854604-11	2011	Decrease in CREB mRNA levels in Abeta-treated neurons was reversed by the antioxidant, N-acetyl cysteine.	Acetylcysteine	87-104	amyloid beta precursor protein	Rattus norvegicus	32-37
21532338-8	2011	N-acetyl-cysteine (NAC; 10 mM) pre-treatment rescued cell viability of RKS262 (23 microM)-treated SMSKCNR cells, and pre-treatment with ascorbic acid (100 muM) and a MAPK inhibitor SB203580 (20 muM) reversed SAPK/JNK, caspase-3 activation, PARP-1 cleavage, and suppression of IGF-1R, PI3K, and PKC phosphorylation.	Acetylcysteine	0-17	insulin like growth factor 1 receptor	Homo sapiens	276-282
21532338-8	2011	N-acetyl-cysteine (NAC; 10 mM) pre-treatment rescued cell viability of RKS262 (23 microM)-treated SMSKCNR cells, and pre-treatment with ascorbic acid (100 muM) and a MAPK inhibitor SB203580 (20 muM) reversed SAPK/JNK, caspase-3 activation, PARP-1 cleavage, and suppression of IGF-1R, PI3K, and PKC phosphorylation.	Acetylcysteine	19-22	insulin like growth factor 1 receptor	Homo sapiens	276-282
21467033-4	2011	Pretreatment with N-acetyl-l-cysteine and catalase expression ameliorated cell death induced by the combination treatment, indicating a role of oxidative stress in mediating HRG/TGZ-induced cell death.	Acetylcysteine	18-37	histidine rich glycoprotein	Homo sapiens	174-177
21455648-10	2011	Subsequent sulfation occurred at C-3 on the unconjugated BAs that had been formed from the BA-NACs.	Acetylcysteine	94-98	complement C3	Rattus norvegicus	33-36
21349322-7	2011	Apoptosis but not cell cycle arrest was susceptible to N-acetyl-L-cysteine (NAC) treatment.	Acetylcysteine	55-74	X-linked Kx blood group	Homo sapiens	76-79
21401696-15	2011	Furthermore, NAC treatment increased eNOS protein expression, but decreased iNOS expression, in lung tissues after infection.	Acetylcysteine	13-16	nitric oxide synthase 3	Rattus norvegicus	37-41
21401696-19	2011	The results suggest that this effect maybe due to regulation of iNOS and eNOS protein expression by NAC.	Acetylcysteine	100-103	nitric oxide synthase 3	Rattus norvegicus	73-77
21303669-10	2011	NAC also up-regulated Bcl-2 and Xiap.	Acetylcysteine	0-3	X-linked inhibitor of apoptosis	Homo sapiens	32-36
21345685-6	2011	N-acetylcysteine (NAC) treatment abolished p38 phosphorylation as well as HO-1 induction caused by SC-1, indicating that ROS are upstream signals of p38 in Nrf2/ARE activation by SC-1.	Acetylcysteine	0-16	heme oxygenase 1	Rattus norvegicus	74-78
21345685-6	2011	N-acetylcysteine (NAC) treatment abolished p38 phosphorylation as well as HO-1 induction caused by SC-1, indicating that ROS are upstream signals of p38 in Nrf2/ARE activation by SC-1.	Acetylcysteine	18-21	heme oxygenase 1	Rattus norvegicus	74-78
21446024-0	2011	N-acetylcysteine prevents loss of dopaminergic neurons in the EAAC1-/- mouse.	Acetylcysteine	0-16	solute carrier family 1 (neuronal/epithelial high affinity glutamate transporter, system Xag), member 1	Mus musculus	62-67
21195169-6	2011	Further studies reveal that Cd induction of ROS increased phosphorylation of the type I insulin-like growth factor receptor (IGFR) beta subunit, which was abrogated by NAC.	Acetylcysteine	168-171	insulin like growth factor 1 receptor	Homo sapiens	125-129
21046465-8	2011	Pre-treatment with N-acetyl-L: -cysteine (NAC), an intracellular reactive oxygen species (ROS) scavenger, significantly decreased apoptosis in plasma-treated cells at 5 and 15 J/cm(2).	Acetylcysteine	19-40	X-linked Kx blood group	Homo sapiens	42-45
20383709-10	2011	Treatment of cells with N-acetyl L-cysteine and 17 beta-estradiol 2 reversed the effects of Ral and Tam.	Acetylcysteine	24-43	RAS like proto-oncogene A	Homo sapiens	92-95
20959139-6	2011	In addition, NAD(P)H oxidase inhibitor DPI and N-acetylcysteine (NAC), a scavenger of superoxide anion (O2-) also inhibited the enhanced phosphorylation of PDGFR and IGF-1R and c-Src in VSMC from SHR to control levels.	Acetylcysteine	47-63	SRC proto-oncogene, non-receptor tyrosine kinase	Rattus norvegicus	177-182
20959139-6	2011	In addition, NAD(P)H oxidase inhibitor DPI and N-acetylcysteine (NAC), a scavenger of superoxide anion (O2-) also inhibited the enhanced phosphorylation of PDGFR and IGF-1R and c-Src in VSMC from SHR to control levels.	Acetylcysteine	65-68	SRC proto-oncogene, non-receptor tyrosine kinase	Rattus norvegicus	177-182
21170508-5	2011	Pretreatment with N-acetyl-L-cysteine (NAC) significantly inhibited the cell death induced by the combined treatment with BBR and TRAIL as well as recovered the expression levels of c-FLIP and Mcl-1 downregulated by treatment with BBR.	Acetylcysteine	18-37	X-linked Kx blood group	Homo sapiens	39-42
21254278-0	2011	N-acetyl-L-cysteine counteracts oxidative stress and prevents H2O2 induced germ cell apoptosis through down-regulation of caspase-9 and JNK/c-Jun.	Acetylcysteine	0-19	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	140-145
21254278-2	2011	In the present study, we investigated the mechanisms by which N-acetyl-L-cysteine (NAC, which is highly cell specific with strong antioxidant and anti-genotoxic properties), stimulated cell survival under such conditions.	Acetylcysteine	62-81	X-linked Kx blood group	Homo sapiens	83-86
21069346-16	2011	Increased immunoreactivity of SOD2 and CAT was also observed in NAC + Cd(-) as compared to Cd(+) and NAC + Cd(+).	Acetylcysteine	101-104	superoxide dismutase 2, mitochondrial	Gallus gallus	30-34
20845026-10	2011	Additionally, NAC significantly reduced the immunostaining of endothelial NOS (e-NOS) and i-NOS in the lung tissue.	Acetylcysteine	14-17	nitric oxide synthase 3	Rattus norvegicus	62-77
20845026-10	2011	Additionally, NAC significantly reduced the immunostaining of endothelial NOS (e-NOS) and i-NOS in the lung tissue.	Acetylcysteine	14-17	nitric oxide synthase 3	Rattus norvegicus	79-84
21873804-0	2011	The antioxidant N-acetylcysteine promotes atherosclerotic plaque stabilization through suppression of RAGE, MMPs and NF-kappaB in ApoE-deficient mice.	Acetylcysteine	16-32	matrix metallopeptidase 2	Mus musculus	108-112
20953987-7	2011	In addition, N-acetyl-cysteine (NAC) was found to decrease Txnip protein expression under high glucose condition.	Acetylcysteine	13-30	thioredoxin interacting protein	Rattus norvegicus	59-64
20953987-7	2011	In addition, N-acetyl-cysteine (NAC) was found to decrease Txnip protein expression under high glucose condition.	Acetylcysteine	32-35	thioredoxin interacting protein	Rattus norvegicus	59-64
21912612-0	2011	N-acetylcysteine and allopurinol synergistically enhance cardiac adiponectin content and reduce myocardial reperfusion injury in diabetic rats.	Acetylcysteine	0-16	adiponectin, C1Q and collagen domain containing	Rattus norvegicus	65-76
21912612-7	2011	NAC but not ALP increased cardiac APN concentrations and AdipoR2 expression in diabetic rats.	Acetylcysteine	0-3	adiponectin, C1Q and collagen domain containing	Rattus norvegicus	34-37
21912612-12	2011	CONCLUSIONS/SIGNIFICANCE: NAC and ALP synergistically restore myocardial APN and AdipoR2 mediated eNOS activation.	Acetylcysteine	26-29	adiponectin, C1Q and collagen domain containing	Rattus norvegicus	73-76
21888768-10	2011	In contrast, the Dexa+NAC group demonstrated an increased expression of SYT VII compared to controls.	Acetylcysteine	22-25	synaptotagmin 7	Rattus norvegicus	72-79
20852045-8	2010	The phosphorylation of c-Src was significantly augmented in VSMC from SHR compared with VSMC from WKY and was attenuated by DPI and NAC.	Acetylcysteine	132-135	SRC proto-oncogene, non-receptor tyrosine kinase	Rattus norvegicus	23-28
20524045-7	2010	Treatment with the antioxidant N-acetyl-L-cysteine (NAC) blunted the increase in Zn(2+) levels and reduced LC3-II conversion, cathepsin D release and cell death induced by tamoxifen.	Acetylcysteine	31-50	X-linked Kx blood group	Homo sapiens	52-55
20408853-10	2010	CONCLUSIONS: A mouse model of incisional wound treated with NAC resulted in lower levels of tissue oxidative stress, higher levels of tissue glutathione, and downregulation of iNOS expression coupled with upregulation of VEGF expression, producing an overall favourable clinical outcome of higher WBS and a shorter wound-healing period both in diabetic and nondiabetic mice.	Acetylcysteine	60-63	vascular endothelial growth factor A	Mus musculus	221-225
21121367-6	2010	SWCNT induced nuclear NF-kB/P65 translocation can be inhibited by N-acetylcysteine, indicating elevated ICAM-1 and VCAM-1 expression is mediated by oxidative stress in RAECs, and may play important inflammatory roles in SWCNT-induced vascular endothelium damage.	Acetylcysteine	66-82	intercellular adhesion molecule 1	Rattus norvegicus	104-110
21084597-6	2010	Treatment of the EAAC1(-/-) mice with N-acetyl cysteine restored neuronal glutathione concentrations and normalized basal zinc levels in the EAAC1(-/-) mice.	Acetylcysteine	38-55	solute carrier family 1 (neuronal/epithelial high affinity glutamate transporter, system Xag), member 1	Mus musculus	17-22
21084597-6	2010	Treatment of the EAAC1(-/-) mice with N-acetyl cysteine restored neuronal glutathione concentrations and normalized basal zinc levels in the EAAC1(-/-) mice.	Acetylcysteine	38-55	solute carrier family 1 (neuronal/epithelial high affinity glutamate transporter, system Xag), member 1	Mus musculus	141-146
21084597-7	2010	Treatment of the EAAC1(-/-) mice with either N-acetyl cysteine or with zinc chelators reduced ischemia-induced zinc translocation, superoxide production, and neuron death.	Acetylcysteine	45-62	solute carrier family 1 (neuronal/epithelial high affinity glutamate transporter, system Xag), member 1	Mus musculus	17-22
20954712-10	2010	Furthermore, both antioxidant (N-acetyl cysteine and tempol) and the VEGF antibody treatments significantly lowered the arsenite-induced permeability of the bEnd3 monolayer as well as VEGF expression.	Acetylcysteine	31-48	BEN domain containing 3	Mus musculus	157-162
20954712-10	2010	Furthermore, both antioxidant (N-acetyl cysteine and tempol) and the VEGF antibody treatments significantly lowered the arsenite-induced permeability of the bEnd3 monolayer as well as VEGF expression.	Acetylcysteine	31-48	vascular endothelial growth factor A	Mus musculus	184-188
20958190-10	2010	Macrophage and neutrophil recruitment were inhibited and the levels of MCP-1, CXCL1, VEGF, and VEGFR-1 were also lower in NAC-treated mice compared to vehicle-treated mice.	Acetylcysteine	122-125	chemokine (C-C motif) ligand 2	Mus musculus	71-76
20958190-10	2010	Macrophage and neutrophil recruitment were inhibited and the levels of MCP-1, CXCL1, VEGF, and VEGFR-1 were also lower in NAC-treated mice compared to vehicle-treated mice.	Acetylcysteine	122-125	vascular endothelial growth factor A	Mus musculus	85-89
20958190-10	2010	Macrophage and neutrophil recruitment were inhibited and the levels of MCP-1, CXCL1, VEGF, and VEGFR-1 were also lower in NAC-treated mice compared to vehicle-treated mice.	Acetylcysteine	122-125	FMS-like tyrosine kinase 1	Mus musculus	95-102
20850416-8	2010	Moreover, Fyn kinase was activated by CoCl2 in WT cells and this activation was prevented by treatment with antioxidants such as Trolox and N-acetylcysteine.	Acetylcysteine	140-156	Fyn proto-oncogene	Mus musculus	10-13
20824644-0	2010	N-acetylcysteine counteracts oxidative stress and prevents hCG-induced apoptosis in rat Leydig cells through down regulation of caspase-8 and JNK.	Acetylcysteine	0-16	caspase 8	Rattus norvegicus	128-137
20808797-7	2010	NAC significantly decreased the levels of human SNCA in the brains of PDGFb-SNCA transgenic mice compared to alanine treated transgenics.	Acetylcysteine	0-3	platelet derived growth factor subunit B	Homo sapiens	70-75
20479336-7	2010	Antioxidants ebselen and N-acetylcysteine decreased the association of Axl with MHC-IIB in response to both Gas6 and reactive oxygen species.	Acetylcysteine	25-41	growth arrest specific 6	Rattus norvegicus	108-112
20421134-1	2010	Diorganotin(IV) complexes of N-acetyl-L-cysteine (H(2)NAC; (R)-2-acetamido-3-sulfanylpropanoic acid) have been synthesized and their solid and solution-phase structural configurations investigated by FTIR, Mossbauer, (1)H, (13)C and (119)Sn NMR spectroscopy.	Acetylcysteine	29-48	X-linked Kx blood group	Homo sapiens	54-57
20219070-5	2010	The cells were also pretreated with antioxidant agents N-acetyl-L-cysteine (NAC) or butylated hydroxyanisole (BHA).	Acetylcysteine	55-74	X-linked Kx blood group	Homo sapiens	76-79
20080177-7	2010	NAC treatment suppressed the contraction-mediated increase in 2-DG uptake; lactate production; hexokinase, PFK, and G6PDH activities; and gene expression of GLUT4, HKII, and PFK.	Acetylcysteine	0-3	hexokinase 2	Rattus norvegicus	164-168
20105176-6	2010	c-Jun N-terminal kinase-mediated p21(Waf1/Cip1) expression and caspase activation cascades were up-regulated by DET, effects suppressed by N-acetyl-L-cysteine.	Acetylcysteine	139-158	cyclin-dependent kinase inhibitor 1A (P21)	Mus musculus	33-36
20105176-6	2010	c-Jun N-terminal kinase-mediated p21(Waf1/Cip1) expression and caspase activation cascades were up-regulated by DET, effects suppressed by N-acetyl-L-cysteine.	Acetylcysteine	139-158	cyclin-dependent kinase inhibitor 1A (P21)	Mus musculus	37-41
20105176-6	2010	c-Jun N-terminal kinase-mediated p21(Waf1/Cip1) expression and caspase activation cascades were up-regulated by DET, effects suppressed by N-acetyl-L-cysteine.	Acetylcysteine	139-158	cyclin-dependent kinase inhibitor 1A (P21)	Mus musculus	42-46
19874809-8	2010	In addition, treatment with antioxidant N-acetyl-l-cysteine (NAC) and broad-spectrum caspase inhibitor z-VAD-fmk partially prevented apoptosis but did not abrogate GHSC-74-induced nuclear translocation of AIF.	Acetylcysteine	40-59	X-linked Kx blood group	Homo sapiens	61-64
20368026-0	2010	[N-acetyl-L-cysteine inhibits adenoviral E1A-involved transactivation of nuclear factor-kappaB in rat alveolar epithelial cells.].	Acetylcysteine	1-20	branched chain keto acid dehydrogenase E1 subunit alpha	Rattus norvegicus	41-44
20368026-2	2010	The aim of this study was to illustrate the roles of adenovirus E1A protein on the transactivation of NF-kappaB, AP-1 in response to inflammatory stimuli and the effect of N-Acetylcysteine (NAC) upon the transactivation of NF-kappaB and AP-1 in cells stably expressing E1A protein.	Acetylcysteine	190-193	branched chain keto acid dehydrogenase E1 subunit alpha	Rattus norvegicus	269-272
20368026-6	2010	The cell model of stably expressing adenoviral E1A was stimulated by LPS or TNF-alpha and treated with NAC, a precursor for cysteine.	Acetylcysteine	103-106	branched chain keto acid dehydrogenase E1 subunit alpha	Rattus norvegicus	47-50
20368026-14	2010	The densitometry of the NF-kappaB expression in E1A-positive clones were 3.2 +/- 0.1 and 3.3 +/- 0.1 respectively under LPS and TNF-alpha-stimulation and 1.98 +/- 0.2 and 1.9 +/- 0.2 respectively upon treatment for LPS and TNF-alpha with NAC pre-incubation.	Acetylcysteine	238-241	branched chain keto acid dehydrogenase E1 subunit alpha	Rattus norvegicus	48-51
20368026-15	2010	CONCLUSIONS: these results indicate that E1A protein upregulated NF-kappaB transcription activity induced by LPS and TNF-alpha in rat alveolar epithelial cells and this effect could be repressed by NAC.	Acetylcysteine	198-201	branched chain keto acid dehydrogenase E1 subunit alpha	Rattus norvegicus	41-44
22272000-4	2009	Although the expression level of tumor protein p53 (Tp53) mRNA decreased in the DEN+FF+NAC group as compared with that in the DEN+FF group, no significant differences between the DEN+FF and DEN+FF+NAC groups were observed in the number of hepatocellular altered foci and activities of hepatocellular proliferation.	Acetylcysteine	87-90	tumor protein p53	Rattus norvegicus	47-50
22272000-4	2009	Although the expression level of tumor protein p53 (Tp53) mRNA decreased in the DEN+FF+NAC group as compared with that in the DEN+FF group, no significant differences between the DEN+FF and DEN+FF+NAC groups were observed in the number of hepatocellular altered foci and activities of hepatocellular proliferation.	Acetylcysteine	87-90	tumor protein p53	Rattus norvegicus	52-56
19442767-10	2009	The monomer/NAC mixture that was pre-reacted for 24h nearly completely restored cell viability, proliferation and ALP activity to the level of an untreated control culture.	Acetylcysteine	12-15	PDZ and LIM domain 3	Rattus norvegicus	114-117
19523508-7	2009	Administration of the antioxidant N-acetylcysteine (NAC) for a period of 14 days (prior to and during AraC treatment), which was previously shown to ameliorate the AraC-induced motor deficits in these animals, largely prevented the reduction in NF-H isoform.	Acetylcysteine	34-50	neurofilament heavy chain	Rattus norvegicus	245-249
19523508-7	2009	Administration of the antioxidant N-acetylcysteine (NAC) for a period of 14 days (prior to and during AraC treatment), which was previously shown to ameliorate the AraC-induced motor deficits in these animals, largely prevented the reduction in NF-H isoform.	Acetylcysteine	52-55	neurofilament heavy chain	Rattus norvegicus	245-249
19328227-7	2009	The antioxidant N-acetylcysteine abolished As(3+)-induced Gclc expression and attenuated induction of Gclm.	Acetylcysteine	16-32	glutamate-cysteine ligase, catalytic subunit	Mus musculus	58-62
19326266-6	2009	Treatment of the ROS scavenger N-acetyl-cysteine (NAC) inhibited EGFR transactivation and ERK phosphorylation induced by hUII.	Acetylcysteine	31-48	epidermal growth factor receptor	Rattus norvegicus	65-69
19326266-6	2009	Treatment of the ROS scavenger N-acetyl-cysteine (NAC) inhibited EGFR transactivation and ERK phosphorylation induced by hUII.	Acetylcysteine	50-53	epidermal growth factor receptor	Rattus norvegicus	65-69
19326266-8	2009	In SHP-2 knockdown cells, UII-induced phosphorylation of EGFR was less influenced by NAC, and significantly suppressed by heparin binding (HB)-EGF neutralizing antibody.	Acetylcysteine	85-88	epidermal growth factor receptor	Rattus norvegicus	57-61
19350554-7	2009	In contrast, N-acetylcysteine, a potent cysteine reductive compound, significantly prevents up-regulation of HMOX1, GCLM, and CXCL2 genes, and repression of MMP9 and CCL22 genes induced by As(2)O(3).	Acetylcysteine	13-29	matrix metallopeptidase 9	Homo sapiens	157-161
19505374-12	2009	Treatment of rats with N-acetylcysteine decreased P-glycoprotein upregulation induced by diethyl maleate.	Acetylcysteine	23-39	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	50-64
19595187-8	2009	The effect of N-acetylcysteine (a free radical scavenger) on GM-CSF production post-exposure to 5-Fu was examined.	Acetylcysteine	14-30	colony stimulating factor 2 (granulocyte-macrophage)	Mus musculus	61-67
19595187-15	2009	N-acetylcysteine significantly decreased the concentration of GM-CSF in HFCL/EG cells treated with 5-FU.	Acetylcysteine	0-16	colony stimulating factor 2 (granulocyte-macrophage)	Mus musculus	62-68
18948301-7	2009	The PBDE-47 groups coincubated with NAC, however, considerably increased Xrcc1 while decreasing Xrcc3 mRNA expression (p &lt; 0.05).	Acetylcysteine	36-39	X-ray repair cross complementing 1	Homo sapiens	73-78
18948301-7	2009	The PBDE-47 groups coincubated with NAC, however, considerably increased Xrcc1 while decreasing Xrcc3 mRNA expression (p &lt; 0.05).	Acetylcysteine	36-39	X-ray repair cross complementing 3	Homo sapiens	96-101
19566031-9	2009	However, both NAC and ALA pathway includes inactivation of MMP-2.	Acetylcysteine	14-17	matrix metallopeptidase 2	Mus musculus	59-64
19067133-6	2008	NAC (N-acetyl-L: -cysteine), an antioxidant, blocked 3-BrPA-induced ROS production, loss of mitochondrial membrane potential and cell death.	Acetylcysteine	5-26	X-linked Kx blood group	Homo sapiens	0-3
19010165-0	2008	Effect of N-acetylcysteine administration on intraoperative plasma levels of interleukin-4 and interleukin-10 in liver transplant recipients.	Acetylcysteine	10-26	interleukin 10	Homo sapiens	95-109
19010165-1	2008	We investigated whether intraoperative administration of N-acetylcysteine (NAC) in liver transplant recipients ameliorated their inflammatory responses by increasing intraoperative plasma levels of interleukin (IL)-4 and IL-10.	Acetylcysteine	57-73	interleukin 10	Homo sapiens	221-226
19010165-1	2008	We investigated whether intraoperative administration of N-acetylcysteine (NAC) in liver transplant recipients ameliorated their inflammatory responses by increasing intraoperative plasma levels of interleukin (IL)-4 and IL-10.	Acetylcysteine	75-78	interleukin 10	Homo sapiens	221-226
19010165-7	2008	Plasma IL-10 levels showed significant enhancement in the NAC-treated group at 5 minutes before reperfusion (I-3; P = .007).	Acetylcysteine	58-61	interleukin 10	Homo sapiens	7-12
18469310-7	2008	Renal cortices and BUO rats presented decreased eNOS protein expression of eNOS in the renal cortex of BUO group rats, whereas it was partially recovered in BUO + NAC-pre group rats.	Acetylcysteine	163-166	nitric oxide synthase 3	Rattus norvegicus	48-52
18469310-7	2008	Renal cortices and BUO rats presented decreased eNOS protein expression of eNOS in the renal cortex of BUO group rats, whereas it was partially recovered in BUO + NAC-pre group rats.	Acetylcysteine	163-166	nitric oxide synthase 3	Rattus norvegicus	75-79
18679109-8	2008	Additionally, the smoke extract-induced heme oxygenase-1 induction was significantly attenuated by mitogen-activated protein kinases inhibitors, by small interfering RNA targeting mitogen-activated protein kinases or by N-acetylcysteine.	Acetylcysteine	220-236	heme oxygenase 1	Rattus norvegicus	40-56
18657320-6	2008	The NAC-induced DNA-binding activity of NF-kappaB and phosphorylation of p65 were sensitive to a phosphatidylinositol (PI) 3-kinase inhibitor, partially sensitive to an IkappaB kinase (IKK) inhibitor, but not sensitive to a Bruton"s tyrosine kinase (Btk) inhibitor.	Acetylcysteine	4-7	Bruton tyrosine kinase	Homo sapiens	250-253
18486599-3	2008	Unexpectedly LPS in the presence of ROS inhibitor N-acetyl-L-cysteine rapidly induced phosphorylation of eIF2alpha and induction of GADD34 expression.	Acetylcysteine	50-69	protein phosphatase 1, regulatory subunit 15A	Mus musculus	132-138
18441204-8	2008	The HNP-induced COX-2 and ET-1 production was attenuated by the treatment with the oxygen free radical scavenger N-acetyl-L-cysteine and the inhibitors of p38 MAPK and NF-kappaB, respectively.	Acetylcysteine	113-132	kallikrein related peptidase 8	Homo sapiens	4-7
18266932-6	2008	The glutathione (GSH) precursor, N-acetyl cysteine, induced HIF-1alpha protein expression in hypoxic neurons while the GSH synthesis inhibitor, l-buthionine sulfoximine, inhibited the expression.	Acetylcysteine	33-50	hypoxia inducible factor 1 subunit alpha	Rattus norvegicus	60-70
18477646-5	2008	We prepared standard mercapturic acids by reactions of syn- or anti-Phe-1,2-diol-3,4-epoxide and syn- or anti-Phe-3,4-diol-1,2-epoxide with N-acetylcysteine.	Acetylcysteine	21-38	synemin	Homo sapiens	55-58
18477646-5	2008	We prepared standard mercapturic acids by reactions of syn- or anti-Phe-1,2-diol-3,4-epoxide and syn- or anti-Phe-3,4-diol-1,2-epoxide with N-acetylcysteine.	Acetylcysteine	21-38	synemin	Homo sapiens	97-100
18073202-8	2008	The accumulation of IRP2 protein was independent of zinc deficiency-induced intracellular nitric oxide production but was attenuated by the addition of the antioxidant N-acetylcysteine or ascorbate to the D medium.	Acetylcysteine	168-184	iron responsive element binding protein 2	Mus musculus	20-24
17647273-5	2008	The activating effect of anisomycin on c-fos transcription could be abrogated by a prior treatment with N-acetyl-L-cysteine.	Acetylcysteine	104-123	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	39-44
18078828-6	2008	An antioxidant N-acetyl-cysteine inhibited both the reduction of phosphorylated dUTPase and the induction of apoptosis by beta-HIVS treatment of DMS114 cells.	Acetylcysteine	15-32	Deoxyuridine triphosphatase	Drosophila melanogaster	80-87
17651528-6	2008	NAC, SEC or SPC treatment also significantly suppressed high saturated fat-induced hepatic mRNA expression of sterol regulatory element-binding protein (SREBP)-1c and SREBP-2 (P &lt; 0.05).	Acetylcysteine	0-3	sterol regulatory element binding factor 2	Mus musculus	167-174
18523380-8	2008	PD98059, a specific inhibitor of extracellular signal-regulated kinase (ERK), and N-acetylcysteine (NAC), an antioxidant, partially abrogated the stretch-induced ICAM-1 protein upregulation at the 3-hour loading.	Acetylcysteine	82-98	intercellular adhesion molecule 1	Homo sapiens	162-168
18523380-8	2008	PD98059, a specific inhibitor of extracellular signal-regulated kinase (ERK), and N-acetylcysteine (NAC), an antioxidant, partially abrogated the stretch-induced ICAM-1 protein upregulation at the 3-hour loading.	Acetylcysteine	100-103	intercellular adhesion molecule 1	Homo sapiens	162-168
20020852-3	2008	The GSH synthesis inhibitor L-Buthionine (S, R)-sulfoximine (BSO) significantly potentiated toxicity of clivorine, while GSH and GSH synthesis precursors N-Acetyl-L-cysteine (NAC) and S-adenosyl-L-methionine (SAM) protected cells against toxicity of clivorine.	Acetylcysteine	154-173	X-linked Kx blood group	Homo sapiens	175-178
17947235-12	2007	Moreover AVD, K+ conductances, and caspase-3 were strongly impaired by ROS scavenger N-acetylcysteine.	Acetylcysteine	85-101	caspase 3	Mus musculus	35-44
17714694-7	2007	Data on membrane localization, Mg2+ dependence, sensitivity to thiol oxidizing agents and protection by N-acetylcysteine (NAC) and DTT strongly suggest the involvement of PTP1B, the major PTP of human RBC associated to and acting on Band 3.	Acetylcysteine	104-120	protein tyrosine phosphatase non-receptor type 1	Homo sapiens	171-176
17714694-7	2007	Data on membrane localization, Mg2+ dependence, sensitivity to thiol oxidizing agents and protection by N-acetylcysteine (NAC) and DTT strongly suggest the involvement of PTP1B, the major PTP of human RBC associated to and acting on Band 3.	Acetylcysteine	122-125	protein tyrosine phosphatase non-receptor type 1	Homo sapiens	171-176
17519395-7	2007	Softness (sigma) was closely correlated to corresponding second-order rate constants (k(2)) for electrophile reactions with sulfhydryl groups on N-acetyl-L-cysteine (NAC).	Acetylcysteine	145-164	X-linked Kx blood group	Homo sapiens	166-169
17462539-5	2007	NAC is shown to decrease glioma cell proliferation, inducing a cell cycle arrest in the G(0)/G(1) phase and markedly up-regulating p21 expression.	Acetylcysteine	0-3	KRAS proto-oncogene, GTPase	Rattus norvegicus	131-134
17448897-8	2007	We observed that BzATP stimulates MAP kinase (ERK1/ERK2, p38, and JNK1/JNK2) phosphorylation and that the antioxidants N-acetylcysteine and ascorbic acid strongly attenuate BzATP-mediated JNK1/JNK2 and p38 phosphorylation but only slightly reduce BzATP-induced ERK1/ERK2 phosphorylation.	Acetylcysteine	119-135	mitogen-activated protein kinase 8	Mus musculus	188-192
17122189-8	2007	Subsequently, the levels of cardiac free 15-F(2t)-isoprostane, HO-1, Cu-Zn-SOD, total SOD, IL-6, and COX-2 in diabetic rats were decreased by NAC.	Acetylcysteine	142-145	heme oxygenase 1	Rattus norvegicus	63-67
17242209-5	2007	Treatment with the antioxidant N-acetylcysteine prevented colitis and colitis-associated tumorigenesis more efficiently in WT mice than in Trp53inp1-deficient mice, suggesting a higher oxidative load in the latter.	Acetylcysteine	31-47	transformation related protein 53 inducible nuclear protein 1	Mus musculus	139-148
17334226-8	2007	Inhibition of Tat-induced ROS generation by N-acetyl cysteine, vitamin C and diphenyl iodonium suppressed Tat-induced NF-kappaB activation, ICAM-1 and VCAM-1 expression, and monocyte adhesion in CRT-MG.	Acetylcysteine	44-61	intercellular adhesion molecule 1	Homo sapiens	140-146
17189831-6	2007	Incubation with the thiol antioxidant N-acetylcysteine strongly inhibited both the Nrf2 accumulation and the expression of Nrf2-regulated genes such as HO-1, GCLM, and SQSTM1.	Acetylcysteine	38-54	sequestosome 1	Homo sapiens	168-174
17051330-3	2006	PTL-mediated apoptosis correlated well with ROS generation and was almost completely inhibited by L-N-acetylcysteine (L-NAC), indicating the crucial role of oxidative stress in the mechanism.	Acetylcysteine	98-116	X-linked Kx blood group	Homo sapiens	120-123
16916625-0	2006	Developmental cell death in the liver and newborn lethality of Ku86 deficient mice suppressed by antioxidant N-acetyl-cysteine.	Acetylcysteine	109-126	X-ray repair complementing defective repair in Chinese hamster cells 5	Mus musculus	63-67
16923159-10	2006	The ROS scavenger N-acetylcysteine prevented ROS generation and attenuated the changes of both expression and activity of Pgp induced by BSO.	Acetylcysteine	18-34	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	122-125
16473382-8	2006	NAC, but not DTT, also decreased the phosphorylation of p38 and JNK supporting a role for oxidative processes in activating these kinases.	Acetylcysteine	0-3	mitogen-activated protein kinase 8	Mus musculus	64-67
16473382-10	2006	The release of cytochrome c and activation of caspase-3 induced by NDGA were inhibited by NAC.	Acetylcysteine	90-93	caspase 3	Mus musculus	46-55
16781197-3	2006	We examined the effect of long-term dietary supplementation with the thiol-containing antioxidant, N-acetyl-L-cysteine (NAC), on survival and cancer formation in Atm (AT-mutated) deficient mice, used as an animal model of AT.	Acetylcysteine	99-118	X-linked Kx blood group	Homo sapiens	120-123
16781197-6	2006	In addition, NAC suppresses carcinogenesis-associated biological markers in Atm deficient mice, such as DNA deletions and oxidative DNA damage (R. Reliene, E. Fischer, R.H. Schiestl, Effect of N-acetyl cysteine on oxidative DNA damage and the frequency of DNA deletions in atm-deficient mice, Cancer Res.	Acetylcysteine	193-210	X-linked Kx blood group	Homo sapiens	13-16
16728380-8	2006	NAC inhibited cadmium-induced activation of mitogen-activated protein kinases, the c-Jun NH2-terminal protein kinase (JNK) and extracellular signal-regulated kinase (ERK).	Acetylcysteine	0-3	mitogen-activated protein kinase 8	Mus musculus	83-116
16728380-8	2006	NAC inhibited cadmium-induced activation of mitogen-activated protein kinases, the c-Jun NH2-terminal protein kinase (JNK) and extracellular signal-regulated kinase (ERK).	Acetylcysteine	0-3	mitogen-activated protein kinase 8	Mus musculus	118-121
16261333-4	2006	Both NAD(P)H oxidase inhibitor, diphenyliodonium (DPI) and ROS scavenger N-acetylcysteine (NAC), inhibited EGFR transactivation and extracellular signal-regulated kinase (ERK) phosphorylation caused by ET-1.	Acetylcysteine	73-89	epidermal growth factor receptor	Rattus norvegicus	107-111
16261333-4	2006	Both NAD(P)H oxidase inhibitor, diphenyliodonium (DPI) and ROS scavenger N-acetylcysteine (NAC), inhibited EGFR transactivation and extracellular signal-regulated kinase (ERK) phosphorylation caused by ET-1.	Acetylcysteine	91-94	epidermal growth factor receptor	Rattus norvegicus	107-111
16497268-7	2006	Antioxidants such as trolox and N-acetylcysteine increased GRP78 and GRP94 levels in the E47 cells, suggesting that CYP2E1- derived oxidant stress was responsible for down regulation of these GRPs in the E47 cells.	Acetylcysteine	32-48	heat shock protein 90 beta family member 1	Homo sapiens	69-74
16487264-13	2006	In addition, 25 mmol/L glucose increased cellular reactive oxygen species and the glucose-induced inhibition of 2-DG uptake were blocked by the anti-oxidants N-acetylcysteine (NAC; 10(-5) mol/L) or taurine (2 yen 10(-3) mol/L).	Acetylcysteine	158-174	NLR family, pyrin domain containing 1A	Mus musculus	176-179
16547393-4	2006	On the other hand, when N-acetyl-L-cysteine (NAC) with the removal ability of a mucin layer was combined with the ibuprofen entrapped O/W microemulsion at the concentration of 3 and 10 mmol/L, it was shown that the permeation clearance of free ibuprofen did not decrease, but that of ibuprofen entrapped in the O/W microemulsion decreased with the increase of the NAC concentration.	Acetylcysteine	24-43	solute carrier family 13 member 2	Rattus norvegicus	80-85
16547393-4	2006	On the other hand, when N-acetyl-L-cysteine (NAC) with the removal ability of a mucin layer was combined with the ibuprofen entrapped O/W microemulsion at the concentration of 3 and 10 mmol/L, it was shown that the permeation clearance of free ibuprofen did not decrease, but that of ibuprofen entrapped in the O/W microemulsion decreased with the increase of the NAC concentration.	Acetylcysteine	45-48	solute carrier family 13 member 2	Rattus norvegicus	80-85
16449798-6	2006	This mechanism is supported by the ability of N-acetyl cysteine (NAC) to prevent dissociation of Trx-ASK1 and activation of the p38 MAPK pathway.	Acetylcysteine	46-63	thioredoxin 1	Mus musculus	97-100
16449798-6	2006	This mechanism is supported by the ability of N-acetyl cysteine (NAC) to prevent dissociation of Trx-ASK1 and activation of the p38 MAPK pathway.	Acetylcysteine	65-68	thioredoxin 1	Mus musculus	97-100
16263740-11	2006	Blocking of ROS by using N-acetyl-l-cysteine abolished CML and H(2)O(2)-induced MCP-1 expression.	Acetylcysteine	25-44	chemokine (C-C motif) ligand 2	Mus musculus	80-85
16174550-9	2006	Administration of antioxidant N-acetylcysteine (NAC) can obviously affected the level of MLK3, JNK3 and Akt1 binding to JIP-1 and JNK3 activation in the hippocampus at 15min ischemia.	Acetylcysteine	30-46	mitogen activated protein kinase 10	Rattus norvegicus	95-99
16174550-9	2006	Administration of antioxidant N-acetylcysteine (NAC) can obviously affected the level of MLK3, JNK3 and Akt1 binding to JIP-1 and JNK3 activation in the hippocampus at 15min ischemia.	Acetylcysteine	30-46	mitogen-activated protein kinase 8 interacting protein 1	Rattus norvegicus	120-125
16174550-9	2006	Administration of antioxidant N-acetylcysteine (NAC) can obviously affected the level of MLK3, JNK3 and Akt1 binding to JIP-1 and JNK3 activation in the hippocampus at 15min ischemia.	Acetylcysteine	30-46	mitogen activated protein kinase 10	Rattus norvegicus	130-134
16174550-9	2006	Administration of antioxidant N-acetylcysteine (NAC) can obviously affected the level of MLK3, JNK3 and Akt1 binding to JIP-1 and JNK3 activation in the hippocampus at 15min ischemia.	Acetylcysteine	48-51	mitogen activated protein kinase 10	Rattus norvegicus	95-99
16174550-9	2006	Administration of antioxidant N-acetylcysteine (NAC) can obviously affected the level of MLK3, JNK3 and Akt1 binding to JIP-1 and JNK3 activation in the hippocampus at 15min ischemia.	Acetylcysteine	48-51	mitogen-activated protein kinase 8 interacting protein 1	Rattus norvegicus	120-125
16174550-9	2006	Administration of antioxidant N-acetylcysteine (NAC) can obviously affected the level of MLK3, JNK3 and Akt1 binding to JIP-1 and JNK3 activation in the hippocampus at 15min ischemia.	Acetylcysteine	48-51	mitogen activated protein kinase 10	Rattus norvegicus	130-134
16298762-0	2006	alpha-Lipoic acid and N-acetyl cysteine prevent zinc deficiency-induced activation of NF-kappaB and AP-1 transcription factors in human neuroblastoma IMR-32 cells.	Acetylcysteine	22-39	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	100-104
16328008-8	2006	These data clearly indicate that increased cell proliferation was associated with the induction of cyclin D1 expression which was regulated by ERK in 4-HNE-treated young SMCs for 36 h. In contrast, we found that the cytotoxicity of aged SMCs to 4-HNE was partly related to generation of ROS and that pretreatment with N-acetyl-L-cysteine prevented 4-HNE-induced cell death in aged SMCs.	Acetylcysteine	318-337	cyclin D1	Mus musculus	99-108
16311588-6	2006	These changes were reversed by treating the EAAC1(-/-) mice with N-acetylcysteine, a membrane-permeable cysteine precursor.	Acetylcysteine	65-81	solute carrier family 1 (neuronal/epithelial high affinity glutamate transporter, system Xag), member 1	Mus musculus	44-49
16086031-7	2005	Reactive oxygen species (ROS) were also detected within 1 h after AF treatment, and the antioxidant N-acetyl-L-cysteine (NAC) effectively protected the cells from apoptosis by inhibiting the phosphorylation of p38 MAPK and the activation of caspases.	Acetylcysteine	100-119	X-linked Kx blood group	Homo sapiens	121-124
16382175-5	2005	In H9C2 cells, NAC pretreatment blocked cocaine-mediated increases in CRP, FAS, FAS ligand, and cytokine receptor-like factor1 (CRLF1) expression.	Acetylcysteine	15-18	cytokine receptor-like factor 1	Rattus norvegicus	96-126
16382175-5	2005	In H9C2 cells, NAC pretreatment blocked cocaine-mediated increases in CRP, FAS, FAS ligand, and cytokine receptor-like factor1 (CRLF1) expression.	Acetylcysteine	15-18	cytokine receptor-like factor 1	Rattus norvegicus	128-133
16148150-7	2005	The thiol antioxidant N-acetyl cysteine, extracellular catalase, and inducible NO synthase inhibitors inhibited ICAM-1 and IL-8 increases in response to both phenazines.	Acetylcysteine	22-39	intercellular adhesion molecule 1	Homo sapiens	112-118
15989974-6	2005	c-Jun was also induced by the ITCs in other bladder cancer cell lines (both human and rat) and by their N-acetylcysteine derivatives--their main urinary metabolites.	Acetylcysteine	104-120	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	0-5
16117612-7	2005	One potential concern is that SF is highly reactive and has a very short half-life in the body, forming a glutathione conjugate that is further metabolized to the N-acetyl-L-cysteine conjugate (SF-NAC), the major excretory product found in the urine.	Acetylcysteine	163-182	NLR family, pyrin domain containing 1A	Mus musculus	197-200
15788408-11	2005	In addition, the ability of a thiol antioxidant, N-acetylcysteine, to inhibit the effect of arsenite on VEGF expression coincided with its ability to inhibit phosphorylation of eIF2alpha and ATF4 protein expression.	Acetylcysteine	49-65	eukaryotic translation initiation factor 2A	Homo sapiens	177-186
15788408-11	2005	In addition, the ability of a thiol antioxidant, N-acetylcysteine, to inhibit the effect of arsenite on VEGF expression coincided with its ability to inhibit phosphorylation of eIF2alpha and ATF4 protein expression.	Acetylcysteine	49-65	activating transcription factor 4	Homo sapiens	191-195
15705601-7	2005	Interestingly, inhibitor of JNK signaling pathway as well as antioxidant N-acetyl-L-cysteine (NAC) blocked EGCG-induced apoptosis.	Acetylcysteine	73-92	X-linked Kx blood group	Homo sapiens	94-97
15728246-3	2005	Induction of IFI16 by H2O2 was concentration- and time-dependent (maximum at 50 microM, 6 h after treatment) and down-regulated by pretreatment with N-acetyl-L-cysteine, which acts as an antioxidant.	Acetylcysteine	149-168	interferon gamma inducible protein 16	Homo sapiens	13-18
15721278-8	2005	The binding of nucleolin to gadd45alpha mRNA could be prevented by the antioxidant, N-acetyl-cysteine.	Acetylcysteine	84-101	nucleolin	Mus musculus	15-24
15816852-9	2005	To further elucidate the possible mechanism of MKK7 activation and translocation, the antioxidant N-acetylcysteine was injected into the rats 20 min before ischemia.	Acetylcysteine	98-114	mitogen activated protein kinase kinase 7	Rattus norvegicus	47-51
15816852-10	2005	The result showed that the levels of MKK7 activation, translocation and binding of p-MKK7 to JIP-1 were obviously limited by N-acetylcysteine in the cytosol at 30 min after reperfusion.	Acetylcysteine	125-141	mitogen activated protein kinase kinase 7	Rattus norvegicus	37-41
15816852-10	2005	The result showed that the levels of MKK7 activation, translocation and binding of p-MKK7 to JIP-1 were obviously limited by N-acetylcysteine in the cytosol at 30 min after reperfusion.	Acetylcysteine	125-141	mitogen activated protein kinase kinase 7	Rattus norvegicus	85-89
15816852-10	2005	The result showed that the levels of MKK7 activation, translocation and binding of p-MKK7 to JIP-1 were obviously limited by N-acetylcysteine in the cytosol at 30 min after reperfusion.	Acetylcysteine	125-141	mitogen-activated protein kinase 8 interacting protein 1	Rattus norvegicus	93-98
15788229-4	2005	Furthermore, N-acetyl-L-cysteine and L-cysteine lowered TPA-induced MMP-9 secretion, suggesting an involvement of reactive oxygen species(ROS).	Acetylcysteine	13-32	matrix metallopeptidase 9	Homo sapiens	68-73
15823179-9	2005	CC16 production by Clara cells in the OVA groups was significantly lower than that of the control group (P &lt; 0.01), but was elevated following NAC treatment (P &lt; 0.05).	Acetylcysteine	146-149	secretoglobin, family 1A, member 1 (uteroglobin)	Mus musculus	0-4
15823179-10	2005	The CC16 level in BALF of the OVA group was lower than that of the control group (P &lt; 0.01), but was elevated by NAC treatment (P &lt; 0.05).	Acetylcysteine	116-119	secretoglobin, family 1A, member 1 (uteroglobin)	Mus musculus	4-8
15654955-6	2005	We found that pre-treatment of skin with N-acetyl cysteine or genistein for 24 h prior to heat treatment inhibited the heat-induced expression of tropoelastin, but not of fibrillin-1.	Acetylcysteine	41-58	elastin	Homo sapiens	146-158
15573404-0	2005	Downregulation of complexin I and complexin II in the medial thalamus is blocked by N-acetylcysteine in experimental Wernicke"s encephalopathy.	Acetylcysteine	84-100	complexin 1	Rattus norvegicus	18-29
15632668-6	2005	Relative to nonexercised mice, protein levels of caspase 3 (P &lt; 0.001) and cytosolic cytochrome c (P &lt; 0.005) were significantly elevated, whereas Bcl-2 (P &lt; 0.05) was significantly lower immediately after exercise in mice receiving saline (EX + SAL + Imm) but not in animals receiving NAC (EX + NAC + Imm) or both 24 h postgroups (EX + SAL + 24 h and EX + NAC + 24 h).	Acetylcysteine	295-298	caspase 3	Mus musculus	49-58
15632668-6	2005	Relative to nonexercised mice, protein levels of caspase 3 (P &lt; 0.001) and cytosolic cytochrome c (P &lt; 0.005) were significantly elevated, whereas Bcl-2 (P &lt; 0.05) was significantly lower immediately after exercise in mice receiving saline (EX + SAL + Imm) but not in animals receiving NAC (EX + NAC + Imm) or both 24 h postgroups (EX + SAL + 24 h and EX + NAC + 24 h).	Acetylcysteine	305-308	caspase 3	Mus musculus	49-58
15632668-6	2005	Relative to nonexercised mice, protein levels of caspase 3 (P &lt; 0.001) and cytosolic cytochrome c (P &lt; 0.005) were significantly elevated, whereas Bcl-2 (P &lt; 0.05) was significantly lower immediately after exercise in mice receiving saline (EX + SAL + Imm) but not in animals receiving NAC (EX + NAC + Imm) or both 24 h postgroups (EX + SAL + 24 h and EX + NAC + 24 h).	Acetylcysteine	305-308	caspase 3	Mus musculus	49-58
15541757-9	2004	Furthermore, these effects of DEP on either HO-1 or TGM-2 were reduced by N-acetyl-l-cysteine (NAC), thus suggesting that oxidative stress caused by this organic fraction of DEP may have induced these cellular responses.	Acetylcysteine	95-98	heme oxygenase 1	Rattus norvegicus	44-48
15375156-3	2004	N-Acetyl-l-cysteine (NAC) but not other antioxidants, such as the vitamin E analog trolox and epigallocatechin-3-gallate, enhanced hypoxia-induced caspase-3 activation and apoptosis.	Acetylcysteine	0-19	X-linked Kx blood group	Homo sapiens	21-24
15375156-3	2004	N-Acetyl-l-cysteine (NAC) but not other antioxidants, such as the vitamin E analog trolox and epigallocatechin-3-gallate, enhanced hypoxia-induced caspase-3 activation and apoptosis.	Acetylcysteine	0-19	caspase 3	Mus musculus	147-156
15292218-8	2004	The suppression of the level of TRAP1 by either beta-HIVS or VP16 was blocked by N-acetyl-cysteine, indicating the involvement of reactive oxygen species (ROS) in the regulation of the expression of TRAP1.	Acetylcysteine	81-98	TNF receptor associated protein 1	Homo sapiens	32-37
15292218-8	2004	The suppression of the level of TRAP1 by either beta-HIVS or VP16 was blocked by N-acetyl-cysteine, indicating the involvement of reactive oxygen species (ROS) in the regulation of the expression of TRAP1.	Acetylcysteine	81-98	host cell factor C1	Homo sapiens	61-65
15292218-8	2004	The suppression of the level of TRAP1 by either beta-HIVS or VP16 was blocked by N-acetyl-cysteine, indicating the involvement of reactive oxygen species (ROS) in the regulation of the expression of TRAP1.	Acetylcysteine	81-98	TNF receptor associated protein 1	Homo sapiens	199-204
15289320-10	2004	The antioxidant N-acetylcysteine significantly reversed the inhibition by 15d-PGJ(2) of AP-1 activity and COX-2 or VEGF transcriptional induction.	Acetylcysteine	16-32	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	88-92
15114627-7	2004	After intrastriatal injection, both cysteine and N-acetylcysteine had clear neuroprotective effects on the striatal dopaminergic terminals, but also led to neuronal degeneration (as revealed by fluoro-jade staining) and astroglial and microglial activation, as well as intense induction of heme-oxygenase-1 in astrocytes and microglial cells.	Acetylcysteine	49-65	heme oxygenase 1	Rattus norvegicus	290-306
15001526-7	2004	Activation of these kinases was inhibited by the antioxidant N-acetyl-L-cysteine (NAC) and by the PKCbeta inhibitor LY379196.	Acetylcysteine	61-80	X-linked Kx blood group	Homo sapiens	82-85
15019093-4	2004	In these experiments, a pre-treatment of the cells with antioxidants N-acetyl-l-cysteine (NAC) and dimethylthiourea (DMTU) or an iNOS inhibitor l-N6-1-iminoethyl-lysine (L-NIL) clearly inhibited the NFkappaB activation by PM2.5.	Acetylcysteine	69-88	X-linked Kx blood group	Homo sapiens	90-93
14734137-8	2004	N-acetylcysteine (NAC) was able to decrease IL-17-induced 8-isoprostane production, with a maximum decrease of 59.3 +/- 9% (p &lt; 0.001, n = 12) with 10 mmol/liter of N-acetylcysteine, which also decreased IL-17-induced IL-8 production in a concentration-dependent manner (with maximum inhibition of 86.3% when combined with NAC 10 mmol/liter as compared with IL-17 alone).	Acetylcysteine	168-184	interleukin 17A	Homo sapiens	44-49
14734137-8	2004	N-acetylcysteine (NAC) was able to decrease IL-17-induced 8-isoprostane production, with a maximum decrease of 59.3 +/- 9% (p &lt; 0.001, n = 12) with 10 mmol/liter of N-acetylcysteine, which also decreased IL-17-induced IL-8 production in a concentration-dependent manner (with maximum inhibition of 86.3% when combined with NAC 10 mmol/liter as compared with IL-17 alone).	Acetylcysteine	326-329	interleukin 17A	Homo sapiens	44-49
15123225-1	2004	N-acetylcysteine (NAC) has antioxidant properties and its oral administration decreased H(2)O(2) exhalation in patients with chronic obstructive pulmonary disease.	Acetylcysteine	0-16	X-linked Kx blood group	Homo sapiens	18-21
12839837-11	2003	MHb treatment activated cellular NF-kappaB and NF-kappaB inhibitors; N-acetyl cysteine, SN50, and caffeic acid phenylethyl ester inhibited the MHb-induced responses.	Acetylcysteine	69-86	hemoglobin subunit gamma 2	Homo sapiens	143-146
14612525-9	2003	The antioxidant N-acetylcysteine partially reversed the increase in P-gp mRNA and protein levels induced by DG, as well as the enhancement of c-Jun phosphorylation and activator protein binding activity.	Acetylcysteine	16-32	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	68-72
14605526-14	2003	CONCLUSIONS: Administration of N-acetylcysteine results in decreased nuclear factor-kappa B activation in patients with sepsis, associated with decreases in interleukin-8 but not interleukin-6 or soluble intercellular adhesion molecule-1.	Acetylcysteine	31-47	intercellular adhesion molecule 1	Homo sapiens	204-237
14636438-0	2003	[Effects of N-acetylcysteine on serum IL-18 level in severe hepatitis patients].	Acetylcysteine	12-28	interleukin 18	Homo sapiens	38-43
12821181-2	2003	Here we evaluated the effects of NMDA receptor antagonist (ketamine) and antioxidant (N-acetylcysteine) on ischemia- and reperfusion-induced activation of tyrosine kinase c-Src.	Acetylcysteine	86-102	SRC proto-oncogene, non-receptor tyrosine kinase	Rattus norvegicus	171-176
12818576-5	2003	N-acetylcysteine (NAC, 10 mM) and probucol (50 microM), and to a lesser extent, vitamin C (500 microM) and reduced glutathione (1 mM), inhibited AngII-induced [(3)H]-leucine uptake and atrial natriuretic factor (ANF) promoter activity.	Acetylcysteine	0-16	natriuretic peptide A	Rattus norvegicus	185-210
12818576-5	2003	N-acetylcysteine (NAC, 10 mM) and probucol (50 microM), and to a lesser extent, vitamin C (500 microM) and reduced glutathione (1 mM), inhibited AngII-induced [(3)H]-leucine uptake and atrial natriuretic factor (ANF) promoter activity.	Acetylcysteine	0-16	natriuretic peptide A	Rattus norvegicus	212-215
12818576-8	2003	Furthermore, NAC blocked AngII-induced increase in myocardial oxidative stress, decreased the expression of ANF and myosin light chain-2v, and inhibited the re-organization of cytoskeletal proteins, desmin and alpha-actinin.	Acetylcysteine	13-16	natriuretic peptide A	Rattus norvegicus	108-111
12681446-4	2003	The induced grp78 expression is sensitive to antioxidant N-acetylcysteine (NAC) addition, indicating the involvement of reactive oxygen species (ROS) in GA-induced ER stress.	Acetylcysteine	57-73	heat shock protein family A (Hsp70) member 5	Rattus norvegicus	12-17
12681446-4	2003	The induced grp78 expression is sensitive to antioxidant N-acetylcysteine (NAC) addition, indicating the involvement of reactive oxygen species (ROS) in GA-induced ER stress.	Acetylcysteine	75-78	heat shock protein family A (Hsp70) member 5	Rattus norvegicus	12-17
12681446-7	2003	The critical ROS-dependent elements in grp78 promoter can be confined within ER stress responsive element (ERSE) region, since reporter constructs loss of ERSE elements that lost the susceptibility to be modulated by NAC after GA treatment.	Acetylcysteine	217-220	heat shock protein family A (Hsp70) member 5	Rattus norvegicus	39-44
12767482-0	2003	Antioxidant NAC and AMPA/KA receptor antagonist DNQX inhibited JNK3 activation following global ischemia in rat hippocampus.	Acetylcysteine	12-15	mitogen activated protein kinase 10	Rattus norvegicus	63-67
12767482-6	2003	The results showed that NAC obviously inhibited JNK3 activation during the early reperfusion, whereas DNQX preferably attenuated JNK3 activation during the latter reperfusion.	Acetylcysteine	24-27	mitogen activated protein kinase 10	Rattus norvegicus	48-52
12825870-4	2003	METHODS: We evaluated whether ICAM-1 expression was linked with a potential protective effect of N-acetyl-L-cysteine (NAC) and the platelet activating factor (PAF) inhibitor (Lexipafant), administered 15 min after the start of reperfusion, in a model of intestinal ischemia (40 min) and reperfusion (12 h) in the rat.	Acetylcysteine	97-116	intercellular adhesion molecule 1	Rattus norvegicus	30-36
12825870-4	2003	METHODS: We evaluated whether ICAM-1 expression was linked with a potential protective effect of N-acetyl-L-cysteine (NAC) and the platelet activating factor (PAF) inhibitor (Lexipafant), administered 15 min after the start of reperfusion, in a model of intestinal ischemia (40 min) and reperfusion (12 h) in the rat.	Acetylcysteine	118-121	intercellular adhesion molecule 1	Rattus norvegicus	30-36
12699905-9	2003	The transcription levels of HO-1 and HSP72 in OE-DEP- and OE-UFP-exposed cells were also reduced by NAC.	Acetylcysteine	100-103	heme oxygenase 1	Rattus norvegicus	28-32
12727827-5	2003	NAC treatment also showed a 70% decrease in cyclin D1 protein levels and a 3-4-fold increase in p27 protein levels, which correlated with decreased retinoblastoma protein phosphorylation.	Acetylcysteine	0-3	cyclin D1	Mus musculus	44-53
12727827-5	2003	NAC treatment also showed a 70% decrease in cyclin D1 protein levels and a 3-4-fold increase in p27 protein levels, which correlated with decreased retinoblastoma protein phosphorylation.	Acetylcysteine	0-3	cyclin-dependent kinase inhibitor 1B	Mus musculus	96-99
12846046-10	2003	In addition, treatment with antioxidant (N-acetyl-L-cysteine) inhibited anti-Id-induced apoptosis in G1-2 and M2-10.	Acetylcysteine	41-60	proline rich protein BstNI subfamily 3	Homo sapiens	101-105
12716756-7	2003	Supplementing the high-glucose culture with the antioxidant N-acetylcysteine (NAC) increased GAPDH activity and diminished embryonic dysmorphogenesis.	Acetylcysteine	60-76	glyceraldehyde-3-phosphate dehydrogenase	Rattus norvegicus	93-98
12716756-7	2003	Supplementing the high-glucose culture with the antioxidant N-acetylcysteine (NAC) increased GAPDH activity and diminished embryonic dysmorphogenesis.	Acetylcysteine	78-81	glyceraldehyde-3-phosphate dehydrogenase	Rattus norvegicus	93-98
12713590-12	2003	Both genistein and n-acetyl cysteine prevented ultraviolet induction of cJun protein.	Acetylcysteine	19-36	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	72-76
12713590-13	2003	Consistent with this, genistein and n-acetyl cysteine blocked ultraviolet induction of cJun-driven enzyme, collagenase.	Acetylcysteine	36-53	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	87-91
12679464-9	2003	Treatment of fetal membranes with NAC significantly suppressed lipopolysaccharide-stimulated type II phospholipase A(2) release and content; PGF(2alpha), IL-6, IL-8, TNFalpha, and 8-isoprostane release; and matrix metalloproteinase-9 and urokinase-type plasminogen activator enzyme activity and suppressed NF-kappaB DNA-binding activity (by ANOVA, P &lt; 0.05).	Acetylcysteine	34-37	matrix metallopeptidase 9	Homo sapiens	207-233
12556365-5	2003	N-acetylcysteine completely blocked hemin-induced expression of HO-1 and MCP-1 mRNA, thereby providing added evidence for redox regulation of expression of these genes.	Acetylcysteine	0-16	heme oxygenase 1	Rattus norvegicus	64-68
12485928-1	2002	Increased expression of the type I insulin-like growth factor receptor (IGF-1R) is associated with colon cancer, while the antioxidant N-acetyl-l-cysteine (NAC) is known to suppress colonic proliferation.	Acetylcysteine	135-154	X-linked Kx blood group	Homo sapiens	156-159
12368900-3	2002	Here we report additional structural and functional studies on ESA1 that demonstrate that histone acetylation proceeds through an acetyl-cysteine enzyme intermediate.	Acetylcysteine	130-145	NuA4 histone acetyltransferase complex catalytic subunit ESA1	Saccharomyces cerevisiae S288C	63-67
12237339-0	2002	Identification of a mechanism by which the methylmercury antidotes N-acetylcysteine and dimercaptopropanesulfonate enhance urinary metal excretion: transport by the renal organic anion transporter-1.	Acetylcysteine	67-83	solute carrier family 22 member 6	Rattus norvegicus	165-198
12237339-4	2002	Xenopus laevis oocytes expressing rat Oat1 showed increased uptake of [(14)C]MeHg when complexed with either NAC or DMPS but not when complexed with L-cysteine, glutathione, dimercaptosuccinate, penicillamine, or gamma-glutamylcysteine.	Acetylcysteine	109-112	solute carrier family 22 member 6	Rattus norvegicus	38-42
12237339-6	2002	The apparent K(m) values for Oat1-mediated transport were 31 +/- 2 microM for MeHg-NAC and 9 +/- 2 microM for MeHg-DMPS, indicating that these are relatively high-affinity substrates.	Acetylcysteine	83-86	solute carrier family 22 member 6	Rattus norvegicus	29-33
12237339-7	2002	Oat1-mediated uptake of [(14)C]MeHg-NAC and [(14)C]MeHg-DMPS was inhibited by prototypical substrates for Oat1, including p-aminohippurate (PAH), and was trans-stimulated when oocytes were preloaded with 2 mM glutarate but not glutamate.	Acetylcysteine	36-39	solute carrier family 22 member 6	Rattus norvegicus	0-4
12237339-7	2002	Oat1-mediated uptake of [(14)C]MeHg-NAC and [(14)C]MeHg-DMPS was inhibited by prototypical substrates for Oat1, including p-aminohippurate (PAH), and was trans-stimulated when oocytes were preloaded with 2 mM glutarate but not glutamate.	Acetylcysteine	36-39	solute carrier family 22 member 6	Rattus norvegicus	106-110
12237339-8	2002	Conversely, efflux of [(3)H]PAH from Oat1-expressing oocytes was trans-stimulated by glutarate, PAH, NAC, DMPS, MeHg-NAC, MeHg-DMPS, and a mercapturic acid, indicating that these are transported solutes.	Acetylcysteine	101-104	solute carrier family 22 member 6	Rattus norvegicus	37-41
12237339-8	2002	Conversely, efflux of [(3)H]PAH from Oat1-expressing oocytes was trans-stimulated by glutarate, PAH, NAC, DMPS, MeHg-NAC, MeHg-DMPS, and a mercapturic acid, indicating that these are transported solutes.	Acetylcysteine	117-120	solute carrier family 22 member 6	Rattus norvegicus	37-41
12237339-8	2002	Conversely, efflux of [(3)H]PAH from Oat1-expressing oocytes was trans-stimulated by glutarate, PAH, NAC, DMPS, MeHg-NAC, MeHg-DMPS, and a mercapturic acid, indicating that these are transported solutes.	Acetylcysteine	139-155	solute carrier family 22 member 6	Rattus norvegicus	37-41
12237339-9	2002	[(3)H]PAH uptake was competitively inhibited by NAC (K(i) of 2.0 +/- 0.3 mM) and DMPS (K(i) of 0.10 +/- 0.02 mM), providing further evidence that these chelating agents are substrates for Oat1.	Acetylcysteine	48-51	solute carrier family 22 member 6	Rattus norvegicus	188-192
12237339-10	2002	These results indicate that the MeHg antidotes NAC and DMPS and their mercaptide complexes are transported by Oat1 but are comparatively poor substrates for Oat3.	Acetylcysteine	47-50	solute carrier family 22 member 6	Rattus norvegicus	110-114
12065237-10	2002	When the conditioned medium was incubated with plasminogen and N-acetylcysteine, this stimulatory effect was lost, consistent with the production of a growth inhibitory factor.	Acetylcysteine	63-79	metallothionein 3	Homo sapiens	151-175
12006386-10	2002	Induction of c-fos expression and enhanced AP-1 binding activity by lysoPC were also inhibited by DPI and NAC.	Acetylcysteine	106-109	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	13-18
11932951-9	2002	Elevations of (*)NO were also inhibited by treatment with the relatively specific nNOS inhibitor, 7 nitroindazole, by the ansamycin antibiotics herbimycin and geldanamycin, by the antioxidant N-acetylcysteine, by the calcium channel blocker nimodipine, and by the N-methyl-D-aspartate inhibitor, MK 801.	Acetylcysteine	192-208	nitric oxide synthase 1	Rattus norvegicus	82-86
11897769-8	2002	Methylglyoxal activated NF-kappaB p65 and increased ICAM-1 expression in hypertensive cells, which was inhibited by N-acetylcysteine.	Acetylcysteine	116-132	intercellular adhesion molecule 1	Rattus norvegicus	52-58
11859152-6	2002	Our data demonstrate that NAC and BUC effectively inhibited the adjuvant effects of DEP in the induction of OVA-specific IgE and IgG1 production.	Acetylcysteine	26-29	LOC105243590	Mus musculus	129-133
11855796-5	2001	Addition of N-acetyl cysteine, LY333531, or L-NAME significantly inhibited glucose-induced elevation in oxidative stress, NO and PKC.	Acetylcysteine	12-29	protein kinase C, gamma	Rattus norvegicus	129-132
11855796-7	2001	In diabetic rats, elevations in retinal TBARS, PKC and NO were observed at 2 months of diabetes, and administration of N-acetyl cysteine, LY333531 or aminoguanidine prevented diabetes-induced elevation in retinal TBARS and NO levels, and PKC activity.	Acetylcysteine	119-136	protein kinase C, gamma	Rattus norvegicus	47-50
11719447-1	2001	The thiol N-acetyl-L-cysteine (NAC), an analogue and precursor of reduced glutathione, has cancer chemopreventive properties attributable to its nucleophilicity, antioxidant activity, and a variety of other mechanisms.	Acetylcysteine	10-29	X-linked Kx blood group	Homo sapiens	31-34
11673494-7	2001	The L-PAM-induced accumulation of IFN-beta mRNA was mimicked with H(2)O(2) and was prevented with the antioxidant N-acetyl-L-cysteine, indicating that reactive oxygen species are involved in the transcriptional regulation of L-PAM-induced IFN-beta gene expression.	Acetylcysteine	114-133	interferon beta 1, fibroblast	Mus musculus	34-42
11673494-7	2001	The L-PAM-induced accumulation of IFN-beta mRNA was mimicked with H(2)O(2) and was prevented with the antioxidant N-acetyl-L-cysteine, indicating that reactive oxygen species are involved in the transcriptional regulation of L-PAM-induced IFN-beta gene expression.	Acetylcysteine	114-133	interferon beta 1, fibroblast	Mus musculus	239-247
11641438-0	2001	Mercapturic acids (N-acetylcysteine S-conjugates) as endogenous substrates for the renal organic anion transporter-1.	Acetylcysteine	0-17	solute carrier family 22 member 6	Rattus norvegicus	83-116
11641438-0	2001	Mercapturic acids (N-acetylcysteine S-conjugates) as endogenous substrates for the renal organic anion transporter-1.	Acetylcysteine	19-35	solute carrier family 22 member 6	Rattus norvegicus	83-116
11641438-3	2001	The present study examined whether mercapturic acids are substrates for the renal basolateral organic anion transporter-1 (Oat1) from rat kidney.	Acetylcysteine	35-52	solute carrier family 22 member 6	Rattus norvegicus	94-121
11641438-3	2001	The present study examined whether mercapturic acids are substrates for the renal basolateral organic anion transporter-1 (Oat1) from rat kidney.	Acetylcysteine	35-52	solute carrier family 22 member 6	Rattus norvegicus	123-127
11641438-5	2001	Uptake of [(3)H]p-aminohippuric acid (PAH) in Oat1-expressing Xenopus laevis oocytes was strongly inhibited by S-(2,4-dinitrophenyl)-N-acetyl-L-cysteine (DNP-NAC) and by all other mercapturic acids tested, including the endogenous mercapturic acid N-acetyl-leukotriene E(4).	Acetylcysteine	180-197	solute carrier family 22 member 6	Rattus norvegicus	46-50
11641438-6	2001	Inhibition by the mercapturic acids was competitive, which is consistent with the hypothesis that these compounds are substrates for Oat1.	Acetylcysteine	18-35	solute carrier family 22 member 6	Rattus norvegicus	133-137
11641438-7	2001	This conclusion was supported by the direct demonstration of saturable [(35)S]DNP-NAC uptake in Oat1-expressing oocytes.	Acetylcysteine	82-85	solute carrier family 22 member 6	Rattus norvegicus	96-100
11641438-9	2001	The apparent K(m) value for DNP-NAC uptake was only 2 microM, indicating that this mercapturic acid is a high affinity substrate for Oat1.	Acetylcysteine	32-35	solute carrier family 22 member 6	Rattus norvegicus	133-137
11641438-9	2001	The apparent K(m) value for DNP-NAC uptake was only 2 microM, indicating that this mercapturic acid is a high affinity substrate for Oat1.	Acetylcysteine	83-99	solute carrier family 22 member 6	Rattus norvegicus	133-137
11207438-5	2001	Incubation with SNP plus N-acetyl-L-cysteine (NAC) further augmented the percentage of cell death with respect to SNP used alone, and this process is seen earlier, i.e. after 24 h. Moreover, the induction of apoptosis in the presence of NAC is time- and concentration-dependent.	Acetylcysteine	25-44	X-linked Kx blood group	Homo sapiens	46-49
11207438-5	2001	Incubation with SNP plus N-acetyl-L-cysteine (NAC) further augmented the percentage of cell death with respect to SNP used alone, and this process is seen earlier, i.e. after 24 h. Moreover, the induction of apoptosis in the presence of NAC is time- and concentration-dependent.	Acetylcysteine	25-44	X-linked Kx blood group	Homo sapiens	237-240
11935096-5	2001	As is the case for MHBs(t167), MHBsKDEL-dependent activation of NFkappaB is inhibited by the antioxidant N-acetyl-L-cysteine indicating the involvement of reactive oxygen intermediates and suggesting a similar mechanism of activation.	Acetylcysteine	105-124	MHB	Homo sapiens	31-39
11237096-4	2000	MDA and HNE induce an increase in intracellular peroxide levels; N-Acetyl-L-cysteine (NAC) suppressed MDA- and HNE-induced ALR gene expression.	Acetylcysteine	65-84	aldo-keto reductase family 1 member A1	Homo sapiens	123-126
11237096-4	2000	MDA and HNE induce an increase in intracellular peroxide levels; N-Acetyl-L-cysteine (NAC) suppressed MDA- and HNE-induced ALR gene expression.	Acetylcysteine	86-89	aldo-keto reductase family 1 member A1	Homo sapiens	123-126
11198153-1	2000	Digital imaging fluorescence microscopy was used to study the effect of two antioxidants, N-acetyl-cysteine (NAC) and glutathione, on the cytosolic free calcium concentration ([Ca2+]i) induced by cholecystokinin-octapeptide (CCK-8) of mouse pancreatic acinar cells.	Acetylcysteine	90-107	cholecystokinin	Mus musculus	196-211
10694352-11	2000	N-acetylcysteine reduced basal activity of both matrix metalloproteinase 9 and matrix metalloproteinase 2 to 20%.	Acetylcysteine	0-16	matrix metallopeptidase 9	Homo sapiens	48-74
10634927-4	2000	Treatment of cells with 20 or 40 mM N-acetyl-L-cysteine, which traps free radicals, was found to increase by 30% the glutathione level and to suppress the HSP over-expression.	Acetylcysteine	36-55	heat shock protein 90 beta family member 2, pseudogene	Homo sapiens	155-158
11124650-0	2000	Effects of N-acetylcysteine and ambroxol on the production of IL-12 and IL-10 in human alveolar macrophages.	Acetylcysteine	11-27	interleukin 10	Homo sapiens	72-77
10629763-7	1999	Addition of glutathione and N-acetyl-L-cysteine, two well-known antioxidants, at 1.5 and 0.5 mM, respectively, decreased A beta (25-35) stimulated adenylate cyclase activity in both tissues.	Acetylcysteine	28-47	amyloid beta precursor protein	Rattus norvegicus	121-127
10559009-6	1999	Both the PDGF-mediated generation of reactive oxygen species and the induction of HO-1 protein was inhibited by the antioxidant N-acetyl-L-cysteine.	Acetylcysteine	128-147	heme oxygenase 1	Rattus norvegicus	82-86
10549609-1	1999	PURPOSE: The effects of antioxidants (N-acetyl-L-cysteine [NAC] and pyrrolidine dithiocarbamate [PDTC]) on radiation-induced ICAM-1 expression on human umbilical vein endothelial cells (HUVEC) were investigated.	Acetylcysteine	38-57	intercellular adhesion molecule 1	Homo sapiens	125-131
10549609-1	1999	PURPOSE: The effects of antioxidants (N-acetyl-L-cysteine [NAC] and pyrrolidine dithiocarbamate [PDTC]) on radiation-induced ICAM-1 expression on human umbilical vein endothelial cells (HUVEC) were investigated.	Acetylcysteine	59-62	intercellular adhesion molecule 1	Homo sapiens	125-131
10549609-5	1999	In fact, by themselves, these antioxidants induced a significant increase of ICAM-1 expression, which in comparison with a radiation dose of 7 Gy after 24h was nine times higher for PDTC, and more than double for NAC.	Acetylcysteine	213-216	intercellular adhesion molecule 1	Homo sapiens	77-83
10549609-9	1999	The inhibition of TNF-alpha-induced ICAM-1 expression by NAC might have clinical implications because this substance is used as a radioprotector in radiotherapy.	Acetylcysteine	57-60	intercellular adhesion molecule 1	Homo sapiens	36-42
10490932-16	1999	Endothelial cells pretreated with a glutathione precursor, N-acetylcysteine, or glutathione ester, showed a decrease in heme-induced ICAM-1 expression of 37 and 44%, respectively, suggesting that the mechanism of ICAM-1 induction by heme may be partly dependent on the levels of antioxidant.	Acetylcysteine	59-75	intercellular adhesion molecule 1	Homo sapiens	133-139
10490932-16	1999	Endothelial cells pretreated with a glutathione precursor, N-acetylcysteine, or glutathione ester, showed a decrease in heme-induced ICAM-1 expression of 37 and 44%, respectively, suggesting that the mechanism of ICAM-1 induction by heme may be partly dependent on the levels of antioxidant.	Acetylcysteine	59-75	intercellular adhesion molecule 1	Homo sapiens	213-219
10448097-4	1999	Moreover, intracellular reactive oxygen species were involved in mediating osmotic stress-induced Syk activation, with osmotic stress-induced Syk activation being inhibited by the pretreatment of cells with N-acetyl-cysteine and reduced glutathione.	Acetylcysteine	207-224	spleen associated tyrosine kinase	Homo sapiens	98-101
10448097-4	1999	Moreover, intracellular reactive oxygen species were involved in mediating osmotic stress-induced Syk activation, with osmotic stress-induced Syk activation being inhibited by the pretreatment of cells with N-acetyl-cysteine and reduced glutathione.	Acetylcysteine	207-224	spleen associated tyrosine kinase	Homo sapiens	142-145
10391952-4	1999	N-Acetylcysteine also significantly reduced serum-stimulated elevation of c-Fos but did not prevent the normal mitogen-induced increase in c-fos mRNA.	Acetylcysteine	0-16	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	74-79
10026227-4	1999	NAC inhibited agonist-induced ERK2, JNK1, and p38 MAP kinase activation and c-Fos, c-Jun, and JunB expression except for platelet-derived growth factor BB-induced ERK2 activation.	Acetylcysteine	0-3	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	76-81
10026227-4	1999	NAC inhibited agonist-induced ERK2, JNK1, and p38 MAP kinase activation and c-Fos, c-Jun, and JunB expression except for platelet-derived growth factor BB-induced ERK2 activation.	Acetylcysteine	0-3	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	83-88
9990295-8	1999	The effects of NAC on TNF-alpha-induced cell death are more complex, with NAC being marginally protective and itself enhancing the formation of c-Rel containing complexes at higher concentrations (25 mM).	Acetylcysteine	15-18	REL proto-oncogene, NF-kB subunit	Homo sapiens	144-149
9712025-9	1998	N-acetyl-L-cysteine pretreatment, which blocks CD40-mediated JNK activation, does not affect the ability of CD40 to inhibit anti-IgM-mediated ERK2 activation and apoptosis.	Acetylcysteine	0-19	mitogen-activated protein kinase 8	Mus musculus	61-64
9618303-4	1998	Pretreatment of cells with antioxidants N-acetylcysteine (NAC) and glutathione (GSH) almost completely blocked tyrosine phosphorylations of Syk, Fc gamma receptor(s) and PLC gamma 2.	Acetylcysteine	40-56	spleen associated tyrosine kinase	Homo sapiens	140-143
9618303-4	1998	Pretreatment of cells with antioxidants N-acetylcysteine (NAC) and glutathione (GSH) almost completely blocked tyrosine phosphorylations of Syk, Fc gamma receptor(s) and PLC gamma 2.	Acetylcysteine	58-61	spleen associated tyrosine kinase	Homo sapiens	140-143
9523930-0	1998	N-acetylcysteine reduces methemoglobin in an in-vitro model of glucose-6-phosphate dehydrogenase deficiency.	Acetylcysteine	0-16	hemoglobin subunit gamma 2	Homo sapiens	25-38
9523930-1	1998	OBJECTIVE: To determine whether N-acetylcysteine (NAC) reduces methemoglobin (MHB) in an in-vitro model of glucose-6-phosphate dehydrogenase (G6PD) deficiency, given that methylene blue is an ineffective MHB antidote in G6PD deficiency.	Acetylcysteine	32-48	hemoglobin subunit gamma 2	Homo sapiens	63-76
9523930-1	1998	OBJECTIVE: To determine whether N-acetylcysteine (NAC) reduces methemoglobin (MHB) in an in-vitro model of glucose-6-phosphate dehydrogenase (G6PD) deficiency, given that methylene blue is an ineffective MHB antidote in G6PD deficiency.	Acetylcysteine	32-48	hemoglobin subunit gamma 2	Homo sapiens	78-81
9523930-1	1998	OBJECTIVE: To determine whether N-acetylcysteine (NAC) reduces methemoglobin (MHB) in an in-vitro model of glucose-6-phosphate dehydrogenase (G6PD) deficiency, given that methylene blue is an ineffective MHB antidote in G6PD deficiency.	Acetylcysteine	50-53	hemoglobin subunit gamma 2	Homo sapiens	63-76
9523930-1	1998	OBJECTIVE: To determine whether N-acetylcysteine (NAC) reduces methemoglobin (MHB) in an in-vitro model of glucose-6-phosphate dehydrogenase (G6PD) deficiency, given that methylene blue is an ineffective MHB antidote in G6PD deficiency.	Acetylcysteine	50-53	hemoglobin subunit gamma 2	Homo sapiens	78-81
9523930-9	1998	CONCLUSION: In this in-vitro model of G6PD deficiency, NAC efficiently reduced MHB.	Acetylcysteine	55-58	hemoglobin subunit gamma 2	Homo sapiens	79-82
9530210-0	1998	Induction of HSP 32 gene in hypoxic cardiomyocytes is attenuated by treatment with N-acetyl-L-cysteine.	Acetylcysteine	83-102	heme oxygenase 1	Rattus norvegicus	13-19
9449403-12	1998	ECs treated with an antioxidant (N-acetylcysteine or catalase) inhibited strain-induced ROS generation and ICAM-1 mRNA levels followed by decreased ICAM-1 expression on EC surfaces.	Acetylcysteine	33-49	intercellular adhesion molecule 1	Homo sapiens	107-113
9449403-12	1998	ECs treated with an antioxidant (N-acetylcysteine or catalase) inhibited strain-induced ROS generation and ICAM-1 mRNA levels followed by decreased ICAM-1 expression on EC surfaces.	Acetylcysteine	33-49	intercellular adhesion molecule 1	Homo sapiens	148-154
9115810-3	1997	Pretreatment of ACH-2 T cells by NAC followed by stimulation with PMA, TNF-alpha, or hydrogen peroxide (H2O2) resulted in strong suppression of NF-kappa B activation.	Acetylcysteine	33-36	acyl-CoA thioesterase 1	Homo sapiens	16-21
9269467-12	1997	Five and 10 U/ml of NAC decreased ICAM-1 expression in HPAEC (141 +/- 26% and 113 +/- 11%) and HUVEC (119 +/- 23% and 106 +/- 7%), respectively.	Acetylcysteine	20-23	intercellular adhesion molecule 1	Homo sapiens	34-40
8981478-3	1996	Percoll gradient purified granule cells maintained without IGF-I, in minimal medium alone or in medium containing the antioxidant N-acetylcysteine (NAC), also express MEF2A and GABAA alpha 6.	Acetylcysteine	130-146	myocyte enhancer factor 2A	Mus musculus	167-172
8981478-3	1996	Percoll gradient purified granule cells maintained without IGF-I, in minimal medium alone or in medium containing the antioxidant N-acetylcysteine (NAC), also express MEF2A and GABAA alpha 6.	Acetylcysteine	148-151	myocyte enhancer factor 2A	Mus musculus	167-172
9216201-2	1996	N-acetylcysteine, an antioxidant, decreased the TNF alpha-induced expression of intercellular adhesion molecule-1 on cultured epithelial cells from human bronchi (BEAS-2A), and inhibited IL-8 production by those cells.	Acetylcysteine	0-16	intercellular adhesion molecule 1	Homo sapiens	80-113
8909270-0	1996	N-acetylcysteine reduces methemoglobin in vitro.	Acetylcysteine	0-16	hemoglobin subunit gamma 2	Homo sapiens	25-38
8909270-1	1996	STUDY OBJECTIVE: To determine whether N-acetylcysteine (NAC reduces methemoglobin.	Acetylcysteine	38-54	X-linked Kx blood group	Homo sapiens	56-59
8909270-1	1996	STUDY OBJECTIVE: To determine whether N-acetylcysteine (NAC reduces methemoglobin.	Acetylcysteine	38-54	hemoglobin subunit gamma 2	Homo sapiens	68-81
8810635-7	1996	The ICAM-1 expression was decreased and the GSH concentration was increased with the addition of NAC.	Acetylcysteine	97-100	intercellular adhesion molecule 1	Homo sapiens	4-10
8810635-9	1996	Negative relationships were also demonstrated between the level of ICAM-1 expression and the total extracellular glutathione concentrations in NAC-treated HPAEC (R = 0.877, P &lt; 0.0005) and HUVEC (R = 0.727, P &lt; 0.0005).	Acetylcysteine	143-146	intercellular adhesion molecule 1	Homo sapiens	67-73
8853906-3	1996	We found that both TGF-beta 1 and an oxidant, hydrogen peroxide, rapidly increase the expression of c-fos and c-jun genes and induce cell death by apoptosis; these effects are inhibited by the antioxidant N-acetylcysteine.	Acetylcysteine	205-221	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	100-105
8853906-3	1996	We found that both TGF-beta 1 and an oxidant, hydrogen peroxide, rapidly increase the expression of c-fos and c-jun genes and induce cell death by apoptosis; these effects are inhibited by the antioxidant N-acetylcysteine.	Acetylcysteine	205-221	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	110-115
8555249-5	1996	UVB-induced synthesis and phosphorylation of cPLA2 could be inhibited by pretreatment with the antioxidants 2,2,5,7,8-pentamethyl-6-hydroxychromane (50 microM) or N-acetylcysteine (10 mM).	Acetylcysteine	163-179	phospholipase A2 group IVA	Homo sapiens	45-50
7761402-9	1995	N-Acetylcysteine does not affect the immediate early pathway but can inhibit the TPA-mediated induction of cyclin D1 and DNA synthesis.	Acetylcysteine	0-16	cyclin D1	Mus musculus	107-116
7963551-8	1994	In accordance with the oxidation dependence of this suppressive mechanism, N-acetylcysteine (NAC; an antioxidant) significantly reversed the polyamine oxidase effects on lymphokine production and signal transduction.	Acetylcysteine	75-91	polyamine oxidase	Homo sapiens	141-158
7963551-8	1994	In accordance with the oxidation dependence of this suppressive mechanism, N-acetylcysteine (NAC; an antioxidant) significantly reversed the polyamine oxidase effects on lymphokine production and signal transduction.	Acetylcysteine	93-96	polyamine oxidase	Homo sapiens	141-158
7811547-1	1994	N-Acetyl-L-cysteine (NAC) and L-2-oxothiazolidine 4-carboxylate (OTC) are pro-GSH drugs that been proposed for AIDS therapy.	Acetylcysteine	0-19	X-linked Kx blood group	Homo sapiens	21-24
8035787-5	1994	This superinduction was blocked by preincubation of cells with the glutathione precursor N-acetyl cysteine or with phorbol 12-myristate 13-acetate, which indicates redox control of c-jun expression and probable involvement of protein kinase C. By gel retardation assay, no increase in AP-1 DNA binding activity was found to be concomitant with the transcriptional activation of c-jun.	Acetylcysteine	89-106	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	181-186
8035787-5	1994	This superinduction was blocked by preincubation of cells with the glutathione precursor N-acetyl cysteine or with phorbol 12-myristate 13-acetate, which indicates redox control of c-jun expression and probable involvement of protein kinase C. By gel retardation assay, no increase in AP-1 DNA binding activity was found to be concomitant with the transcriptional activation of c-jun.	Acetylcysteine	89-106	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	285-289
8035787-5	1994	This superinduction was blocked by preincubation of cells with the glutathione precursor N-acetyl cysteine or with phorbol 12-myristate 13-acetate, which indicates redox control of c-jun expression and probable involvement of protein kinase C. By gel retardation assay, no increase in AP-1 DNA binding activity was found to be concomitant with the transcriptional activation of c-jun.	Acetylcysteine	89-106	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	378-383
8207209-3	1994	N-Acetyl cysteine (NAc-cys) was used to increase intracellular glutathione levels during lymphokine-activated killer (LAK) cell activation by IL-2.	Acetylcysteine	0-17	NLR family, pyrin domain containing 1A	Mus musculus	19-22
7909525-0	1994	Effect of glutathione depletion and oral N-acetyl-cysteine treatment on CD4+ and CD8+ cells.	Acetylcysteine	41-58	CD8a molecule	Homo sapiens	81-84
8238538-2	1993	Since N-acetyl-L-cysteine (NAC) increases glutathione (GSH) levels in vivo and scavenges oxygen radicals in vitro, we tested the effect of NAC given intravenously on lung changes following intratracheal IL-1 administration.	Acetylcysteine	6-25	X-linked Kx blood group	Homo sapiens	27-30
8250542-1	1993	N-acetyl-L-cysteine (NAC) is known to antagonize the PMA- or cytokine-stimulated HIV-1 replication in latently and acutely infected monocytic and lymphocytic cell lines, and to reduce the virus multiplication in acutely infected, PHA-stimulated PBMC.	Acetylcysteine	0-19	X-linked Kx blood group	Homo sapiens	21-24
8487592-3	1993	An estimation was made of the 50% inhibitory concentration (IC50) of mesna and NAC for PMA-induced H2O2 production by human neutrophils, the results being 70 mcM and 77 mcM, respectively.	Acetylcysteine	79-82	methylmalonyl-CoA mutase	Homo sapiens	158-161
8487592-3	1993	An estimation was made of the 50% inhibitory concentration (IC50) of mesna and NAC for PMA-induced H2O2 production by human neutrophils, the results being 70 mcM and 77 mcM, respectively.	Acetylcysteine	79-82	methylmalonyl-CoA mutase	Homo sapiens	169-172
8487592-4	1993	The mechanism which governs mesna and NAC reactions results from a scavenging effect of H2O2: the calculated IC50s of this effect were 30 mcM and 42 mcM, respectively, in free cellular experimentation.	Acetylcysteine	38-41	methylmalonyl-CoA mutase	Homo sapiens	138-141
8487592-4	1993	The mechanism which governs mesna and NAC reactions results from a scavenging effect of H2O2: the calculated IC50s of this effect were 30 mcM and 42 mcM, respectively, in free cellular experimentation.	Acetylcysteine	38-41	methylmalonyl-CoA mutase	Homo sapiens	149-152
2038747-6	1991	Urinary recoveries of AAP and metabolites indicated that more AAP-glucuronide was formed at the expense of other major metabolites (AAP-GSH, -N-acetylcysteine, and -sulfate) in OTP-treated hamsters, while plasma toxicokinetic modeling suggested a greater rate of AAP systemic clearance.	Acetylcysteine	141-158	orthopedia homeobox	Homo sapiens	177-180
2123045-1	1990	This report demonstrates that an Ehrlich-reagent-positive metabolite of monocrotaline and senecionine is excreted in the urine of male rats as an N-acetylcysteine conjugate of (+/-)-6,7-dihydro-7-hydroxy-1-hydroxymethyl-5H-pyrrolizine (NAC-DHP).	Acetylcysteine	146-162	dihydropyrimidinase	Rattus norvegicus	240-243
33761438-11	2021	ROS-mediated Syk phosphorylation at tyrosine 525/526 was confirmed by treatment with H2O2, hypoxia, and CoCl2, and attenuated with NAC treatment.	Acetylcysteine	131-134	spleen associated tyrosine kinase	Homo sapiens	13-16
32890923-10	2020	In addition, NAC pretreatment promoted the phagocytic activity of Cd-exposed chicken peritoneal macrophages, and significantly inhibited expression of pro-inflammatory factors (IL-1beta, IL-6 and TNF-alpha) in both Cd-exposed macrophages and Cd-treated cells in response to LPS stimuli.	Acetylcysteine	13-16	interleukin 6	Gallus gallus	187-191
28828308-13	2017	Thus, NAC may be a useful adjuvant to DOTS in PTB.	Acetylcysteine	6-9	polypyrimidine tract binding protein 1	Homo sapiens	46-49
25028117-8	2014	Upregulation of elastin-, hyaluronic acid-, and GDF6-encoding genes supports the evidence of clinical improvement induced by NAC biostimulation in the prevention and correction of skin aging.	Acetylcysteine	125-128	elastin	Homo sapiens	16-23
25028117-8	2014	Upregulation of elastin-, hyaluronic acid-, and GDF6-encoding genes supports the evidence of clinical improvement induced by NAC biostimulation in the prevention and correction of skin aging.	Acetylcysteine	125-128	growth differentiation factor 6	Homo sapiens	48-52
34619980-9	2021	NAC treatment reduced TGF-beta signaling, p-Smad2 and collagen levels, and mesenchymal transition from Isolectin-B4 and CD45-positive cells in LDLR mice.	Acetylcysteine	0-3	low density lipoprotein receptor	Mus musculus	143-147
34619980-11	2021	CONCLUSIONS: Short-term treatment with NAC inhibits AS progression, by inhibiting WSS-induced TGF-beta1 activation in the LDLR mouse model of AS, motivating a clinical trial of NAC and/or other thiol-reactive agent(s) as a potential therapy for AS.	Acetylcysteine	39-42	low density lipoprotein receptor	Mus musculus	122-126
34425375-7	2021	The mechanistic analysis further demonstrated that N-acetylcysteine pretreatment attenuated the decreased expression of target genes (UBC and PPP2CA) induced by PQ.	Acetylcysteine	51-67	ubiquitin C	Mus musculus	134-137
34850077-8	2021	Finally, we demonstrated that NAC selectively normalized uterine leukemia inhibitory factor, osteopontin/secreted phosphoprotein 1, progesterone receptor, and homeobox A11 mRNA expression and placental estrogen related receptor beta and trophoblast specific protein alpha mRNA expression.	Acetylcysteine	30-33	LIF, interleukin 6 family cytokine	Rattus norvegicus	65-91
34850077-8	2021	Finally, we demonstrated that NAC selectively normalized uterine leukemia inhibitory factor, osteopontin/secreted phosphoprotein 1, progesterone receptor, and homeobox A11 mRNA expression and placental estrogen related receptor beta and trophoblast specific protein alpha mRNA expression.	Acetylcysteine	30-33	estrogen-related receptor beta	Rattus norvegicus	202-232
34884437-8	2021	In U937 cells, the weak cytotoxicity of NAC is probably caused by lower expression of NOX2, SOD1, SOD3, and by the absence of MOP expression.	Acetylcysteine	40-43	cytochrome b-245 beta chain	Homo sapiens	86-90
34820428-11	2021	Finally, the administered N-acetyl cysteine (NAC) or mitochondrial division inhibitor-1 (Mdivi-1), which decreased the mROS or mitochondrial fission, inhibited the expressions of RIPK3 and p-MLKL, attenuating AS and macrophage M1-type polarization in the Cd-treated group.	Acetylcysteine	26-43	receptor-interacting serine-threonine kinase 3	Mus musculus	179-184
34820428-11	2021	Finally, the administered N-acetyl cysteine (NAC) or mitochondrial division inhibitor-1 (Mdivi-1), which decreased the mROS or mitochondrial fission, inhibited the expressions of RIPK3 and p-MLKL, attenuating AS and macrophage M1-type polarization in the Cd-treated group.	Acetylcysteine	26-43	mixed lineage kinase domain-like	Mus musculus	191-195
34820428-11	2021	Finally, the administered N-acetyl cysteine (NAC) or mitochondrial division inhibitor-1 (Mdivi-1), which decreased the mROS or mitochondrial fission, inhibited the expressions of RIPK3 and p-MLKL, attenuating AS and macrophage M1-type polarization in the Cd-treated group.	Acetylcysteine	45-48	receptor-interacting serine-threonine kinase 3	Mus musculus	179-184
34820428-11	2021	Finally, the administered N-acetyl cysteine (NAC) or mitochondrial division inhibitor-1 (Mdivi-1), which decreased the mROS or mitochondrial fission, inhibited the expressions of RIPK3 and p-MLKL, attenuating AS and macrophage M1-type polarization in the Cd-treated group.	Acetylcysteine	45-48	mixed lineage kinase domain-like	Mus musculus	191-195
34745415-6	2021	In addition, blocking of the RIPK1/RIPK3/MLKL signaling by necrostatin-1 (Nec-1), a key inhibitor of RIPK1 kinase in the necroptosis pathway, or antioxidant N-acetylcysteine (NAC), an inhibitor of ROS, could decrease the activation of osteoblast necroptosis and ameliorate alcohol-induced osteopenia both in vivo and in vitro.	Acetylcysteine	157-173	receptor-interacting serine-threonine kinase 3	Mus musculus	35-40
34420083-7	2021	Delayed NAC treatment had no effect on APAP-induced liver injury at 24 h but reduced the decline of plasma ALT activities and prevented the shrinkage of the areas of necrosis at 48 h. This effect correlated with down-regulation of key activators of mitochondrial biogenesis (AMPK, PGC-1alpha, Nrf1/2, TFAM) and reduced expression of Tom 20 (mitochondrial mass) and PCNA (cell proliferation).	Acetylcysteine	8-11	proliferating cell nuclear antigen	Mus musculus	365-369
34534560-6	2021	Those were the conjugates of CEES with glutathione (GSH-CEES), cysteine (Cys-CEES) and N-acetyl-cysteine (NAC-CEES), as well as the guanine adduct (N7Gua-CEES).	Acetylcysteine	87-104	NLR family, pyrin domain containing 1A	Mus musculus	106-109
34572983-9	2021	N-acetylcysteine not only improved the redox balance in Dusp1-/- mice but also inhibited cytokine production and reduced macrophage recruitment.	Acetylcysteine	0-16	dual specificity phosphatase 1	Mus musculus	56-61
34417577-6	2022	Additionally, inhibition of TFEB activation by ROS scavenger N-acetyl cysteine or inhibition of protein synthesis by cycloheximide effectively compromises ATF4 upregulation and apoptosis in response to 15d-PGJ2.	Acetylcysteine	61-78	activating transcription factor 4	Homo sapiens	155-159
34236028-10	2021	Immunocytochemical staining confirmed that the isolated and cultured cells were AA-FLS; NAC inhibited the proliferation of AA-FLS treated with H2O2 in a concentration-dependent manner, and the mitochondrial ROS content and the protein expressions of Nrf2 and Keap1 decreased.	Acetylcysteine	88-91	Kelch-like ECH-associated protein 1	Rattus norvegicus	259-264
34236028-11	2021	Conclusion NAC can inhibit the proliferation of AA-FLS treated with H2O2, which may be related to blocking Nrf2/Keap1 pathway.	Acetylcysteine	11-14	Kelch-like ECH-associated protein 1	Rattus norvegicus	112-117
34203104-7	2021	Our results showed that the high NAC dose stimulated cFOS expression in the NAcc, and that this effect was suppressed in the presence of MTEP, thus suggesting the implication of mGluR5.	Acetylcysteine	33-36	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	53-57
35623294-6	2022	As intracellular reactive oxygen species (ROS) has been reported to be involved in p-MLKL oligomerization, we assessed the effects of N-acetyl-L-cysteine (NAC), an ROS scavenger, on necroptosis and found that NAC significantly attenuated TSI-induced necroptosis and intracellular ROS production concomitantly with reduced levels of oligomerized p-MLKL, mirroring the effect of baicalin.	Acetylcysteine	134-153	mixed lineage kinase domain-like	Mus musculus	85-89
35151835-13	2022	GLA perturbed the redox homeostasis, and cell apoptosis was totally rescued by Z-VAD(OMe)-FMK and NAC.	Acetylcysteine	98-101	galactosidase alpha	Homo sapiens	0-3
35594827-13	2022	Furthermore, NAC significantly attenuated the production of total protein, VEGF, nitrite, and MDA in the mice with PM2.5-induced lung injury in a dose-dependent manner.	Acetylcysteine	13-16	vascular endothelial growth factor A	Mus musculus	75-79
35615146-7	2022	Conversely, inhibiting ROS production with N-acetylcysteine (NAC) elevated AD-decreased ER-alpha expression, which could be alleviated by FOXM1 knockdown.	Acetylcysteine	61-64	forkhead box M1	Homo sapiens	138-143
35473933-9	2022	In addition, we showed that necrotic TECs-induced activation of TLR2/caspase-5/Panx1 axis could be decreased in macrophages when TECs was protected by N-acetylcysteine (NAC).	Acetylcysteine	151-167	pannexin 1	Homo sapiens	79-84
35473933-9	2022	In addition, we showed that necrotic TECs-induced activation of TLR2/caspase-5/Panx1 axis could be decreased in macrophages when TECs was protected by N-acetylcysteine (NAC).	Acetylcysteine	169-172	pannexin 1	Homo sapiens	79-84
35246254-10	2022	CONCLUSIONS: MSCs are comparable to NAC against APAP-induced liver failure by secreting HGF with less regenerative retardation concerns, thus facilitating the application of MSCs in clinical therapy for APAP liver failure.	Acetylcysteine	36-39	hepatocyte growth factor	Mus musculus	88-91
35217818-11	2022	In vitro, N-acetylcysteine (NAC) inhibited NLRP3 inflammasome activation and NLRP3 knockdown reduced GSDMD expression, in MOVAS cells treated with TNF-alpha.	Acetylcysteine	10-26	gasdermin D	Mus musculus	101-106
35217818-11	2022	In vitro, N-acetylcysteine (NAC) inhibited NLRP3 inflammasome activation and NLRP3 knockdown reduced GSDMD expression, in MOVAS cells treated with TNF-alpha.	Acetylcysteine	28-31	gasdermin D	Mus musculus	101-106
35083332-11	2022	More importantly, N-acetylcysteine induced reduction of ROS in HPDLCs, downregulated TXNIP expression, inhibited the expression and aggregation of NLRP3 inflammasome-related factors, and abrogated the inflammatory response to hypoxia.	Acetylcysteine	18-34	thioredoxin interacting protein	Rattus norvegicus	85-90