PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
30886645-5	2019	According to the results from imaging analyses and bioanalytical experiments, acetaminophen (APAP) caused cytotoxicity in the zone-3 region of the 3D hepatic zonal channel, and the levels of nonphosphorylated beta-catenin, CYP2E, and apoptotic proteins were remarkably increased in the zone-3-like region.	4-amino-N-acetyl-N-methylaniline	93-97	cytochrome P450 family 2 subfamily E member 1	Homo sapiens	223-228
31029706-2	2019	Mitochondrial SH3BP5 (also called SAB) and phosphorylation of c-Jun N-terminal kinase (JNK) mediate the hepatotoxic effects of APAP.	4-amino-N-acetyl-N-methylaniline	127-131	SH3-domain binding protein 5 (BTK-associated)	Mus musculus	14-20
31029706-2	2019	Mitochondrial SH3BP5 (also called SAB) and phosphorylation of c-Jun N-terminal kinase (JNK) mediate the hepatotoxic effects of APAP.	4-amino-N-acetyl-N-methylaniline	127-131	mitogen-activated protein kinase 8	Mus musculus	62-85
31029706-2	2019	Mitochondrial SH3BP5 (also called SAB) and phosphorylation of c-Jun N-terminal kinase (JNK) mediate the hepatotoxic effects of APAP.	4-amino-N-acetyl-N-methylaniline	127-131	mitogen-activated protein kinase 8	Mus musculus	87-90
31029706-15	2019	CONCLUSIONS: In studies of mice, we found that upregulation of STARD1 following ER stress mediates APAP hepatoxicity via SH3BP5 and phosphorylation of JNK1 and JNK2.	4-amino-N-acetyl-N-methylaniline	99-103	steroidogenic acute regulatory protein	Mus musculus	63-69
31029706-15	2019	CONCLUSIONS: In studies of mice, we found that upregulation of STARD1 following ER stress mediates APAP hepatoxicity via SH3BP5 and phosphorylation of JNK1 and JNK2.	4-amino-N-acetyl-N-methylaniline	99-103	SH3-domain binding protein 5 (BTK-associated)	Mus musculus	121-127
30886645-5	2019	According to the results from imaging analyses and bioanalytical experiments, acetaminophen (APAP) caused cytotoxicity in the zone-3 region of the 3D hepatic zonal channel, and the levels of nonphosphorylated beta-catenin, CYP2E, and apoptotic proteins were remarkably increased in the zone-3-like region.	4-amino-N-acetyl-N-methylaniline	93-97	catenin beta 1	Homo sapiens	209-221
31029706-15	2019	CONCLUSIONS: In studies of mice, we found that upregulation of STARD1 following ER stress mediates APAP hepatoxicity via SH3BP5 and phosphorylation of JNK1 and JNK2.	4-amino-N-acetyl-N-methylaniline	99-103	mitogen-activated protein kinase 8	Mus musculus	151-155
31029706-15	2019	CONCLUSIONS: In studies of mice, we found that upregulation of STARD1 following ER stress mediates APAP hepatoxicity via SH3BP5 and phosphorylation of JNK1 and JNK2.	4-amino-N-acetyl-N-methylaniline	99-103	mitogen-activated protein kinase 9	Mus musculus	160-164
29374630-8	2019	Mice lacking TREM-2 exhibited heightened liver damage and inflammation during acute and repetitive carbon tetrachloride and acetaminophen (APAP) intoxication, the latter of which TREM-2 deficiency was remarkably associated with worsened survival.	4-amino-N-acetyl-N-methylaniline	139-143	triggering receptor expressed on myeloid cells 2	Mus musculus	13-19
29374630-9	2019	Liver damage in Trem-2-/- mice following chronic injury and APAP challenge was associated with elevated hepatic lipid peroxidation and macrophage content.	4-amino-N-acetyl-N-methylaniline	60-64	triggering receptor expressed on myeloid cells 2	Mus musculus	16-22
30425454-8	2018	In vivo, the vitamins and their combination effectively reduced APAP-induced serum liver enzymes levels, namely ALT, AST, and ALP, and also attenuated oxidative stress and lipids peroxidation confirmed by the results of glutathione, superoxide dismutase, and maloondialdehyde.	4-amino-N-acetyl-N-methylaniline	64-68	PDZ and LIM domain 3	Rattus norvegicus	126-129
31933721-10	2019	Nrf2-silenced LOS cells were sensitive to APAP-induced injury, while Hype did not exhibit any further effects on LO2 cells, which demonstrate the critical role of Nrf2 in this process.	4-amino-N-acetyl-N-methylaniline	42-46	NFE2 like bZIP transcription factor 2	Homo sapiens	0-4
31933721-11	2019	Taken together, our results demonstrated the ability of Hype to inhibit APAP-induced acute hepatic injury and its potential use in the treatment of Nrf2-associated diseases.	4-amino-N-acetyl-N-methylaniline	72-76	NFE2 like bZIP transcription factor 2	Homo sapiens	148-152
30546306-0	2018	Isoorientin Ameliorates APAP-Induced Hepatotoxicity via Activation Nrf2 Antioxidative Pathway: The Involvement of AMPK/Akt/GSK3beta.	4-amino-N-acetyl-N-methylaniline	24-28	nuclear factor, erythroid derived 2, like 2	Mus musculus	67-71
30546306-0	2018	Isoorientin Ameliorates APAP-Induced Hepatotoxicity via Activation Nrf2 Antioxidative Pathway: The Involvement of AMPK/Akt/GSK3beta.	4-amino-N-acetyl-N-methylaniline	24-28	thymoma viral proto-oncogene 1	Mus musculus	119-122
30546306-0	2018	Isoorientin Ameliorates APAP-Induced Hepatotoxicity via Activation Nrf2 Antioxidative Pathway: The Involvement of AMPK/Akt/GSK3beta.	4-amino-N-acetyl-N-methylaniline	24-28	glycogen synthase kinase 3 beta	Mus musculus	123-131
30546306-6	2018	We found that Iso treatment significantly reduced APAP-induced hepatotoxicity by reducing the lethality, histopathological liver changes, and alanine transaminase (ALT) and aspartate aminotransferase (AST) levels in serum.	4-amino-N-acetyl-N-methylaniline	50-54	glutamic pyruvic transaminase, soluble	Mus musculus	142-162
30546306-12	2018	In summary, Iso ameliorated APAP-induced hepatotoxicity by activating Nrf2 via the AMPK/Akt/GSK3beta pathway.	4-amino-N-acetyl-N-methylaniline	28-32	nuclear factor, erythroid derived 2, like 2	Mus musculus	70-74
30546306-12	2018	In summary, Iso ameliorated APAP-induced hepatotoxicity by activating Nrf2 via the AMPK/Akt/GSK3beta pathway.	4-amino-N-acetyl-N-methylaniline	28-32	thymoma viral proto-oncogene 1	Mus musculus	88-91
30546306-12	2018	In summary, Iso ameliorated APAP-induced hepatotoxicity by activating Nrf2 via the AMPK/Akt/GSK3beta pathway.	4-amino-N-acetyl-N-methylaniline	28-32	glycogen synthase kinase 3 beta	Mus musculus	92-100
30006487-4	2018	We also provide novel evidence that APAP-induced glutathionylation of carnitine O-palmitoyltransferase 1 (CPT1) and voltage-dependent anion-selective channel protein 1 are respectively involved in inhibition of fatty acid beta-oxidation and opening of the mitochondrial permeability transition pore.	4-amino-N-acetyl-N-methylaniline	36-40	carnitine palmitoyltransferase 1A	Homo sapiens	70-104
30006487-4	2018	We also provide novel evidence that APAP-induced glutathionylation of carnitine O-palmitoyltransferase 1 (CPT1) and voltage-dependent anion-selective channel protein 1 are respectively involved in inhibition of fatty acid beta-oxidation and opening of the mitochondrial permeability transition pore.	4-amino-N-acetyl-N-methylaniline	36-40	carnitine palmitoyltransferase 1A	Homo sapiens	106-110
30006487-4	2018	We also provide novel evidence that APAP-induced glutathionylation of carnitine O-palmitoyltransferase 1 (CPT1) and voltage-dependent anion-selective channel protein 1 are respectively involved in inhibition of fatty acid beta-oxidation and opening of the mitochondrial permeability transition pore.	4-amino-N-acetyl-N-methylaniline	36-40	voltage dependent anion channel 1	Homo sapiens	116-167
28442342-1	2017	Thioredoxin reductase 1 (TXNRD1) is associated with susceptibility to acetaminophen (APAP)-induced liver damage.	4-amino-N-acetyl-N-methylaniline	85-89	thioredoxin reductase 1	Homo sapiens	0-23
28442342-9	2017	In addition, APAP treatment significantly increased TXNRD1 expression in MsrA-/- hepatocytes, while no significant change was observed in MsrA+/+ cells.	4-amino-N-acetyl-N-methylaniline	13-17	thioredoxin reductase 1	Homo sapiens	52-58
28442342-9	2017	In addition, APAP treatment significantly increased TXNRD1 expression in MsrA-/- hepatocytes, while no significant change was observed in MsrA+/+ cells.	4-amino-N-acetyl-N-methylaniline	13-17	methionine sulfoxide reductase A	Homo sapiens	73-77
30309416-1	2018	OBJECTIVE: To investigate whether GLT25D2 gene regulates autophagy in acetaminophen (APAP)-induced hepatotoxicity injury.	4-amino-N-acetyl-N-methylaniline	85-89	collagen beta(1-O)galactosyltransferase 2	Mus musculus	34-41
30309416-14	2018	RESULTS: (1) In vivo experiment: compared with the corresponding PBS control group, the expressions of the positive-associated proteins ATG5, ATG7 and LC3-II in liver tissue of the APAP intervention group were down-regulated in the wild-type and GLT25D2-/- mice, while the expression of the negative correlation protein P62 was up-regulated, indicating that the overall level of autophagy decreased after treatment with APAP.	4-amino-N-acetyl-N-methylaniline	181-185	autophagy related 5	Mus musculus	136-140
30309416-14	2018	RESULTS: (1) In vivo experiment: compared with the corresponding PBS control group, the expressions of the positive-associated proteins ATG5, ATG7 and LC3-II in liver tissue of the APAP intervention group were down-regulated in the wild-type and GLT25D2-/- mice, while the expression of the negative correlation protein P62 was up-regulated, indicating that the overall level of autophagy decreased after treatment with APAP.	4-amino-N-acetyl-N-methylaniline	181-185	autophagy related 7	Mus musculus	142-146
30309416-14	2018	RESULTS: (1) In vivo experiment: compared with the corresponding PBS control group, the expressions of the positive-associated proteins ATG5, ATG7 and LC3-II in liver tissue of the APAP intervention group were down-regulated in the wild-type and GLT25D2-/- mice, while the expression of the negative correlation protein P62 was up-regulated, indicating that the overall level of autophagy decreased after treatment with APAP.	4-amino-N-acetyl-N-methylaniline	181-185	microtubule-associated protein 1 light chain 3 alpha	Mus musculus	151-154
30309416-14	2018	RESULTS: (1) In vivo experiment: compared with the corresponding PBS control group, the expressions of the positive-associated proteins ATG5, ATG7 and LC3-II in liver tissue of the APAP intervention group were down-regulated in the wild-type and GLT25D2-/- mice, while the expression of the negative correlation protein P62 was up-regulated, indicating that the overall level of autophagy decreased after treatment with APAP.	4-amino-N-acetyl-N-methylaniline	181-185	collagen beta(1-O)galactosyltransferase 2	Mus musculus	246-253
30309416-14	2018	RESULTS: (1) In vivo experiment: compared with the corresponding PBS control group, the expressions of the positive-associated proteins ATG5, ATG7 and LC3-II in liver tissue of the APAP intervention group were down-regulated in the wild-type and GLT25D2-/- mice, while the expression of the negative correlation protein P62 was up-regulated, indicating that the overall level of autophagy decreased after treatment with APAP.	4-amino-N-acetyl-N-methylaniline	181-185	nucleoporin 62	Mus musculus	320-323
30309416-21	2018	Fluorescence microscopy showed that GFP-LC3 positive cells in both wild-type and GLT25D2-/- mice hepatocytes were significantly increased after APAP intervention as compared with those of PBS control group, and the proportion of GFP-LC3 positive cells in GLT25D2-/- mice was significantly higher than that in wild-type mice (0.64+-0.08 vs. 0.36+-0.05, P > 0.05).	4-amino-N-acetyl-N-methylaniline	144-148	microtubule-associated protein 1 light chain 3 alpha	Mus musculus	40-43
30309416-21	2018	Fluorescence microscopy showed that GFP-LC3 positive cells in both wild-type and GLT25D2-/- mice hepatocytes were significantly increased after APAP intervention as compared with those of PBS control group, and the proportion of GFP-LC3 positive cells in GLT25D2-/- mice was significantly higher than that in wild-type mice (0.64+-0.08 vs. 0.36+-0.05, P > 0.05).	4-amino-N-acetyl-N-methylaniline	144-148	collagen beta(1-O)galactosyltransferase 2	Mus musculus	81-88
30309416-21	2018	Fluorescence microscopy showed that GFP-LC3 positive cells in both wild-type and GLT25D2-/- mice hepatocytes were significantly increased after APAP intervention as compared with those of PBS control group, and the proportion of GFP-LC3 positive cells in GLT25D2-/- mice was significantly higher than that in wild-type mice (0.64+-0.08 vs. 0.36+-0.05, P > 0.05).	4-amino-N-acetyl-N-methylaniline	144-148	microtubule-associated protein 1 light chain 3 alpha	Mus musculus	233-236
30309416-21	2018	Fluorescence microscopy showed that GFP-LC3 positive cells in both wild-type and GLT25D2-/- mice hepatocytes were significantly increased after APAP intervention as compared with those of PBS control group, and the proportion of GFP-LC3 positive cells in GLT25D2-/- mice was significantly higher than that in wild-type mice (0.64+-0.08 vs. 0.36+-0.05, P > 0.05).	4-amino-N-acetyl-N-methylaniline	144-148	collagen beta(1-O)galactosyltransferase 2	Mus musculus	255-262
29192844-12	2018	However, in the APAP group, iNOS immunostaining was most evident in pericentral hepatocytes.	4-amino-N-acetyl-N-methylaniline	16-20	nitric oxide synthase 2	Rattus norvegicus	28-32
29192844-13	2018	In the same areas in APAP+RSV group, intensity of iNOS immunostaining decreased.	4-amino-N-acetyl-N-methylaniline	21-25	nitric oxide synthase 2	Rattus norvegicus	50-54
29192844-14	2018	A significant increase in MDA and decreases in GSH level, CAT, and SOD activity indicated that APAP-induced hepatotoxicity was mediated through oxidative stress.	4-amino-N-acetyl-N-methylaniline	95-99	catalase	Rattus norvegicus	58-61
29042982-4	2017	GSTA1 protein content was 3.8, 1.3 and 2.6 times lower in the CCl4, APAP and ethanol model groups, respectively.	4-amino-N-acetyl-N-methylaniline	68-72	glutathione S-transferase, alpha 1 (Ya)	Mus musculus	0-5
29042982-5	2017	Furthermore, GSTA1 mRNA expression levels decreased by 4.9, 2.1 and 3.7 times in the CCl4, APAP and ethanol model groups, respectively.	4-amino-N-acetyl-N-methylaniline	91-95	glutathione S-transferase, alpha 1 (Ya)	Mus musculus	13-18
28442342-10	2017	Overexpression of MsrA reduced APAP-induced cytotoxicity and TXNRD1 expression levels in APAP-treated MsrA-/- hepatocytes.	4-amino-N-acetyl-N-methylaniline	31-35	methionine sulfoxide reductase A	Homo sapiens	18-22
28442342-10	2017	Overexpression of MsrA reduced APAP-induced cytotoxicity and TXNRD1 expression levels in APAP-treated MsrA-/- hepatocytes.	4-amino-N-acetyl-N-methylaniline	89-93	methionine sulfoxide reductase A	Homo sapiens	18-22
28442342-10	2017	Overexpression of MsrA reduced APAP-induced cytotoxicity and TXNRD1 expression levels in APAP-treated MsrA-/- hepatocytes.	4-amino-N-acetyl-N-methylaniline	89-93	thioredoxin reductase 1	Homo sapiens	61-67
28442342-10	2017	Overexpression of MsrA reduced APAP-induced cytotoxicity and TXNRD1 expression levels in APAP-treated MsrA-/- hepatocytes.	4-amino-N-acetyl-N-methylaniline	89-93	methionine sulfoxide reductase A	Homo sapiens	102-106
28442342-1	2017	Thioredoxin reductase 1 (TXNRD1) is associated with susceptibility to acetaminophen (APAP)-induced liver damage.	4-amino-N-acetyl-N-methylaniline	85-89	thioredoxin reductase 1	Homo sapiens	25-31
28442342-4	2017	In this study, we used primary hepatocytes to investigate the underlying mechanism of the protective effect of MsrA against APAP-induced hepatotoxicity.	4-amino-N-acetyl-N-methylaniline	124-128	methionine sulfoxide reductase A	Homo sapiens	111-115
28442342-5	2017	MsrA gene-deleted (MsrA-/-) hepatocytes showed higher susceptibility to APAP-induced cytotoxicity than wild-type (MsrA+/+) cells, consistent with our previous in vivo results.	4-amino-N-acetyl-N-methylaniline	72-76	methionine sulfoxide reductase A	Homo sapiens	0-4
28442342-5	2017	MsrA gene-deleted (MsrA-/-) hepatocytes showed higher susceptibility to APAP-induced cytotoxicity than wild-type (MsrA+/+) cells, consistent with our previous in vivo results.	4-amino-N-acetyl-N-methylaniline	72-76	methionine sulfoxide reductase A	Homo sapiens	19-23
28442342-5	2017	MsrA gene-deleted (MsrA-/-) hepatocytes showed higher susceptibility to APAP-induced cytotoxicity than wild-type (MsrA+/+) cells, consistent with our previous in vivo results.	4-amino-N-acetyl-N-methylaniline	72-76	methionine sulfoxide reductase A	Homo sapiens	19-23
28442342-7	2017	APAP treatment increased Nrf2 activation more profoundly in MsrA-/- than in MsrA+/+ hepatocytes.	4-amino-N-acetyl-N-methylaniline	0-4	NFE2 like bZIP transcription factor 2	Homo sapiens	25-29
28442342-7	2017	APAP treatment increased Nrf2 activation more profoundly in MsrA-/- than in MsrA+/+ hepatocytes.	4-amino-N-acetyl-N-methylaniline	0-4	methionine sulfoxide reductase A	Homo sapiens	60-64
28442342-7	2017	APAP treatment increased Nrf2 activation more profoundly in MsrA-/- than in MsrA+/+ hepatocytes.	4-amino-N-acetyl-N-methylaniline	0-4	methionine sulfoxide reductase A	Homo sapiens	76-80
28330995-7	2017	As such, global or liver-specific deletion of FcRn results in resistance to APAP-induced liver injury through increased albumin loss into the bile and increased intracellular albumin scavenging of reactive oxygen species.	4-amino-N-acetyl-N-methylaniline	76-80	Fc fragment of IgG receptor and transporter	Mus musculus	46-50
26304691-3	2015	Our in vitro experiments indicated that the formation of these novel APAP metabolites is, at least in part, attributable to the interaction of CysSSnSH produced by CSE and GSH persulfide with APAP-derived NAPQI.	4-amino-N-acetyl-N-methylaniline	69-73	cystathionase (cystathionine gamma-lyase)	Mus musculus	164-167
27151180-7	2016	APAP-AD displayed a punctate pattern and were colocalized with GFP-LC3 positive autophagosomes and Lamp1 positive lysosomes in APAP-treated primary hepatocytes.	4-amino-N-acetyl-N-methylaniline	0-4	lysosomal-associated membrane protein 1	Mus musculus	99-104
26454172-2	2015	Structures of AAA were determined in its native form and in complex with the analgesic acetanilide, p-acetaminophenol, at 1.70 A and 1.73 A resolutions, respectively.	4-amino-N-acetyl-N-methylaniline	100-117	AAA1	Homo sapiens	14-17
26304691-1	2015	While N-acetyl-p-benzoquinoneimine (NAPQI), an electrophilic metabolite of acetaminophen (APAP), has been found to undergo GSH conjugation associated with its detoxification, interaction of NAPQI with nucleophilic per- and polysulfides produced by cystathionine gamma-lyase (CSE), cystathionine beta-synthase, and/or other enzymes is not known.	4-amino-N-acetyl-N-methylaniline	90-94	cystathionase (cystathionine gamma-lyase)	Mus musculus	248-273
26304691-1	2015	While N-acetyl-p-benzoquinoneimine (NAPQI), an electrophilic metabolite of acetaminophen (APAP), has been found to undergo GSH conjugation associated with its detoxification, interaction of NAPQI with nucleophilic per- and polysulfides produced by cystathionine gamma-lyase (CSE), cystathionine beta-synthase, and/or other enzymes is not known.	4-amino-N-acetyl-N-methylaniline	90-94	cystathionase (cystathionine gamma-lyase)	Mus musculus	275-278
27965156-12	2017	Induction of Mmp12, was dramatically reduced in APAP-treated Fibgamma390-396A mice.	4-amino-N-acetyl-N-methylaniline	48-52	matrix metallopeptidase 12	Mus musculus	13-18
27965156-13	2017	Mice lacking Mmp12 displayed exacerbated APAP-induced liver injury, resembling Fibgamma390-396A mice.	4-amino-N-acetyl-N-methylaniline	41-45	matrix metallopeptidase 12	Mus musculus	13-18
27965156-16	2017	CONCLUSIONS: These studies highlight a novel pathway of liver repair after APAP overdose, mediated by fibrin(ogen)-alphaMbeta2 integrin engagement, and demonstrate a protective role of Mmp12 expression after APAP overdose.	4-amino-N-acetyl-N-methylaniline	208-212	matrix metallopeptidase 12	Mus musculus	185-190
27866976-2	2017	The aim of the present study was to investigate the effects of rosiglitazone (RSG), a synthetic PPAR-gamma agonist, on acetaminophen (APAP)-induced acute liver injury.	4-amino-N-acetyl-N-methylaniline	134-138	peroxisome proliferator activated receptor gamma	Mus musculus	96-106
27866976-8	2017	In addition, RSG pretreatment suppressed activation of hepatic nuclear factor kappa B (NF-kappaB) and extracellular signal-related kinase (ERK)/mitogen-activated protein kinase (MAPK) signaling during APAP-induced acute liver injury.	4-amino-N-acetyl-N-methylaniline	201-205	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	87-96
27866976-8	2017	In addition, RSG pretreatment suppressed activation of hepatic nuclear factor kappa B (NF-kappaB) and extracellular signal-related kinase (ERK)/mitogen-activated protein kinase (MAPK) signaling during APAP-induced acute liver injury.	4-amino-N-acetyl-N-methylaniline	201-205	mitogen-activated protein kinase 1	Mus musculus	102-137
27866976-8	2017	In addition, RSG pretreatment suppressed activation of hepatic nuclear factor kappa B (NF-kappaB) and extracellular signal-related kinase (ERK)/mitogen-activated protein kinase (MAPK) signaling during APAP-induced acute liver injury.	4-amino-N-acetyl-N-methylaniline	201-205	mitogen-activated protein kinase 1	Mus musculus	139-142
27866976-8	2017	In addition, RSG pretreatment suppressed activation of hepatic nuclear factor kappa B (NF-kappaB) and extracellular signal-related kinase (ERK)/mitogen-activated protein kinase (MAPK) signaling during APAP-induced acute liver injury.	4-amino-N-acetyl-N-methylaniline	201-205	mitogen-activated protein kinase 1	Mus musculus	178-182
27866976-10	2017	The present results suggest that synthetic PPAR-gamma agonists might be effective agents for preventing the progression of APAP-induced acute liver injury.	4-amino-N-acetyl-N-methylaniline	123-127	peroxisome proliferator activated receptor gamma	Mus musculus	43-53
27830004-6	2016	These data suggested that FA could effectively protect against APAP-induced liver injury by down-regulated expression of CYP 2E1 and the suppression of TLR4-mediated inflammatory responses.	4-amino-N-acetyl-N-methylaniline	63-67	cytochrome P450, family 2, subfamily e, polypeptide 1	Mus musculus	121-128
27830004-6	2016	These data suggested that FA could effectively protect against APAP-induced liver injury by down-regulated expression of CYP 2E1 and the suppression of TLR4-mediated inflammatory responses.	4-amino-N-acetyl-N-methylaniline	63-67	toll-like receptor 4	Mus musculus	152-156
26806302-11	2016	CONCLUSION: SolB exhibits a remarkable protective effect against APAP-induced hepatotoxicity, partially via activation of the NRF2/ARE pathway and regulation of NRF2 target genes, which induce detoxification and increase antioxidant capacity.	4-amino-N-acetyl-N-methylaniline	65-69	nuclear factor, erythroid derived 2, like 2	Mus musculus	126-130
26806302-11	2016	CONCLUSION: SolB exhibits a remarkable protective effect against APAP-induced hepatotoxicity, partially via activation of the NRF2/ARE pathway and regulation of NRF2 target genes, which induce detoxification and increase antioxidant capacity.	4-amino-N-acetyl-N-methylaniline	65-69	nuclear factor, erythroid derived 2, like 2	Mus musculus	161-165
26304691-1	2015	While N-acetyl-p-benzoquinoneimine (NAPQI), an electrophilic metabolite of acetaminophen (APAP), has been found to undergo GSH conjugation associated with its detoxification, interaction of NAPQI with nucleophilic per- and polysulfides produced by cystathionine gamma-lyase (CSE), cystathionine beta-synthase, and/or other enzymes is not known.	4-amino-N-acetyl-N-methylaniline	90-94	cystathionine beta-synthase	Mus musculus	281-308
26304691-3	2015	Our in vitro experiments indicated that the formation of these novel APAP metabolites is, at least in part, attributable to the interaction of CysSSnSH produced by CSE and GSH persulfide with APAP-derived NAPQI.	4-amino-N-acetyl-N-methylaniline	192-196	cystathionase (cystathionine gamma-lyase)	Mus musculus	164-167
25681557-10	2015	Notably, subtoxic doses of APAP caused cell death and sustained JNK phosphorylation in Gadd45beta-deficient primary hepatocytes.	4-amino-N-acetyl-N-methylaniline	27-31	mitogen-activated protein kinase 8	Mus musculus	64-67
25681557-10	2015	Notably, subtoxic doses of APAP caused cell death and sustained JNK phosphorylation in Gadd45beta-deficient primary hepatocytes.	4-amino-N-acetyl-N-methylaniline	27-31	growth arrest and DNA-damage-inducible 45 beta	Mus musculus	87-97
25681557-7	2015	RESULTS: Metformin pretreatment protected against APAP toxicity with decreased liver damage, and inhibited APAP-induced prolonged hepatic JNK phosphorylation in WT mice.	4-amino-N-acetyl-N-methylaniline	107-111	mitogen-activated protein kinase 8	Mus musculus	138-141
25681557-13	2015	CONCLUSIONS: This study is the first to demonstrate that metformin shows protective and therapeutic effects against APAP overdose-evoked hepatotoxicity via Gadd45beta-dependent JNK regulation.	4-amino-N-acetyl-N-methylaniline	116-120	growth arrest and DNA-damage-inducible 45 beta	Mus musculus	156-166
25681557-13	2015	CONCLUSIONS: This study is the first to demonstrate that metformin shows protective and therapeutic effects against APAP overdose-evoked hepatotoxicity via Gadd45beta-dependent JNK regulation.	4-amino-N-acetyl-N-methylaniline	116-120	mitogen-activated protein kinase 8	Mus musculus	177-180
25681557-9	2015	The effects of metformin on APAP-induced liver injury and JNK phosphorylation were abolished in Gadd45beta KO mice.	4-amino-N-acetyl-N-methylaniline	28-32	growth arrest and DNA-damage-inducible 45 beta	Mus musculus	96-106
25645193-1	2015	OBJECTIVES: This study aimed to investigate the protective effects of Danshen (Salvia miltiorrhiza) water extract (DSE) and its major phenolic acid components against CYP2E1-mediated paracetamol (APAP)-induced hepatic toxicity.	4-amino-N-acetyl-N-methylaniline	196-200	cytochrome P450, family 2, subfamily e, polypeptide 1	Rattus norvegicus	167-173
25752611-8	2015	In contrast to chronic deletion of Parkin, acute knockdown of Parkin in mouse livers using adenovirus shRNA reduced mitophagy and Mcl-1 expression but increased JNK activation after APAP administration, which exacerbated APAP-induced liver injury.	4-amino-N-acetyl-N-methylaniline	182-186	mitogen-activated protein kinase 8	Mus musculus	161-164
25752611-8	2015	In contrast to chronic deletion of Parkin, acute knockdown of Parkin in mouse livers using adenovirus shRNA reduced mitophagy and Mcl-1 expression but increased JNK activation after APAP administration, which exacerbated APAP-induced liver injury.	4-amino-N-acetyl-N-methylaniline	221-225	mitogen-activated protein kinase 8	Mus musculus	161-164
25667042-0	2015	Role of nuclear factor-erythroid 2-related factor 2 (Nrf2) in the transcriptional regulation of brain ABC transporters during acute acetaminophen (APAP) intoxication in mice.	4-amino-N-acetyl-N-methylaniline	147-151	nuclear factor, erythroid derived 2, like 2	Mus musculus	8-51
25667042-0	2015	Role of nuclear factor-erythroid 2-related factor 2 (Nrf2) in the transcriptional regulation of brain ABC transporters during acute acetaminophen (APAP) intoxication in mice.	4-amino-N-acetyl-N-methylaniline	147-151	nuclear factor, erythroid derived 2, like 2	Mus musculus	53-57
25667042-9	2015	Furthermore, APAP treated Nrf2 knockout mice did not increase mRNA or protein expression of Mrp2 and Mrp4 as observed in wildtypes.	4-amino-N-acetyl-N-methylaniline	13-17	nuclear factor, erythroid derived 2, like 2	Mus musculus	26-30
25667042-10	2015	In contrast, P-gp induction by APAP was observed in both genotypes.	4-amino-N-acetyl-N-methylaniline	31-35	phosphoglycolate phosphatase	Mus musculus	13-17
25667042-12	2015	This study also suggests that brain changes in Mrp2 and Mrp4 expression may be due to in situ Nrf2 activation by APAP, while P-gp induction is independent of Nrf2 function.	4-amino-N-acetyl-N-methylaniline	113-117	prolactin family 2, subfamily c, member 3	Mus musculus	47-51
25667042-12	2015	This study also suggests that brain changes in Mrp2 and Mrp4 expression may be due to in situ Nrf2 activation by APAP, while P-gp induction is independent of Nrf2 function.	4-amino-N-acetyl-N-methylaniline	113-117	prolactin family 2, subfamily c, member 5	Mus musculus	56-60
25667042-12	2015	This study also suggests that brain changes in Mrp2 and Mrp4 expression may be due to in situ Nrf2 activation by APAP, while P-gp induction is independent of Nrf2 function.	4-amino-N-acetyl-N-methylaniline	113-117	nuclear factor, erythroid derived 2, like 2	Mus musculus	94-98
25666961-5	2015	Administration of APAP, significantly increased, lactate dehydrogenase (LDH) and catalase (CAT) activity in liver tissue and pretreatment with TSBE returned these parameters to control group, moreover TSBE reduces APAP-induced hepatic Glutathione (GSH) depletion.	4-amino-N-acetyl-N-methylaniline	18-22	catalase	Rattus norvegicus	81-89
25666961-5	2015	Administration of APAP, significantly increased, lactate dehydrogenase (LDH) and catalase (CAT) activity in liver tissue and pretreatment with TSBE returned these parameters to control group, moreover TSBE reduces APAP-induced hepatic Glutathione (GSH) depletion.	4-amino-N-acetyl-N-methylaniline	18-22	catalase	Rattus norvegicus	91-94
24779639-5	2014	The contents of 4-acetamidophenol, 6beta-hydroxyltestosterone and 4-hydroxydiclofenac, the metabolites of phenacetin, testosterone and diclofenac, which were selected as specific probe drugs of CYP1A2, CYP2C9 and CYP3A4, respectively, were analyzed by high-performance liquid chromatography.	4-amino-N-acetyl-N-methylaniline	16-33	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	194-200
24882054-4	2014	METHODS: Adiponectin knockout (ADN KO) and C57 wild type mice were treated with an overdose of APAP, followed by histological and biochemical evaluation of liver injury and activation of autophagy.	4-amino-N-acetyl-N-methylaniline	95-99	adiponectin, C1Q and collagen domain containing	Mus musculus	9-20
24882054-5	2014	The mechanism of adiponectin in APAP-induced hepatocytic toxicity was also explored in primary cultured hepatocytes.	4-amino-N-acetyl-N-methylaniline	32-36	adiponectin, C1Q and collagen domain containing	Mus musculus	17-28
24882054-6	2014	RESULTS: APAP overdose triggers a marked accumulation of adiponectin in injured liver tissues.	4-amino-N-acetyl-N-methylaniline	9-13	adiponectin, C1Q and collagen domain containing	Mus musculus	57-68
24882054-7	2014	ADN KO mice exhibit severely exacerbated mitochondrial dysfunction and damage, oxidative stress and necrosis and much higher mortality in response to APAP overdose, whereas these changes are reversed by a single injection of adiponectin.	4-amino-N-acetyl-N-methylaniline	150-154	adiponectin, C1Q and collagen domain containing	Mus musculus	225-236
24882054-10	2014	CONCLUSIONS: Our findings suggest that the APAP-induced accumulation of adiponectin in liver tissues serves as an adaptive mechanism to ameliorate hepatotoxicity by promoting autophagy-mediated clearance of damaged mitochondria.	4-amino-N-acetyl-N-methylaniline	43-47	adiponectin, C1Q and collagen domain containing	Mus musculus	72-83
25139304-9	2014	CONCLUSIONS: Neostigmine is an acetylcholinesterase inhibitor that ameliorates the effects of APAP-induced acute liver failure in the mouse and therefore may provide new treatment options for affected patients.	4-amino-N-acetyl-N-methylaniline	94-98	acetylcholinesterase	Mus musculus	31-51
21654829-8	2011	Consequently, TRAIL- or Bim-deficient mice were substantially protected from APAP-induced liver damage.	4-amino-N-acetyl-N-methylaniline	77-81	BCL2-like 11 (apoptosis facilitator)	Mus musculus	24-27
23661004-5	2013	We have assessed PTP1B expression in APAP-induced liver failure in humans and its role in the molecular mechanisms that regulate the balance between cell death and survival in human and mouse hepatocytes, as well as in a mouse model of APAP-induced hepatotoxicity.	4-amino-N-acetyl-N-methylaniline	37-41	protein tyrosine phosphatase non-receptor type 1	Homo sapiens	17-22
23661004-10	2013	APAP-treated PTP1B(-/-) hepatocytes showed enhanced antioxidant defense through the glycogen synthase kinase 3 (GSK3)beta/Src kinase family (SKF) axis, delaying tyrosine phosphorylation of the transcription factor nuclear factor-erythroid 2-related factor (Nrf2) and its nuclear exclusion, ubiquitination and degradation.	4-amino-N-acetyl-N-methylaniline	0-4	protein tyrosine phosphatase, non-receptor type 1	Mus musculus	13-18
23661004-10	2013	APAP-treated PTP1B(-/-) hepatocytes showed enhanced antioxidant defense through the glycogen synthase kinase 3 (GSK3)beta/Src kinase family (SKF) axis, delaying tyrosine phosphorylation of the transcription factor nuclear factor-erythroid 2-related factor (Nrf2) and its nuclear exclusion, ubiquitination and degradation.	4-amino-N-acetyl-N-methylaniline	0-4	glycogen synthase kinase 3 beta	Mus musculus	112-121
23661004-10	2013	APAP-treated PTP1B(-/-) hepatocytes showed enhanced antioxidant defense through the glycogen synthase kinase 3 (GSK3)beta/Src kinase family (SKF) axis, delaying tyrosine phosphorylation of the transcription factor nuclear factor-erythroid 2-related factor (Nrf2) and its nuclear exclusion, ubiquitination and degradation.	4-amino-N-acetyl-N-methylaniline	0-4	nuclear factor, erythroid derived 2, like 2	Mus musculus	214-255
23661004-10	2013	APAP-treated PTP1B(-/-) hepatocytes showed enhanced antioxidant defense through the glycogen synthase kinase 3 (GSK3)beta/Src kinase family (SKF) axis, delaying tyrosine phosphorylation of the transcription factor nuclear factor-erythroid 2-related factor (Nrf2) and its nuclear exclusion, ubiquitination and degradation.	4-amino-N-acetyl-N-methylaniline	0-4	nuclear factor, erythroid derived 2, like 2	Mus musculus	257-261
23661004-11	2013	Insulin-like growth factor-I receptor-mediated signaling decreased in APAP-treated wild-type hepatocytes, but was maintained in PTP1B(-/-) cells or in wild-type hepatocytes with reduced PTP1B levels by RNA interference.	4-amino-N-acetyl-N-methylaniline	70-74	insulin-like growth factor I receptor	Mus musculus	0-37
22107450-1	2012	In a recent study, we reported that interleukin (IL)-4 had a protective role against acetaminophen (APAP)-induced liver injury (AILI), although the mechanism of protection was unclear.	4-amino-N-acetyl-N-methylaniline	100-104	interleukin 4	Mus musculus	36-54
22107450-6	2012	We also report that the prolonged reduction of GSH in APAP-treated IL-4(-/-) mice appeared to contribute toward increased liver injury by causing a sustained activation of c-Jun-N-terminal kinase (JNK) since levels of phosphorylated JNK remained significantly higher in the IL-4(-/-) mice up to 24 h after APAP treatment.	4-amino-N-acetyl-N-methylaniline	54-58	interleukin 4	Mus musculus	67-71
22107450-6	2012	We also report that the prolonged reduction of GSH in APAP-treated IL-4(-/-) mice appeared to contribute toward increased liver injury by causing a sustained activation of c-Jun-N-terminal kinase (JNK) since levels of phosphorylated JNK remained significantly higher in the IL-4(-/-) mice up to 24 h after APAP treatment.	4-amino-N-acetyl-N-methylaniline	54-58	mitogen-activated protein kinase 8	Mus musculus	172-195
22107450-6	2012	We also report that the prolonged reduction of GSH in APAP-treated IL-4(-/-) mice appeared to contribute toward increased liver injury by causing a sustained activation of c-Jun-N-terminal kinase (JNK) since levels of phosphorylated JNK remained significantly higher in the IL-4(-/-) mice up to 24 h after APAP treatment.	4-amino-N-acetyl-N-methylaniline	54-58	mitogen-activated protein kinase 8	Mus musculus	197-200
22107450-6	2012	We also report that the prolonged reduction of GSH in APAP-treated IL-4(-/-) mice appeared to contribute toward increased liver injury by causing a sustained activation of c-Jun-N-terminal kinase (JNK) since levels of phosphorylated JNK remained significantly higher in the IL-4(-/-) mice up to 24 h after APAP treatment.	4-amino-N-acetyl-N-methylaniline	54-58	mitogen-activated protein kinase 8	Mus musculus	233-236
22107450-6	2012	We also report that the prolonged reduction of GSH in APAP-treated IL-4(-/-) mice appeared to contribute toward increased liver injury by causing a sustained activation of c-Jun-N-terminal kinase (JNK) since levels of phosphorylated JNK remained significantly higher in the IL-4(-/-) mice up to 24 h after APAP treatment.	4-amino-N-acetyl-N-methylaniline	54-58	interleukin 4	Mus musculus	274-278
22107450-6	2012	We also report that the prolonged reduction of GSH in APAP-treated IL-4(-/-) mice appeared to contribute toward increased liver injury by causing a sustained activation of c-Jun-N-terminal kinase (JNK) since levels of phosphorylated JNK remained significantly higher in the IL-4(-/-) mice up to 24 h after APAP treatment.	4-amino-N-acetyl-N-methylaniline	306-310	interleukin 4	Mus musculus	67-71
22107450-6	2012	We also report that the prolonged reduction of GSH in APAP-treated IL-4(-/-) mice appeared to contribute toward increased liver injury by causing a sustained activation of c-Jun-N-terminal kinase (JNK) since levels of phosphorylated JNK remained significantly higher in the IL-4(-/-) mice up to 24 h after APAP treatment.	4-amino-N-acetyl-N-methylaniline	306-310	mitogen-activated protein kinase 8	Mus musculus	172-195
22107450-6	2012	We also report that the prolonged reduction of GSH in APAP-treated IL-4(-/-) mice appeared to contribute toward increased liver injury by causing a sustained activation of c-Jun-N-terminal kinase (JNK) since levels of phosphorylated JNK remained significantly higher in the IL-4(-/-) mice up to 24 h after APAP treatment.	4-amino-N-acetyl-N-methylaniline	306-310	mitogen-activated protein kinase 8	Mus musculus	197-200
21654829-7	2011	Furthermore, we found that APAP strongly induces the expression of Bim in a c-JNK-dependent manner.	4-amino-N-acetyl-N-methylaniline	27-31	BCL2-like 11 (apoptosis facilitator)	Mus musculus	67-70
21654829-7	2011	Furthermore, we found that APAP strongly induces the expression of Bim in a c-JNK-dependent manner.	4-amino-N-acetyl-N-methylaniline	27-31	mitogen-activated protein kinase 8	Mus musculus	78-81
21654829-8	2011	Consequently, TRAIL- or Bim-deficient mice were substantially protected from APAP-induced liver damage.	4-amino-N-acetyl-N-methylaniline	77-81	tumor necrosis factor (ligand) superfamily, member 10	Mus musculus	14-19
22902588-3	2012	Since hypoxia inducible factor-one alpha (HIF-1alpha) is induced very early in APAP toxicity, a role for oxidative stress in the induction has been postulated.	4-amino-N-acetyl-N-methylaniline	79-83	hypoxia inducible factor 1, alpha subunit	Mus musculus	42-52
22902588-12	2012	In summary, the MPT inhibitor TFP delayed the onset of toxicity and lowered HIF-1alpha induction in APAP treated mice.	4-amino-N-acetyl-N-methylaniline	100-104	hypoxia inducible factor 1, alpha subunit	Mus musculus	76-86
21654829-9	2011	This study identifies the TRAIL-JNK-Bim axis as a novel target in the treatment of APAP-induced liver damage and substantiates its general role in hepatocyte death.	4-amino-N-acetyl-N-methylaniline	83-87	tumor necrosis factor (ligand) superfamily, member 10	Mus musculus	26-31
21654829-9	2011	This study identifies the TRAIL-JNK-Bim axis as a novel target in the treatment of APAP-induced liver damage and substantiates its general role in hepatocyte death.	4-amino-N-acetyl-N-methylaniline	83-87	mitogen-activated protein kinase 8	Mus musculus	32-35
21654829-9	2011	This study identifies the TRAIL-JNK-Bim axis as a novel target in the treatment of APAP-induced liver damage and substantiates its general role in hepatocyte death.	4-amino-N-acetyl-N-methylaniline	83-87	BCL2-like 11 (apoptosis facilitator)	Mus musculus	36-39
21316383-5	2011	We previously reported the induction of HIF-1alpha in mice with APAP toxicity and have shown that VEGF is important in hepatocyte regeneration following APAP toxicity.	4-amino-N-acetyl-N-methylaniline	64-68	hypoxia inducible factor 1, alpha subunit	Mus musculus	40-50
21316383-9	2011	Subsequent studies with the MPT inhibitor cyclosporine A showed that cyclosporine A (CYC; 10mg/kg) reduced HIF-1alpha induction in APAP treated mice at 1 and 4h and did not inhibit the metabolism of APAP (depletion of hepatic non-protein sulfhydryls and hepatic protein adduct levels).	4-amino-N-acetyl-N-methylaniline	131-135	hypoxia inducible factor 1, alpha subunit	Mus musculus	107-117
20207720-3	2010	The amount of SAA needed for the metabolism of two doses of APAP is equivalent to 62% of the recommended dietary allowance (RDA) for SAA in humans.	4-amino-N-acetyl-N-methylaniline	60-64	serum amyloid A1 cluster	Homo sapiens	14-17
21135413-2	2011	The objective of the present study was to examine the role of VEGF receptor 1 (VEGFR1) signaling in hepatic tissue repair after acetaminophen (N-acetyl-para-aminophenol) (APAP)-induced liver injury.	4-amino-N-acetyl-N-methylaniline	143-168	FMS-like tyrosine kinase 1	Mus musculus	62-77
21135413-2	2011	The objective of the present study was to examine the role of VEGF receptor 1 (VEGFR1) signaling in hepatic tissue repair after acetaminophen (N-acetyl-para-aminophenol) (APAP)-induced liver injury.	4-amino-N-acetyl-N-methylaniline	143-168	FMS-like tyrosine kinase 1	Mus musculus	79-85
21205919-15	2011	The data indicate that MnSOD inactivation by nitration is an early event in APAP-induced hepatic toxicity.	4-amino-N-acetyl-N-methylaniline	76-80	superoxide dismutase 2, mitochondrial	Mus musculus	23-28
20207720-3	2010	The amount of SAA needed for the metabolism of two doses of APAP is equivalent to 62% of the recommended dietary allowance (RDA) for SAA in humans.	4-amino-N-acetyl-N-methylaniline	60-64	serum amyloid A1 cluster	Homo sapiens	133-136
19969075-0	2010	Arjunolic acid, a triterpenoid saponin, prevents acetaminophen (APAP)-induced liver and hepatocyte injury via the inhibition of APAP bioactivation and JNK-mediated mitochondrial protection.	4-amino-N-acetyl-N-methylaniline	64-68	mitogen-activated protein kinase 8	Rattus norvegicus	151-154
20067817-4	2010	APAP exposure for 24h significantly increased plasma level of blood urea nitrogen (BUN), creatinine, uric acid, TNF-alpha, NO production, urinary gamma-glutamyl transpeptidase (gamma-GT) activity, total urinary protein and urinary glucose level accompanied by a decrease in Na(+)-K(+)-ATPase activity.	4-amino-N-acetyl-N-methylaniline	0-4	tumor necrosis factor	Mus musculus	112-121
20067817-7	2010	Besides, APAP exposure significantly reduced mitochondrial membrane potential and induced up-regulation of CYP2E1 in renal tissues although JNK did not play any significant role in this APAP-induced renal pathophysiology.	4-amino-N-acetyl-N-methylaniline	9-13	cytochrome P450, family 2, subfamily e, polypeptide 1	Mus musculus	107-113
20024105-6	2009	In contrast, the efficacy of ApAP as an inhibitor of lipid hydroperoxide biosynthesis by soybean LOX-1 (sLOX-1) increased upon incorporation of nitrogen into the ring, suggesting a different mechanism of inhibition dependent on the acidity of the phenolic O-H which may involve chelation of the catalytic non-heme iron atom.	4-amino-N-acetyl-N-methylaniline	29-33	oxidized low density lipoprotein receptor 1	Homo sapiens	104-110
19117117-11	2009	A significant increase in MDA and decreases in GSH level and GSH-Px, CAT, and SOD activity indicated that APAP-induced renal damage was mediated through oxidative stress.	4-amino-N-acetyl-N-methylaniline	106-110	catalase	Rattus norvegicus	69-72
16552707-8	2006	An HO-1 inhibitor, tin-protoporphyrin-IX, significantly increased APAP-induced mortality, implicating HO-1 as a protective molecule for APAP-induced liver injury.	4-amino-N-acetyl-N-methylaniline	66-70	heme oxygenase 1	Mus musculus	3-7
17584759-10	2007	Additionally, male Gclm wild-type mice demonstrated greater APAP-induced hepatotoxicity than female wild-type mice.	4-amino-N-acetyl-N-methylaniline	60-64	glutamate-cysteine ligase, modifier subunit	Mus musculus	19-23
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.	4-amino-N-acetyl-N-methylaniline	62-66	glutamate-cysteine ligase, modifier subunit	Mus musculus	70-74
16552707-4	2006	APAP injection markedly augmented intrahepatic gene expression of inducible nitric oxide synthase (iNOS) and heme oxygenase (HO)-1.	4-amino-N-acetyl-N-methylaniline	0-4	nitric oxide synthase 2, inducible	Mus musculus	66-97
16552707-4	2006	APAP injection markedly augmented intrahepatic gene expression of inducible nitric oxide synthase (iNOS) and heme oxygenase (HO)-1.	4-amino-N-acetyl-N-methylaniline	0-4	nitric oxide synthase 2, inducible	Mus musculus	99-103
16552707-5	2006	Moreover, neutrophils expressed iNOS, which is presumed to be an aggravating molecule for APAP-induced liver injury, while HO-1 was mainly expressed by macrophages.	4-amino-N-acetyl-N-methylaniline	90-94	nitric oxide synthase 2, inducible	Mus musculus	32-36
18700144-11	2008	Primary hepatocyte culture also revealed that ASK1 and JNK, but not p38, contributed to direct APAP-induced cellular damage.	4-amino-N-acetyl-N-methylaniline	95-99	mitogen-activated protein kinase kinase kinase 5	Mus musculus	46-50
18700144-11	2008	Primary hepatocyte culture also revealed that ASK1 and JNK, but not p38, contributed to direct APAP-induced cellular damage.	4-amino-N-acetyl-N-methylaniline	95-99	mitogen-activated protein kinase 8	Mus musculus	55-58
17935745-2	2008	Mice deficient in Nrf2 (Nrf2-null) are highly susceptible to acetaminophen (APAP) hepatotoxicity and exhibit lower basal and inducible expression of cytoprotective genes, including NADPH quinone oxidoreductase 1 (Nqo1) and glutamate cysteine ligase (catalytic subunit, or Gclc).	4-amino-N-acetyl-N-methylaniline	76-80	nuclear factor, erythroid derived 2, like 2	Mus musculus	18-22
17935745-2	2008	Mice deficient in Nrf2 (Nrf2-null) are highly susceptible to acetaminophen (APAP) hepatotoxicity and exhibit lower basal and inducible expression of cytoprotective genes, including NADPH quinone oxidoreductase 1 (Nqo1) and glutamate cysteine ligase (catalytic subunit, or Gclc).	4-amino-N-acetyl-N-methylaniline	76-80	nuclear factor, erythroid derived 2, like 2	Mus musculus	24-28
17935745-4	2008	It was hypothesized that induction of hepatic Mrp1-4 expression following APAP is Nrf2 dependent.	4-amino-N-acetyl-N-methylaniline	74-78	S100 calcium binding protein A9 (calgranulin B)	Mus musculus	46-52
17935745-4	2008	It was hypothesized that induction of hepatic Mrp1-4 expression following APAP is Nrf2 dependent.	4-amino-N-acetyl-N-methylaniline	74-78	nuclear factor, erythroid derived 2, like 2	Mus musculus	82-86
17935745-9	2008	Similarly, APAP treatment increased hepatic Mrp3 and Mrp4 mRNA and protein in WT, but not Nrf2-null mice.	4-amino-N-acetyl-N-methylaniline	11-15	prolactin family 2, subfamily c, member 4	Mus musculus	44-48
17935745-9	2008	Similarly, APAP treatment increased hepatic Mrp3 and Mrp4 mRNA and protein in WT, but not Nrf2-null mice.	4-amino-N-acetyl-N-methylaniline	11-15	prolactin family 2, subfamily c, member 5	Mus musculus	53-57
17935745-12	2008	These results show that Nrf2 mediates induction of Mrp3 and Mrp4 after APAP but does not affect Mrp1 or Mrp2.	4-amino-N-acetyl-N-methylaniline	71-75	nuclear factor, erythroid derived 2, like 2	Mus musculus	24-28
17935745-12	2008	These results show that Nrf2 mediates induction of Mrp3 and Mrp4 after APAP but does not affect Mrp1 or Mrp2.	4-amino-N-acetyl-N-methylaniline	71-75	prolactin family 2, subfamily c, member 4	Mus musculus	51-55
17935745-12	2008	These results show that Nrf2 mediates induction of Mrp3 and Mrp4 after APAP but does not affect Mrp1 or Mrp2.	4-amino-N-acetyl-N-methylaniline	71-75	prolactin family 2, subfamily c, member 5	Mus musculus	60-64
17053928-3	2007	The purpose of this study was to assess the combination of autoadjusting CPAP (APAP) and C-Flex in terms of (1) treatment efficacy, and (2) patient preference when compared to standard CPAP.	4-amino-N-acetyl-N-methylaniline	79-83	centromere protein J	Homo sapiens	73-77
16552707-6	2006	All anti-granulocyte antibody-treated neutropenic WT and most CXC chemokine receptor 2 (CXCR2)-deficient mice survived the same dose of APAP, with reduced neutrophil infiltration and iNOS expression, indicating the pathogenic roles of neutrophils in APAP-induced liver injury.	4-amino-N-acetyl-N-methylaniline	136-140	chemokine (C-X-C motif) receptor 2	Mus musculus	62-86
16552707-6	2006	All anti-granulocyte antibody-treated neutropenic WT and most CXC chemokine receptor 2 (CXCR2)-deficient mice survived the same dose of APAP, with reduced neutrophil infiltration and iNOS expression, indicating the pathogenic roles of neutrophils in APAP-induced liver injury.	4-amino-N-acetyl-N-methylaniline	136-140	chemokine (C-X-C motif) receptor 2	Mus musculus	88-93
16552707-8	2006	An HO-1 inhibitor, tin-protoporphyrin-IX, significantly increased APAP-induced mortality, implicating HO-1 as a protective molecule for APAP-induced liver injury.	4-amino-N-acetyl-N-methylaniline	66-70	heme oxygenase 1	Mus musculus	102-106
12143040-1	2002	Chronic alcohol consumption may potentiate acetaminophen (APAP) hepatotoxicity through enhanced formation of N-acetyl-p-benzoquinone imine (NAPQI) via induction of cytochrome P450 2E1 (CYP2E1).	4-amino-N-acetyl-N-methylaniline	58-62	cytochrome P450, family 2, subfamily e, polypeptide 1	Rattus norvegicus	164-183
16548897-6	2006	The more recent development of auto-adjusting CPAP (APAP) is a reflection of the understanding that the pressure required to prevent UA collapse fluctuates throughout the night and results in a lower mean pressure that may be more comfortable for some patients.	4-amino-N-acetyl-N-methylaniline	52-56	centromere protein J	Homo sapiens	46-50
15205452-8	2004	CYP2E1 activity and hepatic glutathione (GSH) levels in untreated mice showed significant 24-h rhythms associated with APAP toxicity rhythm.	4-amino-N-acetyl-N-methylaniline	119-123	cytochrome P450, family 2, subfamily e, polypeptide 1	Mus musculus	0-6
16420515-2	2006	In the present study, the possible influence of PAF-R antagonist (BN52021) on the protection of liver injury after 4-hydroxyacetanilide, N-acetyl-p-aminophenol, paracetamol (APAP) intoxication was investigated.	4-amino-N-acetyl-N-methylaniline	174-178	platelet-activating factor receptor	Rattus norvegicus	48-53
16420515-5	2006	RESULTS: APAP was found to cause an acute hepatic injury, evident by alterations of biochemical (serum enzymes: aspartate aminotransferase (AST), alanine aminotransferase (ALT) and alkaline phosphatase) and liver histopathological (degree of necrosis and apoptosis) indices, which was followed by liver regeneration, evident by three independent indices ([3H] thymidine incorporation into hepatic DNA, liver thymidine kinase activity and hepatocyte mitotic index).	4-amino-N-acetyl-N-methylaniline	9-13	glutamic-oxaloacetic transaminase 2	Rattus norvegicus	112-138
16420515-5	2006	RESULTS: APAP was found to cause an acute hepatic injury, evident by alterations of biochemical (serum enzymes: aspartate aminotransferase (AST), alanine aminotransferase (ALT) and alkaline phosphatase) and liver histopathological (degree of necrosis and apoptosis) indices, which was followed by liver regeneration, evident by three independent indices ([3H] thymidine incorporation into hepatic DNA, liver thymidine kinase activity and hepatocyte mitotic index).	4-amino-N-acetyl-N-methylaniline	9-13	glutamic-oxaloacetic transaminase 2	Rattus norvegicus	140-143
12143040-1	2002	Chronic alcohol consumption may potentiate acetaminophen (APAP) hepatotoxicity through enhanced formation of N-acetyl-p-benzoquinone imine (NAPQI) via induction of cytochrome P450 2E1 (CYP2E1).	4-amino-N-acetyl-N-methylaniline	58-62	cytochrome P450, family 2, subfamily e, polypeptide 1	Rattus norvegicus	185-191
12143040-8	2002	Partial inhibition of NAPQI formation by CYP2E1 inhibitor diethyldithiocarbamate to that of pair-fed controls abolished APAP toxicity in the 10-day ethanol group only.	4-amino-N-acetyl-N-methylaniline	120-124	cytochrome P450, family 2, subfamily e, polypeptide 1	Rattus norvegicus	41-47
11995823-8	2001	Non growing suspended cells of strain ST1 degraded 68, 96 and 76.8% of 4-aminophenol (1,000 ppm), phenol (500 ppm) and 4-acetamidophenol (1,000 ppm), respectively, in 72 hrs.	4-amino-N-acetyl-N-methylaniline	119-136	syndecan binding protein	Homo sapiens	38-41
34289451-3	2021	RESULTS: In this present study, by employing an acute liver injury induced by APAP overdose mouse model, we demonstrated that DJ-1 knockout (DJ-1-/-) mice showed reduced liver injury and lower mortality.	4-amino-N-acetyl-N-methylaniline	78-82	Parkinson disease (autosomal recessive, early onset) 7	Mus musculus	126-130
10535745-1	1999	The role of NAD(P)H:quinone reductase (QR; EC 1.6.99.2) in the alcohol-derived protective effect against hepatotoxicity caused by acetaminophen (APAP) was studied.	4-amino-N-acetyl-N-methylaniline	145-149	crystallin, zeta	Mus musculus	39-41
10535745-2	1999	In mice pretreated with dicoumarol (30 mg/kg), an inhibitor of QR, hepatic necrosis caused by APAP (400 mg/kg) was potentiated.	4-amino-N-acetyl-N-methylaniline	94-98	crystallin, zeta	Mus musculus	63-65
10535745-9	1999	These results suggest that ethanol inhibited not only the microsomal (CYP2E1 mediated) formation of a toxic quinone metabolite from APAP, but also accelerated the conversion of the toxic quinone metabolite produced back to APAP by stimulating cytoplasmic QR activity.	4-amino-N-acetyl-N-methylaniline	132-136	cytochrome P450, family 2, subfamily e, polypeptide 1	Mus musculus	70-76
10535745-9	1999	These results suggest that ethanol inhibited not only the microsomal (CYP2E1 mediated) formation of a toxic quinone metabolite from APAP, but also accelerated the conversion of the toxic quinone metabolite produced back to APAP by stimulating cytoplasmic QR activity.	4-amino-N-acetyl-N-methylaniline	223-227	crystallin, zeta	Mus musculus	255-257
9704905-3	1998	at 08:00, 14:00 or 20:00 h. APAP at this dose was markedly hepatotoxic to mice when administered at 20:00 h as determined by increases in serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities, and by decreases in hepatic glucose-6-phosphatase (G-6-Pase) activity.	4-amino-N-acetyl-N-methylaniline	28-32	glutamic pyruvic transaminase, soluble	Mus musculus	144-168
9704905-3	1998	at 08:00, 14:00 or 20:00 h. APAP at this dose was markedly hepatotoxic to mice when administered at 20:00 h as determined by increases in serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities, and by decreases in hepatic glucose-6-phosphatase (G-6-Pase) activity.	4-amino-N-acetyl-N-methylaniline	28-32	glutamic pyruvic transaminase, soluble	Mus musculus	170-173
9704905-3	1998	at 08:00, 14:00 or 20:00 h. APAP at this dose was markedly hepatotoxic to mice when administered at 20:00 h as determined by increases in serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities, and by decreases in hepatic glucose-6-phosphatase (G-6-Pase) activity.	4-amino-N-acetyl-N-methylaniline	28-32	solute carrier family 17 (anion/sugar transporter), member 5	Mus musculus	179-205
9704905-3	1998	at 08:00, 14:00 or 20:00 h. APAP at this dose was markedly hepatotoxic to mice when administered at 20:00 h as determined by increases in serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities, and by decreases in hepatic glucose-6-phosphatase (G-6-Pase) activity.	4-amino-N-acetyl-N-methylaniline	28-32	solute carrier family 17 (anion/sugar transporter), member 5	Mus musculus	207-210
9704905-3	1998	at 08:00, 14:00 or 20:00 h. APAP at this dose was markedly hepatotoxic to mice when administered at 20:00 h as determined by increases in serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities, and by decreases in hepatic glucose-6-phosphatase (G-6-Pase) activity.	4-amino-N-acetyl-N-methylaniline	28-32	glucose-6-phosphatase, catalytic	Mus musculus	252-273
9704905-3	1998	at 08:00, 14:00 or 20:00 h. APAP at this dose was markedly hepatotoxic to mice when administered at 20:00 h as determined by increases in serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities, and by decreases in hepatic glucose-6-phosphatase (G-6-Pase) activity.	4-amino-N-acetyl-N-methylaniline	28-32	glucose-6-phosphatase, catalytic	Mus musculus	275-283
34558831-8	2021	Here, we identify hepatic NIK as a previously unrecognized mediator for acetaminophen (APAP)-induced acute liver failure.	4-amino-N-acetyl-N-methylaniline	87-91	mitogen-activated protein kinase kinase kinase 14	Mus musculus	26-29
34558831-9	2021	APAP treatment increased both NIK transcription and NIK protein stability in primary hepatocytes as well as in liver in mice.	4-amino-N-acetyl-N-methylaniline	0-4	mitogen-activated protein kinase kinase kinase 14	Mus musculus	30-33
34558831-9	2021	APAP treatment increased both NIK transcription and NIK protein stability in primary hepatocytes as well as in liver in mice.	4-amino-N-acetyl-N-methylaniline	0-4	mitogen-activated protein kinase kinase kinase 14	Mus musculus	52-55
34558831-10	2021	Hepatocyte-specific overexpression of NIK augmented APAP-induced liver oxidative stress in mice and increased hepatocyte death and mortality in a ROS-dependent manner.	4-amino-N-acetyl-N-methylaniline	52-56	mitogen-activated protein kinase kinase kinase 14	Mus musculus	38-41
34558831-12	2021	NIK increased lipid peroxidation and cell death in APAP-stimulated primary hepatocytes.	4-amino-N-acetyl-N-methylaniline	51-55	mitogen-activated protein kinase kinase kinase 14	Mus musculus	0-3
34558831-13	2021	Pretreatment with antioxidants or ferroptosis inhibitors blocked NIK/APAP-induced hepatocyte death.	4-amino-N-acetyl-N-methylaniline	69-73	mitogen-activated protein kinase kinase kinase 14	Mus musculus	65-68
34289451-3	2021	RESULTS: In this present study, by employing an acute liver injury induced by APAP overdose mouse model, we demonstrated that DJ-1 knockout (DJ-1-/-) mice showed reduced liver injury and lower mortality.	4-amino-N-acetyl-N-methylaniline	78-82	Parkinson disease (autosomal recessive, early onset) 7	Mus musculus	141-145
34289451-9	2021	CONCLUSION: our findings clearly defined that deletion of DJ-1 protects APAP-induced acute liver injury through decreasing inflammatory response, and suggest DJ-1 as a potential therapeutic and/or prophylactic target of APAP-induced acute liver injury.	4-amino-N-acetyl-N-methylaniline	72-76	Parkinson disease (autosomal recessive, early onset) 7	Mus musculus	58-62
34289451-9	2021	CONCLUSION: our findings clearly defined that deletion of DJ-1 protects APAP-induced acute liver injury through decreasing inflammatory response, and suggest DJ-1 as a potential therapeutic and/or prophylactic target of APAP-induced acute liver injury.	4-amino-N-acetyl-N-methylaniline	220-224	Parkinson disease (autosomal recessive, early onset) 7	Mus musculus	58-62
34289451-9	2021	CONCLUSION: our findings clearly defined that deletion of DJ-1 protects APAP-induced acute liver injury through decreasing inflammatory response, and suggest DJ-1 as a potential therapeutic and/or prophylactic target of APAP-induced acute liver injury.	4-amino-N-acetyl-N-methylaniline	220-224	Parkinson disease (autosomal recessive, early onset) 7	Mus musculus	158-162
32517496-8	2021	INNOVATION: This work demonstrates that both Trx and GSH systems are susceptible to APAP toxicity in vivo, and that the thiol-dependent redox environment is a key factor in determining the extent of APAP-induced hepatotoxicity.	4-amino-N-acetyl-N-methylaniline	84-88	thioredoxin 1	Mus musculus	45-48
3806412-1	1987	Pretreatment of mice with multiple doses of phenobarbital (PB) potentiates N-acetyl-para-aminophenol (APAP) hepatotoxicity through induction of cytochrome P-450, thus increasing the formation of APAP-reactive metabolites.	4-amino-N-acetyl-N-methylaniline	75-100	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	144-160
3806412-1	1987	Pretreatment of mice with multiple doses of phenobarbital (PB) potentiates N-acetyl-para-aminophenol (APAP) hepatotoxicity through induction of cytochrome P-450, thus increasing the formation of APAP-reactive metabolites.	4-amino-N-acetyl-N-methylaniline	102-106	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	144-160
3806412-1	1987	Pretreatment of mice with multiple doses of phenobarbital (PB) potentiates N-acetyl-para-aminophenol (APAP) hepatotoxicity through induction of cytochrome P-450, thus increasing the formation of APAP-reactive metabolites.	4-amino-N-acetyl-N-methylaniline	195-199	cytochrome P450, family 21, subfamily a, polypeptide 1	Mus musculus	144-160
3965129-8	1985	With livers of animals fed 4-acetamidophenol, a hepatotoxin chemically related to AAF, small decreases were noted in NADH:ferricyanide reductase, but not in xanthine dehydrogenase nor in DT-diaphorase.	4-amino-N-acetyl-N-methylaniline	27-44	xanthine dehydrogenase	Rattus norvegicus	157-179
3965129-8	1985	With livers of animals fed 4-acetamidophenol, a hepatotoxin chemically related to AAF, small decreases were noted in NADH:ferricyanide reductase, but not in xanthine dehydrogenase nor in DT-diaphorase.	4-amino-N-acetyl-N-methylaniline	27-44	NAD(P)H quinone dehydrogenase 1	Rattus norvegicus	187-200
699902-3	1978	The conversion of [4-(3)H]acetanilide to 4-hydroxyacetanilide by rat liver microsomes (or purified cytochrome P-450) in the presence of either cumene hydroperoxide or NADPH is attended by comparable "NIH shifts".	4-amino-N-acetyl-N-methylaniline	41-61	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	99-115
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).	4-amino-N-acetyl-N-methylaniline	174-178	transforming growth factor alpha	Homo sapiens	68-75
34141985-4	2021	We found that both high-fructose diet feeding before APAP injection and fructose gavage after APAP injection reduced APAP-induced liver injury with a concomitant induction of the hepatic carbohydrate-response element-binding protein alpha (ChREBPalpha)-fibroblast growth factor 21 (FGF21) pathway.	4-amino-N-acetyl-N-methylaniline	53-57	fibroblast growth factor 21	Mus musculus	253-280
34141985-4	2021	We found that both high-fructose diet feeding before APAP injection and fructose gavage after APAP injection reduced APAP-induced liver injury with a concomitant induction of the hepatic carbohydrate-response element-binding protein alpha (ChREBPalpha)-fibroblast growth factor 21 (FGF21) pathway.	4-amino-N-acetyl-N-methylaniline	53-57	fibroblast growth factor 21	Mus musculus	282-287
34141985-4	2021	We found that both high-fructose diet feeding before APAP injection and fructose gavage after APAP injection reduced APAP-induced liver injury with a concomitant induction of the hepatic carbohydrate-response element-binding protein alpha (ChREBPalpha)-fibroblast growth factor 21 (FGF21) pathway.	4-amino-N-acetyl-N-methylaniline	94-98	fibroblast growth factor 21	Mus musculus	253-280
34141985-4	2021	We found that both high-fructose diet feeding before APAP injection and fructose gavage after APAP injection reduced APAP-induced liver injury with a concomitant induction of the hepatic carbohydrate-response element-binding protein alpha (ChREBPalpha)-fibroblast growth factor 21 (FGF21) pathway.	4-amino-N-acetyl-N-methylaniline	94-98	fibroblast growth factor 21	Mus musculus	282-287
34141985-4	2021	We found that both high-fructose diet feeding before APAP injection and fructose gavage after APAP injection reduced APAP-induced liver injury with a concomitant induction of the hepatic carbohydrate-response element-binding protein alpha (ChREBPalpha)-fibroblast growth factor 21 (FGF21) pathway.	4-amino-N-acetyl-N-methylaniline	117-121	fibroblast growth factor 21	Mus musculus	253-280
34141985-7	2021	Furthermore, overexpression of FGF21 in the liver was sufficient to reverse liver toxicity in APAP-injected Chrebpalpha-LKO mice.	4-amino-N-acetyl-N-methylaniline	94-98	fibroblast growth factor 21	Mus musculus	31-36
34141985-8	2021	Conclusion: Fructose protects against APAP-induced hepatotoxicity likely through its ability to activate the hepatocyte ChREBPalpha-FGF21 axis.	4-amino-N-acetyl-N-methylaniline	38-42	fibroblast growth factor 21	Mus musculus	132-137
35259261-4	2022	STUDY DESIGN, SIZE, DURATION: This study consists of (i) an in vivo human pharmaceutical APAP exposure experiment to understand to what degree APAP reaches the sperm cells in the seminal fluid; (ii) in vitro calcium imaging and functional experiments in freshly donated human sperm cells to investigate CatSper channel-dependent activation by APAP and its metabolites; and (iii) experiments to understand the in situ capabilities of human sperm cells to form APAP metabolite AM404.	4-amino-N-acetyl-N-methylaniline	143-147	cation channel sperm associated 1	Homo sapiens	303-310
32517496-3	2021	RESULTS: APAP treatment affected mouse liver selenoprotein thioredoxin reductase (TrxR) activity and glutathione level in a dose- and time-dependent manner.	4-amino-N-acetyl-N-methylaniline	9-13	peroxiredoxin 2	Mus musculus	59-80
32517496-3	2021	RESULTS: APAP treatment affected mouse liver selenoprotein thioredoxin reductase (TrxR) activity and glutathione level in a dose- and time-dependent manner.	4-amino-N-acetyl-N-methylaniline	9-13	peroxiredoxin 2	Mus musculus	82-86
32517496-5	2021	The decreases of ratio of GSH/GSSG, TrxR activity and the increase of protein S-glutathionylation were correlated with the APAP-induced hepatotoxicity.	4-amino-N-acetyl-N-methylaniline	123-127	peroxiredoxin 2	Mus musculus	36-40
32517496-7	2021	An increase in the oxidation state of the TrxR-mediated system, including cytosolic thioredoxin1 (Trx1) and peroxiredoxin1/2, and mitochondrial Trx2 and Prx3, were found in the livers from mice reared on selenium-deficient and excess selenium-supplemented diets upon APAP-treatment.	4-amino-N-acetyl-N-methylaniline	267-271	peroxiredoxin 2	Mus musculus	42-46
32517496-8	2021	INNOVATION: This work demonstrates that both Trx and GSH systems are susceptible to APAP toxicity in vivo, and that the thiol-dependent redox environment is a key factor in determining the extent of APAP-induced hepatotoxicity.	4-amino-N-acetyl-N-methylaniline	199-203	thioredoxin 1	Mus musculus	45-48
32517496-10	2021	CONCLUSION: APAP treatment in mice interrupts the function of the Trx and GSH system which are the main enzymatic antioxidant systems, in both cytosol and mitochondria.	4-amino-N-acetyl-N-methylaniline	12-16	thioredoxin 1	Mus musculus	66-69
32682928-4	2020	Baicalin alleviated APAP-induced hepatic parenchymal cells injury and enhanced the number of mitotic and proliferating cell nuclear antigen (PCNA)-positive hepatocytes in APAP-intoxicated mice.	4-amino-N-acetyl-N-methylaniline	171-175	proliferating cell nuclear antigen	Mus musculus	105-139
33795997-10	2021	Moreover, the test chalcones (3a, 3f & 3 g) antagonized the effect of 4-acetaminophenol and thus, raised the catalase (CAT) and superoxide dismutase (SOD) while decreased the malondialdehyde (MDA) in experimental animals.	4-amino-N-acetyl-N-methylaniline	70-87	catalase	Rattus norvegicus	109-117
33795997-10	2021	Moreover, the test chalcones (3a, 3f & 3 g) antagonized the effect of 4-acetaminophenol and thus, raised the catalase (CAT) and superoxide dismutase (SOD) while decreased the malondialdehyde (MDA) in experimental animals.	4-amino-N-acetyl-N-methylaniline	70-87	catalase	Rattus norvegicus	119-122
33382198-2	2021	During the course of a study examining interactions between the common antipyretic acetaminophen (APAP; paracetamol) and interleukin-1beta (IL-1beta)-induced inflammation in neonatal mice we observed that subcutaneous (s.c.) injection of IL-1beta often leads to significantly shorter, blunt-tipped tails.	4-amino-N-acetyl-N-methylaniline	98-102	interleukin 1 alpha	Mus musculus	238-246
32846216-7	2020	3, 293 T cells overexpressing Selenov gene (OE) were treated with APAP (0 to 4 mM) for 24 h or H2O2 (0 to 0.4 mM) for 12 h.Compared with the WT, the DQ- and APAP-injected KO mice had higher (P < 0.05) serum alanine aminotransferase activities and hepatic malondialdehyde (MDA), protein carbonyl, endoplasmic reticulum (ER) stress-related proteins (BIP and CHOP), apoptosis-related proteins (FAK and caspase-9), and 3-nitrotyrosine, along with lower total anti-oxidizing-capability (T-AOC) and severer hepatic necrosis.	4-amino-N-acetyl-N-methylaniline	66-70	selenoprotein V	Homo sapiens	30-37
32682928-10	2020	Furthermore, the baicalin-provided NLRP3 inflammasome activation and promotion on liver regeneration after APAP-induced liver injury in wild-type mice were diminished in Nrf2 knockout mice.	4-amino-N-acetyl-N-methylaniline	107-111	NLR family, pyrin domain containing 3	Mus musculus	35-40
32682928-4	2020	Baicalin alleviated APAP-induced hepatic parenchymal cells injury and enhanced the number of mitotic and proliferating cell nuclear antigen (PCNA)-positive hepatocytes in APAP-intoxicated mice.	4-amino-N-acetyl-N-methylaniline	171-175	proliferating cell nuclear antigen	Mus musculus	141-145
32682928-6	2020	Baicalin induced the activation of NOD-like receptor pyrin domain containing 3 (NLRP3) inflammasome, leading to the increased hepatic expression of interleukin-18 (IL-18) and IL-1beta in APAP-intoxicated mice.	4-amino-N-acetyl-N-methylaniline	187-191	NLR family, pyrin domain containing 3	Mus musculus	80-85
32682928-6	2020	Baicalin induced the activation of NOD-like receptor pyrin domain containing 3 (NLRP3) inflammasome, leading to the increased hepatic expression of interleukin-18 (IL-18) and IL-1beta in APAP-intoxicated mice.	4-amino-N-acetyl-N-methylaniline	187-191	interleukin 18	Mus musculus	148-162
32682928-6	2020	Baicalin induced the activation of NOD-like receptor pyrin domain containing 3 (NLRP3) inflammasome, leading to the increased hepatic expression of interleukin-18 (IL-18) and IL-1beta in APAP-intoxicated mice.	4-amino-N-acetyl-N-methylaniline	187-191	interleukin 18	Mus musculus	164-169
32682928-6	2020	Baicalin induced the activation of NOD-like receptor pyrin domain containing 3 (NLRP3) inflammasome, leading to the increased hepatic expression of interleukin-18 (IL-18) and IL-1beta in APAP-intoxicated mice.	4-amino-N-acetyl-N-methylaniline	187-191	interleukin 1 alpha	Mus musculus	175-183
32682928-8	2020	Moreover, the baicalin-provided promotion on liver regeneration in APAP-intoxicated mice was diminished after the application of NLRP3 inhibitor MCC950 and the recombinant mouse IL-18 binding protein (rmIL-18BP).	4-amino-N-acetyl-N-methylaniline	67-71	NLR family, pyrin domain containing 3	Mus musculus	129-134
32682928-9	2020	Baicalin induced the cytosolic accumulation of nuclear factor erythroid 2-related factor 2 (Nrf2), and increased the interaction between Nrf2 with Nlrp3, ASC and pro-caspase-1 in livers from APAP-intoxicated mice.	4-amino-N-acetyl-N-methylaniline	191-195	nuclear factor, erythroid derived 2, like 2	Mus musculus	137-141
32793668-17	2020	Conclusions: These data indicate that DB alleviated hepatotoxicity caused by APAP at least in part via Neu1 inhibition, Akt/mTOR pathway is involved in the detoxification effect of DB on acetaminophen-induced hepatotoxicity.	4-amino-N-acetyl-N-methylaniline	77-81	neuraminidase 1	Mus musculus	103-107
32793668-17	2020	Conclusions: These data indicate that DB alleviated hepatotoxicity caused by APAP at least in part via Neu1 inhibition, Akt/mTOR pathway is involved in the detoxification effect of DB on acetaminophen-induced hepatotoxicity.	4-amino-N-acetyl-N-methylaniline	77-81	thymoma viral proto-oncogene 1	Mus musculus	120-123
32793668-17	2020	Conclusions: These data indicate that DB alleviated hepatotoxicity caused by APAP at least in part via Neu1 inhibition, Akt/mTOR pathway is involved in the detoxification effect of DB on acetaminophen-induced hepatotoxicity.	4-amino-N-acetyl-N-methylaniline	77-81	mechanistic target of rapamycin kinase	Mus musculus	124-128
32484845-4	2020	We provide the means to challenge the ability of closely related model mechanisms to generate patterns of simulated hepatic injury and ALT release that scale (or not) to be quantitatively similar to the wet-lab validation targets, which are elevated plasma ALT values following acetaminophen (APAP) exposure in mice.	4-amino-N-acetyl-N-methylaniline	293-297	glutamic pyruvic transaminase, soluble	Mus musculus	135-138
32213564-4	2020	In this report, using genetic and pharmacological approaches, we demonstrate that whereas Gpbar1 gene deletion worsens the severity of liver injury, its pharmacological activation by 6beta-ethyl-3a,7b-dihydroxy-5b-cholan-24-ol rescues mice from liver injury caused by APAP.	4-amino-N-acetyl-N-methylaniline	268-272	G protein-coupled bile acid receptor 1	Mus musculus	90-96
32029527-7	2020	Specifically, HNF1alpha-AS1 knockdown decreased APAP toxicity with increased cell viability and decreased LDH release, whereas HNF4alpha-AS1 knockdown exacerbated APAP toxicity, with opposite effects in the MTT and LDH assays.	4-amino-N-acetyl-N-methylaniline	48-52	HNF1 homeobox A	Homo sapiens	14-23
32029527-7	2020	Specifically, HNF1alpha-AS1 knockdown decreased APAP toxicity with increased cell viability and decreased LDH release, whereas HNF4alpha-AS1 knockdown exacerbated APAP toxicity, with opposite effects in the MTT and LDH assays.	4-amino-N-acetyl-N-methylaniline	48-52	prostaglandin D2 receptor	Homo sapiens	24-27
32029527-7	2020	Specifically, HNF1alpha-AS1 knockdown decreased APAP toxicity with increased cell viability and decreased LDH release, whereas HNF4alpha-AS1 knockdown exacerbated APAP toxicity, with opposite effects in the MTT and LDH assays.	4-amino-N-acetyl-N-methylaniline	163-167	hepatocyte nuclear factor 4 alpha	Homo sapiens	127-136
32029527-7	2020	Specifically, HNF1alpha-AS1 knockdown decreased APAP toxicity with increased cell viability and decreased LDH release, whereas HNF4alpha-AS1 knockdown exacerbated APAP toxicity, with opposite effects in the MTT and LDH assays.	4-amino-N-acetyl-N-methylaniline	163-167	prostaglandin D2 receptor	Homo sapiens	137-140
30669860-7	2019	SAG-Sh-SeNPs showed enhanced protection against APAP toxicity in comparison to Sh-SeNPs due to synergistic effect of SAG and Sh-SeNPs.	4-amino-N-acetyl-N-methylaniline	48-52	S-antigen visual arrestin	Rattus norvegicus	0-3
30669860-7	2019	SAG-Sh-SeNPs showed enhanced protection against APAP toxicity in comparison to Sh-SeNPs due to synergistic effect of SAG and Sh-SeNPs.	4-amino-N-acetyl-N-methylaniline	48-52	S-antigen visual arrestin	Rattus norvegicus	117-120
30669860-8	2019	SAG-Sh-SeNPs protected the liver and kidney against APAP toxicity through reducing oxidative stress, enhancing endogenous antioxidants and protecting mitochondrial functions.	4-amino-N-acetyl-N-methylaniline	52-56	S-antigen visual arrestin	Rattus norvegicus	0-3