PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
34963515-0	2022	Corrigendum to Acacetin inhibits RANKL-induced osteoclastogenesis and LPS-induced bone loss by modulating NFATc1 transcription.	acacetin	15-23	TNF superfamily member 11	Homo sapiens	33-38
34963515-0	2022	Corrigendum to Acacetin inhibits RANKL-induced osteoclastogenesis and LPS-induced bone loss by modulating NFATc1 transcription.	acacetin	15-23	nuclear factor of activated T cells 1	Homo sapiens	106-112
34763194-0	2021	Acacetin inhibits RANKL-induced osteoclastogenesis and LPS-induced bone loss by modulating NFATc1 transcription.	acacetin	0-8	TNF superfamily member 11	Homo sapiens	18-23
34886812-0	2021	Amelioration of human peritoneal mesothelial cell co-culture-evoked malignant potential of ovarian cancer cells by acacetin involves LPA release-activated RAGE-PI3K/AKT signaling.	acacetin	115-123	advanced glycosylation end-product specific receptor	Homo sapiens	155-159
34886812-0	2021	Amelioration of human peritoneal mesothelial cell co-culture-evoked malignant potential of ovarian cancer cells by acacetin involves LPA release-activated RAGE-PI3K/AKT signaling.	acacetin	115-123	AKT serine/threonine kinase 1	Homo sapiens	165-168
34886812-11	2021	Furthermore, mesothelial cell-evoked malignant characteristics were inhibited when mesothelial cells were pre-treated with acacetin via restraining cell proliferation and invasion, concomitant with decreases in proliferation-related PCNA, MMP-2 and MMP-9 levels.	acacetin	123-131	matrix metallopeptidase 2	Homo sapiens	239-244
34886812-11	2021	Furthermore, mesothelial cell-evoked malignant characteristics were inhibited when mesothelial cells were pre-treated with acacetin via restraining cell proliferation and invasion, concomitant with decreases in proliferation-related PCNA, MMP-2 and MMP-9 levels.	acacetin	123-131	matrix metallopeptidase 9	Homo sapiens	249-254
34886812-12	2021	Simultaneously, acacetin reduced mesothelial cell-induced transcripts and production of pro-inflammatory cytokine IL-6 and IL-8 in ovarian cancer cells.	acacetin	16-24	interleukin 6	Homo sapiens	114-118
34886812-12	2021	Simultaneously, acacetin reduced mesothelial cell-induced transcripts and production of pro-inflammatory cytokine IL-6 and IL-8 in ovarian cancer cells.	acacetin	16-24	C-X-C motif chemokine ligand 8	Homo sapiens	123-127
34886812-13	2021	Mechanically, acacetin decreased lysophosphatidic acid (LPA) release from mesothelial cells, and subsequent activation of receptor for advanced glycation end-products (RAGE)-PI3K/AKT signaling in ovarian cancer cells.	acacetin	14-22	advanced glycosylation end-product specific receptor	Homo sapiens	122-166
34886812-13	2021	Mechanically, acacetin decreased lysophosphatidic acid (LPA) release from mesothelial cells, and subsequent activation of receptor for advanced glycation end-products (RAGE)-PI3K/AKT signaling in ovarian cancer cells.	acacetin	14-22	advanced glycosylation end-product specific receptor	Homo sapiens	168-172
34886812-13	2021	Mechanically, acacetin decreased lysophosphatidic acid (LPA) release from mesothelial cells, and subsequent activation of receptor for advanced glycation end-products (RAGE)-PI3K/AKT signaling in ovarian cancer cells.	acacetin	14-22	AKT serine/threonine kinase 1	Homo sapiens	179-182
34886812-15	2021	CONCLUSIONS: Acacetin may not only engender direct inhibition of ovarian cancer cell malignancy, but also antagonize mesothelial cell-evoked malignancy by blocking LPA release-activated RAGE-PI3K/AKT signaling.	acacetin	13-21	advanced glycosylation end-product specific receptor	Homo sapiens	186-190
34886812-15	2021	CONCLUSIONS: Acacetin may not only engender direct inhibition of ovarian cancer cell malignancy, but also antagonize mesothelial cell-evoked malignancy by blocking LPA release-activated RAGE-PI3K/AKT signaling.	acacetin	13-21	AKT serine/threonine kinase 1	Homo sapiens	196-199
34950037-8	2021	In vitro, Quercetin, Methyl rosmarinate, Kaempferol, Diosmetin and Acacetin were demonstrated to retard podocyte proliferation by inhibiting DPP4 activity and were the top five compounds predicted by molecular docking to be the most likely to affect DPP4 activity.	acacetin	67-75	dipeptidylpeptidase 4	Mus musculus	141-145
34950037-8	2021	In vitro, Quercetin, Methyl rosmarinate, Kaempferol, Diosmetin and Acacetin were demonstrated to retard podocyte proliferation by inhibiting DPP4 activity and were the top five compounds predicted by molecular docking to be the most likely to affect DPP4 activity.	acacetin	67-75	dipeptidylpeptidase 4	Mus musculus	250-254
34763194-0	2021	Acacetin inhibits RANKL-induced osteoclastogenesis and LPS-induced bone loss by modulating NFATc1 transcription.	acacetin	0-8	nuclear factor of activated T cells 1	Homo sapiens	91-97
34763194-5	2021	Here, we demonstrated, for the first time, that acacetin repressed osteoclastogenesis, formation of F-actin rings, bone resorption activity, and osteoclast-related gene expression in vitro through modulating ERK, P38, and NF-kappaB signaling pathways and preventing expression of NFATc1.	acacetin	48-56	mitogen-activated protein kinase 1	Homo sapiens	208-211
34763194-5	2021	Here, we demonstrated, for the first time, that acacetin repressed osteoclastogenesis, formation of F-actin rings, bone resorption activity, and osteoclast-related gene expression in vitro through modulating ERK, P38, and NF-kappaB signaling pathways and preventing expression of NFATc1.	acacetin	48-56	mitogen-activated protein kinase 14	Homo sapiens	213-216
34763194-5	2021	Here, we demonstrated, for the first time, that acacetin repressed osteoclastogenesis, formation of F-actin rings, bone resorption activity, and osteoclast-related gene expression in vitro through modulating ERK, P38, and NF-kappaB signaling pathways and preventing expression of NFATc1.	acacetin	48-56	nuclear factor of activated T cells 1	Homo sapiens	280-286
34684783-0	2021	Acacetin Inhibits the Growth of STAT3-Activated DU145 Prostate Cancer Cells by Directly Binding to Signal Transducer and Activator of Transcription 3 (STAT3).	acacetin	0-8	signal transducer and activator of transcription 3	Homo sapiens	32-37
34684783-0	2021	Acacetin Inhibits the Growth of STAT3-Activated DU145 Prostate Cancer Cells by Directly Binding to Signal Transducer and Activator of Transcription 3 (STAT3).	acacetin	0-8	signal transducer and activator of transcription 3	Homo sapiens	99-149
34684783-0	2021	Acacetin Inhibits the Growth of STAT3-Activated DU145 Prostate Cancer Cells by Directly Binding to Signal Transducer and Activator of Transcription 3 (STAT3).	acacetin	0-8	signal transducer and activator of transcription 3	Homo sapiens	151-156
34684783-3	2021	Acacetin, a flavone present in various plants, inhibits constitutive and inducible STAT3 activation in STAT3-activated DU145 prostate cancer cells.	acacetin	0-8	signal transducer and activator of transcription 3	Homo sapiens	83-88
34684783-3	2021	Acacetin, a flavone present in various plants, inhibits constitutive and inducible STAT3 activation in STAT3-activated DU145 prostate cancer cells.	acacetin	0-8	signal transducer and activator of transcription 3	Homo sapiens	103-108
34684783-4	2021	Acacetin inhibits STAT3 activity by directly binding to STAT3, which we confirmed by a pull-down assay with a biotinylated compound and two level-free methods, namely, a drug affinity responsive target stability (DARTS) experiment and a cellular thermal shift assay (CETSA).	acacetin	0-8	signal transducer and activator of transcription 3	Homo sapiens	18-23
34684783-4	2021	Acacetin inhibits STAT3 activity by directly binding to STAT3, which we confirmed by a pull-down assay with a biotinylated compound and two level-free methods, namely, a drug affinity responsive target stability (DARTS) experiment and a cellular thermal shift assay (CETSA).	acacetin	0-8	signal transducer and activator of transcription 3	Homo sapiens	56-61
34684783-5	2021	Acacetin inhibits STAT3 phosphorylation at the tyrosine 705 residue and nuclear translocation in DU145 cells, which leads to the downregulation of STAT3 target genes.	acacetin	0-8	signal transducer and activator of transcription 3	Homo sapiens	18-23
34684783-5	2021	Acacetin inhibits STAT3 phosphorylation at the tyrosine 705 residue and nuclear translocation in DU145 cells, which leads to the downregulation of STAT3 target genes.	acacetin	0-8	signal transducer and activator of transcription 3	Homo sapiens	147-152
34684783-7	2021	Interestingly, acacetin induces the production of reactive oxygen species (ROS) that are not involved in the acacetin-induced inhibition of STAT3 activation because the suppressed p-STAT3 level is not rescued by treatment with GSH or NAC, which are general ROS inhibitors.	acacetin	15-23	signal transducer and activator of transcription 3	Homo sapiens	182-187
34684783-9	2021	These results suggest that acacetin, as a STAT3 inhibitor, could be a possible drug candidate for targeting STAT3 for the treatment of cancer in humans.	acacetin	27-35	signal transducer and activator of transcription 3	Homo sapiens	42-47
34684783-9	2021	These results suggest that acacetin, as a STAT3 inhibitor, could be a possible drug candidate for targeting STAT3 for the treatment of cancer in humans.	acacetin	27-35	signal transducer and activator of transcription 3	Homo sapiens	108-113
34307696-5	2021	In addition, lentiviral infection of H9c2 cardiomyocytes revealed that acacetin pretreatment significantly enhanced the fluorescence intensity of autophagy proteins Beclin 1, LC3-II, and p62.	acacetin	71-79	beclin 1	Rattus norvegicus	165-173
34175838-4	2021	Acacetin significantly countered the increased serum advanced glycation end products, the myocardial telomere length shortening, the increased cellular senescence marker proteins p21 and p53, and the reduced mitophagy signaling proteins PINK1/Parkin and Sirt6 expression in aging mice.	acacetin	0-8	cyclin-dependent kinase inhibitor 1A (P21)	Mus musculus	179-182
34175838-4	2021	Acacetin significantly countered the increased serum advanced glycation end products, the myocardial telomere length shortening, the increased cellular senescence marker proteins p21 and p53, and the reduced mitophagy signaling proteins PINK1/Parkin and Sirt6 expression in aging mice.	acacetin	0-8	transformation related protein 53, pseudogene	Mus musculus	187-190
34175838-4	2021	Acacetin significantly countered the increased serum advanced glycation end products, the myocardial telomere length shortening, the increased cellular senescence marker proteins p21 and p53, and the reduced mitophagy signaling proteins PINK1/Parkin and Sirt6 expression in aging mice.	acacetin	0-8	PTEN induced putative kinase 1	Mus musculus	237-242
34175838-4	2021	Acacetin significantly countered the increased serum advanced glycation end products, the myocardial telomere length shortening, the increased cellular senescence marker proteins p21 and p53, and the reduced mitophagy signaling proteins PINK1/Parkin and Sirt6 expression in aging mice.	acacetin	0-8	sirtuin 6	Mus musculus	254-259
34175838-6	2021	Acacetin decreased p21 and p53 expression, up-regulated PINK1/Parkin, LC3II/LC3I ratio, pLKB1, pAMPK and Sirt6, and reversed the depolarized mitochondrial membrane potential in aging cardiac cells.	acacetin	0-8	KRAS proto-oncogene, GTPase	Rattus norvegicus	19-22
34175838-6	2021	Acacetin decreased p21 and p53 expression, up-regulated PINK1/Parkin, LC3II/LC3I ratio, pLKB1, pAMPK and Sirt6, and reversed the depolarized mitochondrial membrane potential in aging cardiac cells.	acacetin	0-8	Wistar clone pR53P1 p53 pseudogene	Rattus norvegicus	27-30
34175838-6	2021	Acacetin decreased p21 and p53 expression, up-regulated PINK1/Parkin, LC3II/LC3I ratio, pLKB1, pAMPK and Sirt6, and reversed the depolarized mitochondrial membrane potential in aging cardiac cells.	acacetin	0-8	PTEN induced kinase 1	Rattus norvegicus	56-61
34175838-6	2021	Acacetin decreased p21 and p53 expression, up-regulated PINK1/Parkin, LC3II/LC3I ratio, pLKB1, pAMPK and Sirt6, and reversed the depolarized mitochondrial membrane potential in aging cardiac cells.	acacetin	0-8	microtubule-associated protein 1 light chain 3 alpha	Rattus norvegicus	70-80
34175838-6	2021	Acacetin decreased p21 and p53 expression, up-regulated PINK1/Parkin, LC3II/LC3I ratio, pLKB1, pAMPK and Sirt6, and reversed the depolarized mitochondrial membrane potential in aging cardiac cells.	acacetin	0-8	sirtuin 6	Rattus norvegicus	105-110
34175838-7	2021	Mitophagy inhibition with 3-methyladenine or silencing Sirt6 abolished the protective effects of acacetin against cardiac senescence.	acacetin	97-105	sirtuin 6	Rattus norvegicus	55-60
34175838-8	2021	Further analysis revealed that acacetin effect on Sirt6 was mediated by Sirt1 activation and increase of NAD+/NADH ratio.	acacetin	31-39	sirtuin 6	Rattus norvegicus	50-55
34175838-8	2021	Further analysis revealed that acacetin effect on Sirt6 was mediated by Sirt1 activation and increase of NAD+/NADH ratio.	acacetin	31-39	sirtuin 1	Rattus norvegicus	72-77
34175838-9	2021	These results demonstrate that acacetin significantly inhibits in vivo and in vitro cardiac senescence induced by D-galactose via Sirt1-mediated activation of Sirt6/AMPK signaling pathway, thereby enhancing mitophagy and preserving mitochondrial function, which suggests that acacetin may be a drug candidate for treating cardiovascular disorders related to aging.	acacetin	31-39	sirtuin 1	Rattus norvegicus	130-135
34175838-9	2021	These results demonstrate that acacetin significantly inhibits in vivo and in vitro cardiac senescence induced by D-galactose via Sirt1-mediated activation of Sirt6/AMPK signaling pathway, thereby enhancing mitophagy and preserving mitochondrial function, which suggests that acacetin may be a drug candidate for treating cardiovascular disorders related to aging.	acacetin	31-39	sirtuin 6	Rattus norvegicus	159-164
34175838-9	2021	These results demonstrate that acacetin significantly inhibits in vivo and in vitro cardiac senescence induced by D-galactose via Sirt1-mediated activation of Sirt6/AMPK signaling pathway, thereby enhancing mitophagy and preserving mitochondrial function, which suggests that acacetin may be a drug candidate for treating cardiovascular disorders related to aging.	acacetin	31-39	protein kinase AMP-activated catalytic subunit alpha 2	Rattus norvegicus	165-169
34175838-9	2021	These results demonstrate that acacetin significantly inhibits in vivo and in vitro cardiac senescence induced by D-galactose via Sirt1-mediated activation of Sirt6/AMPK signaling pathway, thereby enhancing mitophagy and preserving mitochondrial function, which suggests that acacetin may be a drug candidate for treating cardiovascular disorders related to aging.	acacetin	276-284	sirtuin 1	Rattus norvegicus	130-135
34175838-9	2021	These results demonstrate that acacetin significantly inhibits in vivo and in vitro cardiac senescence induced by D-galactose via Sirt1-mediated activation of Sirt6/AMPK signaling pathway, thereby enhancing mitophagy and preserving mitochondrial function, which suggests that acacetin may be a drug candidate for treating cardiovascular disorders related to aging.	acacetin	276-284	sirtuin 6	Rattus norvegicus	159-164
34175838-9	2021	These results demonstrate that acacetin significantly inhibits in vivo and in vitro cardiac senescence induced by D-galactose via Sirt1-mediated activation of Sirt6/AMPK signaling pathway, thereby enhancing mitophagy and preserving mitochondrial function, which suggests that acacetin may be a drug candidate for treating cardiovascular disorders related to aging.	acacetin	276-284	protein kinase AMP-activated catalytic subunit alpha 2	Rattus norvegicus	165-169
34594156-9	2021	Results: Based on network pharmacological method, the key active ingredient of WSD was identified as Acacetin, and the enrichment signaling pathway was the PI3K-AKT signaling pathway.	acacetin	101-109	thymoma viral proto-oncogene 1	Mus musculus	161-164
34594156-11	2021	The levels of GAS and MTL were increased after using Acacetin.	acacetin	53-61	gastrin	Mus musculus	14-17
34594156-16	2021	The detection of the PI3K-AKT signaling pathway-related proteins showed that Acacetin improved gastrointestinal motility disorder by inhibiting the activation of the PI3K-AKT signaling pathway.	acacetin	77-85	thymoma viral proto-oncogene 1	Mus musculus	26-29
34594156-16	2021	The detection of the PI3K-AKT signaling pathway-related proteins showed that Acacetin improved gastrointestinal motility disorder by inhibiting the activation of the PI3K-AKT signaling pathway.	acacetin	77-85	thymoma viral proto-oncogene 1	Mus musculus	171-174
34594156-17	2021	Conclusion: The key ingredient Acacetin in WSD could alleviate gastrointestinal motility disorder by inhibiting the activation of the PI3K-AKT signaling pathway based on network pharmacology analysis.	acacetin	31-39	thymoma viral proto-oncogene 1	Mus musculus	139-142
34483900-8	2021	Finally, molecular docking verified that acacetin bound to the active sites of the four targets predicted by network pharmacology, and in vitro experiments further confirmed that acacetin significantly inhibited the upregulation of p-src induced by LPS and attenuated LPS-induced M1 polarization through gap junctions.	acacetin	41-49	Rous sarcoma oncogene	Mus musculus	234-237
34483900-8	2021	Finally, molecular docking verified that acacetin bound to the active sites of the four targets predicted by network pharmacology, and in vitro experiments further confirmed that acacetin significantly inhibited the upregulation of p-src induced by LPS and attenuated LPS-induced M1 polarization through gap junctions.	acacetin	179-187	Rous sarcoma oncogene	Mus musculus	234-237
34307696-5	2021	In addition, lentiviral infection of H9c2 cardiomyocytes revealed that acacetin pretreatment significantly enhanced the fluorescence intensity of autophagy proteins Beclin 1, LC3-II, and p62.	acacetin	71-79	annexin A3	Rattus norvegicus	175-178
34307696-5	2021	In addition, lentiviral infection of H9c2 cardiomyocytes revealed that acacetin pretreatment significantly enhanced the fluorescence intensity of autophagy proteins Beclin 1, LC3-II, and p62.	acacetin	71-79	KH RNA binding domain containing, signal transduction associated 1	Rattus norvegicus	187-190
34307696-7	2021	Moreover, we found that application of acacetin increased activation of the PI3K/Akt signaling pathway, whereas cotreatment with the PI3K inhibitor LY294002 reversed the inhibition of apoptosis and autophagy induced by acacetin.	acacetin	39-47	AKT serine/threonine kinase 1	Rattus norvegicus	81-84
34307696-7	2021	Moreover, we found that application of acacetin increased activation of the PI3K/Akt signaling pathway, whereas cotreatment with the PI3K inhibitor LY294002 reversed the inhibition of apoptosis and autophagy induced by acacetin.	acacetin	219-227	AKT serine/threonine kinase 1	Rattus norvegicus	81-84
34307696-8	2021	In conclusion, acacetin mitigated H/R injury by promoting autophagy through activating the PI3K/Akt/mTOR signaling pathway.	acacetin	15-23	AKT serine/threonine kinase 1	Rattus norvegicus	96-99
34307696-8	2021	In conclusion, acacetin mitigated H/R injury by promoting autophagy through activating the PI3K/Akt/mTOR signaling pathway.	acacetin	15-23	mechanistic target of rapamycin kinase	Rattus norvegicus	100-104
34060409-2	2021	The time-dependent inhibition of CYP3A4 by acacetin, apigenin, chrysin, and pinocembrin was experimentally detected, but not entirely elaborated so far.	acacetin	43-51	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	33-39
34125845-15	2021	The molecular docking experiment confirmed the correlation between five core compounds (quercetin, stigmasterol, kaempferol, baicalein, and acacetin) just as well as PTGS2, NR3C2, CA2, and MMP1.	acacetin	140-148	nuclear receptor subfamily 3 group C member 2	Homo sapiens	173-178
35405252-18	2022	Moreover, acacetin and apigenin, two components of Cortex Lycii, reduced the protein level of p-AKT and p-mTOR, and the reduction was also inhibited by Terazosin.	acacetin	10-18	AKT serine/threonine kinase 1	Homo sapiens	96-99
35405252-18	2022	Moreover, acacetin and apigenin, two components of Cortex Lycii, reduced the protein level of p-AKT and p-mTOR, and the reduction was also inhibited by Terazosin.	acacetin	10-18	mechanistic target of rapamycin kinase	Homo sapiens	106-110
33998937-0	2022	Effects of cisplatin and acacetin on total antioxidant status, apoptosis and expression of OCTN3 in mouse testis.	acacetin	25-33	solute carrier family 22 (organic cation transporter), member 21	Mus musculus	91-96
35341782-0	2022	Acacetin attenuates diabetes-induced cardiomyopathy by inhibiting oxidative stress and energy metabolism via PPAR-alpha/AMPK pathway.	acacetin	0-8	peroxisome proliferator activated receptor alpha	Rattus norvegicus	109-119
35341782-0	2022	Acacetin attenuates diabetes-induced cardiomyopathy by inhibiting oxidative stress and energy metabolism via PPAR-alpha/AMPK pathway.	acacetin	0-8	protein kinase AMP-activated catalytic subunit alpha 2	Rattus norvegicus	120-124
35341782-6	2022	Acacetin countered high glucose-induced increase of Bax and decrease of Bcl-2, SOD1, and SOD2.	acacetin	0-8	BCL2 associated X, apoptosis regulator	Rattus norvegicus	52-55
35341782-6	2022	Acacetin countered high glucose-induced increase of Bax and decrease of Bcl-2, SOD1, and SOD2.	acacetin	0-8	BCL2, apoptosis regulator	Rattus norvegicus	72-77
35341782-6	2022	Acacetin countered high glucose-induced increase of Bax and decrease of Bcl-2, SOD1, and SOD2.	acacetin	0-8	superoxide dismutase 1	Rattus norvegicus	79-83
35341782-6	2022	Acacetin countered high glucose-induced increase of Bax and decrease of Bcl-2, SOD1, and SOD2.	acacetin	0-8	superoxide dismutase 2	Rattus norvegicus	89-93
35341782-8	2022	significantly improved the cardiac function and reduced myocardial injury, and reversed the increase of serum MDA, Ang II, and IL-6 levels and myocardial Bax and IL-6, and the decrease of serum SOD, indicating that acacetin plays a cardioprotective effect by inhibiting oxidative stress, inflammation, and apoptosis.	acacetin	215-223	angiotensinogen	Rattus norvegicus	115-121
35341782-8	2022	significantly improved the cardiac function and reduced myocardial injury, and reversed the increase of serum MDA, Ang II, and IL-6 levels and myocardial Bax and IL-6, and the decrease of serum SOD, indicating that acacetin plays a cardioprotective effect by inhibiting oxidative stress, inflammation, and apoptosis.	acacetin	215-223	interleukin 6	Rattus norvegicus	127-131
35341782-8	2022	significantly improved the cardiac function and reduced myocardial injury, and reversed the increase of serum MDA, Ang II, and IL-6 levels and myocardial Bax and IL-6, and the decrease of serum SOD, indicating that acacetin plays a cardioprotective effect by inhibiting oxidative stress, inflammation, and apoptosis.	acacetin	215-223	BCL2 associated X, apoptosis regulator	Rattus norvegicus	154-157
35341782-8	2022	significantly improved the cardiac function and reduced myocardial injury, and reversed the increase of serum MDA, Ang II, and IL-6 levels and myocardial Bax and IL-6, and the decrease of serum SOD, indicating that acacetin plays a cardioprotective effect by inhibiting oxidative stress, inflammation, and apoptosis.	acacetin	215-223	interleukin 6	Rattus norvegicus	162-166
35341782-9	2022	In addition, both in vitro and in vivo experimental results showed that acacetin increased the expression of PPAR-alpha and pAMPK, indicating that PPAR-alpha and pAMPK are potential targets of acacetin for the protection against diabetic cardiomyopathy.	acacetin	72-80	peroxisome proliferator activated receptor alpha	Rattus norvegicus	109-119
35341782-9	2022	In addition, both in vitro and in vivo experimental results showed that acacetin increased the expression of PPAR-alpha and pAMPK, indicating that PPAR-alpha and pAMPK are potential targets of acacetin for the protection against diabetic cardiomyopathy.	acacetin	72-80	peroxisome proliferator activated receptor alpha	Rattus norvegicus	147-157
35341782-9	2022	In addition, both in vitro and in vivo experimental results showed that acacetin increased the expression of PPAR-alpha and pAMPK, indicating that PPAR-alpha and pAMPK are potential targets of acacetin for the protection against diabetic cardiomyopathy.	acacetin	193-201	peroxisome proliferator activated receptor alpha	Rattus norvegicus	109-119
35341782-9	2022	In addition, both in vitro and in vivo experimental results showed that acacetin increased the expression of PPAR-alpha and pAMPK, indicating that PPAR-alpha and pAMPK are potential targets of acacetin for the protection against diabetic cardiomyopathy.	acacetin	193-201	peroxisome proliferator activated receptor alpha	Rattus norvegicus	147-157
35563076-7	2022	Acacetin decreased low-density lipoprotein and leptin concentrations, but increased high-density lipoprotein and adiponectin levels in obese mice.	acacetin	0-8	leptin	Mus musculus	47-53
35517504-6	2022	In this study, we found that acacetin inhibits osteoclast formation and bone resorption of BMMs induced by the macrophage colony stimulating factor (M-CSF) and receptor activator of nuclear factor-kappaB ligand (RANKL) in a concentration of 20 muM without exerting cytotoxic effects.	acacetin	29-37	colony stimulating factor 1 (macrophage)	Mus musculus	111-147
35517504-6	2022	In this study, we found that acacetin inhibits osteoclast formation and bone resorption of BMMs induced by the macrophage colony stimulating factor (M-CSF) and receptor activator of nuclear factor-kappaB ligand (RANKL) in a concentration of 20 muM without exerting cytotoxic effects.	acacetin	29-37	colony stimulating factor 1 (macrophage)	Mus musculus	149-154
35517504-6	2022	In this study, we found that acacetin inhibits osteoclast formation and bone resorption of BMMs induced by the macrophage colony stimulating factor (M-CSF) and receptor activator of nuclear factor-kappaB ligand (RANKL) in a concentration of 20 muM without exerting cytotoxic effects.	acacetin	29-37	tumor necrosis factor (ligand) superfamily, member 11	Mus musculus	212-217
35517504-9	2022	Mechanistic analysis revealed that acacetin not only inhibits the expression of the major transcription factor NFATc1 and NF-kappaB during RANKL-induced osteoclast formation, but also suppresses RANKL-induced the phosphorylation of Akt, GSK3beta, IkappaBalpha, and p65.	acacetin	35-43	nuclear factor of activated T cells, cytoplasmic, calcineurin dependent 1	Mus musculus	111-117
35517504-9	2022	Mechanistic analysis revealed that acacetin not only inhibits the expression of the major transcription factor NFATc1 and NF-kappaB during RANKL-induced osteoclast formation, but also suppresses RANKL-induced the phosphorylation of Akt, GSK3beta, IkappaBalpha, and p65.	acacetin	35-43	tumor necrosis factor (ligand) superfamily, member 11	Mus musculus	139-144
35517504-9	2022	Mechanistic analysis revealed that acacetin not only inhibits the expression of the major transcription factor NFATc1 and NF-kappaB during RANKL-induced osteoclast formation, but also suppresses RANKL-induced the phosphorylation of Akt, GSK3beta, IkappaBalpha, and p65.	acacetin	35-43	tumor necrosis factor (ligand) superfamily, member 11	Mus musculus	195-200
35517504-9	2022	Mechanistic analysis revealed that acacetin not only inhibits the expression of the major transcription factor NFATc1 and NF-kappaB during RANKL-induced osteoclast formation, but also suppresses RANKL-induced the phosphorylation of Akt, GSK3beta, IkappaBalpha, and p65.	acacetin	35-43	thymoma viral proto-oncogene 1	Mus musculus	232-235
35517504-9	2022	Mechanistic analysis revealed that acacetin not only inhibits the expression of the major transcription factor NFATc1 and NF-kappaB during RANKL-induced osteoclast formation, but also suppresses RANKL-induced the phosphorylation of Akt, GSK3beta, IkappaBalpha, and p65.	acacetin	35-43	glycogen synthase kinase 3 alpha	Mus musculus	237-245
35517504-9	2022	Mechanistic analysis revealed that acacetin not only inhibits the expression of the major transcription factor NFATc1 and NF-kappaB during RANKL-induced osteoclast formation, but also suppresses RANKL-induced the phosphorylation of Akt, GSK3beta, IkappaBalpha, and p65.	acacetin	35-43	nuclear factor of kappa light polypeptide gene enhancer in B cells inhibitor, alpha	Mus musculus	247-259
35517504-9	2022	Mechanistic analysis revealed that acacetin not only inhibits the expression of the major transcription factor NFATc1 and NF-kappaB during RANKL-induced osteoclast formation, but also suppresses RANKL-induced the phosphorylation of Akt, GSK3beta, IkappaBalpha, and p65.	acacetin	35-43	v-rel reticuloendotheliosis viral oncogene homolog A (avian)	Mus musculus	265-268
35517504-10	2022	Additionally, acacetin enhanced the ability of M-CSF and RANKL-stimulated BMMs to promote angiogenesis and migration of EPCs.	acacetin	14-22	colony stimulating factor 1 (macrophage)	Mus musculus	47-52
35517504-10	2022	Additionally, acacetin enhanced the ability of M-CSF and RANKL-stimulated BMMs to promote angiogenesis and migration of EPCs.	acacetin	14-22	tumor necrosis factor (ligand) superfamily, member 11	Mus musculus	57-62
35517504-12	2022	These data demonstrate that acacetin prevents OVX-induced bone loss in mice through inhibition of osteoclast function and promotion of type H vessel formation via Akt/GSK3beta and NF-kappaB signalling pathway, suggesting that acacetin may be a novel therapeutic agent for the treatment of osteoporosis.	acacetin	28-36	thymoma viral proto-oncogene 1	Mus musculus	163-166
35517504-12	2022	These data demonstrate that acacetin prevents OVX-induced bone loss in mice through inhibition of osteoclast function and promotion of type H vessel formation via Akt/GSK3beta and NF-kappaB signalling pathway, suggesting that acacetin may be a novel therapeutic agent for the treatment of osteoporosis.	acacetin	28-36	glycogen synthase kinase 3 alpha	Mus musculus	167-175
35219729-0	2022	Acacetin ameliorates cardiac hypertrophy by activating Sirt1/AMPK/PGC-1alpha pathway.	acacetin	0-8	sirtuin 1	Rattus norvegicus	55-60
35219729-0	2022	Acacetin ameliorates cardiac hypertrophy by activating Sirt1/AMPK/PGC-1alpha pathway.	acacetin	0-8	protein kinase AMP-activated catalytic subunit alpha 2	Rattus norvegicus	61-65
35219729-0	2022	Acacetin ameliorates cardiac hypertrophy by activating Sirt1/AMPK/PGC-1alpha pathway.	acacetin	0-8	PPARG coactivator 1 alpha	Rattus norvegicus	66-76
35219729-4	2022	In addition, acacetin rescued Ang II-induced impairment of PGC-1alpha, PPARalpha and pAMPK.	acacetin	13-21	angiotensinogen	Rattus norvegicus	30-36
35219729-4	2022	In addition, acacetin rescued Ang II-induced impairment of PGC-1alpha, PPARalpha and pAMPK.	acacetin	13-21	PPARG coactivator 1 alpha	Rattus norvegicus	59-69
35219729-4	2022	In addition, acacetin rescued Ang II-induced impairment of PGC-1alpha, PPARalpha and pAMPK.	acacetin	13-21	peroxisome proliferator activated receptor alpha	Rattus norvegicus	71-80
35219729-5	2022	These beneficial effects of acacetin were mediated by activation of Sirt1, which was confirmed in cardiac hypertrophy induced by abdominal aorta constriction (AAC) in SD rats.	acacetin	28-36	sirtuin 1	Rattus norvegicus	68-73
35219729-8	2022	Our results demonstrate the novel pharmacological effect that acacetin ameliorates cardiac hypertrophy via Sirt1-mediated activation of AMPK/PGC-1alpha signal molecules followed by reducing oxidation, inflammation and apoptosis.	acacetin	62-70	sirtuin 1	Rattus norvegicus	107-112
35219729-8	2022	Our results demonstrate the novel pharmacological effect that acacetin ameliorates cardiac hypertrophy via Sirt1-mediated activation of AMPK/PGC-1alpha signal molecules followed by reducing oxidation, inflammation and apoptosis.	acacetin	62-70	protein kinase AMP-activated catalytic subunit alpha 2	Rattus norvegicus	136-140
35219729-8	2022	Our results demonstrate the novel pharmacological effect that acacetin ameliorates cardiac hypertrophy via Sirt1-mediated activation of AMPK/PGC-1alpha signal molecules followed by reducing oxidation, inflammation and apoptosis.	acacetin	62-70	PPARG coactivator 1 alpha	Rattus norvegicus	141-151
35433930-15	2022	Acacetin, wogonin, baicalein, oroxylin A, and beta-sitosterol, which are rich in RS, are closely related to hemagglutinin (HA), NeurAminidase (NA), nucleoprotein (NP), polymerase basic protein 1 (PB1), polymerase basic protein 2 (PB2), polymerase acidic (PA), matrix protein 1 (M1), matrix protein 2 (M2), and non-structural protein (NS), which are the main RNA coding proteins of influenza A virus.	acacetin	0-8	neuraminidase 1	Homo sapiens	128-141
35433930-15	2022	Acacetin, wogonin, baicalein, oroxylin A, and beta-sitosterol, which are rich in RS, are closely related to hemagglutinin (HA), NeurAminidase (NA), nucleoprotein (NP), polymerase basic protein 1 (PB1), polymerase basic protein 2 (PB2), polymerase acidic (PA), matrix protein 1 (M1), matrix protein 2 (M2), and non-structural protein (NS), which are the main RNA coding proteins of influenza A virus.	acacetin	0-8	polybromo 1	Homo sapiens	196-199
35387543-4	2022	4 -Methoxy-5,7-dihydroxyflavone (acacetin) was found to be demethylated by CYP1B1 and 2A13 to form 4 ,5,7-trihydroxyflavone (apigenin) at rates of 0.098-1 and 0.42 min-1, respectively.	acacetin	33-41	cytochrome P450 family 1 subfamily B member 1	Homo sapiens	75-90
35000605-0	2022	Acacetin inhibits invasion, migration and TGF-beta1-induced EMT of gastric cancer cells through the PI3K/Akt/Snail pathway.	acacetin	0-8	AKT serine/threonine kinase 1	Homo sapiens	105-108
35000605-0	2022	Acacetin inhibits invasion, migration and TGF-beta1-induced EMT of gastric cancer cells through the PI3K/Akt/Snail pathway.	acacetin	0-8	snail family transcriptional repressor 1	Homo sapiens	109-114
35000605-9	2022	In TGF-beta1-induced EMT models, acacetin reversed the morphological changes from epithelial to mesenchymal cells, and invasion and migration were limited by regulating EMT.	acacetin	33-41	transforming growth factor beta 1	Homo sapiens	3-12
35000605-10	2022	In addition, acacetin suppressed the activation of PI3K/Akt signalling and decreased the phosphorylation levels of TGF-beta1-treated GC cells.	acacetin	13-21	AKT serine/threonine kinase 1	Homo sapiens	56-59
35000605-10	2022	In addition, acacetin suppressed the activation of PI3K/Akt signalling and decreased the phosphorylation levels of TGF-beta1-treated GC cells.	acacetin	13-21	transforming growth factor beta 1	Homo sapiens	115-124
35000605-13	2022	CONCLUSION: Our study showed that the invasion, metastasis and TGF-beta1-induced EMT of GC are inhibited by acacetin, and the mechanism may involve the suppression of the PI3K/Akt/Snail signalling pathway.	acacetin	108-116	transforming growth factor beta 1	Homo sapiens	63-72
35000605-13	2022	CONCLUSION: Our study showed that the invasion, metastasis and TGF-beta1-induced EMT of GC are inhibited by acacetin, and the mechanism may involve the suppression of the PI3K/Akt/Snail signalling pathway.	acacetin	108-116	AKT serine/threonine kinase 1	Homo sapiens	176-179
35000605-13	2022	CONCLUSION: Our study showed that the invasion, metastasis and TGF-beta1-induced EMT of GC are inhibited by acacetin, and the mechanism may involve the suppression of the PI3K/Akt/Snail signalling pathway.	acacetin	108-116	snail family transcriptional repressor 1	Homo sapiens	180-185
33647348-5	2021	Among flavonoids acacetin showed highest binding-energy against JAK-2 following FYN > VEGF > PI3K > MKK4 > MAPK > BRAF > STAT5 > STAT1 > STAT4 whereas pinostrobin depicts higher binding-energy with JAK-2 followed by BRAF > MKK4 > VEGF > PI3K > MAPK > STAT1 > STAT4 > STAT5.	acacetin	17-25	Janus kinase 2	Homo sapiens	64-69
33647348-5	2021	Among flavonoids acacetin showed highest binding-energy against JAK-2 following FYN > VEGF > PI3K > MKK4 > MAPK > BRAF > STAT5 > STAT1 > STAT4 whereas pinostrobin depicts higher binding-energy with JAK-2 followed by BRAF > MKK4 > VEGF > PI3K > MAPK > STAT1 > STAT4 > STAT5.	acacetin	17-25	FYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	80-83
33647348-5	2021	Among flavonoids acacetin showed highest binding-energy against JAK-2 following FYN > VEGF > PI3K > MKK4 > MAPK > BRAF > STAT5 > STAT1 > STAT4 whereas pinostrobin depicts higher binding-energy with JAK-2 followed by BRAF > MKK4 > VEGF > PI3K > MAPK > STAT1 > STAT4 > STAT5.	acacetin	17-25	vascular endothelial growth factor A	Homo sapiens	86-90
33647348-5	2021	Among flavonoids acacetin showed highest binding-energy against JAK-2 following FYN > VEGF > PI3K > MKK4 > MAPK > BRAF > STAT5 > STAT1 > STAT4 whereas pinostrobin depicts higher binding-energy with JAK-2 followed by BRAF > MKK4 > VEGF > PI3K > MAPK > STAT1 > STAT4 > STAT5.	acacetin	17-25	mitogen-activated protein kinase kinase 4	Homo sapiens	100-104
33647348-5	2021	Among flavonoids acacetin showed highest binding-energy against JAK-2 following FYN > VEGF > PI3K > MKK4 > MAPK > BRAF > STAT5 > STAT1 > STAT4 whereas pinostrobin depicts higher binding-energy with JAK-2 followed by BRAF > MKK4 > VEGF > PI3K > MAPK > STAT1 > STAT4 > STAT5.	acacetin	17-25	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	114-118
33647348-5	2021	Among flavonoids acacetin showed highest binding-energy against JAK-2 following FYN > VEGF > PI3K > MKK4 > MAPK > BRAF > STAT5 > STAT1 > STAT4 whereas pinostrobin depicts higher binding-energy with JAK-2 followed by BRAF > MKK4 > VEGF > PI3K > MAPK > STAT1 > STAT4 > STAT5.	acacetin	17-25	signal transducer and activator of transcription 5A	Homo sapiens	121-126
33647348-5	2021	Among flavonoids acacetin showed highest binding-energy against JAK-2 following FYN > VEGF > PI3K > MKK4 > MAPK > BRAF > STAT5 > STAT1 > STAT4 whereas pinostrobin depicts higher binding-energy with JAK-2 followed by BRAF > MKK4 > VEGF > PI3K > MAPK > STAT1 > STAT4 > STAT5.	acacetin	17-25	signal transducer and activator of transcription 1	Homo sapiens	129-134
33647348-5	2021	Among flavonoids acacetin showed highest binding-energy against JAK-2 following FYN > VEGF > PI3K > MKK4 > MAPK > BRAF > STAT5 > STAT1 > STAT4 whereas pinostrobin depicts higher binding-energy with JAK-2 followed by BRAF > MKK4 > VEGF > PI3K > MAPK > STAT1 > STAT4 > STAT5.	acacetin	17-25	signal transducer and activator of transcription 4	Homo sapiens	137-142
33647348-5	2021	Among flavonoids acacetin showed highest binding-energy against JAK-2 following FYN > VEGF > PI3K > MKK4 > MAPK > BRAF > STAT5 > STAT1 > STAT4 whereas pinostrobin depicts higher binding-energy with JAK-2 followed by BRAF > MKK4 > VEGF > PI3K > MAPK > STAT1 > STAT4 > STAT5.	acacetin	17-25	Janus kinase 2	Homo sapiens	198-203
33647348-5	2021	Among flavonoids acacetin showed highest binding-energy against JAK-2 following FYN > VEGF > PI3K > MKK4 > MAPK > BRAF > STAT5 > STAT1 > STAT4 whereas pinostrobin depicts higher binding-energy with JAK-2 followed by BRAF > MKK4 > VEGF > PI3K > MAPK > STAT1 > STAT4 > STAT5.	acacetin	17-25	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	216-220
33647348-5	2021	Among flavonoids acacetin showed highest binding-energy against JAK-2 following FYN > VEGF > PI3K > MKK4 > MAPK > BRAF > STAT5 > STAT1 > STAT4 whereas pinostrobin depicts higher binding-energy with JAK-2 followed by BRAF > MKK4 > VEGF > PI3K > MAPK > STAT1 > STAT4 > STAT5.	acacetin	17-25	mitogen-activated protein kinase kinase 4	Homo sapiens	223-227
33647348-5	2021	Among flavonoids acacetin showed highest binding-energy against JAK-2 following FYN > VEGF > PI3K > MKK4 > MAPK > BRAF > STAT5 > STAT1 > STAT4 whereas pinostrobin depicts higher binding-energy with JAK-2 followed by BRAF > MKK4 > VEGF > PI3K > MAPK > STAT1 > STAT4 > STAT5.	acacetin	17-25	vascular endothelial growth factor A	Homo sapiens	230-234
33647348-5	2021	Among flavonoids acacetin showed highest binding-energy against JAK-2 following FYN > VEGF > PI3K > MKK4 > MAPK > BRAF > STAT5 > STAT1 > STAT4 whereas pinostrobin depicts higher binding-energy with JAK-2 followed by BRAF > MKK4 > VEGF > PI3K > MAPK > STAT1 > STAT4 > STAT5.	acacetin	17-25	signal transducer and activator of transcription 1	Homo sapiens	251-256
33647348-5	2021	Among flavonoids acacetin showed highest binding-energy against JAK-2 following FYN > VEGF > PI3K > MKK4 > MAPK > BRAF > STAT5 > STAT1 > STAT4 whereas pinostrobin depicts higher binding-energy with JAK-2 followed by BRAF > MKK4 > VEGF > PI3K > MAPK > STAT1 > STAT4 > STAT5.	acacetin	17-25	signal transducer and activator of transcription 4	Homo sapiens	259-264
33647348-5	2021	Among flavonoids acacetin showed highest binding-energy against JAK-2 following FYN > VEGF > PI3K > MKK4 > MAPK > BRAF > STAT5 > STAT1 > STAT4 whereas pinostrobin depicts higher binding-energy with JAK-2 followed by BRAF > MKK4 > VEGF > PI3K > MAPK > STAT1 > STAT4 > STAT5.	acacetin	17-25	signal transducer and activator of transcription 5A	Homo sapiens	267-272
33647348-6	2021	Further, molecular-dynamic simulation revealed that pinostrobin interacted with JAK-2 protein with binding-energy of -25.068 +- 1.08 kJ/mol whereas acacetin interacted with both JAK-2 and Fyn with binding-energies of -23.466 +- 0.9508 kJ/mol and-8.935+-1.3108 kJ/mol respectively.	acacetin	148-156	Janus kinase 2	Homo sapiens	178-183
33647348-6	2021	Further, molecular-dynamic simulation revealed that pinostrobin interacted with JAK-2 protein with binding-energy of -25.068 +- 1.08 kJ/mol whereas acacetin interacted with both JAK-2 and Fyn with binding-energies of -23.466 +- 0.9508 kJ/mol and-8.935+-1.3108 kJ/mol respectively.	acacetin	148-156	FYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	188-191
33647348-7	2021	High binding-energy, low inhibition-constant, and drug-likeness of acacetin and pinostrobin provide a clue for their usage as a JAK-2 inhibitor which could be useful for molecular/cell- target based in-vitro and in-vivo investigations.	acacetin	67-75	Janus kinase 2	Homo sapiens	128-133
33998937-9	2022	All ACA groups exhibited decreased apoptosis and ROS levels, and increased TAC and OCTN3 gene expression compared to the cisplatin treated mice.	acacetin	4-7	solute carrier family 22 (organic cation transporter), member 21	Mus musculus	83-88
33109424-0	2021	Corrigendum to "Acacetin enhances glucose uptake through insulin-independent GLUT4 translocation in L6 myotubes" [Phytomedicine 68 (2020)/153178].	acacetin	16-24	insulin	Homo sapiens	57-64
33781239-0	2021	Acacetin ameliorates insulin resistance in obesity mice through regulating Treg/Th17 balance via MiR-23b-3p/NEU1 Axis.	acacetin	0-8	neuraminidase 1	Mus musculus	108-112
33781239-10	2021	CONCLUSION: Upregulation of miR-23b-3p offset the effects of acacetin on obesity-induced IR through regulating Treg/Th17 cell balance via targeting NEU1.The present findings provide a possible prevention strategy for obesity-induced IR.	acacetin	61-69	neuraminidase 1	Mus musculus	148-152
33241629-0	2021	Acacetin exerts antioxidant potential against atherosclerosis through Nrf2 pathway in apoE-/- Mice.	acacetin	0-8	nuclear factor, erythroid derived 2, like 2	Mus musculus	70-74
33241629-0	2021	Acacetin exerts antioxidant potential against atherosclerosis through Nrf2 pathway in apoE-/- Mice.	acacetin	0-8	apolipoprotein E	Mus musculus	86-90
33241629-9	2021	Moreover, 3 mumol/L acacetin clearly decreased ROS levels and enhanced reductase protein expression through MsrA and Nrf2 pathway through phosphorylation of Nrf2 and degradation of Keap1.	acacetin	20-28	methionine sulfoxide reductase A	Mus musculus	108-112
33241629-9	2021	Moreover, 3 mumol/L acacetin clearly decreased ROS levels and enhanced reductase protein expression through MsrA and Nrf2 pathway through phosphorylation of Nrf2 and degradation of Keap1.	acacetin	20-28	nuclear factor, erythroid derived 2, like 2	Mus musculus	117-121
33241629-9	2021	Moreover, 3 mumol/L acacetin clearly decreased ROS levels and enhanced reductase protein expression through MsrA and Nrf2 pathway through phosphorylation of Nrf2 and degradation of Keap1.	acacetin	20-28	nuclear factor, erythroid derived 2, like 2	Mus musculus	157-161
33241629-9	2021	Moreover, 3 mumol/L acacetin clearly decreased ROS levels and enhanced reductase protein expression through MsrA and Nrf2 pathway through phosphorylation of Nrf2 and degradation of Keap1.	acacetin	20-28	kelch-like ECH-associated protein 1	Mus musculus	181-186
33241629-10	2021	In vivo, acacetin treatment remarkably attenuated atherosclerosis by increasing reductase levels in circulation and aortic roots, decreasing plasma inflammatory factor levels as well as accelerating lipid metabolism in Western diet-fed apoE-/- mice.	acacetin	9-17	apolipoprotein E	Mus musculus	236-240
33394232-0	2021	The natural flavones, acacetin and apigenin, induce Cdk-Cyclin mediated G2/M phase arrest and trigger ROS-mediated apoptosis in glioblastoma cells.	acacetin	22-30	proliferating cell nuclear antigen	Homo sapiens	56-62
33109424-0	2021	Corrigendum to "Acacetin enhances glucose uptake through insulin-independent GLUT4 translocation in L6 myotubes" [Phytomedicine 68 (2020)/153178].	acacetin	16-24	solute carrier family 2 member 4	Homo sapiens	77-82
33519472-0	2020	Acacetin Protects Against High Glucose-Induced Endothelial Cells Injury by Preserving Mitochondrial Function via Activating Sirt1/Sirt3/AMPK Signals.	acacetin	0-8	sirtuin 1	Homo sapiens	124-129
33519472-0	2020	Acacetin Protects Against High Glucose-Induced Endothelial Cells Injury by Preserving Mitochondrial Function via Activating Sirt1/Sirt3/AMPK Signals.	acacetin	0-8	sirtuin 3	Homo sapiens	130-135
33519472-0	2020	Acacetin Protects Against High Glucose-Induced Endothelial Cells Injury by Preserving Mitochondrial Function via Activating Sirt1/Sirt3/AMPK Signals.	acacetin	0-8	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	136-140
33519472-2	2020	The aim of this study was to investigate whether the natural flavone acacetin could protect against endothelial injury induced by high glucose and attenuate diabetes-accelerated atherosclerosis in streptozotocin-(STZ) induced diabetic ApoE-/- mice model.	acacetin	69-77	apolipoprotein E	Mus musculus	235-239
33519472-5	2020	Silencing Sirt3 abolished the beneficial effects of acacetin.	acacetin	52-60	sirtuin 3	Homo sapiens	10-15
33519472-6	2020	Further analysis revealed that these effects of acacetin rely on Sirt1 activation by increasing NAD+ followed by increasing Sirt3, pAMPK and PGC-1alpha.	acacetin	48-56	sirtuin 1	Homo sapiens	65-70
33519472-6	2020	Further analysis revealed that these effects of acacetin rely on Sirt1 activation by increasing NAD+ followed by increasing Sirt3, pAMPK and PGC-1alpha.	acacetin	48-56	sirtuin 3	Homo sapiens	124-129
33519472-6	2020	Further analysis revealed that these effects of acacetin rely on Sirt1 activation by increasing NAD+ followed by increasing Sirt3, pAMPK and PGC-1alpha.	acacetin	48-56	PPARG coactivator 1 alpha	Homo sapiens	141-151
33519472-7	2020	In STZ-diabetic mice, acacetin significantly upregulated the decreased signaling molecules (i.e. SOD, Bcl-2, PGC-1alpha, pAMPK, Sirt3 and Sirt1) in aorta tissue and attenuated atherosclerosis.	acacetin	22-30	superoxide dismutase 1	Homo sapiens	97-100
33519472-7	2020	In STZ-diabetic mice, acacetin significantly upregulated the decreased signaling molecules (i.e. SOD, Bcl-2, PGC-1alpha, pAMPK, Sirt3 and Sirt1) in aorta tissue and attenuated atherosclerosis.	acacetin	22-30	BCL2 apoptosis regulator	Homo sapiens	102-107
33519472-7	2020	In STZ-diabetic mice, acacetin significantly upregulated the decreased signaling molecules (i.e. SOD, Bcl-2, PGC-1alpha, pAMPK, Sirt3 and Sirt1) in aorta tissue and attenuated atherosclerosis.	acacetin	22-30	PPARG coactivator 1 alpha	Homo sapiens	109-119
33519472-7	2020	In STZ-diabetic mice, acacetin significantly upregulated the decreased signaling molecules (i.e. SOD, Bcl-2, PGC-1alpha, pAMPK, Sirt3 and Sirt1) in aorta tissue and attenuated atherosclerosis.	acacetin	22-30	sirtuin 3	Mus musculus	128-133
33519472-7	2020	In STZ-diabetic mice, acacetin significantly upregulated the decreased signaling molecules (i.e. SOD, Bcl-2, PGC-1alpha, pAMPK, Sirt3 and Sirt1) in aorta tissue and attenuated atherosclerosis.	acacetin	22-30	sirtuin 1	Mus musculus	138-143
33519472-8	2020	These results indicate that vascular endothelial protection of acacetin by activating Sirt1/Sirt3/AMPK signals is likely involved in alleviating diabetes-accelerated atherosclerosis by preserving mitochondrial function, which suggests that acacetin may be a drug candidate for treating cardiovascular disorder in patients with diabetes.	acacetin	63-71	sirtuin 1	Homo sapiens	86-91
33519472-8	2020	These results indicate that vascular endothelial protection of acacetin by activating Sirt1/Sirt3/AMPK signals is likely involved in alleviating diabetes-accelerated atherosclerosis by preserving mitochondrial function, which suggests that acacetin may be a drug candidate for treating cardiovascular disorder in patients with diabetes.	acacetin	63-71	sirtuin 3	Homo sapiens	92-97
33519472-8	2020	These results indicate that vascular endothelial protection of acacetin by activating Sirt1/Sirt3/AMPK signals is likely involved in alleviating diabetes-accelerated atherosclerosis by preserving mitochondrial function, which suggests that acacetin may be a drug candidate for treating cardiovascular disorder in patients with diabetes.	acacetin	63-71	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	98-102
33519472-8	2020	These results indicate that vascular endothelial protection of acacetin by activating Sirt1/Sirt3/AMPK signals is likely involved in alleviating diabetes-accelerated atherosclerosis by preserving mitochondrial function, which suggests that acacetin may be a drug candidate for treating cardiovascular disorder in patients with diabetes.	acacetin	240-248	sirtuin 1	Homo sapiens	86-91
33519472-8	2020	These results indicate that vascular endothelial protection of acacetin by activating Sirt1/Sirt3/AMPK signals is likely involved in alleviating diabetes-accelerated atherosclerosis by preserving mitochondrial function, which suggests that acacetin may be a drug candidate for treating cardiovascular disorder in patients with diabetes.	acacetin	240-248	sirtuin 3	Homo sapiens	92-97
33519472-8	2020	These results indicate that vascular endothelial protection of acacetin by activating Sirt1/Sirt3/AMPK signals is likely involved in alleviating diabetes-accelerated atherosclerosis by preserving mitochondrial function, which suggests that acacetin may be a drug candidate for treating cardiovascular disorder in patients with diabetes.	acacetin	240-248	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	98-102
32522955-11	2020	Similar to SSO, acacetin also inhibited UVB-induced MMP-1 protein and mRNA levels in HaCaT cells and HDF.	acacetin	16-24	matrix metallopeptidase 1	Homo sapiens	52-57
33394232-10	2021	The up-regulation of p21 and down-regulation of Cyclin-A1, Cyclin-B1, and Cdk-1 revealed the G2/M phase arrest mechanism of acacetin and apigenin.	acacetin	124-132	H3 histone pseudogene 16	Homo sapiens	21-24
33394232-10	2021	The up-regulation of p21 and down-regulation of Cyclin-A1, Cyclin-B1, and Cdk-1 revealed the G2/M phase arrest mechanism of acacetin and apigenin.	acacetin	124-132	cyclin A1	Homo sapiens	48-57
33394232-10	2021	The up-regulation of p21 and down-regulation of Cyclin-A1, Cyclin-B1, and Cdk-1 revealed the G2/M phase arrest mechanism of acacetin and apigenin.	acacetin	124-132	cyclin B1	Homo sapiens	59-68
33394232-10	2021	The up-regulation of p21 and down-regulation of Cyclin-A1, Cyclin-B1, and Cdk-1 revealed the G2/M phase arrest mechanism of acacetin and apigenin.	acacetin	124-132	cyclin dependent kinase 1	Homo sapiens	74-79
33394232-13	2021	Acacetin and apigenin-induced ROS is responsible for the induction of cell cycle arrest and activation of caspase-cascade pathways in U87 cells.	acacetin	0-8	caspase 8	Homo sapiens	106-113
32987362-4	2020	PURPOSE: This study aimed to determine whether linarin present in Cirsium setidens water extracts (CSE) and its aglycone acacetin inhibited osteoclastogenesis of RANKL-exposed RAW 264.7 murine macrophages for 5 days.	acacetin	121-129	tumor necrosis factor (ligand) superfamily, member 11	Mus musculus	162-167
32987362-5	2020	METHODS: This study assessed the osteoprotective effects of CSE, linarin and acacetin on RANKL-induced differentiation and activation of osteoclasts by using MTT assay, TRAP staining, Western blot analysis, bone resorption assay actin ring staining, adhesion assay and immunocytochemical assay.	acacetin	77-85	tumor necrosis factor (ligand) superfamily, member 11	Mus musculus	89-94
33239866-0	2020	Acacetin Induces Apoptosis in Human Osteosarcoma Cells by Modulation of ROS/JNK Activation.	acacetin	0-8	mitogen-activated protein kinase 8	Homo sapiens	76-79
33239866-13	2020	The acacetin treatment resulted in the activation of caspase-3, -8, and -9 and cleaved PARP.	acacetin	4-12	caspase 3	Homo sapiens	53-74
33239866-13	2020	The acacetin treatment resulted in the activation of caspase-3, -8, and -9 and cleaved PARP.	acacetin	4-12	poly(ADP-ribose) polymerase 1	Homo sapiens	87-91
33239866-15	2020	In addition, we found that acacetin induced the activation of the downstream c-Jun N-terminal kinase (JNK) signaling pathway.	acacetin	27-35	mitogen-activated protein kinase 8	Homo sapiens	77-100
33239866-15	2020	In addition, we found that acacetin induced the activation of the downstream c-Jun N-terminal kinase (JNK) signaling pathway.	acacetin	27-35	mitogen-activated protein kinase 8	Homo sapiens	102-105
33239866-16	2020	Subsequently, after treatment with the ROS scavenger GSH and the JNK inhibitor SP600125, the apoptosis-inducing effect triggered by acacetin was significantly attenuated.	acacetin	132-140	mitogen-activated protein kinase 8	Homo sapiens	65-68
33239866-17	2020	Conclusion: The results of the present study indicate that acacetin may induce apoptosis to inhibit cell growth by activating the ROS/JNK signaling pathway in SJSA and HOS cells, suggesting that acacetin may be a promising candidate for the management of osteosarcomas.	acacetin	59-67	mitogen-activated protein kinase 8	Homo sapiens	134-137
33239866-17	2020	Conclusion: The results of the present study indicate that acacetin may induce apoptosis to inhibit cell growth by activating the ROS/JNK signaling pathway in SJSA and HOS cells, suggesting that acacetin may be a promising candidate for the management of osteosarcomas.	acacetin	195-203	mitogen-activated protein kinase 8	Homo sapiens	134-137
33204066-12	2020	Results: In vitro, acacetin alleviated TBHP-induced ROS generation and upregulated the expression of antioxidant proteins, including HO-1, NQO1, and SOD.	acacetin	19-27	heme oxygenase 1	Rattus norvegicus	133-137
33204066-12	2020	Results: In vitro, acacetin alleviated TBHP-induced ROS generation and upregulated the expression of antioxidant proteins, including HO-1, NQO1, and SOD.	acacetin	19-27	NAD(P)H quinone dehydrogenase 1	Rattus norvegicus	139-143
33204066-13	2020	In addition, acacetin relieved the TBHP-induced generation of inflammatory mediators (COX-2, iNOS) and degradation of the extracellular matrix (aggrecan, collagen II, MMP13, MMP9, and MMP3).	acacetin	13-21	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	86-91
33204066-13	2020	In addition, acacetin relieved the TBHP-induced generation of inflammatory mediators (COX-2, iNOS) and degradation of the extracellular matrix (aggrecan, collagen II, MMP13, MMP9, and MMP3).	acacetin	13-21	nitric oxide synthase 2	Rattus norvegicus	93-97
33204066-13	2020	In addition, acacetin relieved the TBHP-induced generation of inflammatory mediators (COX-2, iNOS) and degradation of the extracellular matrix (aggrecan, collagen II, MMP13, MMP9, and MMP3).	acacetin	13-21	matrix metallopeptidase 13	Rattus norvegicus	167-172
33204066-13	2020	In addition, acacetin relieved the TBHP-induced generation of inflammatory mediators (COX-2, iNOS) and degradation of the extracellular matrix (aggrecan, collagen II, MMP13, MMP9, and MMP3).	acacetin	13-21	matrix metallopeptidase 9	Rattus norvegicus	174-178
33204066-13	2020	In addition, acacetin relieved the TBHP-induced generation of inflammatory mediators (COX-2, iNOS) and degradation of the extracellular matrix (aggrecan, collagen II, MMP13, MMP9, and MMP3).	acacetin	13-21	matrix metallopeptidase 3	Rattus norvegicus	184-188
33204066-14	2020	Acacetin exerted its effect by activating the Nrf2 pathway and inhibiting p38, JNK and ERK1/2 phosphorylation.	acacetin	0-8	NFE2 like bZIP transcription factor 2	Rattus norvegicus	46-50
33204066-14	2020	Acacetin exerted its effect by activating the Nrf2 pathway and inhibiting p38, JNK and ERK1/2 phosphorylation.	acacetin	0-8	mitogen activated protein kinase 14	Rattus norvegicus	74-77
33204066-14	2020	Acacetin exerted its effect by activating the Nrf2 pathway and inhibiting p38, JNK and ERK1/2 phosphorylation.	acacetin	0-8	mitogen-activated protein kinase 8	Rattus norvegicus	79-82
33204066-14	2020	Acacetin exerted its effect by activating the Nrf2 pathway and inhibiting p38, JNK and ERK1/2 phosphorylation.	acacetin	0-8	mitogen activated protein kinase 3	Rattus norvegicus	87-93
32522955-13	2020	Acacetin regulated the phosphorylation of JNK1/2 and c-jun, but did not inhibit the phosphorylation of ERK1/2, p38 and AKT.	acacetin	0-8	mitogen-activated protein kinase 8	Homo sapiens	42-48
32522955-13	2020	Acacetin regulated the phosphorylation of JNK1/2 and c-jun, but did not inhibit the phosphorylation of ERK1/2, p38 and AKT.	acacetin	0-8	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	53-58
32522955-14	2020	Taken together, these results indicate that SSO and its active compound acacetin can prevent UVB-induced MMP-1 expression that lead to skin photoaging.	acacetin	72-80	matrix metallopeptidase 1	Homo sapiens	105-110
32746771-7	2021	This study mainly represents that Galuteolin and Linarin in the Akt pathway can be perceived for OSCC treatment and other five CYP inhibitors - Diosmetin, Acacetin, Epicatechin, Eriodictyol and Capillin for the treatment of other diseases and cancers caused by overexpression of MAOB.	acacetin	155-163	AKT serine/threonine kinase 1	Homo sapiens	64-67
33195691-0	2020	Acacetin Suppresses IL-1beta-Induced Expression of Matrix Metalloproteinases in Chondrocytes and Protects against Osteoarthritis in a Mouse Model by Inhibiting NF-kappaB Signaling Pathways.	acacetin	0-8	interleukin 1 alpha	Mus musculus	20-28
33195691-6	2020	Acacetin inhibited the interleukin-1beta- (IL-1beta-) induced expression of MMP-1, MMP-3, and MMP-13in chondrocytes by blocking nuclear factor-kappaB (NF-kappaB) signaling pathways.	acacetin	0-8	interleukin 1 beta	Mus musculus	23-40
33195691-6	2020	Acacetin inhibited the interleukin-1beta- (IL-1beta-) induced expression of MMP-1, MMP-3, and MMP-13in chondrocytes by blocking nuclear factor-kappaB (NF-kappaB) signaling pathways.	acacetin	0-8	interleukin 1 alpha	Mus musculus	43-52
33195691-6	2020	Acacetin inhibited the interleukin-1beta- (IL-1beta-) induced expression of MMP-1, MMP-3, and MMP-13in chondrocytes by blocking nuclear factor-kappaB (NF-kappaB) signaling pathways.	acacetin	0-8	matrix metallopeptidase 13	Mus musculus	76-81
33195691-6	2020	Acacetin inhibited the interleukin-1beta- (IL-1beta-) induced expression of MMP-1, MMP-3, and MMP-13in chondrocytes by blocking nuclear factor-kappaB (NF-kappaB) signaling pathways.	acacetin	0-8	matrix metallopeptidase 3	Mus musculus	83-88
33195691-6	2020	Acacetin inhibited the interleukin-1beta- (IL-1beta-) induced expression of MMP-1, MMP-3, and MMP-13in chondrocytes by blocking nuclear factor-kappaB (NF-kappaB) signaling pathways.	acacetin	0-8	matrix metallopeptidase 13	Mus musculus	94-100
33195691-7	2020	Furthermore, we found that acacetin suppressed OA progression and inhibited the expression of MMP-1, MMP-3, and MMP-13 in ACLT-induced OA mice.	acacetin	27-35	matrix metallopeptidase 13	Mus musculus	94-99
33195691-7	2020	Furthermore, we found that acacetin suppressed OA progression and inhibited the expression of MMP-1, MMP-3, and MMP-13 in ACLT-induced OA mice.	acacetin	27-35	matrix metallopeptidase 3	Mus musculus	101-106
33195691-7	2020	Furthermore, we found that acacetin suppressed OA progression and inhibited the expression of MMP-1, MMP-3, and MMP-13 in ACLT-induced OA mice.	acacetin	27-35	matrix metallopeptidase 13	Mus musculus	112-118
32918384-0	2020	Doxorubicin cardiomyopathy is ameliorated by acacetin via Sirt1-mediated activation of AMPK/Nrf2 signal molecules.	acacetin	45-53	sirtuin 1	Rattus norvegicus	58-63
32918384-0	2020	Doxorubicin cardiomyopathy is ameliorated by acacetin via Sirt1-mediated activation of AMPK/Nrf2 signal molecules.	acacetin	45-53	protein kinase AMP-activated catalytic subunit alpha 2	Rattus norvegicus	87-91
32918384-0	2020	Doxorubicin cardiomyopathy is ameliorated by acacetin via Sirt1-mediated activation of AMPK/Nrf2 signal molecules.	acacetin	45-53	NFE2 like bZIP transcription factor 2	Rattus norvegicus	92-96
32918384-3	2020	It was found that the cardiac dysfunction and myocardial fibrosis induced by doxorubicin were significantly improved by acacetin in mice with impaired Nrf2/HO-1 and Sirt1/pAMPK molecules, which is reversed by acacetin treatment.	acacetin	120-128	nuclear factor, erythroid derived 2, like 2	Mus musculus	151-155
32918384-3	2020	It was found that the cardiac dysfunction and myocardial fibrosis induced by doxorubicin were significantly improved by acacetin in mice with impaired Nrf2/HO-1 and Sirt1/pAMPK molecules, which is reversed by acacetin treatment.	acacetin	120-128	heme oxygenase 1	Mus musculus	156-160
32918384-3	2020	It was found that the cardiac dysfunction and myocardial fibrosis induced by doxorubicin were significantly improved by acacetin in mice with impaired Nrf2/HO-1 and Sirt1/pAMPK molecules, which is reversed by acacetin treatment.	acacetin	120-128	sirtuin 1	Mus musculus	165-170
32918384-4	2020	Doxorubicin decreased cell viability and increased ROS production in rat cardiomyoblasts; these effects are significantly countered by acacetin (0.3-3 muM) in a concentration-dependent manner via activating Sirt1/pAMPK signals and enhancing antioxidation (Nrf2/HO-1 and SOD1/SOD2) and anti-apoptosis.	acacetin	135-143	sirtuin 1	Rattus norvegicus	207-212
32918384-4	2020	Doxorubicin decreased cell viability and increased ROS production in rat cardiomyoblasts; these effects are significantly countered by acacetin (0.3-3 muM) in a concentration-dependent manner via activating Sirt1/pAMPK signals and enhancing antioxidation (Nrf2/HO-1 and SOD1/SOD2) and anti-apoptosis.	acacetin	135-143	NFE2 like bZIP transcription factor 2	Rattus norvegicus	256-260
32918384-4	2020	Doxorubicin decreased cell viability and increased ROS production in rat cardiomyoblasts; these effects are significantly countered by acacetin (0.3-3 muM) in a concentration-dependent manner via activating Sirt1/pAMPK signals and enhancing antioxidation (Nrf2/HO-1 and SOD1/SOD2) and anti-apoptosis.	acacetin	135-143	heme oxygenase 1	Rattus norvegicus	261-265
32918384-4	2020	Doxorubicin decreased cell viability and increased ROS production in rat cardiomyoblasts; these effects are significantly countered by acacetin (0.3-3 muM) in a concentration-dependent manner via activating Sirt1/pAMPK signals and enhancing antioxidation (Nrf2/HO-1 and SOD1/SOD2) and anti-apoptosis.	acacetin	135-143	superoxide dismutase 1	Rattus norvegicus	270-274
32918384-4	2020	Doxorubicin decreased cell viability and increased ROS production in rat cardiomyoblasts; these effects are significantly countered by acacetin (0.3-3 muM) in a concentration-dependent manner via activating Sirt1/pAMPK signals and enhancing antioxidation (Nrf2/HO-1 and SOD1/SOD2) and anti-apoptosis.	acacetin	135-143	superoxide dismutase 2	Rattus norvegicus	275-279
32918384-6	2020	The results demonstrate for the first time that doxorubicin cardiotoxicity is antagonized by acacetin via Sirt1-mediated activation of AMPK/Nrf2 signal molecules, indicating that acacetin may be a drug candidate used clinically for protecting against doxorubicin cardiomyopathy.	acacetin	93-101	sirtuin 1	Rattus norvegicus	106-111
32918384-6	2020	The results demonstrate for the first time that doxorubicin cardiotoxicity is antagonized by acacetin via Sirt1-mediated activation of AMPK/Nrf2 signal molecules, indicating that acacetin may be a drug candidate used clinically for protecting against doxorubicin cardiomyopathy.	acacetin	93-101	protein kinase AMP-activated catalytic subunit alpha 2	Rattus norvegicus	135-139
32918384-6	2020	The results demonstrate for the first time that doxorubicin cardiotoxicity is antagonized by acacetin via Sirt1-mediated activation of AMPK/Nrf2 signal molecules, indicating that acacetin may be a drug candidate used clinically for protecting against doxorubicin cardiomyopathy.	acacetin	93-101	NFE2 like bZIP transcription factor 2	Rattus norvegicus	140-144
32918384-6	2020	The results demonstrate for the first time that doxorubicin cardiotoxicity is antagonized by acacetin via Sirt1-mediated activation of AMPK/Nrf2 signal molecules, indicating that acacetin may be a drug candidate used clinically for protecting against doxorubicin cardiomyopathy.	acacetin	179-187	sirtuin 1	Rattus norvegicus	106-111
32918384-6	2020	The results demonstrate for the first time that doxorubicin cardiotoxicity is antagonized by acacetin via Sirt1-mediated activation of AMPK/Nrf2 signal molecules, indicating that acacetin may be a drug candidate used clinically for protecting against doxorubicin cardiomyopathy.	acacetin	179-187	protein kinase AMP-activated catalytic subunit alpha 2	Rattus norvegicus	135-139
32918384-6	2020	The results demonstrate for the first time that doxorubicin cardiotoxicity is antagonized by acacetin via Sirt1-mediated activation of AMPK/Nrf2 signal molecules, indicating that acacetin may be a drug candidate used clinically for protecting against doxorubicin cardiomyopathy.	acacetin	179-187	NFE2 like bZIP transcription factor 2	Rattus norvegicus	140-144
32738202-2	2020	The aim of the present study was to investigate the effects of acacetin on the activities of the cytochrome P450 family members CYP1A2, CYP2B1, CYP2C11, CYP2D1, CYP2E1, and CYP3A2 in rat liver microsomes in vitro and rats in vivo to evaluate potential herb-drug interactions by using a cocktail approach.	acacetin	63-71	cytochrome P450, family 1, subfamily a, polypeptide 2	Rattus norvegicus	128-134
32738202-2	2020	The aim of the present study was to investigate the effects of acacetin on the activities of the cytochrome P450 family members CYP1A2, CYP2B1, CYP2C11, CYP2D1, CYP2E1, and CYP3A2 in rat liver microsomes in vitro and rats in vivo to evaluate potential herb-drug interactions by using a cocktail approach.	acacetin	63-71	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	136-142
32738202-2	2020	The aim of the present study was to investigate the effects of acacetin on the activities of the cytochrome P450 family members CYP1A2, CYP2B1, CYP2C11, CYP2D1, CYP2E1, and CYP3A2 in rat liver microsomes in vitro and rats in vivo to evaluate potential herb-drug interactions by using a cocktail approach.	acacetin	63-71	cytochrome P450, subfamily 2, polypeptide 11	Rattus norvegicus	144-151
32738202-2	2020	The aim of the present study was to investigate the effects of acacetin on the activities of the cytochrome P450 family members CYP1A2, CYP2B1, CYP2C11, CYP2D1, CYP2E1, and CYP3A2 in rat liver microsomes in vitro and rats in vivo to evaluate potential herb-drug interactions by using a cocktail approach.	acacetin	63-71	cytochrome P450, family 2, subfamily d, polypeptide 1	Rattus norvegicus	153-159
32738202-2	2020	The aim of the present study was to investigate the effects of acacetin on the activities of the cytochrome P450 family members CYP1A2, CYP2B1, CYP2C11, CYP2D1, CYP2E1, and CYP3A2 in rat liver microsomes in vitro and rats in vivo to evaluate potential herb-drug interactions by using a cocktail approach.	acacetin	63-71	cytochrome P450, family 2, subfamily e, polypeptide 1	Rattus norvegicus	161-167
32738202-2	2020	The aim of the present study was to investigate the effects of acacetin on the activities of the cytochrome P450 family members CYP1A2, CYP2B1, CYP2C11, CYP2D1, CYP2E1, and CYP3A2 in rat liver microsomes in vitro and rats in vivo to evaluate potential herb-drug interactions by using a cocktail approach.	acacetin	63-71	cytochrome P450, family 3, subfamily a, polypeptide 2	Rattus norvegicus	173-179
32738202-5	2020	In vitro, the mode of acacetin inhibition of CYP2B1, CYP2C11, and CYP2E1 was competitive, while mixed inhibition was observed for CYP1A2 and CYP3A2.	acacetin	22-30	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	45-51
32738202-5	2020	In vitro, the mode of acacetin inhibition of CYP2B1, CYP2C11, and CYP2E1 was competitive, while mixed inhibition was observed for CYP1A2 and CYP3A2.	acacetin	22-30	cytochrome P450, subfamily 2, polypeptide 11	Rattus norvegicus	53-60
32738202-5	2020	In vitro, the mode of acacetin inhibition of CYP2B1, CYP2C11, and CYP2E1 was competitive, while mixed inhibition was observed for CYP1A2 and CYP3A2.	acacetin	22-30	cytochrome P450, family 2, subfamily e, polypeptide 1	Rattus norvegicus	66-72
32738202-5	2020	In vitro, the mode of acacetin inhibition of CYP2B1, CYP2C11, and CYP2E1 was competitive, while mixed inhibition was observed for CYP1A2 and CYP3A2.	acacetin	22-30	cytochrome P450, family 3, subfamily a, polypeptide 2	Rattus norvegicus	141-147
32892299-11	2020	Cell experiments showed that acacetin could reduce the apoptosis of HUVEC cells, the levels of inflammatory cytokines and the expression of TGF-beta, Collagen I and Smad3 in endothelial cell injury model.	acacetin	29-37	transforming growth factor alpha	Rattus norvegicus	140-148
32892299-11	2020	Cell experiments showed that acacetin could reduce the apoptosis of HUVEC cells, the levels of inflammatory cytokines and the expression of TGF-beta, Collagen I and Smad3 in endothelial cell injury model.	acacetin	29-37	SMAD family member 3	Rattus norvegicus	165-170
32797769-3	2020	Moreover, ELISA assay showed that acacetin dose-dependently attenuated LPS-induced increases of TNF-alpha, IL-6 and IL-1beta in PDL cells.	acacetin	34-42	tumor necrosis factor	Homo sapiens	96-105
32797769-3	2020	Moreover, ELISA assay showed that acacetin dose-dependently attenuated LPS-induced increases of TNF-alpha, IL-6 and IL-1beta in PDL cells.	acacetin	34-42	interleukin 6	Homo sapiens	107-111
32797769-3	2020	Moreover, ELISA assay showed that acacetin dose-dependently attenuated LPS-induced increases of TNF-alpha, IL-6 and IL-1beta in PDL cells.	acacetin	34-42	interleukin 1 alpha	Homo sapiens	116-124
32797769-4	2020	Western blot analysis showed that administration of acacetin dose-dependently increased the ratio of LC3II/LC3I, as well as the expression of beclin-1, as compared to LPS-stimulated PDL cells.	acacetin	52-60	beclin 1	Homo sapiens	142-150
32797769-6	2020	In addition, the expression of GSK-3beta, a regulator of autophagy, was suppressed by administration with acacetin in a dose-dependent manner.	acacetin	106-114	glycogen synthase kinase 3 alpha	Homo sapiens	31-40
32797769-7	2020	Acacetin treatment promotes survival and suppresses inflammation in LPS-stimulated PDL cells via regulating autophagy and GSK-3beta signal in PDL cells, suggesting that acacetin may be a potential novel agent for the treatment of chronic periodontitis.	acacetin	0-8	glycogen synthase kinase 3 alpha	Homo sapiens	122-131
32797769-7	2020	Acacetin treatment promotes survival and suppresses inflammation in LPS-stimulated PDL cells via regulating autophagy and GSK-3beta signal in PDL cells, suggesting that acacetin may be a potential novel agent for the treatment of chronic periodontitis.	acacetin	169-177	glycogen synthase kinase 3 alpha	Homo sapiens	122-131
31734898-5	2020	Acacetin reduced the cell survival and proliferation of both types of cells, and induced S- and G2-M phase arrest and also reduced the levels of beta-catenin and its downstream target c-myc.	acacetin	0-8	catenin beta 1	Homo sapiens	145-157
32746771-6	2021	From the investigation of CYP inhibitors against MAOB, five CYP inhibitors- Diosmetin, Acacetin, Epicatechin, Eriodictyol and Capillin have expressed inhibitory action against MAOB without any interference with Akt1 and Akt2.	acacetin	87-95	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	26-29
32746771-6	2021	From the investigation of CYP inhibitors against MAOB, five CYP inhibitors- Diosmetin, Acacetin, Epicatechin, Eriodictyol and Capillin have expressed inhibitory action against MAOB without any interference with Akt1 and Akt2.	acacetin	87-95	monoamine oxidase B	Homo sapiens	49-53
32746771-6	2021	From the investigation of CYP inhibitors against MAOB, five CYP inhibitors- Diosmetin, Acacetin, Epicatechin, Eriodictyol and Capillin have expressed inhibitory action against MAOB without any interference with Akt1 and Akt2.	acacetin	87-95	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	60-63
32746771-6	2021	From the investigation of CYP inhibitors against MAOB, five CYP inhibitors- Diosmetin, Acacetin, Epicatechin, Eriodictyol and Capillin have expressed inhibitory action against MAOB without any interference with Akt1 and Akt2.	acacetin	87-95	monoamine oxidase B	Homo sapiens	176-180
32746771-6	2021	From the investigation of CYP inhibitors against MAOB, five CYP inhibitors- Diosmetin, Acacetin, Epicatechin, Eriodictyol and Capillin have expressed inhibitory action against MAOB without any interference with Akt1 and Akt2.	acacetin	87-95	AKT serine/threonine kinase 2	Homo sapiens	220-224
32126492-0	2020	Acacetin enhances glucose uptake through insulin-independent GLUT4 translocation in L6 myotubes.	acacetin	0-8	insulin	Homo sapiens	41-48
32126492-0	2020	Acacetin enhances glucose uptake through insulin-independent GLUT4 translocation in L6 myotubes.	acacetin	0-8	solute carrier family 2 member 4	Homo sapiens	61-66
32126492-3	2020	METHODS: To determine whether acacetin promotes GLUT4-dependent glucose uptake in cultured L6 skeletal muscle cells, we performed a [14C] 2-deoxy-D-glucose (2-DG) uptake assay after treating differentiated L6-GLUT4myc cells with acacetin.	acacetin	30-38	solute carrier family 2 member 4	Rattus norvegicus	48-53
32126492-4	2020	RESULTS: Acacetin dose-dependently increased 2-DG uptake by enhancing GLUT4 translocation to the plasma membrane.	acacetin	9-17	solute carrier family 2 member 4	Rattus norvegicus	70-75
32126492-5	2020	Our results revealed that acacetin activated the CaMKII-AMPK pathway by increasing intracellular calcium concentrations.	acacetin	26-34	protein kinase AMP-activated catalytic subunit alpha 2	Rattus norvegicus	56-60
32126492-6	2020	We also found that aPKClambda/zeta phosphorylation and intracellular reactive oxygen species (ROS) production were involved in acacetin-induced GLUT4 translocation.	acacetin	127-135	solute carrier family 2 member 4	Rattus norvegicus	144-149
32126492-7	2020	Moreover, acacetin-activated AMPK inhibited intracellular lipid accumulation and increased 2-DG uptake in HepG2 cells.	acacetin	10-18	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	29-33
31734898-5	2020	Acacetin reduced the cell survival and proliferation of both types of cells, and induced S- and G2-M phase arrest and also reduced the levels of beta-catenin and its downstream target c-myc.	acacetin	0-8	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	184-189
31734898-6	2020	Further, acacetin induced apoptosis as examined by Annexin-V FITC and nuclear condensation.	acacetin	9-17	annexin A5	Homo sapiens	51-60
31734898-8	2020	Acacetin increased mitochondrial membrane potential depolarization and Bax:Bcl-2 ratio.	acacetin	0-8	BCL2 associated X, apoptosis regulator	Homo sapiens	71-74
31734898-8	2020	Acacetin increased mitochondrial membrane potential depolarization and Bax:Bcl-2 ratio.	acacetin	0-8	BCL2 apoptosis regulator	Homo sapiens	75-80
31734898-10	2020	In conclusion, Acacetin induces mitochondrial ROS-mediated cell death in a caspase-independent manner in SW480 and HCT-116 colon carcinoma cells by inducing apoptosis inducing factor (AIF), which may potentiate its anticancer and chemotherapeutic prospects against colorectal carcinoma.	acacetin	15-23	caspase 8	Homo sapiens	75-82
30594625-7	2019	Furthermore, docking simulations showed that the binding areas of NHPN, kaempferol and acacetin on UGT1A1 were highly overlapping, and convergence with the binding area of bilirubin within UGT1A1.	acacetin	87-95	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	99-105
31066474-4	2019	Our results showed that 12.5- to 200-muM acacetin inhibited cell viability in dose- and time-dependent manners in HNSCC cells, but a relative higher concentration was needed for oral adenoid cystic carcinoma cells.	acacetin	41-49	latexin	Homo sapiens	37-40
31066474-7	2019	Acacetin promoted mitochondrial cytochrome c release and caspase 9, 3 processing.	acacetin	0-8	cytochrome c, somatic	Homo sapiens	32-44
31066474-7	2019	Acacetin promoted mitochondrial cytochrome c release and caspase 9, 3 processing.	acacetin	0-8	caspase 9	Homo sapiens	57-66
31066474-8	2019	Knocking down of M3 R expression by specific siRNA significantly prevented the acacetin-induced cell viability damage, cell apoptosis, and caspase 3 activation.	acacetin	79-87	caspase 3	Homo sapiens	139-148
31066474-10	2019	These data indicate that acacetin-induced cell apoptosis in HNSCC cells may through M3 R related calcium signaling and caspase 3 activation.	acacetin	25-33	caspase 3	Homo sapiens	119-128
30632500-0	2019	Acacetin protects against cerebral ischemia-reperfusion injury via the NLRP3 signaling pathway.	acacetin	0-8	NLR family, pyrin domain containing 3	Mus musculus	71-76
30632500-2	2019	However, whether acacetin has an effect on inflammatory corpuscle 3 (NLRP3) after cerebral ischemia-reperfusion injury has not been fully determined.	acacetin	17-25	NLR family, pyrin domain containing 3	Mus musculus	69-74
30632500-9	2019	Expression of Iba1, tumor necrosis factor-alpha, interleukin-1beta and interleukin-6 was significantly lower in the acacetin group compared with the middle cerebral artery occlusion group.	acacetin	116-124	tumor necrosis factor	Mus musculus	20-47
30632500-9	2019	Expression of Iba1, tumor necrosis factor-alpha, interleukin-1beta and interleukin-6 was significantly lower in the acacetin group compared with the middle cerebral artery occlusion group.	acacetin	116-124	interleukin 1 beta	Mus musculus	49-66
30632500-9	2019	Expression of Iba1, tumor necrosis factor-alpha, interleukin-1beta and interleukin-6 was significantly lower in the acacetin group compared with the middle cerebral artery occlusion group.	acacetin	116-124	interleukin 6	Mus musculus	71-84
30632500-10	2019	Western blot assay results showed that expression of Toll-like receptor 4, nuclear factor kappa B, NLRP3, procaspase-1, caspase-1, pro-interleukin-1beta, and interleukin-1beta were significantly lower in the acacetin group compared with the middle cerebral artery occlusion group.	acacetin	208-216	toll-like receptor 4	Mus musculus	53-97
30632500-11	2019	Our findings indicate that acacetin has a protective effect on cerebral ischemia-reperfusion injury, and its mechanism of action is associated with inhibition of microglia-mediated inflammation and the NLRP3 signaling pathway.	acacetin	27-35	NLR family, pyrin domain containing 3	Mus musculus	202-207
31734898-0	2020	Induction of growth cessation by acacetin via beta-catenin pathway and apoptosis by apoptosis inducing factor activation in colorectal carcinoma cells.	acacetin	33-41	catenin beta 1	Homo sapiens	46-58
31827551-8	2019	The active compounds of acacetin, kaempferol, luteolin, and quercetin showed a good binding affinity towards TNF (C-score >= 4).	acacetin	24-32	tumor necrosis factor-like	Rattus norvegicus	109-112
31621310-6	2019	In contrast, both 5,7-dihydroxy-4-methoxy substituted isoflavone (biochanin A) and flavone (acacetin) induced all three AhR-responsive genes; 4",5,7-trimethoxyisoflavone was a potent AhR agonist, and the isomeric flavone was AhR-inactive.	acacetin	92-100	aryl hydrocarbon receptor	Homo sapiens	120-123
31621310-6	2019	In contrast, both 5,7-dihydroxy-4-methoxy substituted isoflavone (biochanin A) and flavone (acacetin) induced all three AhR-responsive genes; 4",5,7-trimethoxyisoflavone was a potent AhR agonist, and the isomeric flavone was AhR-inactive.	acacetin	92-100	aryl hydrocarbon receptor	Homo sapiens	183-186
31621310-6	2019	In contrast, both 5,7-dihydroxy-4-methoxy substituted isoflavone (biochanin A) and flavone (acacetin) induced all three AhR-responsive genes; 4",5,7-trimethoxyisoflavone was a potent AhR agonist, and the isomeric flavone was AhR-inactive.	acacetin	92-100	aryl hydrocarbon receptor	Homo sapiens	183-186
31229563-4	2019	Although acacetin-treated mice showed normal circadian hypothalamo-pituitary-adrenal (HPA) axis activity, their endocrine responsivity to both acute restraint stress and intracerebroventricular injection of corticotropin-releasing factor (CRF) was buffered.	acacetin	9-17	corticotropin releasing hormone	Mus musculus	207-237
31229563-7	2019	Moreover, the acacetin-evoked anti-depression was preferentially counteracted by co-administration of 5-HT1A receptor antagonist WAY-100635, but potentiated by 5-HT1A receptor agonist 8-OH-DPAT and sub-effective dose of serotonergic antidepressant fluoxetine, suggesting a pivotal engagement of 5-HT1A related serotonergic system.	acacetin	14-22	5-hydroxytryptamine (serotonin) receptor 1A	Mus musculus	102-117
31229563-7	2019	Moreover, the acacetin-evoked anti-depression was preferentially counteracted by co-administration of 5-HT1A receptor antagonist WAY-100635, but potentiated by 5-HT1A receptor agonist 8-OH-DPAT and sub-effective dose of serotonergic antidepressant fluoxetine, suggesting a pivotal engagement of 5-HT1A related serotonergic system.	acacetin	14-22	5-hydroxytryptamine (serotonin) receptor 1A	Mus musculus	160-175
31229563-7	2019	Moreover, the acacetin-evoked anti-depression was preferentially counteracted by co-administration of 5-HT1A receptor antagonist WAY-100635, but potentiated by 5-HT1A receptor agonist 8-OH-DPAT and sub-effective dose of serotonergic antidepressant fluoxetine, suggesting a pivotal engagement of 5-HT1A related serotonergic system.	acacetin	14-22	5-hydroxytryptamine (serotonin) receptor 1A	Mus musculus	102-108
30594625-5	2019	Further investigation on inhibition kinetics of two strong flavonoid-type UGT1A1 inhibitors, acacetin and kaempferol, yielded interesting results.	acacetin	93-101	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	74-80
30594625-7	2019	Furthermore, docking simulations showed that the binding areas of NHPN, kaempferol and acacetin on UGT1A1 were highly overlapping, and convergence with the binding area of bilirubin within UGT1A1.	acacetin	87-95	UDP glucuronosyltransferase family 1 member A1	Homo sapiens	189-195
30813423-4	2019	However, acacetin 7-methyl ether was >500-fold selective against MAO-B over MAO-A as compared to only two-fold selectivity shown by acacetin.	acacetin	9-17	monoamine oxidase B	Homo sapiens	65-70
30813423-4	2019	However, acacetin 7-methyl ether was >500-fold selective against MAO-B over MAO-A as compared to only two-fold selectivity shown by acacetin.	acacetin	9-17	monoamine oxidase A	Homo sapiens	76-81
31359386-5	2019	We recently reported that acacetin could antagonize the non-genomic action of RARgamma via tipping the balance of AKT-p53 driven by RARgamma from tumor promoting to tumor suppressive effect.	acacetin	26-34	retinoic acid receptor gamma	Homo sapiens	78-86
31359386-5	2019	We recently reported that acacetin could antagonize the non-genomic action of RARgamma via tipping the balance of AKT-p53 driven by RARgamma from tumor promoting to tumor suppressive effect.	acacetin	26-34	tumor protein p53	Homo sapiens	118-121
31359386-5	2019	We recently reported that acacetin could antagonize the non-genomic action of RARgamma via tipping the balance of AKT-p53 driven by RARgamma from tumor promoting to tumor suppressive effect.	acacetin	26-34	retinoic acid receptor gamma	Homo sapiens	132-140
31359386-6	2019	This chapter provides methodology for identification of acacetin as a ligand and regulator of non-genomic signaling of RARgamma.	acacetin	56-64	retinoic acid receptor gamma	Homo sapiens	119-127
30301254-8	2018	Out of the 30 flavonoids tested, 7 significantly inhibited CYP3A4, most prominent being acacetin that inhibited 95% of enzyme activity at 1 microM concentration.	acacetin	88-96	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	59-65
29243040-7	2018	Pulmonary myeloperoxidase (MPO) activity was lower in the acacetin-pre-treated sepsis groups than in the sepsis group.	acacetin	58-66	myeloperoxidase	Mus musculus	10-25
29243040-7	2018	Pulmonary myeloperoxidase (MPO) activity was lower in the acacetin-pre-treated sepsis groups than in the sepsis group.	acacetin	58-66	myeloperoxidase	Mus musculus	27-30
29243040-8	2018	The mechanism underlying the protective effect of acacetin on sepsis is related to the regulation of certain antioxidation genes, including inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), superoxide dismutases (SODs), and heme oxygenase 1 (HO-1).Taken together, our results indicate that acacetin pre-treatment inhibits sepsis-induced ALI through its anti-inflammatory and antioxidative activity, suggesting that acacetin may be a potential protective agent for sepsis-induced ALI.	acacetin	50-58	nitric oxide synthase 2, inducible	Mus musculus	140-171
29243040-8	2018	The mechanism underlying the protective effect of acacetin on sepsis is related to the regulation of certain antioxidation genes, including inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), superoxide dismutases (SODs), and heme oxygenase 1 (HO-1).Taken together, our results indicate that acacetin pre-treatment inhibits sepsis-induced ALI through its anti-inflammatory and antioxidative activity, suggesting that acacetin may be a potential protective agent for sepsis-induced ALI.	acacetin	50-58	nitric oxide synthase 2, inducible	Mus musculus	173-177
29243040-8	2018	The mechanism underlying the protective effect of acacetin on sepsis is related to the regulation of certain antioxidation genes, including inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), superoxide dismutases (SODs), and heme oxygenase 1 (HO-1).Taken together, our results indicate that acacetin pre-treatment inhibits sepsis-induced ALI through its anti-inflammatory and antioxidative activity, suggesting that acacetin may be a potential protective agent for sepsis-induced ALI.	acacetin	50-58	prostaglandin-endoperoxide synthase 2	Mus musculus	180-196
29243040-8	2018	The mechanism underlying the protective effect of acacetin on sepsis is related to the regulation of certain antioxidation genes, including inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), superoxide dismutases (SODs), and heme oxygenase 1 (HO-1).Taken together, our results indicate that acacetin pre-treatment inhibits sepsis-induced ALI through its anti-inflammatory and antioxidative activity, suggesting that acacetin may be a potential protective agent for sepsis-induced ALI.	acacetin	50-58	prostaglandin-endoperoxide synthase 2	Mus musculus	198-203
29243040-8	2018	The mechanism underlying the protective effect of acacetin on sepsis is related to the regulation of certain antioxidation genes, including inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), superoxide dismutases (SODs), and heme oxygenase 1 (HO-1).Taken together, our results indicate that acacetin pre-treatment inhibits sepsis-induced ALI through its anti-inflammatory and antioxidative activity, suggesting that acacetin may be a potential protective agent for sepsis-induced ALI.	acacetin	50-58	heme oxygenase 1	Mus musculus	240-256
30187077-7	2018	Among non-prenylated flavonoids, acacetin and chrysin inhibited Kv1.3 channels in Jurkat T cells when applied at the concentration of 30 microM, whereas baicalein, wogonin, and luteolin were ineffective at this concentration.	acacetin	33-41	potassium voltage-gated channel subfamily A member 3	Homo sapiens	64-69
30187077-8	2018	The inhibitory effects of acacetin and chrysin on Kv1.3 channels were significantly less potent than the inhibition caused by 6-PR.	acacetin	26-34	potassium voltage-gated channel subfamily A member 3	Homo sapiens	50-55
30187077-12	2018	The inhibition of Kv1.3 channels by 6-PR, acacetin, and chrysin was not related to cytotoxicity of these compounds.	acacetin	42-50	potassium voltage-gated channel subfamily A member 3	Homo sapiens	18-23
29626627-6	2018	In MDA-MB-468 cells that were coincubated with the CYP1 inhibitor acacetin, an approximately 70-fold increase was noted in the IC50 (18 +- 1.6 muM) of tangeretin.	acacetin	66-74	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	51-55
30176062-3	2018	METHODS AND RESULTS: In a type II collagen (CII)-induced autoimmune arthritis model, acacetin significantly repressed the incidence of CIA, prevented the pathological alteration, and reduced CII-specific IgG and IgG1 levels.	acacetin	85-93	LOC105243590	Mus musculus	212-216
30176062-6	2018	The addition of acacetin inhibited the T cell proliferation, as well as the expression of the transcriptional coactivator TAZ, which regulated the balance of Treg/Th17 immunity, in a dose-dependent manner.	acacetin	16-24	tafazzin, phospholipid-lysophospholipid transacylase	Mus musculus	122-125
29867499-0	2018	The Natural Flavone Acacetin Confers Cardiomyocyte Protection Against Hypoxia/Reoxygenation Injury via AMPK-Mediated Activation of Nrf2 Signaling Pathway.	acacetin	20-28	protein kinase AMP-activated catalytic subunit alpha 2	Rattus norvegicus	103-107
29867499-0	2018	The Natural Flavone Acacetin Confers Cardiomyocyte Protection Against Hypoxia/Reoxygenation Injury via AMPK-Mediated Activation of Nrf2 Signaling Pathway.	acacetin	20-28	NFE2 like bZIP transcription factor 2	Rattus norvegicus	131-135
29867499-2	2018	It was found that acacetin (0.3-3 muM) significantly decreased the apoptosis and reactive oxygen species production induced by hypoxia/reoxygenation injury in cardiomyocytes and H9C2 cardiomyoblasts via reducing the pro-apoptotic proteins Bax and cleaved-caspase-3 and increasing the anti-apoptotic protein Bcl-2.	acacetin	18-26	BCL2 associated X, apoptosis regulator	Rattus norvegicus	239-242
29867499-2	2018	It was found that acacetin (0.3-3 muM) significantly decreased the apoptosis and reactive oxygen species production induced by hypoxia/reoxygenation injury in cardiomyocytes and H9C2 cardiomyoblasts via reducing the pro-apoptotic proteins Bax and cleaved-caspase-3 and increasing the anti-apoptotic protein Bcl-2.	acacetin	18-26	BCL2, apoptosis regulator	Rattus norvegicus	307-312
29867499-3	2018	In addition, acacetin not only suppressed the release of pro-inflammatory cytokines TLR-4 and IL-6 induced by hypoxia/reoxygenation injury, but also increased the secretion of anti-inflammatory cytokine IL-10.	acacetin	13-21	toll-like receptor 4	Rattus norvegicus	84-89
29867499-3	2018	In addition, acacetin not only suppressed the release of pro-inflammatory cytokines TLR-4 and IL-6 induced by hypoxia/reoxygenation injury, but also increased the secretion of anti-inflammatory cytokine IL-10.	acacetin	13-21	interleukin 6	Rattus norvegicus	94-98
29867499-3	2018	In addition, acacetin not only suppressed the release of pro-inflammatory cytokines TLR-4 and IL-6 induced by hypoxia/reoxygenation injury, but also increased the secretion of anti-inflammatory cytokine IL-10.	acacetin	13-21	interleukin 10	Rattus norvegicus	203-208
29867499-4	2018	Moreover, acacetin increased Nrf2 and HO-1 in a concentration-dependent manner, and rescued SOD1 and SOD2 reduction induced by hypoxia/reoxygenation insult.	acacetin	10-18	NFE2 like bZIP transcription factor 2	Rattus norvegicus	29-33
29867499-4	2018	Moreover, acacetin increased Nrf2 and HO-1 in a concentration-dependent manner, and rescued SOD1 and SOD2 reduction induced by hypoxia/reoxygenation insult.	acacetin	10-18	heme oxygenase 1	Rattus norvegicus	38-42
29867499-4	2018	Moreover, acacetin increased Nrf2 and HO-1 in a concentration-dependent manner, and rescued SOD1 and SOD2 reduction induced by hypoxia/reoxygenation insult.	acacetin	10-18	superoxide dismutase 1	Rattus norvegicus	92-96
29867499-4	2018	Moreover, acacetin increased Nrf2 and HO-1 in a concentration-dependent manner, and rescued SOD1 and SOD2 reduction induced by hypoxia/reoxygenation insult.	acacetin	10-18	superoxide dismutase 2	Rattus norvegicus	101-105
29867499-5	2018	These beneficial effects of acacetin disappeared in cells with silenced Nrf2, suggesting that Nrf2 activation participates in the cardioprotective effect of acacetin against hypoxia/reoxygenation insult.	acacetin	28-36	NFE2 like bZIP transcription factor 2	Rattus norvegicus	72-76
29867499-5	2018	These beneficial effects of acacetin disappeared in cells with silenced Nrf2, suggesting that Nrf2 activation participates in the cardioprotective effect of acacetin against hypoxia/reoxygenation insult.	acacetin	28-36	NFE2 like bZIP transcription factor 2	Rattus norvegicus	94-98
29867499-5	2018	These beneficial effects of acacetin disappeared in cells with silenced Nrf2, suggesting that Nrf2 activation participates in the cardioprotective effect of acacetin against hypoxia/reoxygenation insult.	acacetin	157-165	NFE2 like bZIP transcription factor 2	Rattus norvegicus	94-98
29867499-7	2018	Our results demonstrate for the first time that AMPK-mediated Nrf2 activation is involved in the cardiomyocytes protection of acacetin against hypoxia/reoxygenation injury by activating a series of intracellular signals involved in anti-oxidation, anti-inflammation, and anti-apoptosis.	acacetin	126-134	protein kinase AMP-activated catalytic subunit alpha 2	Rattus norvegicus	48-52
29867499-7	2018	Our results demonstrate for the first time that AMPK-mediated Nrf2 activation is involved in the cardiomyocytes protection of acacetin against hypoxia/reoxygenation injury by activating a series of intracellular signals involved in anti-oxidation, anti-inflammation, and anti-apoptosis.	acacetin	126-134	NFE2 like bZIP transcription factor 2	Rattus norvegicus	62-66
29408579-6	2018	In MDA-MB-468 cells that were coincubated with the CYP1 inhibitor acacetin, an approximately 300-fold increase was noted in the IC50 (30 +- 2.4 muM) of nobiletin.	acacetin	66-74	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	51-55
28988328-0	2018	Acacetin attenuates mice endotoxin-induced acute lung injury via augmentation of heme oxygenase-1 activity.	acacetin	0-8	heme oxygenase 1	Mus musculus	81-97
28988328-7	2018	Acacetin administration notably attenuated these changes and reduced tumor necrosis factor-alpha and interleukin-1beta in lung tissues.	acacetin	0-8	tumor necrosis factor	Mus musculus	69-96
28988328-7	2018	Acacetin administration notably attenuated these changes and reduced tumor necrosis factor-alpha and interleukin-1beta in lung tissues.	acacetin	0-8	interleukin 1 beta	Mus musculus	101-118
28988328-9	2018	Furthermore, Acacetin treatment significantly elevated pulmonary HO-1 and nuclear factor erythroid-2-related factor 2 (Nrf2) activities.	acacetin	13-21	heme oxygenase 1	Mus musculus	65-117
28988328-9	2018	Furthermore, Acacetin treatment significantly elevated pulmonary HO-1 and nuclear factor erythroid-2-related factor 2 (Nrf2) activities.	acacetin	13-21	nuclear factor, erythroid derived 2, like 2	Mus musculus	119-123
28988328-10	2018	However, the beneficial action of Acacetin was markedly abolished when pretreated with zinc protoporphyrin, an inhibitor of HO-1.	acacetin	34-42	heme oxygenase 1	Mus musculus	124-128
28988328-11	2018	In in vitro studies, Acacetin notably increased the HO-1 expression in pulmonary microvascular endothelial cells.	acacetin	21-29	heme oxygenase 1	Mus musculus	52-56
28988328-12	2018	During knockdown of Nrf2 by siRNA, the effect of Acacetin on HO-1 expression was significantly reversed.	acacetin	49-57	nuclear factor, erythroid derived 2, like 2	Mus musculus	20-24
28988328-12	2018	During knockdown of Nrf2 by siRNA, the effect of Acacetin on HO-1 expression was significantly reversed.	acacetin	49-57	heme oxygenase 1	Mus musculus	61-65
28988328-14	2018	This protective effect of Acacetin may be mediated, in part, through an HO-1-dependent pathway.	acacetin	26-34	heme oxygenase 1	Mus musculus	72-76
29408579-6	2018	In MDA-MB-468 cells that were coincubated with the CYP1 inhibitor acacetin, an approximately 300-fold increase was noted in the IC50 (30 +- 2.4 muM) of nobiletin.	acacetin	66-74	latexin	Homo sapiens	144-147
29408579-7	2018	In the presence of the CYP1 inhibitor acacetin, the conversion of nobiletin to NP1 was significantly reduced in MDA-MB-468 cells.	acacetin	38-46	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	23-27
29408579-7	2018	In the presence of the CYP1 inhibitor acacetin, the conversion of nobiletin to NP1 was significantly reduced in MDA-MB-468 cells.	acacetin	38-46	neuronal pentraxin 1	Homo sapiens	79-82
29332599-8	2018	Experiments using the CYP1 inhibitors acacetin and alpha-naphthoflavone provided supporting evidence for the involvement of CYP1 enzymes in the bioactivation of these compounds.	acacetin	38-46	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	22-26
29332599-8	2018	Experiments using the CYP1 inhibitors acacetin and alpha-naphthoflavone provided supporting evidence for the involvement of CYP1 enzymes in the bioactivation of these compounds.	acacetin	38-46	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	124-128
29676234-0	2018	Low Dose of Acacetin Promotes Breast Cancer MCF-7 Cells Proliferation Through the Activation of ERK/ PI3K /AKT and Cyclin Signaling Pathway.	acacetin	12-20	mitogen-activated protein kinase 1	Homo sapiens	96-99
29676234-0	2018	Low Dose of Acacetin Promotes Breast Cancer MCF-7 Cells Proliferation Through the Activation of ERK/ PI3K /AKT and Cyclin Signaling Pathway.	acacetin	12-20	AKT serine/threonine kinase 1	Homo sapiens	107-110
29676234-0	2018	Low Dose of Acacetin Promotes Breast Cancer MCF-7 Cells Proliferation Through the Activation of ERK/ PI3K /AKT and Cyclin Signaling Pathway.	acacetin	12-20	proliferating cell nuclear antigen	Homo sapiens	115-121
29676234-9	2018	RESULTS: According to SRB assay and flow cytometric analysis, low dose of acacetin from 10-3 to 1microM promoted the MCF-7 cells proliferation in a dose-dependent and time-dependent manner.	acacetin	74-82	chaperonin containing TCP1 subunit 4	Homo sapiens	22-25
29676234-10	2018	Moreover, the expressions of cell cycle-related molecules, ERK1/2 and PI3K/AKT were increased after treatment with acacetin, while the increases were effectively reversed by ER antagonist ICI 182,780.	acacetin	115-123	mitogen-activated protein kinase 3	Homo sapiens	59-65
29676234-10	2018	Moreover, the expressions of cell cycle-related molecules, ERK1/2 and PI3K/AKT were increased after treatment with acacetin, while the increases were effectively reversed by ER antagonist ICI 182,780.	acacetin	115-123	AKT serine/threonine kinase 1	Homo sapiens	75-78
29676234-11	2018	Further studies showed that acacetin notably induced increasing mRNA and proteins levels of ERalpha, which were strongly reversed by ERalpha antagonist MPP.	acacetin	28-36	estrogen receptor 1	Homo sapiens	92-99
29676234-11	2018	Further studies showed that acacetin notably induced increasing mRNA and proteins levels of ERalpha, which were strongly reversed by ERalpha antagonist MPP.	acacetin	28-36	estrogen receptor 1	Homo sapiens	133-140
29676234-12	2018	CONCLUSION: Low dose of acacetin from 10-3 microM to microM promoted the proliferation of MCF-7 cells through the ERK/PI3K/AKT pathway and its downstream cyclin signaling.	acacetin	24-32	mitogen-activated protein kinase 1	Homo sapiens	114-117
29676234-12	2018	CONCLUSION: Low dose of acacetin from 10-3 microM to microM promoted the proliferation of MCF-7 cells through the ERK/PI3K/AKT pathway and its downstream cyclin signaling.	acacetin	24-32	AKT serine/threonine kinase 1	Homo sapiens	123-126
29676234-12	2018	CONCLUSION: Low dose of acacetin from 10-3 microM to microM promoted the proliferation of MCF-7 cells through the ERK/PI3K/AKT pathway and its downstream cyclin signaling.	acacetin	24-32	proliferating cell nuclear antigen	Homo sapiens	154-160
29676234-13	2018	And ERalpha is mainly responsible for acacetin promoting proliferation in MCF-7 cells.	acacetin	38-46	estrogen receptor 1	Homo sapiens	4-11
29089232-5	2017	Acacetin also markedly acted on key molecules in apoptotic cell death pathways and reduced phosphorylation of c-Jun N-terminal kinase (JNK), p38 mitogen-activated protein kinase (MAPK), phosphatidylinositol 3-kinases (PI3K)/Akt, and glycogen synthase kinase-3beta (GSK-3beta).	acacetin	0-8	mitogen-activated protein kinase 8	Homo sapiens	110-133
29089232-5	2017	Acacetin also markedly acted on key molecules in apoptotic cell death pathways and reduced phosphorylation of c-Jun N-terminal kinase (JNK), p38 mitogen-activated protein kinase (MAPK), phosphatidylinositol 3-kinases (PI3K)/Akt, and glycogen synthase kinase-3beta (GSK-3beta).	acacetin	0-8	mitogen-activated protein kinase 8	Homo sapiens	135-138
29089232-5	2017	Acacetin also markedly acted on key molecules in apoptotic cell death pathways and reduced phosphorylation of c-Jun N-terminal kinase (JNK), p38 mitogen-activated protein kinase (MAPK), phosphatidylinositol 3-kinases (PI3K)/Akt, and glycogen synthase kinase-3beta (GSK-3beta).	acacetin	0-8	mitogen-activated protein kinase 14	Homo sapiens	141-177
29089232-5	2017	Acacetin also markedly acted on key molecules in apoptotic cell death pathways and reduced phosphorylation of c-Jun N-terminal kinase (JNK), p38 mitogen-activated protein kinase (MAPK), phosphatidylinositol 3-kinases (PI3K)/Akt, and glycogen synthase kinase-3beta (GSK-3beta).	acacetin	0-8	AKT serine/threonine kinase 1	Homo sapiens	224-227
29089232-5	2017	Acacetin also markedly acted on key molecules in apoptotic cell death pathways and reduced phosphorylation of c-Jun N-terminal kinase (JNK), p38 mitogen-activated protein kinase (MAPK), phosphatidylinositol 3-kinases (PI3K)/Akt, and glycogen synthase kinase-3beta (GSK-3beta).	acacetin	0-8	glycogen synthase kinase 3 beta	Homo sapiens	233-263
29089232-5	2017	Acacetin also markedly acted on key molecules in apoptotic cell death pathways and reduced phosphorylation of c-Jun N-terminal kinase (JNK), p38 mitogen-activated protein kinase (MAPK), phosphatidylinositol 3-kinases (PI3K)/Akt, and glycogen synthase kinase-3beta (GSK-3beta).	acacetin	0-8	glycogen synthase kinase 3 alpha	Homo sapiens	265-274
29276114-0	2017	Acacetin protects against cardiac remodeling after myocardial infarction by mediating MAPK and PI3K/Akt signal pathway.	acacetin	0-8	thymoma viral proto-oncogene 1	Mus musculus	100-103
29276114-10	2017	Western blot analysis of various signaling pathway proteins showed that acacetin targets the MAPK and PI3K/Akt signaling pathways.	acacetin	72-80	thymoma viral proto-oncogene 1	Mus musculus	107-110
29276114-11	2017	Collectively, acacetin improves mouse left ventricular function and attenuates cardiac remodeling by inhibiting of the MAPK and PI3K/Akt signaling pathway.	acacetin	14-22	thymoma viral proto-oncogene 1	Mus musculus	133-136
28634060-2	2017	Acacetin, a flavonoid, potently inhibited recombinant human MAO-A and MAO-B (IC50=0.19 and 0.17muM, respectively), and reversibly and competitively inhibited MAO-A and MAO-B (Ki=0.045 and 0.037muM, respectively).	acacetin	0-8	monoamine oxidase A	Homo sapiens	60-65
28634060-2	2017	Acacetin, a flavonoid, potently inhibited recombinant human MAO-A and MAO-B (IC50=0.19 and 0.17muM, respectively), and reversibly and competitively inhibited MAO-A and MAO-B (Ki=0.045 and 0.037muM, respectively).	acacetin	0-8	monoamine oxidase B	Homo sapiens	70-75
28634060-2	2017	Acacetin, a flavonoid, potently inhibited recombinant human MAO-A and MAO-B (IC50=0.19 and 0.17muM, respectively), and reversibly and competitively inhibited MAO-A and MAO-B (Ki=0.045 and 0.037muM, respectively).	acacetin	0-8	monoamine oxidase A	Homo sapiens	158-163
28634060-2	2017	Acacetin, a flavonoid, potently inhibited recombinant human MAO-A and MAO-B (IC50=0.19 and 0.17muM, respectively), and reversibly and competitively inhibited MAO-A and MAO-B (Ki=0.045 and 0.037muM, respectively).	acacetin	0-8	monoamine oxidase B	Homo sapiens	168-173
28634060-5	2017	Molecular docking simulation revealed the binding energy of acacetin for MAO-B (-44.2kcal/mol) was greater than its energy for MAO-A (-27.0kcal/mol), and that the Cys172 residue of MAO-B was important for hydrogen bonding with acacetin.	acacetin	60-68	monoamine oxidase B	Homo sapiens	73-78
28634060-5	2017	Molecular docking simulation revealed the binding energy of acacetin for MAO-B (-44.2kcal/mol) was greater than its energy for MAO-A (-27.0kcal/mol), and that the Cys172 residue of MAO-B was important for hydrogen bonding with acacetin.	acacetin	60-68	monoamine oxidase A	Homo sapiens	127-132
28634060-5	2017	Molecular docking simulation revealed the binding energy of acacetin for MAO-B (-44.2kcal/mol) was greater than its energy for MAO-A (-27.0kcal/mol), and that the Cys172 residue of MAO-B was important for hydrogen bonding with acacetin.	acacetin	60-68	monoamine oxidase B	Homo sapiens	181-186
28634060-5	2017	Molecular docking simulation revealed the binding energy of acacetin for MAO-B (-44.2kcal/mol) was greater than its energy for MAO-A (-27.0kcal/mol), and that the Cys172 residue of MAO-B was important for hydrogen bonding with acacetin.	acacetin	227-235	monoamine oxidase B	Homo sapiens	73-78
29081746-2	2017	The present study investigates whether acacetin inhibits the Ca2+-activated potassium (KCa) currents, including small conductance (SKCa1, SKCa2, and SKCa3), intermediate conductance (IKCa), and large-conductance (BKCa) channels stably expressed in HEK 293 cells.	acacetin	39-47	potassium calcium-activated channel subfamily N member 1	Homo sapiens	131-136
29081746-2	2017	The present study investigates whether acacetin inhibits the Ca2+-activated potassium (KCa) currents, including small conductance (SKCa1, SKCa2, and SKCa3), intermediate conductance (IKCa), and large-conductance (BKCa) channels stably expressed in HEK 293 cells.	acacetin	39-47	potassium calcium-activated channel subfamily N member 2	Homo sapiens	138-143
29081746-4	2017	The results showed that acacetin inhibited the three subtype SKCa channel currents in concentration-dependent manner with IC50 of 12.4 muM for SKCa1, 10.8 muM for SKCa2, and 11.6 muM for SKCa3.	acacetin	24-32	latexin	Homo sapiens	135-138
29081746-4	2017	The results showed that acacetin inhibited the three subtype SKCa channel currents in concentration-dependent manner with IC50 of 12.4 muM for SKCa1, 10.8 muM for SKCa2, and 11.6 muM for SKCa3.	acacetin	24-32	potassium calcium-activated channel subfamily N member 1	Homo sapiens	143-148
29081746-4	2017	The results showed that acacetin inhibited the three subtype SKCa channel currents in concentration-dependent manner with IC50 of 12.4 muM for SKCa1, 10.8 muM for SKCa2, and 11.6 muM for SKCa3.	acacetin	24-32	latexin	Homo sapiens	155-158
29081746-4	2017	The results showed that acacetin inhibited the three subtype SKCa channel currents in concentration-dependent manner with IC50 of 12.4 muM for SKCa1, 10.8 muM for SKCa2, and 11.6 muM for SKCa3.	acacetin	24-32	potassium calcium-activated channel subfamily N member 2	Homo sapiens	163-168
29081746-4	2017	The results showed that acacetin inhibited the three subtype SKCa channel currents in concentration-dependent manner with IC50 of 12.4 muM for SKCa1, 10.8 muM for SKCa2, and 11.6 muM for SKCa3.	acacetin	24-32	latexin	Homo sapiens	155-158
29081746-4	2017	The results showed that acacetin inhibited the three subtype SKCa channel currents in concentration-dependent manner with IC50 of 12.4 muM for SKCa1, 10.8 muM for SKCa2, and 11.6 muM for SKCa3.	acacetin	24-32	potassium calcium-activated channel subfamily N member 3	Homo sapiens	187-192
29081746-6	2017	Acacetin inhibited the mutants with IC50 of 118.5 muM for H490N, 275.2 muM for S512T, 15.3 muM for H521N, and 10.6 muM for A537V, suggesting that acacetin interacts with the P-loop helix of SKCa3 channel.	acacetin	0-8	latexin	Homo sapiens	50-53
29081746-6	2017	Acacetin inhibited the mutants with IC50 of 118.5 muM for H490N, 275.2 muM for S512T, 15.3 muM for H521N, and 10.6 muM for A537V, suggesting that acacetin interacts with the P-loop helix of SKCa3 channel.	acacetin	0-8	latexin	Homo sapiens	71-74
29081746-6	2017	Acacetin inhibited the mutants with IC50 of 118.5 muM for H490N, 275.2 muM for S512T, 15.3 muM for H521N, and 10.6 muM for A537V, suggesting that acacetin interacts with the P-loop helix of SKCa3 channel.	acacetin	0-8	latexin	Homo sapiens	71-74
29081746-6	2017	Acacetin inhibited the mutants with IC50 of 118.5 muM for H490N, 275.2 muM for S512T, 15.3 muM for H521N, and 10.6 muM for A537V, suggesting that acacetin interacts with the P-loop helix of SKCa3 channel.	acacetin	0-8	latexin	Homo sapiens	71-74
29081746-6	2017	Acacetin inhibited the mutants with IC50 of 118.5 muM for H490N, 275.2 muM for S512T, 15.3 muM for H521N, and 10.6 muM for A537V, suggesting that acacetin interacts with the P-loop helix of SKCa3 channel.	acacetin	0-8	potassium calcium-activated channel subfamily N member 3	Homo sapiens	190-195
29081746-7	2017	However, acacetin at 3-10 muM did not decrease, but induced a slight increase of BKCa (+70 mV) by 8% at 30 muM.	acacetin	9-17	latexin	Homo sapiens	26-29
29081746-7	2017	However, acacetin at 3-10 muM did not decrease, but induced a slight increase of BKCa (+70 mV) by 8% at 30 muM.	acacetin	9-17	latexin	Homo sapiens	107-110
27817185-4	2017	Correspondingly, concomitant treatment with the autophagy inhibitor (3-methyladenine or LY294002) appeared to enhance acacetin-induced apoptotic responses, such as Bak activation, Deltapsi loss, activation of caspase-9 and caspase-3, and apoptotic sub-G1 accumulation.	acacetin	118-126	caspase 9	Homo sapiens	209-218
28859099-13	2017	Acacetin also decreased efflux of doxorubicin by 59% after 30 mins of exposure to A549 cells and further increased accumulation of doxorubicin inside the cells upto 55% in 2 h. The modulatory effect of acacetin-doxorubicin combination on doxorubicin influx and efflux was mediated through downregulation of MDR1 treansporter in NSCLC cells.	acacetin	0-8	ATP binding cassette subfamily B member 1	Homo sapiens	307-311
28900399-11	2017	Acacetin reduced the expression of adipogenesis-related transcription factors, including the expression of the CCAAT/enhancer-binding protein; it also increased sirtuin 1 expression and AMPK phosphorylation in adipocytes.	acacetin	0-8	sirtuin 1	Mus musculus	161-170
28540728-8	2017	In conclusion, acacetin sulfonation was mediated mostly by SULT1A1.	acacetin	15-23	sulfotransferase family 1A, phenol-preferring, member 1	Mus musculus	59-66
28336971-0	2017	Targeting to the non-genomic activity of retinoic acid receptor-gamma by acacetin in hepatocellular carcinoma.	acacetin	73-81	retinoic acid receptor gamma	Homo sapiens	41-69
28336971-4	2017	A natural flavonoid acacetin is then identified to be capable of modulating RARgamma-dependent AKT-p53 network.	acacetin	20-28	retinoic acid receptor gamma	Homo sapiens	76-84
28336971-4	2017	A natural flavonoid acacetin is then identified to be capable of modulating RARgamma-dependent AKT-p53 network.	acacetin	20-28	AKT serine/threonine kinase 1	Homo sapiens	95-98
28336971-4	2017	A natural flavonoid acacetin is then identified to be capable of modulating RARgamma-dependent AKT-p53 network.	acacetin	20-28	tumor protein p53	Homo sapiens	99-102
28336971-6	2017	However, the anticancer action of acacetin is independent on its modulation of RARgamma-driven transcriptional activity.	acacetin	34-42	retinoic acid receptor gamma	Homo sapiens	79-87
28336971-7	2017	Acacetin induces cancer cell apoptosis through antagonizing the non-genomic effect of RARgamma on AKT and p53.	acacetin	0-8	retinoic acid receptor gamma	Homo sapiens	86-94
28336971-7	2017	Acacetin induces cancer cell apoptosis through antagonizing the non-genomic effect of RARgamma on AKT and p53.	acacetin	0-8	AKT serine/threonine kinase 1	Homo sapiens	98-101
28336971-7	2017	Acacetin induces cancer cell apoptosis through antagonizing the non-genomic effect of RARgamma on AKT and p53.	acacetin	0-8	tumor protein p53	Homo sapiens	106-109
28336971-8	2017	When bound to RARgamma, acacetin prevents RARgamma from its activation of AKT followed by recovery of the normal p53 signaling.	acacetin	24-32	retinoic acid receptor gamma	Homo sapiens	14-22
28336971-8	2017	When bound to RARgamma, acacetin prevents RARgamma from its activation of AKT followed by recovery of the normal p53 signaling.	acacetin	24-32	retinoic acid receptor gamma	Homo sapiens	42-50
28336971-8	2017	When bound to RARgamma, acacetin prevents RARgamma from its activation of AKT followed by recovery of the normal p53 signaling.	acacetin	24-32	AKT serine/threonine kinase 1	Homo sapiens	74-77
28336971-8	2017	When bound to RARgamma, acacetin prevents RARgamma from its activation of AKT followed by recovery of the normal p53 signaling.	acacetin	24-32	tumor protein p53	Homo sapiens	113-116
27817185-4	2017	Correspondingly, concomitant treatment with the autophagy inhibitor (3-methyladenine or LY294002) appeared to enhance acacetin-induced apoptotic responses, such as Bak activation, Deltapsi loss, activation of caspase-9 and caspase-3, and apoptotic sub-G1 accumulation.	acacetin	118-126	caspase 3	Homo sapiens	223-232
27817185-6	2017	Together, these results demonstrate that acacetin induces not only apoptotic cell death via activation of Bak, loss of Deltapsi, and activation of the mitochondrial caspase cascade, but also cytoprotective autophagy resulting from suppression of the Akt-mTOR pathway.	acacetin	41-49	BCL2 antagonist/killer 1	Homo sapiens	106-109
27817185-6	2017	Together, these results demonstrate that acacetin induces not only apoptotic cell death via activation of Bak, loss of Deltapsi, and activation of the mitochondrial caspase cascade, but also cytoprotective autophagy resulting from suppression of the Akt-mTOR pathway.	acacetin	41-49	AKT serine/threonine kinase 1	Homo sapiens	250-253
27817185-6	2017	Together, these results demonstrate that acacetin induces not only apoptotic cell death via activation of Bak, loss of Deltapsi, and activation of the mitochondrial caspase cascade, but also cytoprotective autophagy resulting from suppression of the Akt-mTOR pathway.	acacetin	41-49	mechanistic target of rapamycin kinase	Homo sapiens	254-258
27819271-5	2016	Molecular mechanism analysis revealed that acacetin prevented the ischemia/reperfusion-induced reduction of the anti-oxidative proteins SOD-2 and thioredoxin, suppressed the release of inflammation cytokines TLR4, IL-6 and TNFalpha, and decreased myocyte apoptosis induced by ischemia/reperfusion.	acacetin	43-51	superoxide dismutase 2	Rattus norvegicus	136-141
27819271-5	2016	Molecular mechanism analysis revealed that acacetin prevented the ischemia/reperfusion-induced reduction of the anti-oxidative proteins SOD-2 and thioredoxin, suppressed the release of inflammation cytokines TLR4, IL-6 and TNFalpha, and decreased myocyte apoptosis induced by ischemia/reperfusion.	acacetin	43-51	thioredoxin 1	Rattus norvegicus	146-157
27819271-5	2016	Molecular mechanism analysis revealed that acacetin prevented the ischemia/reperfusion-induced reduction of the anti-oxidative proteins SOD-2 and thioredoxin, suppressed the release of inflammation cytokines TLR4, IL-6 and TNFalpha, and decreased myocyte apoptosis induced by ischemia/reperfusion.	acacetin	43-51	toll-like receptor 4	Rattus norvegicus	208-212
27819271-5	2016	Molecular mechanism analysis revealed that acacetin prevented the ischemia/reperfusion-induced reduction of the anti-oxidative proteins SOD-2 and thioredoxin, suppressed the release of inflammation cytokines TLR4, IL-6 and TNFalpha, and decreased myocyte apoptosis induced by ischemia/reperfusion.	acacetin	43-51	interleukin 6	Rattus norvegicus	214-218
27819271-5	2016	Molecular mechanism analysis revealed that acacetin prevented the ischemia/reperfusion-induced reduction of the anti-oxidative proteins SOD-2 and thioredoxin, suppressed the release of inflammation cytokines TLR4, IL-6 and TNFalpha, and decreased myocyte apoptosis induced by ischemia/reperfusion.	acacetin	43-51	tumor necrosis factor	Rattus norvegicus	223-231
27779444-6	2016	We have found that acacetin (10 muM) can selectively induce apoptosis on CLL B-lymphocyte (25% at 24 h) by directly targeting mitochondria, through increased reactive oxygen species (ROS) formation, MMP collapse, MPT, release of cytochrome c, caspase 3 activation, and finally apoptosis, while sparing normal healthy B-lymphocytes unaffected at similar concentrations.	acacetin	19-27	caspase 3	Mus musculus	243-252
27754693-0	2016	Isolation of Acacetin from Calea urticifolia with Inhibitory Properties against Human Monoamine Oxidase-A and -B.	acacetin	13-21	monoamine oxidase A	Homo sapiens	86-112
27754693-3	2016	Further bioassay-guided fractionation led to the isolation of a flavonoid, acacetin, as the most prominent MAO inhibitory constituent, with IC50 values of 121 and 49 nM for MAO-A and -B, respectively.	acacetin	75-83	monoamine oxidase A	Homo sapiens	173-185
27754693-4	2016	The potency of MAO inhibition by acacetin was >5-fold higher for MAO-A (0.121 muM vs 0.640 muM) and >22-fold higher for MAO-B (0.049 muM vs 1.12 muM) as compared to apigenin, the closest flavone structural analogue.	acacetin	33-41	monoamine oxidase A	Homo sapiens	68-73
27754693-4	2016	The potency of MAO inhibition by acacetin was >5-fold higher for MAO-A (0.121 muM vs 0.640 muM) and >22-fold higher for MAO-B (0.049 muM vs 1.12 muM) as compared to apigenin, the closest flavone structural analogue.	acacetin	33-41	monoamine oxidase B	Homo sapiens	126-131
27754693-5	2016	Interaction and binding characteristics of acacetin with MAO-A and -B were determined by enzyme-kinetic assays, enzyme-inhibitor complex binding, equilibrium-dialysis dissociation analyses, and computation analysis.	acacetin	43-51	monoamine oxidase A	Homo sapiens	57-69
27754693-6	2016	Follow-up studies showed reversible binding of acacetin with human MAO-A and -B, resulting in competitive inhibition.	acacetin	47-55	monoamine oxidase A	Homo sapiens	67-79
27754693-7	2016	Acacetin showed more preference toward MAO-B than to MAO-A, suggesting its potential for eliciting selective pharmacological effects that might be useful in the treatment of neurological and psychiatric disorders.	acacetin	0-8	monoamine oxidase B	Homo sapiens	39-44
27754693-8	2016	In addition, the binding modes of acacetin at the enzymatic site of MAO-A and -B were predicted through molecular modeling algorithms, illustrating the high importance of ligand interaction with negative and positive free energy regions of the enzyme active site.	acacetin	34-42	monoamine oxidase A	Homo sapiens	68-80
26317684-7	2015	Tilianin and acacetin were metabolized into different glucuronides, with UGT1A8 produced as the main isoform.	acacetin	13-21	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	73-79
26317684-8	2015	Assessment of enzyme kinetics in UGT1A8, human liver microsomes and human intestinal microsomes revealed that compared with tilianin, acacetin displayed lower Km (0.6-, 0.7- and 0.6-fold, respectively), higher Vmax (20-, 60- and 230-fold, respectively) and higher clearance (30-, 80- and 300-fold, respectively).	acacetin	134-142	UDP glucuronosyltransferase family 1 member A8	Homo sapiens	33-39
26530776-2	2015	This study was conducted to determine if acacetin extracted from the whole Agastache rugosa plant had anti-BACE-1 and behavioral activities in Drosophila melanogaster AD models and to determine acacetin"s mechanism of action.	acacetin	41-49	beta-secretase 1	Homo sapiens	107-113
26530776-3	2015	Acacetin (100, 300, and 500 muM) rescued amyloid precursor protein (APP)/BACE1-expressing flies and kept them from developing both eye morphology (dark deposits, ommatidial collapse and fusion, and the absence of ommatidial bristles) and behavioral (motor abnormalities) defects.	acacetin	0-8	amyloid beta precursor protein	Homo sapiens	41-66
26530776-3	2015	Acacetin (100, 300, and 500 muM) rescued amyloid precursor protein (APP)/BACE1-expressing flies and kept them from developing both eye morphology (dark deposits, ommatidial collapse and fusion, and the absence of ommatidial bristles) and behavioral (motor abnormalities) defects.	acacetin	0-8	beta-secretase 1	Homo sapiens	73-78
26530776-4	2015	The reverse transcription polymerase chain reaction analysis revealed that acacetin reduced both the human APP and BACE-1 mRNA levels in the transgenic flies, suggesting that it plays an important role in the transcriptional regulation of human BACE-1 and APP.	acacetin	75-83	beta-secretase 1	Homo sapiens	115-121
26530776-4	2015	The reverse transcription polymerase chain reaction analysis revealed that acacetin reduced both the human APP and BACE-1 mRNA levels in the transgenic flies, suggesting that it plays an important role in the transcriptional regulation of human BACE-1 and APP.	acacetin	75-83	beta-secretase 1	Homo sapiens	245-251
26530776-5	2015	Western blot analysis revealed that acacetin reduced Abeta production by interfering with BACE-1 activity and APP synthesis, resulting in a decrease in the levels of the APP carboxy-terminal fragments and the APP intracellular domain.	acacetin	36-44	amyloid beta precursor protein	Homo sapiens	53-58
26530776-5	2015	Western blot analysis revealed that acacetin reduced Abeta production by interfering with BACE-1 activity and APP synthesis, resulting in a decrease in the levels of the APP carboxy-terminal fragments and the APP intracellular domain.	acacetin	36-44	beta-secretase 1	Homo sapiens	90-96
26530776-6	2015	Therefore, the protective effect of acacetin on Abeta production is mediated by transcriptional regulation of BACE-1 and APP, resulting in decreased APP protein expression and BACE-1 activity.	acacetin	36-44	amyloid beta precursor protein	Homo sapiens	48-53
26530776-6	2015	Therefore, the protective effect of acacetin on Abeta production is mediated by transcriptional regulation of BACE-1 and APP, resulting in decreased APP protein expression and BACE-1 activity.	acacetin	36-44	beta-secretase 1	Homo sapiens	110-116
26530776-6	2015	Therefore, the protective effect of acacetin on Abeta production is mediated by transcriptional regulation of BACE-1 and APP, resulting in decreased APP protein expression and BACE-1 activity.	acacetin	36-44	beta-secretase 1	Homo sapiens	176-182
25856795-6	2015	We found that acacetin inhibits p38 and JNK phosphorylation and reduces MMP-1, MMP-3 and MMP-13 expression in interleukin-1beta-induced FLSs.	acacetin	14-22	mitogen-activated protein kinase 14	Homo sapiens	32-35
25856795-6	2015	We found that acacetin inhibits p38 and JNK phosphorylation and reduces MMP-1, MMP-3 and MMP-13 expression in interleukin-1beta-induced FLSs.	acacetin	14-22	mitogen-activated protein kinase 8	Homo sapiens	40-43
25856795-6	2015	We found that acacetin inhibits p38 and JNK phosphorylation and reduces MMP-1, MMP-3 and MMP-13 expression in interleukin-1beta-induced FLSs.	acacetin	14-22	matrix metallopeptidase 1	Homo sapiens	72-77
25856795-6	2015	We found that acacetin inhibits p38 and JNK phosphorylation and reduces MMP-1, MMP-3 and MMP-13 expression in interleukin-1beta-induced FLSs.	acacetin	14-22	matrix metallopeptidase 3	Homo sapiens	79-84
25856795-6	2015	We found that acacetin inhibits p38 and JNK phosphorylation and reduces MMP-1, MMP-3 and MMP-13 expression in interleukin-1beta-induced FLSs.	acacetin	14-22	matrix metallopeptidase 13	Homo sapiens	89-95
25856795-6	2015	We found that acacetin inhibits p38 and JNK phosphorylation and reduces MMP-1, MMP-3 and MMP-13 expression in interleukin-1beta-induced FLSs.	acacetin	14-22	interleukin 1 beta	Homo sapiens	110-127
25301362-5	2014	RESULTS: Acacetin decreased the Kv1.3 current, accelerated the decay rate and negatively shifted the steady-state inactivation curves in a concentration-dependent manner.	acacetin	9-17	potassium voltage-gated channel subfamily A member 3	Homo sapiens	32-37
24520409-7	2014	Furthermore, the inhibitory effect of acacetin on evoked glutamate release was prevented by the Cav2.2 (N-type) and Cav2.1 (P/Q-type) channel blocker known as omega-conotoxin MVIIC.	acacetin	38-46	calcium voltage-gated channel subunit alpha1 A	Rattus norvegicus	116-122
24285354-0	2014	Acacetin (5,7-dihydroxy-4"-methoxyflavone) exhibits in vitro and in vivo anticancer activity through the suppression of NF-kappaB/Akt signaling in prostate cancer cells.	acacetin	0-8	nuclear factor kappa B subunit 1	Homo sapiens	120-129
24285354-0	2014	Acacetin (5,7-dihydroxy-4"-methoxyflavone) exhibits in vitro and in vivo anticancer activity through the suppression of NF-kappaB/Akt signaling in prostate cancer cells.	acacetin	0-8	AKT serine/threonine kinase 1	Homo sapiens	130-133
24285354-0	2014	Acacetin (5,7-dihydroxy-4"-methoxyflavone) exhibits in vitro and in vivo anticancer activity through the suppression of NF-kappaB/Akt signaling in prostate cancer cells.	acacetin	10-41	nuclear factor kappa B subunit 1	Homo sapiens	120-129
24285354-0	2014	Acacetin (5,7-dihydroxy-4"-methoxyflavone) exhibits in vitro and in vivo anticancer activity through the suppression of NF-kappaB/Akt signaling in prostate cancer cells.	acacetin	10-41	AKT serine/threonine kinase 1	Homo sapiens	130-133
24285354-7	2014	Western blot anlaysis of various markers of signaling pathways revealed that acacetin targets the Akt and nuclear factor (NF)-kappaB signaling pathways by inhibiting the phosphorylation of IkappaBalpha and NF-kappaB in a dose-dependent manner.	acacetin	77-85	AKT serine/threonine kinase 1	Homo sapiens	98-101
24285354-7	2014	Western blot anlaysis of various markers of signaling pathways revealed that acacetin targets the Akt and nuclear factor (NF)-kappaB signaling pathways by inhibiting the phosphorylation of IkappaBalpha and NF-kappaB in a dose-dependent manner.	acacetin	77-85	nuclear factor kappa B subunit 1	Homo sapiens	106-132
24285354-7	2014	Western blot anlaysis of various markers of signaling pathways revealed that acacetin targets the Akt and nuclear factor (NF)-kappaB signaling pathways by inhibiting the phosphorylation of IkappaBalpha and NF-kappaB in a dose-dependent manner.	acacetin	77-85	NFKB inhibitor alpha	Homo sapiens	189-201
24285354-7	2014	Western blot anlaysis of various markers of signaling pathways revealed that acacetin targets the Akt and nuclear factor (NF)-kappaB signaling pathways by inhibiting the phosphorylation of IkappaBalpha and NF-kappaB in a dose-dependent manner.	acacetin	77-85	nuclear factor kappa B subunit 1	Homo sapiens	206-215
24285354-8	2014	Consistent with its ability to induce apoptosis, the acacetin-mediated inhibition of the pro-survival pathway, Akt, and of the NF-kappaB pathway was accompanied by a marked reduction in the levels of the NF-kappaB-regulated anti-apoptotic proteins, Bcl-2 and X-linked inhibitor of apoptosis protein (XIAP), as well as of the proliferative protein, cyclooxygenase (COX)-2.	acacetin	53-61	AKT serine/threonine kinase 1	Homo sapiens	111-114
24285354-8	2014	Consistent with its ability to induce apoptosis, the acacetin-mediated inhibition of the pro-survival pathway, Akt, and of the NF-kappaB pathway was accompanied by a marked reduction in the levels of the NF-kappaB-regulated anti-apoptotic proteins, Bcl-2 and X-linked inhibitor of apoptosis protein (XIAP), as well as of the proliferative protein, cyclooxygenase (COX)-2.	acacetin	53-61	nuclear factor kappa B subunit 1	Homo sapiens	127-136
24285354-8	2014	Consistent with its ability to induce apoptosis, the acacetin-mediated inhibition of the pro-survival pathway, Akt, and of the NF-kappaB pathway was accompanied by a marked reduction in the levels of the NF-kappaB-regulated anti-apoptotic proteins, Bcl-2 and X-linked inhibitor of apoptosis protein (XIAP), as well as of the proliferative protein, cyclooxygenase (COX)-2.	acacetin	53-61	nuclear factor kappa B subunit 1	Homo sapiens	204-213
24285354-8	2014	Consistent with its ability to induce apoptosis, the acacetin-mediated inhibition of the pro-survival pathway, Akt, and of the NF-kappaB pathway was accompanied by a marked reduction in the levels of the NF-kappaB-regulated anti-apoptotic proteins, Bcl-2 and X-linked inhibitor of apoptosis protein (XIAP), as well as of the proliferative protein, cyclooxygenase (COX)-2.	acacetin	53-61	BCL2 apoptosis regulator	Homo sapiens	249-254
24285354-8	2014	Consistent with its ability to induce apoptosis, the acacetin-mediated inhibition of the pro-survival pathway, Akt, and of the NF-kappaB pathway was accompanied by a marked reduction in the levels of the NF-kappaB-regulated anti-apoptotic proteins, Bcl-2 and X-linked inhibitor of apoptosis protein (XIAP), as well as of the proliferative protein, cyclooxygenase (COX)-2.	acacetin	53-61	X-linked inhibitor of apoptosis	Homo sapiens	259-298
24285354-8	2014	Consistent with its ability to induce apoptosis, the acacetin-mediated inhibition of the pro-survival pathway, Akt, and of the NF-kappaB pathway was accompanied by a marked reduction in the levels of the NF-kappaB-regulated anti-apoptotic proteins, Bcl-2 and X-linked inhibitor of apoptosis protein (XIAP), as well as of the proliferative protein, cyclooxygenase (COX)-2.	acacetin	53-61	X-linked inhibitor of apoptosis	Homo sapiens	300-304
24285354-8	2014	Consistent with its ability to induce apoptosis, the acacetin-mediated inhibition of the pro-survival pathway, Akt, and of the NF-kappaB pathway was accompanied by a marked reduction in the levels of the NF-kappaB-regulated anti-apoptotic proteins, Bcl-2 and X-linked inhibitor of apoptosis protein (XIAP), as well as of the proliferative protein, cyclooxygenase (COX)-2.	acacetin	53-61	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	348-370
24285354-11	2014	Our findings suggest that acacetin exerts antitumor effects by targeting the Akt/NF-kappaB signaling pathway.	acacetin	26-34	AKT serine/threonine kinase 1	Homo sapiens	77-80
24285354-11	2014	Our findings suggest that acacetin exerts antitumor effects by targeting the Akt/NF-kappaB signaling pathway.	acacetin	26-34	nuclear factor kappa B subunit 1	Homo sapiens	81-90
24979133-0	2014	Chrysin, apigenin and acacetin inhibit tumor necrosis factor-related apoptosis-inducing ligand receptor-1 (TRAIL-R1) on activated RAW264.7 macrophages.	acacetin	22-30	TNF superfamily member 10	Homo sapiens	39-94
24979133-0	2014	Chrysin, apigenin and acacetin inhibit tumor necrosis factor-related apoptosis-inducing ligand receptor-1 (TRAIL-R1) on activated RAW264.7 macrophages.	acacetin	22-30	TNF receptor superfamily member 10a	Homo sapiens	107-115
24979133-5	2014	We demonstrate that RAW264.7 macrophages exhibit TRAIL-R1 surface expression and that the tested compounds: chrysin, apigenin and acacetin can inhibit TRAIL-R1 death receptor expression level on macrophages.	acacetin	130-138	TNF receptor superfamily member 10a	Homo sapiens	49-57
24979133-5	2014	We demonstrate that RAW264.7 macrophages exhibit TRAIL-R1 surface expression and that the tested compounds: chrysin, apigenin and acacetin can inhibit TRAIL-R1 death receptor expression level on macrophages.	acacetin	130-138	TNF superfamily member 10	Homo sapiens	49-54
25272843-2	2014	METHOD: The model of acacetin enzyme in vitro was established by the determination of fluorescence absorption of NADPH, the inhibition rate of acacetin aldose reductase was calculated, and then the IC50 of hydrolysis was obtained.	acacetin	21-29	aldo-keto reductase family 1 member B	Homo sapiens	152-168
25272843-6	2014	CONCLUSION: Hydrolyzate acacetin has preferable inhibitory activity of aldose reductase.	acacetin	24-32	aldo-keto reductase family 1 member B	Homo sapiens	71-87
23918449-13	2014	In the mechanism of the acacetin antinociceptive effect, 5-HT1A, GABA/BDZs and opioid receptors but not the NO-cGMP-K(+) channel pathway seem to be involved.	acacetin	24-32	5-hydroxytryptamine (serotonin) receptor 1A	Mus musculus	57-63
25301362-0	2014	Acacetin blocks kv1.3 channels and inhibits human T cell activation.	acacetin	0-8	potassium voltage-gated channel subfamily A member 3	Homo sapiens	16-21
25301362-3	2014	The present study was designed to characterize the inhibition of Kv1.3 channels by Acacetin in human T cells and examine its role in T cell activation.	acacetin	83-91	potassium voltage-gated channel subfamily A member 3	Homo sapiens	65-70
25301362-7	2014	Treatment with Acacetin for 24 h significantly inhibited Kv1.3 protein expression.	acacetin	15-23	potassium voltage-gated channel subfamily A member 3	Homo sapiens	57-62
25301362-8	2014	Additionally, paralleling Kv1.3 inhibition, Acacetin also inhibited Ca(2+) influx, the Ca(2+)-activated transcription factors NFAT1, NF-kappaB p65/p50 activity, and proliferation as well as IL-2 production.	acacetin	44-52	nuclear factor of activated T cells 2	Homo sapiens	126-131
25301362-8	2014	Additionally, paralleling Kv1.3 inhibition, Acacetin also inhibited Ca(2+) influx, the Ca(2+)-activated transcription factors NFAT1, NF-kappaB p65/p50 activity, and proliferation as well as IL-2 production.	acacetin	44-52	RELA proto-oncogene, NF-kB subunit	Homo sapiens	143-146
25301362-8	2014	Additionally, paralleling Kv1.3 inhibition, Acacetin also inhibited Ca(2+) influx, the Ca(2+)-activated transcription factors NFAT1, NF-kappaB p65/p50 activity, and proliferation as well as IL-2 production.	acacetin	44-52	nuclear factor kappa B subunit 1	Homo sapiens	147-150
25301362-8	2014	Additionally, paralleling Kv1.3 inhibition, Acacetin also inhibited Ca(2+) influx, the Ca(2+)-activated transcription factors NFAT1, NF-kappaB p65/p50 activity, and proliferation as well as IL-2 production.	acacetin	44-52	interleukin 2	Homo sapiens	190-194
25301362-9	2014	Small interfering RNA against Kv1.3 reduced the inhibitory effect of Acacetin on IL-2 secretion.	acacetin	69-77	potassium voltage-gated channel subfamily A member 3	Homo sapiens	30-35
25301362-9	2014	Small interfering RNA against Kv1.3 reduced the inhibitory effect of Acacetin on IL-2 secretion.	acacetin	69-77	interleukin 2	Homo sapiens	81-85
25301362-10	2014	CONCLUSIONS: Acacetin blocks the Kv1.3 channel and inhibits human T cell activation.	acacetin	13-21	potassium voltage-gated channel subfamily A member 3	Homo sapiens	33-38
23855486-6	2013	Acacetin also inhibited the activation of NF-kappaB by stimulation with TNF-alpha.	acacetin	0-8	nuclear factor kappa B subunit 1	Homo sapiens	42-51
29364964-0	2013	Correction: Properties and Molecular Determinants of the Natural Flavone Acacetin for Blocking hKv4.3 Channels.	acacetin	73-81	potassium voltage-gated channel subfamily D member 3	Homo sapiens	95-101
23943785-0	2013	Acacetin inhibits in vitro and in vivo angiogenesis and downregulates Stat signaling and VEGF expression.	acacetin	0-8	vascular endothelial growth factor A	Homo sapiens	89-93
23943785-3	2013	In the present study, acacetin inhibited growth and survival (up to 92%; P < 0.001), and capillary-like tube formation on Matrigel (up to 98%; P < 0.001) by human umbilical vein endothelial cells (HUVEC) in regular condition, as well as VEGF-induced and tumor cells conditioned medium-stimulated growth conditions.	acacetin	22-30	vascular endothelial growth factor A	Homo sapiens	243-247
23943785-6	2013	Acacetin inhibited Stat-1 (Tyr701) and Stat-3 (Tyr705) phosphorylation, and downregulated proangiogenic factors including VEGF, endothelial nitric oxide synthase (eNOS), inducible nitric oxide synthase (iNOS), matrix metalloproteinase-2 (MMP-2), and basic fibroblast growth factor (bFGF) in HUVEC.	acacetin	0-8	signal transducer and activator of transcription 1	Homo sapiens	19-25
23943785-6	2013	Acacetin inhibited Stat-1 (Tyr701) and Stat-3 (Tyr705) phosphorylation, and downregulated proangiogenic factors including VEGF, endothelial nitric oxide synthase (eNOS), inducible nitric oxide synthase (iNOS), matrix metalloproteinase-2 (MMP-2), and basic fibroblast growth factor (bFGF) in HUVEC.	acacetin	0-8	vascular endothelial growth factor A	Homo sapiens	122-126
23943785-6	2013	Acacetin inhibited Stat-1 (Tyr701) and Stat-3 (Tyr705) phosphorylation, and downregulated proangiogenic factors including VEGF, endothelial nitric oxide synthase (eNOS), inducible nitric oxide synthase (iNOS), matrix metalloproteinase-2 (MMP-2), and basic fibroblast growth factor (bFGF) in HUVEC.	acacetin	0-8	nitric oxide synthase 3	Homo sapiens	128-161
23943785-6	2013	Acacetin inhibited Stat-1 (Tyr701) and Stat-3 (Tyr705) phosphorylation, and downregulated proangiogenic factors including VEGF, endothelial nitric oxide synthase (eNOS), inducible nitric oxide synthase (iNOS), matrix metalloproteinase-2 (MMP-2), and basic fibroblast growth factor (bFGF) in HUVEC.	acacetin	0-8	nitric oxide synthase 2	Homo sapiens	170-201
23943785-6	2013	Acacetin inhibited Stat-1 (Tyr701) and Stat-3 (Tyr705) phosphorylation, and downregulated proangiogenic factors including VEGF, endothelial nitric oxide synthase (eNOS), inducible nitric oxide synthase (iNOS), matrix metalloproteinase-2 (MMP-2), and basic fibroblast growth factor (bFGF) in HUVEC.	acacetin	0-8	nitric oxide synthase 2	Homo sapiens	203-207
23943785-6	2013	Acacetin inhibited Stat-1 (Tyr701) and Stat-3 (Tyr705) phosphorylation, and downregulated proangiogenic factors including VEGF, endothelial nitric oxide synthase (eNOS), inducible nitric oxide synthase (iNOS), matrix metalloproteinase-2 (MMP-2), and basic fibroblast growth factor (bFGF) in HUVEC.	acacetin	0-8	matrix metallopeptidase 2	Homo sapiens	210-236
23943785-6	2013	Acacetin inhibited Stat-1 (Tyr701) and Stat-3 (Tyr705) phosphorylation, and downregulated proangiogenic factors including VEGF, endothelial nitric oxide synthase (eNOS), inducible nitric oxide synthase (iNOS), matrix metalloproteinase-2 (MMP-2), and basic fibroblast growth factor (bFGF) in HUVEC.	acacetin	0-8	matrix metallopeptidase 2	Homo sapiens	238-243
23943785-6	2013	Acacetin inhibited Stat-1 (Tyr701) and Stat-3 (Tyr705) phosphorylation, and downregulated proangiogenic factors including VEGF, endothelial nitric oxide synthase (eNOS), inducible nitric oxide synthase (iNOS), matrix metalloproteinase-2 (MMP-2), and basic fibroblast growth factor (bFGF) in HUVEC.	acacetin	0-8	fibroblast growth factor 2	Homo sapiens	250-280
23943785-6	2013	Acacetin inhibited Stat-1 (Tyr701) and Stat-3 (Tyr705) phosphorylation, and downregulated proangiogenic factors including VEGF, endothelial nitric oxide synthase (eNOS), inducible nitric oxide synthase (iNOS), matrix metalloproteinase-2 (MMP-2), and basic fibroblast growth factor (bFGF) in HUVEC.	acacetin	0-8	fibroblast growth factor 2	Homo sapiens	282-286
23943785-10	2013	Acacetin also inhibited tyrosine phosphorylation of Stat-1 and -3, and expression of VEGF in cancer cells.	acacetin	0-8	signal transducer and activator of transcription 1	Homo sapiens	52-65
23943785-10	2013	Acacetin also inhibited tyrosine phosphorylation of Stat-1 and -3, and expression of VEGF in cancer cells.	acacetin	0-8	vascular endothelial growth factor A	Homo sapiens	85-89
23855486-0	2013	Acacetin inhibits expression of E-selectin on endothelial cells through regulation of the MAP kinase signaling pathway and activation of NF-kappaB.	acacetin	0-8	selectin E	Homo sapiens	32-42
23855486-0	2013	Acacetin inhibits expression of E-selectin on endothelial cells through regulation of the MAP kinase signaling pathway and activation of NF-kappaB.	acacetin	0-8	nuclear factor kappa B subunit 1	Homo sapiens	137-146
23855486-4	2013	Among 11 flavones, acacetin strongly inhibited TNF-alpha-induced E-selectin expression in HUVECs.	acacetin	19-27	tumor necrosis factor	Homo sapiens	47-56
23855486-4	2013	Among 11 flavones, acacetin strongly inhibited TNF-alpha-induced E-selectin expression in HUVECs.	acacetin	19-27	selectin E	Homo sapiens	65-75
23855486-5	2013	Acacetin suppressed the TNF-alpha-induced phosphorylation of p38 but did not inhibit TNF-alpha-induced phosphorylations of JNK and ERK.	acacetin	0-8	tumor necrosis factor	Homo sapiens	24-33
23855486-5	2013	Acacetin suppressed the TNF-alpha-induced phosphorylation of p38 but did not inhibit TNF-alpha-induced phosphorylations of JNK and ERK.	acacetin	0-8	mitogen-activated protein kinase 14	Homo sapiens	61-64
23855486-6	2013	Acacetin also inhibited the activation of NF-kappaB by stimulation with TNF-alpha.	acacetin	0-8	tumor necrosis factor	Homo sapiens	72-81
23855486-7	2013	Furthermore, adhesion of monocytes to TNF-alpha-treated endothelial cells was inhibited by cotreatment with acacetin.	acacetin	108-116	tumor necrosis factor	Homo sapiens	38-47
23855486-8	2013	These results suggest that acacetin inhibits the expression of E-selectin by regulation of the p38 MAPK signaling pathway and activation of NF-kappaB.	acacetin	27-35	selectin E	Homo sapiens	63-73
23855486-8	2013	These results suggest that acacetin inhibits the expression of E-selectin by regulation of the p38 MAPK signaling pathway and activation of NF-kappaB.	acacetin	27-35	mitogen-activated protein kinase 14	Homo sapiens	95-98
23855486-8	2013	These results suggest that acacetin inhibits the expression of E-selectin by regulation of the p38 MAPK signaling pathway and activation of NF-kappaB.	acacetin	27-35	mitogen-activated protein kinase 1	Homo sapiens	99-103
23855486-8	2013	These results suggest that acacetin inhibits the expression of E-selectin by regulation of the p38 MAPK signaling pathway and activation of NF-kappaB.	acacetin	27-35	nuclear factor kappa B subunit 1	Homo sapiens	140-149
22447574-0	2012	Acacetin attenuates neuroinflammation via regulation the response to LPS stimuli in vitro and in vivo.	acacetin	0-8	toll-like receptor 4	Mus musculus	69-72
22438130-7	2013	Moreover, the major components of the MCI were bioactive compounds such as sudachitin, hesperetin, chrysoeriol, and acacetin.	acacetin	116-124	multiciliate differentiation and DNA synthesis associated cell cycle protein	Homo sapiens	38-41
22438130-8	2013	Sudachitin, chrysoeriol, and acacetin also exerted significantly cytotoxicity, clearly suppressed constitutive STAT3 activation, and induced apoptosis, although hesperetin did not show any significant effect in DU145 cells.	acacetin	29-37	signal transducer and activator of transcription 3	Homo sapiens	111-116
23526953-0	2013	Properties and molecular determinants of the natural flavone acacetin for blocking hKv4.3 channels.	acacetin	61-69	potassium voltage-gated channel subfamily D member 3	Homo sapiens	83-89
23526953-4	2013	It was found that acacetin inhibited hKv4.3 current by binding to both the closed and open channels, and decreased the recovery from inactivation.	acacetin	18-26	potassium voltage-gated channel subfamily D member 3	Homo sapiens	37-43
23526953-5	2013	The blockade of hKv4.3 channels by acacetin was use- and frequency-dependent, and IC50s of acacetin for inhibiting hKv4.3 were 7.9, 6.1, 3.9, and 3.2 microM, respectively, at 0.2, 0.5, 1, and 3.3 Hz.	acacetin	35-43	potassium voltage-gated channel subfamily D member 3	Homo sapiens	16-22
23526953-5	2013	The blockade of hKv4.3 channels by acacetin was use- and frequency-dependent, and IC50s of acacetin for inhibiting hKv4.3 were 7.9, 6.1, 3.9, and 3.2 microM, respectively, at 0.2, 0.5, 1, and 3.3 Hz.	acacetin	91-99	potassium voltage-gated channel subfamily D member 3	Homo sapiens	16-22
23526953-5	2013	The blockade of hKv4.3 channels by acacetin was use- and frequency-dependent, and IC50s of acacetin for inhibiting hKv4.3 were 7.9, 6.1, 3.9, and 3.2 microM, respectively, at 0.2, 0.5, 1, and 3.3 Hz.	acacetin	91-99	potassium voltage-gated channel subfamily D member 3	Homo sapiens	115-121
23526953-6	2013	The mutagenesis study revealed that the hKv4.3 mutants T366A and T367A in the P-loop helix, and V392A, I395A and V399A in the S6-segment had a reduced channel blocking efficacy of acacetin (IC50, 44.5 microM for T366A, 25.8 microM for T367A, 17.6 microM for V392A, 16.2 microM for I395A, and 19.1 microM for V399A).	acacetin	180-188	potassium voltage-gated channel subfamily D member 3	Homo sapiens	40-46
23526953-8	2013	The use- and rate-dependent blocking of hKv4.3 by acacetin is likely beneficial for managing atrial fibrillation.	acacetin	50-58	potassium voltage-gated channel subfamily D member 3	Homo sapiens	40-46
22743247-6	2012	The intracellular CYP1-mediated bioconversion of the flavone was reduced in the presence of the CYP1A1 and CYP1B1-selective inhibitors alpha-napthoflavone and acacetin.	acacetin	159-167	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	18-22
22743247-6	2012	The intracellular CYP1-mediated bioconversion of the flavone was reduced in the presence of the CYP1A1 and CYP1B1-selective inhibitors alpha-napthoflavone and acacetin.	acacetin	159-167	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	96-102
22743247-6	2012	The intracellular CYP1-mediated bioconversion of the flavone was reduced in the presence of the CYP1A1 and CYP1B1-selective inhibitors alpha-napthoflavone and acacetin.	acacetin	159-167	cytochrome P450 family 1 subfamily B member 1	Homo sapiens	107-113
22447574-4	2012	In this study, we investigated the effects of acacetin (5,7-dihydroxy-4"-methoxyflavone), which is derived from Robinia pseudoacacia, on neuroinflammation in lipopolysaccharide (LPS)-stimulated BV-2 cells and in animal models of neuroinflammation and ischemia.	acacetin	46-54	toll-like receptor 4	Mus musculus	178-181
22447574-4	2012	In this study, we investigated the effects of acacetin (5,7-dihydroxy-4"-methoxyflavone), which is derived from Robinia pseudoacacia, on neuroinflammation in lipopolysaccharide (LPS)-stimulated BV-2 cells and in animal models of neuroinflammation and ischemia.	acacetin	56-87	toll-like receptor 4	Mus musculus	178-181
22447574-5	2012	Acacetin significantly inhibited the release of nitric oxide (NO) and prostaglandin E(2) and the expression of inducible NO synthase and cyclooxygenase-2 in LPS-stimulated BV-2 cells.	acacetin	0-8	nitric oxide synthase 2, inducible	Mus musculus	111-132
22447574-5	2012	Acacetin significantly inhibited the release of nitric oxide (NO) and prostaglandin E(2) and the expression of inducible NO synthase and cyclooxygenase-2 in LPS-stimulated BV-2 cells.	acacetin	0-8	prostaglandin-endoperoxide synthase 2	Mus musculus	137-153
22447574-5	2012	Acacetin significantly inhibited the release of nitric oxide (NO) and prostaglandin E(2) and the expression of inducible NO synthase and cyclooxygenase-2 in LPS-stimulated BV-2 cells.	acacetin	0-8	toll-like receptor 4	Mus musculus	157-160
22447574-7	2012	In an LPS-induced neuroinflammation mouse model, acacetin significantly suppressed microglial activation.	acacetin	49-57	toll-like receptor 4	Mus musculus	6-9
23049614-9	2012	At the molecular level, acacetin significantly reduced IL-6, IL-8, intercellular adhesion molecule-1, and eotaxin-1 in activated BEAS-2B cells.	acacetin	24-32	C-X-C motif chemokine ligand 8	Homo sapiens	61-65
22107990-12	2012	The phytochemical study of Ba-CAE showed the presence of flavones as luteolin and acacetin, caffeoylquinic acids as chlorogenic acid, and tannins.	acacetin	82-90	gap junction protein alpha 8	Homo sapiens	30-33
22863927-4	2012	In primary mesencephalic culture, acacetin protected dopaminergic (DA) cells and inhibited production of inflammatory factors such as nitric oxide, prostaglandin E2, and tumor necrosis factor-alpha against MPP+-induced toxicity in a dose-dependent manner.	acacetin	34-42	tumor necrosis factor	Mus musculus	170-197
22863927-9	2012	Moreover, the acacetin-treated group inhibited microglia activation, accompanied by production of inducible nitric oxide synthases and cyclooxygenase-2.	acacetin	14-22	prostaglandin-endoperoxide synthase 2	Mus musculus	135-151
23049614-9	2012	At the molecular level, acacetin significantly reduced IL-6, IL-8, intercellular adhesion molecule-1, and eotaxin-1 in activated BEAS-2B cells.	acacetin	24-32	intercellular adhesion molecule 1	Homo sapiens	67-100
23049614-9	2012	At the molecular level, acacetin significantly reduced IL-6, IL-8, intercellular adhesion molecule-1, and eotaxin-1 in activated BEAS-2B cells.	acacetin	24-32	C-C motif chemokine ligand 11	Homo sapiens	106-115
21993665-8	2012	Acacetin-induced             apoptosis was also accompanied by upregulation of Bax, and downregulation of Bcl-2.	acacetin	0-8	BCL2 associated X, apoptosis regulator	Homo sapiens	79-82
23049614-0	2012	Dietary acacetin reduces airway hyperresponsiveness and eosinophil infiltration by modulating eotaxin-1 and th2 cytokines in a mouse model of asthma.	acacetin	8-16	C-C motif chemokine ligand 11	Homo sapiens	94-103
23049614-0	2012	Dietary acacetin reduces airway hyperresponsiveness and eosinophil infiltration by modulating eotaxin-1 and th2 cytokines in a mouse model of asthma.	acacetin	8-16	heart and neural crest derivatives expressed 2	Mus musculus	108-111
23049614-3	2012	This study aims to investigate the anti-inflammatory effect of orally administered acacetin in ovalbumin- (OVA-) sensitized asthmatic mice and its underlying molecular mechanism.	acacetin	83-91	serine (or cysteine) peptidase inhibitor, clade B, member 1, pseudogene	Mus musculus	95-104
23049614-9	2012	At the molecular level, acacetin significantly reduced IL-6, IL-8, intercellular adhesion molecule-1, and eotaxin-1 in activated BEAS-2B cells.	acacetin	24-32	interleukin 6	Homo sapiens	55-59
21993665-0	2012	Acacetin induces apoptosis in human T cell leukemia Jurkat cells via             activation of a caspase cascade.	acacetin	0-8	caspase 8	Homo sapiens	97-104
21993665-5	2012	Treatment of Jurkat cells with acacetin also induced             caspase-3, -8 and -9 activities in a time-dependent manner.	acacetin	31-39	caspase 3	Homo sapiens	65-85
21993665-6	2012	Acacetin-induced apoptosis             was blocked by a broad-spectrum caspase inhibitor, a caspase-3 inhibitor and a             caspase-8 inhibitor, but not by a caspase-9 inhibitor.	acacetin	0-8	caspase 8	Homo sapiens	71-78
21993665-6	2012	Acacetin-induced apoptosis             was blocked by a broad-spectrum caspase inhibitor, a caspase-3 inhibitor and a             caspase-8 inhibitor, but not by a caspase-9 inhibitor.	acacetin	0-8	caspase 3	Homo sapiens	92-101
21993665-6	2012	Acacetin-induced apoptosis             was blocked by a broad-spectrum caspase inhibitor, a caspase-3 inhibitor and a             caspase-8 inhibitor, but not by a caspase-9 inhibitor.	acacetin	0-8	caspase 8	Homo sapiens	130-139
21993665-7	2012	In addition, acacetin promoted             the expression of FAF1, phosphor-FADD, Apaf-1 and cytochrome c.	acacetin	13-21	Fas associated factor 1	Homo sapiens	61-65
21993665-7	2012	In addition, acacetin promoted             the expression of FAF1, phosphor-FADD, Apaf-1 and cytochrome c.	acacetin	13-21	Fas associated via death domain	Homo sapiens	76-80
21993665-7	2012	In addition, acacetin promoted             the expression of FAF1, phosphor-FADD, Apaf-1 and cytochrome c.	acacetin	13-21	apoptotic peptidase activating factor 1	Homo sapiens	82-88
21993665-7	2012	In addition, acacetin promoted             the expression of FAF1, phosphor-FADD, Apaf-1 and cytochrome c.	acacetin	13-21	cytochrome c, somatic	Homo sapiens	93-105
21993665-8	2012	Acacetin-induced             apoptosis was also accompanied by upregulation of Bax, and downregulation of Bcl-2.	acacetin	0-8	BCL2 apoptosis regulator	Homo sapiens	106-111
21210297-0	2011	Acacetin inhibits the invasion and migration of human non-small cell lung cancer A549 cells by suppressing the p38alpha MAPK signaling pathway.	acacetin	0-8	mitogen-activated protein kinase 14	Homo sapiens	111-119
21893035-0	2011	Acacetin inhibits VEGF expression, tumor angiogenesis and growth through AKT/HIF-1alpha pathway.	acacetin	0-8	vascular endothelial growth factor A	Homo sapiens	18-22
21893035-0	2011	Acacetin inhibits VEGF expression, tumor angiogenesis and growth through AKT/HIF-1alpha pathway.	acacetin	0-8	AKT serine/threonine kinase 1	Homo sapiens	73-76
21893035-0	2011	Acacetin inhibits VEGF expression, tumor angiogenesis and growth through AKT/HIF-1alpha pathway.	acacetin	0-8	hypoxia inducible factor 1 subunit alpha	Homo sapiens	77-87
21893035-3	2011	In this study, we found that acacetin decreased the steady level of VEGF mRNA level and inhibited VEGF transcriptional activation.	acacetin	29-37	vascular endothelial growth factor A	Homo sapiens	68-72
21893035-3	2011	In this study, we found that acacetin decreased the steady level of VEGF mRNA level and inhibited VEGF transcriptional activation.	acacetin	29-37	vascular endothelial growth factor A	Homo sapiens	98-102
21893035-4	2011	To further determine the potential mechanism of acacetin in inhibiting VEGF expression, we showed that acacetin inhibited HIF-1alpha expression and AKT activation.	acacetin	48-56	vascular endothelial growth factor A	Homo sapiens	71-75
21893035-4	2011	To further determine the potential mechanism of acacetin in inhibiting VEGF expression, we showed that acacetin inhibited HIF-1alpha expression and AKT activation.	acacetin	103-111	vascular endothelial growth factor A	Homo sapiens	71-75
21893035-4	2011	To further determine the potential mechanism of acacetin in inhibiting VEGF expression, we showed that acacetin inhibited HIF-1alpha expression and AKT activation.	acacetin	103-111	hypoxia inducible factor 1 subunit alpha	Homo sapiens	122-132
21893035-4	2011	To further determine the potential mechanism of acacetin in inhibiting VEGF expression, we showed that acacetin inhibited HIF-1alpha expression and AKT activation.	acacetin	103-111	AKT serine/threonine kinase 1	Homo sapiens	148-151
21893035-5	2011	Over-expression of HIF-1alpha or AKT restored acacetin-decreasing VEGF transcriptional activation, indicating that AKT and HIF-1 are the essential downstream targets of acacetin for inhibiting VEGF expression in the cells.	acacetin	46-54	hypoxia inducible factor 1 subunit alpha	Homo sapiens	19-29
21893035-5	2011	Over-expression of HIF-1alpha or AKT restored acacetin-decreasing VEGF transcriptional activation, indicating that AKT and HIF-1 are the essential downstream targets of acacetin for inhibiting VEGF expression in the cells.	acacetin	46-54	AKT serine/threonine kinase 1	Homo sapiens	33-36
21893035-5	2011	Over-expression of HIF-1alpha or AKT restored acacetin-decreasing VEGF transcriptional activation, indicating that AKT and HIF-1 are the essential downstream targets of acacetin for inhibiting VEGF expression in the cells.	acacetin	46-54	vascular endothelial growth factor A	Homo sapiens	66-70
21893035-5	2011	Over-expression of HIF-1alpha or AKT restored acacetin-decreasing VEGF transcriptional activation, indicating that AKT and HIF-1 are the essential downstream targets of acacetin for inhibiting VEGF expression in the cells.	acacetin	46-54	AKT serine/threonine kinase 1	Homo sapiens	115-118
21893035-5	2011	Over-expression of HIF-1alpha or AKT restored acacetin-decreasing VEGF transcriptional activation, indicating that AKT and HIF-1 are the essential downstream targets of acacetin for inhibiting VEGF expression in the cells.	acacetin	46-54	hypoxia inducible factor 1 subunit alpha	Homo sapiens	19-24
21893035-5	2011	Over-expression of HIF-1alpha or AKT restored acacetin-decreasing VEGF transcriptional activation, indicating that AKT and HIF-1 are the essential downstream targets of acacetin for inhibiting VEGF expression in the cells.	acacetin	46-54	vascular endothelial growth factor A	Homo sapiens	193-197
21893035-5	2011	Over-expression of HIF-1alpha or AKT restored acacetin-decreasing VEGF transcriptional activation, indicating that AKT and HIF-1 are the essential downstream targets of acacetin for inhibiting VEGF expression in the cells.	acacetin	169-177	hypoxia inducible factor 1 subunit alpha	Homo sapiens	19-29
21893035-5	2011	Over-expression of HIF-1alpha or AKT restored acacetin-decreasing VEGF transcriptional activation, indicating that AKT and HIF-1 are the essential downstream targets of acacetin for inhibiting VEGF expression in the cells.	acacetin	169-177	AKT serine/threonine kinase 1	Homo sapiens	33-36
21893035-5	2011	Over-expression of HIF-1alpha or AKT restored acacetin-decreasing VEGF transcriptional activation, indicating that AKT and HIF-1 are the essential downstream targets of acacetin for inhibiting VEGF expression in the cells.	acacetin	169-177	vascular endothelial growth factor A	Homo sapiens	66-70
21893035-5	2011	Over-expression of HIF-1alpha or AKT restored acacetin-decreasing VEGF transcriptional activation, indicating that AKT and HIF-1 are the essential downstream targets of acacetin for inhibiting VEGF expression in the cells.	acacetin	169-177	AKT serine/threonine kinase 1	Homo sapiens	115-118
21893035-5	2011	Over-expression of HIF-1alpha or AKT restored acacetin-decreasing VEGF transcriptional activation, indicating that AKT and HIF-1 are the essential downstream targets of acacetin for inhibiting VEGF expression in the cells.	acacetin	169-177	hypoxia inducible factor 1 subunit alpha	Homo sapiens	19-24
21893035-5	2011	Over-expression of HIF-1alpha or AKT restored acacetin-decreasing VEGF transcriptional activation, indicating that AKT and HIF-1 are the essential downstream targets of acacetin for inhibiting VEGF expression in the cells.	acacetin	169-177	vascular endothelial growth factor A	Homo sapiens	193-197
21893035-6	2011	Moreover, acacetin significantly inhibited ovarian cancer cell-induced angiogenesis and tumor growth in vivo through inhibiting HIF-1alpha and VEGF expression.	acacetin	10-18	hypoxia inducible factor 1 subunit alpha	Homo sapiens	128-138
21893035-6	2011	Moreover, acacetin significantly inhibited ovarian cancer cell-induced angiogenesis and tumor growth in vivo through inhibiting HIF-1alpha and VEGF expression.	acacetin	10-18	vascular endothelial growth factor A	Homo sapiens	143-147
21893035-7	2011	Acacetin did not change HIF-1alpha mRNA level, but inhibited HIF-1alpha protein level through increasing its degradation and decreasing its stability.	acacetin	0-8	hypoxia inducible factor 1 subunit alpha	Homo sapiens	61-71
21482471-4	2011	In the present study we have examined the inhibition of CYP1A1 and CYP1B1-catalyzed EROD activity by 14 different flavonoids containing methoxy- and hydroxyl-group substitutions as well as the metabolism of the monomethoxylated CYP1-flavonoid inhibitor acacetin and the poly-methoxylated flavone eupatorin-5-methyl ether by recombinant CYP1A1 and CYP1B1.	acacetin	253-261	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	56-62
21482471-4	2011	In the present study we have examined the inhibition of CYP1A1 and CYP1B1-catalyzed EROD activity by 14 different flavonoids containing methoxy- and hydroxyl-group substitutions as well as the metabolism of the monomethoxylated CYP1-flavonoid inhibitor acacetin and the poly-methoxylated flavone eupatorin-5-methyl ether by recombinant CYP1A1 and CYP1B1.	acacetin	253-261	cytochrome P450 family 1 subfamily B member 1	Homo sapiens	67-73
21482471-4	2011	In the present study we have examined the inhibition of CYP1A1 and CYP1B1-catalyzed EROD activity by 14 different flavonoids containing methoxy- and hydroxyl-group substitutions as well as the metabolism of the monomethoxylated CYP1-flavonoid inhibitor acacetin and the poly-methoxylated flavone eupatorin-5-methyl ether by recombinant CYP1A1 and CYP1B1.	acacetin	253-261	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	56-60
21482471-5	2011	The most potent inhibitors of CYP1-EROD activity were the methoxylated flavones acacetin, diosmetin, eupatorin and the di-hydroxylated flavone chrysin, indicating that the 4"-OCH(3) group at the B ring and the 5,7-dihydroxy motif at the A ring play a prominent role in EROD inhibition.	acacetin	80-88	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	30-34
21482471-7	2011	HPLC metabolism of acacetin by CYP1A1 and CYP1B1 revealed the formation of the structurally similar flavone apigenin by demethylation at the 4"-position of the B ring, whereas the flavone eupatorin-5-methyl ether was metabolized to an as yet unidentified metabolite assigned E(5)M1.	acacetin	19-27	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	31-37
21482471-7	2011	HPLC metabolism of acacetin by CYP1A1 and CYP1B1 revealed the formation of the structurally similar flavone apigenin by demethylation at the 4"-position of the B ring, whereas the flavone eupatorin-5-methyl ether was metabolized to an as yet unidentified metabolite assigned E(5)M1.	acacetin	19-27	cytochrome P450 family 1 subfamily B member 1	Homo sapiens	42-48
21906601-0	2011	Acacetin causes a frequency- and use-dependent blockade of hKv1.5 channels by binding to the S6 domain.	acacetin	0-8	potassium voltage-gated channel subfamily A member 5	Homo sapiens	59-65
21906601-3	2011	The present study was designed to investigate the molecular determinants underlying the ability of acacetin to block hKv1.5 channels (coding I(Kur)) in human atrial myocytes using the whole-cell patch voltage-clamp technique to record membrane current in HEK 293 cells stably expressing the hKv1.5 gene or transiently expressing mutant hKv1.5 genes generated by site-directed mutagenesis.	acacetin	99-107	potassium voltage-gated channel subfamily A member 5	Homo sapiens	117-123
21906601-3	2011	The present study was designed to investigate the molecular determinants underlying the ability of acacetin to block hKv1.5 channels (coding I(Kur)) in human atrial myocytes using the whole-cell patch voltage-clamp technique to record membrane current in HEK 293 cells stably expressing the hKv1.5 gene or transiently expressing mutant hKv1.5 genes generated by site-directed mutagenesis.	acacetin	99-107	potassium voltage-gated channel subfamily A member 5	Homo sapiens	291-297
21906601-3	2011	The present study was designed to investigate the molecular determinants underlying the ability of acacetin to block hKv1.5 channels (coding I(Kur)) in human atrial myocytes using the whole-cell patch voltage-clamp technique to record membrane current in HEK 293 cells stably expressing the hKv1.5 gene or transiently expressing mutant hKv1.5 genes generated by site-directed mutagenesis.	acacetin	99-107	potassium voltage-gated channel subfamily A member 5	Homo sapiens	291-297
21906601-4	2011	It was found that acacetin blocked hKv1.5 channels by binding to both closed and open channels.	acacetin	18-26	potassium voltage-gated channel subfamily A member 5	Homo sapiens	35-41
21906601-5	2011	The blockade of hKv1.5 channels by acacetin was use- and frequency-dependent, and the IC(50) of acacetin for inhibiting hKv1.5 was 3.5, 3.1, 2.9, 2.1, and 1.7muM, respectively, at 0.2, 0.5, 1, 3, and 4Hz.	acacetin	35-43	potassium voltage-gated channel subfamily A member 5	Homo sapiens	16-22
21906601-5	2011	The blockade of hKv1.5 channels by acacetin was use- and frequency-dependent, and the IC(50) of acacetin for inhibiting hKv1.5 was 3.5, 3.1, 2.9, 2.1, and 1.7muM, respectively, at 0.2, 0.5, 1, 3, and 4Hz.	acacetin	96-104	potassium voltage-gated channel subfamily A member 5	Homo sapiens	16-22
21906601-5	2011	The blockade of hKv1.5 channels by acacetin was use- and frequency-dependent, and the IC(50) of acacetin for inhibiting hKv1.5 was 3.5, 3.1, 2.9, 2.1, and 1.7muM, respectively, at 0.2, 0.5, 1, 3, and 4Hz.	acacetin	96-104	potassium voltage-gated channel subfamily A member 5	Homo sapiens	120-126
21906601-6	2011	The mutagenesis study showed that the hKv1.5 mutants V505A, I508A, and V512A in the S6-segment remarkably reduced the channel blocking properties by acacetin (IC(50), 29.5muM for V505A, 19.1muM for I508A, and 6.9muM for V512A).	acacetin	149-157	potassium voltage-gated channel subfamily A member 5	Homo sapiens	38-44
21906601-6	2011	The mutagenesis study showed that the hKv1.5 mutants V505A, I508A, and V512A in the S6-segment remarkably reduced the channel blocking properties by acacetin (IC(50), 29.5muM for V505A, 19.1muM for I508A, and 6.9muM for V512A).	acacetin	149-157	latexin	Homo sapiens	171-174
21906601-7	2011	These results demonstrate the novel information that acacetin mainly blocks open hKv1.5 channels by binding to their S6 domain.	acacetin	53-61	potassium voltage-gated channel subfamily A member 5	Homo sapiens	81-87
21906601-8	2011	The use- and rate-dependent blocking of hKv1.5 by acacetin is beneficial for anti-atrial fibrillation.	acacetin	50-58	potassium voltage-gated channel subfamily A member 5	Homo sapiens	40-46
21210297-6	2011	Next, acacetin significantly decreased in the phosphorylation and degradation of inhibitor of kappaBalpha (IkappaBalpha), and the nuclear levels of nuclear factor kappa B (NF-kappaB), c-Fos, and c-Jun.	acacetin	6-14	NFKB inhibitor alpha	Homo sapiens	107-119
21210297-6	2011	Next, acacetin significantly decreased in the phosphorylation and degradation of inhibitor of kappaBalpha (IkappaBalpha), and the nuclear levels of nuclear factor kappa B (NF-kappaB), c-Fos, and c-Jun.	acacetin	6-14	nuclear factor kappa B subunit 1	Homo sapiens	148-170
21210297-6	2011	Next, acacetin significantly decreased in the phosphorylation and degradation of inhibitor of kappaBalpha (IkappaBalpha), and the nuclear levels of nuclear factor kappa B (NF-kappaB), c-Fos, and c-Jun.	acacetin	6-14	nuclear factor kappa B subunit 1	Homo sapiens	172-181
21210297-6	2011	Next, acacetin significantly decreased in the phosphorylation and degradation of inhibitor of kappaBalpha (IkappaBalpha), and the nuclear levels of nuclear factor kappa B (NF-kappaB), c-Fos, and c-Jun.	acacetin	6-14	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	184-189
21210297-6	2011	Next, acacetin significantly decreased in the phosphorylation and degradation of inhibitor of kappaBalpha (IkappaBalpha), and the nuclear levels of nuclear factor kappa B (NF-kappaB), c-Fos, and c-Jun.	acacetin	6-14	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	195-200
21210297-7	2011	Also, the treatment with acacetin to A549 cells also leads to a concentration-dependent inhibition on the binding abilities of NF-kappaB and activator protein-1 (AP-1).	acacetin	25-33	nuclear factor kappa B subunit 1	Homo sapiens	127-136
21210297-7	2011	Also, the treatment with acacetin to A549 cells also leads to a concentration-dependent inhibition on the binding abilities of NF-kappaB and activator protein-1 (AP-1).	acacetin	25-33	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	141-160
21210297-7	2011	Also, the treatment with acacetin to A549 cells also leads to a concentration-dependent inhibition on the binding abilities of NF-kappaB and activator protein-1 (AP-1).	acacetin	25-33	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	162-166
21210297-9	2011	In addition, acacetin significantly decreased the levels of phospho-p38alpha MAPK, MMP-2/9, and u-PA in p38alpha-cDNA-transfected cells concomitantly with a marked reduction on cell invasion and migration.	acacetin	13-21	mitogen-activated protein kinase 14	Homo sapiens	68-76
21210297-9	2011	In addition, acacetin significantly decreased the levels of phospho-p38alpha MAPK, MMP-2/9, and u-PA in p38alpha-cDNA-transfected cells concomitantly with a marked reduction on cell invasion and migration.	acacetin	13-21	matrix metallopeptidase 2	Homo sapiens	83-90
21210297-9	2011	In addition, acacetin significantly decreased the levels of phospho-p38alpha MAPK, MMP-2/9, and u-PA in p38alpha-cDNA-transfected cells concomitantly with a marked reduction on cell invasion and migration.	acacetin	13-21	plasminogen activator, urokinase	Homo sapiens	96-100
21210297-9	2011	In addition, acacetin significantly decreased the levels of phospho-p38alpha MAPK, MMP-2/9, and u-PA in p38alpha-cDNA-transfected cells concomitantly with a marked reduction on cell invasion and migration.	acacetin	13-21	mitogen-activated protein kinase 14	Homo sapiens	104-112
19693651-0	2010	Acacetin, a flavonoid, inhibits the invasion and migration of human prostate cancer DU145 cells via inactivation of the p38 MAPK signaling pathway.	acacetin	0-8	mitogen-activated protein kinase 14	Homo sapiens	120-123
20492175-0	2010	Acacetin inhibits TPA-induced MMP-2 and u-PA expressions of human lung cancer cells through inactivating JNK signaling pathway and reducing binding activities of NF-kappaB and AP-1.	acacetin	0-8	matrix metallopeptidase 2	Homo sapiens	30-35
20492175-0	2010	Acacetin inhibits TPA-induced MMP-2 and u-PA expressions of human lung cancer cells through inactivating JNK signaling pathway and reducing binding activities of NF-kappaB and AP-1.	acacetin	0-8	plasminogen activator, urokinase	Homo sapiens	40-44
20492175-0	2010	Acacetin inhibits TPA-induced MMP-2 and u-PA expressions of human lung cancer cells through inactivating JNK signaling pathway and reducing binding activities of NF-kappaB and AP-1.	acacetin	0-8	mitogen-activated protein kinase 8	Homo sapiens	105-108
20492175-0	2010	Acacetin inhibits TPA-induced MMP-2 and u-PA expressions of human lung cancer cells through inactivating JNK signaling pathway and reducing binding activities of NF-kappaB and AP-1.	acacetin	0-8	nuclear factor kappa B subunit 1	Homo sapiens	162-171
20492175-0	2010	Acacetin inhibits TPA-induced MMP-2 and u-PA expressions of human lung cancer cells through inactivating JNK signaling pathway and reducing binding activities of NF-kappaB and AP-1.	acacetin	0-8	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	176-180
20492175-2	2010	The effect of acacetin on 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced MMPs and u-PA expressions in human lung cancer A549 cells was investigated.	acacetin	14-22	plasminogen activator, urokinase	Homo sapiens	86-90
20492175-4	2010	Data also showed acacetin could inhibit phosphorylation of c-Jun N-terminal kinase 1 and 2 (JNK1/2) involved in the down-regulating protein expressions and transcriptions of matrix metalloproteinase-2 (MMP-2) and urokinase-type plasminogen activator (u-PA) induced by TPA.	acacetin	17-25	mitogen-activated protein kinase 8	Homo sapiens	59-90
20492175-4	2010	Data also showed acacetin could inhibit phosphorylation of c-Jun N-terminal kinase 1 and 2 (JNK1/2) involved in the down-regulating protein expressions and transcriptions of matrix metalloproteinase-2 (MMP-2) and urokinase-type plasminogen activator (u-PA) induced by TPA.	acacetin	17-25	mitogen-activated protein kinase 8	Homo sapiens	92-98
20492175-4	2010	Data also showed acacetin could inhibit phosphorylation of c-Jun N-terminal kinase 1 and 2 (JNK1/2) involved in the down-regulating protein expressions and transcriptions of matrix metalloproteinase-2 (MMP-2) and urokinase-type plasminogen activator (u-PA) induced by TPA.	acacetin	17-25	matrix metallopeptidase 2	Homo sapiens	174-200
20492175-4	2010	Data also showed acacetin could inhibit phosphorylation of c-Jun N-terminal kinase 1 and 2 (JNK1/2) involved in the down-regulating protein expressions and transcriptions of matrix metalloproteinase-2 (MMP-2) and urokinase-type plasminogen activator (u-PA) induced by TPA.	acacetin	17-25	matrix metallopeptidase 2	Homo sapiens	202-207
20492175-4	2010	Data also showed acacetin could inhibit phosphorylation of c-Jun N-terminal kinase 1 and 2 (JNK1/2) involved in the down-regulating protein expressions and transcriptions of matrix metalloproteinase-2 (MMP-2) and urokinase-type plasminogen activator (u-PA) induced by TPA.	acacetin	17-25	plasminogen activator, urokinase	Homo sapiens	213-249
20492175-4	2010	Data also showed acacetin could inhibit phosphorylation of c-Jun N-terminal kinase 1 and 2 (JNK1/2) involved in the down-regulating protein expressions and transcriptions of matrix metalloproteinase-2 (MMP-2) and urokinase-type plasminogen activator (u-PA) induced by TPA.	acacetin	17-25	plasminogen activator, urokinase	Homo sapiens	251-255
20492175-5	2010	Next, acacetin also strongly inhibited TPA-stimulated the nuclear levels of nuclear factor kappa B (NF-kappaB), c-Fos, and c-Jun.	acacetin	6-14	nuclear factor kappa B subunit 1	Homo sapiens	76-98
20492175-5	2010	Next, acacetin also strongly inhibited TPA-stimulated the nuclear levels of nuclear factor kappa B (NF-kappaB), c-Fos, and c-Jun.	acacetin	6-14	nuclear factor kappa B subunit 1	Homo sapiens	100-109
20492175-5	2010	Next, acacetin also strongly inhibited TPA-stimulated the nuclear levels of nuclear factor kappa B (NF-kappaB), c-Fos, and c-Jun.	acacetin	6-14	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	112-117
20492175-5	2010	Next, acacetin also strongly inhibited TPA-stimulated the nuclear levels of nuclear factor kappa B (NF-kappaB), c-Fos, and c-Jun.	acacetin	6-14	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	123-128
20492175-6	2010	Also, a dose-dependent inhibition on the binding abilities of NF-kappaB and activator protein-1 (AP-1) by acacetin treatment was further observed.	acacetin	106-114	nuclear factor kappa B subunit 1	Homo sapiens	62-71
20492175-6	2010	Also, a dose-dependent inhibition on the binding abilities of NF-kappaB and activator protein-1 (AP-1) by acacetin treatment was further observed.	acacetin	106-114	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	76-95
20492175-6	2010	Also, a dose-dependent inhibition on the binding abilities of NF-kappaB and activator protein-1 (AP-1) by acacetin treatment was further observed.	acacetin	106-114	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	97-101
20492175-8	2010	Taken together, these results suggest the antimetastatic effects of acacetin on the TPA-induced A549 cells might be by reducing MMP-2 and u-PA expressions through inhibiting phosphorylation of JNK and reducing NF-kappaB and AP-1 binding activities.	acacetin	68-76	matrix metallopeptidase 2	Homo sapiens	128-133
20492175-8	2010	Taken together, these results suggest the antimetastatic effects of acacetin on the TPA-induced A549 cells might be by reducing MMP-2 and u-PA expressions through inhibiting phosphorylation of JNK and reducing NF-kappaB and AP-1 binding activities.	acacetin	68-76	plasminogen activator, urokinase	Homo sapiens	138-142
20492175-8	2010	Taken together, these results suggest the antimetastatic effects of acacetin on the TPA-induced A549 cells might be by reducing MMP-2 and u-PA expressions through inhibiting phosphorylation of JNK and reducing NF-kappaB and AP-1 binding activities.	acacetin	68-76	mitogen-activated protein kinase 8	Homo sapiens	193-196
20492175-8	2010	Taken together, these results suggest the antimetastatic effects of acacetin on the TPA-induced A549 cells might be by reducing MMP-2 and u-PA expressions through inhibiting phosphorylation of JNK and reducing NF-kappaB and AP-1 binding activities.	acacetin	68-76	nuclear factor kappa B subunit 1	Homo sapiens	210-219
20492175-8	2010	Taken together, these results suggest the antimetastatic effects of acacetin on the TPA-induced A549 cells might be by reducing MMP-2 and u-PA expressions through inhibiting phosphorylation of JNK and reducing NF-kappaB and AP-1 binding activities.	acacetin	68-76	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	224-228
19693651-4	2010	Data also showed acacetin could inhibit the phosphorylation of p38 mitogen-activated protein kinase (p38 MAPK) involved in the downregulation of the expressions of matrix metalloproteinase-2 (MMP-2), matrix metalloproteinase-9 (MMP-9), and urokinase-type plasminogen activator (u-PA) at both the protein and mRNA levels.	acacetin	17-25	mitogen-activated protein kinase 14	Homo sapiens	63-99
19693651-4	2010	Data also showed acacetin could inhibit the phosphorylation of p38 mitogen-activated protein kinase (p38 MAPK) involved in the downregulation of the expressions of matrix metalloproteinase-2 (MMP-2), matrix metalloproteinase-9 (MMP-9), and urokinase-type plasminogen activator (u-PA) at both the protein and mRNA levels.	acacetin	17-25	mitogen-activated protein kinase 14	Homo sapiens	101-109
19693651-4	2010	Data also showed acacetin could inhibit the phosphorylation of p38 mitogen-activated protein kinase (p38 MAPK) involved in the downregulation of the expressions of matrix metalloproteinase-2 (MMP-2), matrix metalloproteinase-9 (MMP-9), and urokinase-type plasminogen activator (u-PA) at both the protein and mRNA levels.	acacetin	17-25	matrix metallopeptidase 2	Homo sapiens	164-190
19693651-4	2010	Data also showed acacetin could inhibit the phosphorylation of p38 mitogen-activated protein kinase (p38 MAPK) involved in the downregulation of the expressions of matrix metalloproteinase-2 (MMP-2), matrix metalloproteinase-9 (MMP-9), and urokinase-type plasminogen activator (u-PA) at both the protein and mRNA levels.	acacetin	17-25	matrix metallopeptidase 2	Homo sapiens	192-197
19693651-4	2010	Data also showed acacetin could inhibit the phosphorylation of p38 mitogen-activated protein kinase (p38 MAPK) involved in the downregulation of the expressions of matrix metalloproteinase-2 (MMP-2), matrix metalloproteinase-9 (MMP-9), and urokinase-type plasminogen activator (u-PA) at both the protein and mRNA levels.	acacetin	17-25	matrix metallopeptidase 9	Homo sapiens	200-226
19693651-4	2010	Data also showed acacetin could inhibit the phosphorylation of p38 mitogen-activated protein kinase (p38 MAPK) involved in the downregulation of the expressions of matrix metalloproteinase-2 (MMP-2), matrix metalloproteinase-9 (MMP-9), and urokinase-type plasminogen activator (u-PA) at both the protein and mRNA levels.	acacetin	17-25	matrix metallopeptidase 9	Homo sapiens	228-233
19693651-4	2010	Data also showed acacetin could inhibit the phosphorylation of p38 mitogen-activated protein kinase (p38 MAPK) involved in the downregulation of the expressions of matrix metalloproteinase-2 (MMP-2), matrix metalloproteinase-9 (MMP-9), and urokinase-type plasminogen activator (u-PA) at both the protein and mRNA levels.	acacetin	17-25	plasminogen activator, urokinase	Homo sapiens	240-276
19693651-4	2010	Data also showed acacetin could inhibit the phosphorylation of p38 mitogen-activated protein kinase (p38 MAPK) involved in the downregulation of the expressions of matrix metalloproteinase-2 (MMP-2), matrix metalloproteinase-9 (MMP-9), and urokinase-type plasminogen activator (u-PA) at both the protein and mRNA levels.	acacetin	17-25	plasminogen activator, urokinase	Homo sapiens	278-282
19693651-5	2010	Next, acacetin significantly decreased the nuclear levels of nuclear factor kappa B (NF-kappaB), c-Fos, and c-Jun.	acacetin	6-14	nuclear factor kappa B subunit 1	Homo sapiens	61-83
19693651-5	2010	Next, acacetin significantly decreased the nuclear levels of nuclear factor kappa B (NF-kappaB), c-Fos, and c-Jun.	acacetin	6-14	nuclear factor kappa B subunit 1	Homo sapiens	85-94
19693651-5	2010	Next, acacetin significantly decreased the nuclear levels of nuclear factor kappa B (NF-kappaB), c-Fos, and c-Jun.	acacetin	6-14	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	97-102
19693651-5	2010	Next, acacetin significantly decreased the nuclear levels of nuclear factor kappa B (NF-kappaB), c-Fos, and c-Jun.	acacetin	6-14	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	108-113
19693651-6	2010	Also, the treatment with acacetin to DU145 cells also leads to a dose-dependent inhibition on the binding ability of NF-kappaB and activator protein-1 (AP-1).	acacetin	25-33	nuclear factor kappa B subunit 1	Homo sapiens	117-126
19693651-6	2010	Also, the treatment with acacetin to DU145 cells also leads to a dose-dependent inhibition on the binding ability of NF-kappaB and activator protein-1 (AP-1).	acacetin	25-33	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	131-150
19693651-6	2010	Also, the treatment with acacetin to DU145 cells also leads to a dose-dependent inhibition on the binding ability of NF-kappaB and activator protein-1 (AP-1).	acacetin	25-33	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	152-156
19693651-8	2010	These results showed acacetin could inhibit the invasion and migration abilities of DU145 cells by reducing MMP-2, MMP-9, and u-PA expressions through suppressing p38 MAPK signaling pathway and inhibiting NF-kappaB- or AP-1-binding activity.	acacetin	21-29	matrix metallopeptidase 2	Homo sapiens	108-113
19693651-8	2010	These results showed acacetin could inhibit the invasion and migration abilities of DU145 cells by reducing MMP-2, MMP-9, and u-PA expressions through suppressing p38 MAPK signaling pathway and inhibiting NF-kappaB- or AP-1-binding activity.	acacetin	21-29	matrix metallopeptidase 9	Homo sapiens	115-120
19693651-8	2010	These results showed acacetin could inhibit the invasion and migration abilities of DU145 cells by reducing MMP-2, MMP-9, and u-PA expressions through suppressing p38 MAPK signaling pathway and inhibiting NF-kappaB- or AP-1-binding activity.	acacetin	21-29	plasminogen activator, urokinase	Homo sapiens	126-130
19693651-8	2010	These results showed acacetin could inhibit the invasion and migration abilities of DU145 cells by reducing MMP-2, MMP-9, and u-PA expressions through suppressing p38 MAPK signaling pathway and inhibiting NF-kappaB- or AP-1-binding activity.	acacetin	21-29	mitogen-activated protein kinase 14	Homo sapiens	163-166
19693651-8	2010	These results showed acacetin could inhibit the invasion and migration abilities of DU145 cells by reducing MMP-2, MMP-9, and u-PA expressions through suppressing p38 MAPK signaling pathway and inhibiting NF-kappaB- or AP-1-binding activity.	acacetin	21-29	nuclear factor kappa B subunit 1	Homo sapiens	205-214
19693651-8	2010	These results showed acacetin could inhibit the invasion and migration abilities of DU145 cells by reducing MMP-2, MMP-9, and u-PA expressions through suppressing p38 MAPK signaling pathway and inhibiting NF-kappaB- or AP-1-binding activity.	acacetin	21-29	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	219-223
17846503-0	2007	Acacetin-induced apoptosis of human breast cancer MCF-7 cells involves caspase cascade, mitochondria-mediated death signaling and SAPK/JNK1/2-c-Jun activation.	acacetin	0-8	mitogen-activated protein kinase 9	Homo sapiens	130-134
19666078-5	2009	Cotreatment of the CYP1 family inhibitor acacetin reversed the antiproliferative activity noticed for the two flavones in MDA-MB-468 cells to 13 and 14 microM respectively.	acacetin	41-49	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	19-23
18458165-6	2008	Although acacetin caused a weak reduction in the hERG and hKCNQ1/hKCNE1 channels stably expressed in HEK 293 cells, it did not prolong the corrected QT interval in rabbit hearts.	acacetin	9-17	ETS transcription factor ERG	Homo sapiens	49-53
18458165-6	2008	Although acacetin caused a weak reduction in the hERG and hKCNQ1/hKCNE1 channels stably expressed in HEK 293 cells, it did not prolong the corrected QT interval in rabbit hearts.	acacetin	9-17	potassium voltage-gated channel subfamily Q member 1	Homo sapiens	58-64
18458165-6	2008	Although acacetin caused a weak reduction in the hERG and hKCNQ1/hKCNE1 channels stably expressed in HEK 293 cells, it did not prolong the corrected QT interval in rabbit hearts.	acacetin	9-17	potassium voltage-gated channel subfamily E regulatory subunit 1	Homo sapiens	65-71
18454852-12	2008	The effect of eupatorin on the MDA-MB-468 cell cycle could be reversed by co-application of the CYP1 inhibitor acacetin.	acacetin	111-119	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	96-100
17345086-11	2007	Two of the flavones, 3",4",7-trimethoxyflavone and acacetin, showed only low anti-P-gp activity, with the remainder displaying no suppressive effects against P-gp.	acacetin	51-59	ATP binding cassette subfamily B member 1	Homo sapiens	82-86
17846503-8	2007	Stress-activated protein kinase/c-Jun NH4-terminal kinase 1/2 (SAPK/ JNK1/2) and c-Jun were activated by acacetin but extracellular-regulated kinase 1/2 (Erk1/2) nor p38 mitogen-activated protein kinase (MAPK) were not.	acacetin	105-113	mitogen-activated protein kinase 3	Homo sapiens	204-208
17846503-9	2007	Our results show that acacetin-induced apoptosis of MCF-7 cells is mediated by caspase activation cascades, ROS generation, mitochondria-mediated cell death signaling and the SAPK/JNK1/2-c-Jun signaling pathway, activated by acacetin-induced ROS generation.	acacetin	22-30	mitogen-activated protein kinase 9	Homo sapiens	175-179
17846503-9	2007	Our results show that acacetin-induced apoptosis of MCF-7 cells is mediated by caspase activation cascades, ROS generation, mitochondria-mediated cell death signaling and the SAPK/JNK1/2-c-Jun signaling pathway, activated by acacetin-induced ROS generation.	acacetin	22-30	mitogen-activated protein kinase 8	Homo sapiens	180-188
19601638-6	2009	Application of the CYP1 family inhibitor, acacetin, significantly increased the IC(50) value of 2 in MCF7 cells, but did not significantly affect the action of 1.	acacetin	42-50	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	19-23
19020811-2	2009	Since the activity of the other MDR transporter, P-glycoprotein, is sensitive to membrane perturbation, we aimed to check whether the changes in lipid bilayer properties induced by flavones (apigenin, acacetin) and flavonols (morin, myricetin) were related to their MRP1 inhibitory activity.	acacetin	201-209	ATP binding cassette subfamily B member 1	Homo sapiens	49-63
17846503-0	2007	Acacetin-induced apoptosis of human breast cancer MCF-7 cells involves caspase cascade, mitochondria-mediated death signaling and SAPK/JNK1/2-c-Jun activation.	acacetin	0-8	mitogen-activated protein kinase 8	Homo sapiens	135-143
17846503-4	2007	Maximum caspase 7 activity was observed with 100 microM acacetin for 24 h. Caspase 8 and 9 activation cascades mediated the activation of caspase 7.	acacetin	56-64	caspase 7	Homo sapiens	8-17
17846503-4	2007	Maximum caspase 7 activity was observed with 100 microM acacetin for 24 h. Caspase 8 and 9 activation cascades mediated the activation of caspase 7.	acacetin	56-64	caspase 8	Homo sapiens	75-84
17846503-4	2007	Maximum caspase 7 activity was observed with 100 microM acacetin for 24 h. Caspase 8 and 9 activation cascades mediated the activation of caspase 7.	acacetin	56-64	caspase 7	Homo sapiens	138-147
17846503-5	2007	Acacetin caused a reduction of Bcl-2 expression leading to an increase of the Bax:Bcl-2 ratio.	acacetin	0-8	BCL2 apoptosis regulator	Homo sapiens	31-36
17846503-5	2007	Acacetin caused a reduction of Bcl-2 expression leading to an increase of the Bax:Bcl-2 ratio.	acacetin	0-8	BCL2 associated X, apoptosis regulator	Homo sapiens	78-81
17846503-5	2007	Acacetin caused a reduction of Bcl-2 expression leading to an increase of the Bax:Bcl-2 ratio.	acacetin	0-8	BCL2 apoptosis regulator	Homo sapiens	82-87
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.	acacetin	179-187	caspase 8	Homo sapiens	132-141
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.	acacetin	179-187	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.	acacetin	179-187	apoptosis inducing factor mitochondria associated 1	Homo sapiens	269-272
17846503-8	2007	Stress-activated protein kinase/c-Jun NH4-terminal kinase 1/2 (SAPK/ JNK1/2) and c-Jun were activated by acacetin but extracellular-regulated kinase 1/2 (Erk1/2) nor p38 mitogen-activated protein kinase (MAPK) were not.	acacetin	105-113	mitogen-activated protein kinase 9	Homo sapiens	63-67
17846503-8	2007	Stress-activated protein kinase/c-Jun NH4-terminal kinase 1/2 (SAPK/ JNK1/2) and c-Jun were activated by acacetin but extracellular-regulated kinase 1/2 (Erk1/2) nor p38 mitogen-activated protein kinase (MAPK) were not.	acacetin	105-113	mitogen-activated protein kinase 8	Homo sapiens	69-75
17846503-8	2007	Stress-activated protein kinase/c-Jun NH4-terminal kinase 1/2 (SAPK/ JNK1/2) and c-Jun were activated by acacetin but extracellular-regulated kinase 1/2 (Erk1/2) nor p38 mitogen-activated protein kinase (MAPK) were not.	acacetin	105-113	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	32-37
15246561-3	2004	ELISA assay demonstrated that acacetin significantly increased the expression of p53 and p21/WAF1 protein, which caused cell cycle arrest.	acacetin	30-38	tumor protein p53	Homo sapiens	81-84
16949556-0	2006	Acacetin suppressed LPS-induced up-expression of iNOS and COX-2 in murine macrophages and TPA-induced tumor promotion in mice.	acacetin	0-8	nitric oxide synthase 2, inducible	Mus musculus	49-53
16949556-0	2006	Acacetin suppressed LPS-induced up-expression of iNOS and COX-2 in murine macrophages and TPA-induced tumor promotion in mice.	acacetin	0-8	cytochrome c oxidase II, mitochondrial	Mus musculus	58-63
16949556-2	2006	In this study, we investigated the inhibitory effects of acacetin and a related compound, wogonin, on the induction of NO synthase (NOS) and COX-2 in RAW 264.7 cells activated with lipopolysaccharide (LPS).	acacetin	57-65	nitric oxide synthase 1, neuronal	Mus musculus	119-130
16949556-2	2006	In this study, we investigated the inhibitory effects of acacetin and a related compound, wogonin, on the induction of NO synthase (NOS) and COX-2 in RAW 264.7 cells activated with lipopolysaccharide (LPS).	acacetin	57-65	cytochrome c oxidase II, mitochondrial	Mus musculus	141-146
16949556-3	2006	Acacetin markedly and actively inhibited the transcriptional activation of iNOS and COX-2.	acacetin	0-8	nitric oxide synthase 2, inducible	Mus musculus	75-79
16949556-3	2006	Acacetin markedly and actively inhibited the transcriptional activation of iNOS and COX-2.	acacetin	0-8	cytochrome c oxidase II, mitochondrial	Mus musculus	84-89
16949556-4	2006	Western blotting, reverse transcription-polymerase chain reaction (PCR), and real-time PCR analyses demonstrated that acacetin significantly blocked protein and mRNA expression of iNOS and COX-2 in LPS-inducted macrophages.	acacetin	118-126	nitric oxide synthase 2, inducible	Mus musculus	180-184
16949556-4	2006	Western blotting, reverse transcription-polymerase chain reaction (PCR), and real-time PCR analyses demonstrated that acacetin significantly blocked protein and mRNA expression of iNOS and COX-2 in LPS-inducted macrophages.	acacetin	118-126	cytochrome c oxidase II, mitochondrial	Mus musculus	189-194
16949556-5	2006	Treatment with acacetin reduced translocation of nuclear factor-kappa B (NF kappa B) subunit and the dependent transcriptional activity of NF kappa B.	acacetin	15-23	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	73-83
16949556-5	2006	Treatment with acacetin reduced translocation of nuclear factor-kappa B (NF kappa B) subunit and the dependent transcriptional activity of NF kappa B.	acacetin	15-23	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	139-149
16949556-7	2006	Furthermore, acacetin inhibited LPS-induced phosphorylation as well as degradation of I kappa B alpha.	acacetin	13-21	nuclear factor of kappa light polypeptide gene enhancer in B cells inhibitor, alpha	Mus musculus	86-101
16949556-9	2006	We found that acacetin also inhibited LPS-induced activation of PI3K/Akt and p44/42, but not p38 MAPK.	acacetin	14-22	thymoma viral proto-oncogene 1	Mus musculus	69-72
16949556-11	2006	Taken together, these results show that acacetin down regulates inflammatory iNOS and COX-2 gene expression in macrophages by inhibiting the activation of NF kappa B by interfering with the activation PI3K/Akt/IKK and MAPK, suggesting that acacetin is a functionally novel agent capable of preventing inflammation-associated tumorigenesis.	acacetin	40-48	nitric oxide synthase 2, inducible	Mus musculus	77-81
16949556-11	2006	Taken together, these results show that acacetin down regulates inflammatory iNOS and COX-2 gene expression in macrophages by inhibiting the activation of NF kappa B by interfering with the activation PI3K/Akt/IKK and MAPK, suggesting that acacetin is a functionally novel agent capable of preventing inflammation-associated tumorigenesis.	acacetin	40-48	cytochrome c oxidase II, mitochondrial	Mus musculus	86-91
16949556-11	2006	Taken together, these results show that acacetin down regulates inflammatory iNOS and COX-2 gene expression in macrophages by inhibiting the activation of NF kappa B by interfering with the activation PI3K/Akt/IKK and MAPK, suggesting that acacetin is a functionally novel agent capable of preventing inflammation-associated tumorigenesis.	acacetin	40-48	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	155-165
16949556-11	2006	Taken together, these results show that acacetin down regulates inflammatory iNOS and COX-2 gene expression in macrophages by inhibiting the activation of NF kappa B by interfering with the activation PI3K/Akt/IKK and MAPK, suggesting that acacetin is a functionally novel agent capable of preventing inflammation-associated tumorigenesis.	acacetin	40-48	thymoma viral proto-oncogene 1	Mus musculus	206-209
16949556-11	2006	Taken together, these results show that acacetin down regulates inflammatory iNOS and COX-2 gene expression in macrophages by inhibiting the activation of NF kappa B by interfering with the activation PI3K/Akt/IKK and MAPK, suggesting that acacetin is a functionally novel agent capable of preventing inflammation-associated tumorigenesis.	acacetin	240-248	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	155-165
15686411-0	2005	Acacetin induces apoptosis in human gastric carcinoma cells accompanied by activation of caspase cascades and production of reactive oxygen species.	acacetin	0-8	caspase 1	Homo sapiens	89-96
15686411-6	2005	Treatment with acacetin caused induction of caspase-3 activity in a time-dependent manner, but not caspase-1 activity, and induced the degradation of DNA fragmentation factor (DFF-45) and poly(ADP-riobse) polymerase.	acacetin	15-23	caspase 3	Homo sapiens	44-53
15686411-6	2005	Treatment with acacetin caused induction of caspase-3 activity in a time-dependent manner, but not caspase-1 activity, and induced the degradation of DNA fragmentation factor (DFF-45) and poly(ADP-riobse) polymerase.	acacetin	15-23	DNA fragmentation factor subunit alpha	Homo sapiens	176-182
15686411-8	2005	Furthermore, treatment with acacetin caused a rapid loss of mitochondrial transmembrane potential, stimulation of reactive oxygen species (ROS), release of mitochondrial cytochrome c into cytosol, and subsequent induction of procaspase-9 processing.	acacetin	28-36	cytochrome c, somatic	Homo sapiens	170-182
15686411-10	2005	In addition, it was found that acacetin promoted the up-regulation of Fas and FasL prior to the processing and activation of pro-caspase-8 and cleavage of Bid, suggesting the involvement of a Fas-mediated pathway in acacetin-induced apoptosis.	acacetin	31-39	Fas ligand	Homo sapiens	78-82
15686411-10	2005	In addition, it was found that acacetin promoted the up-regulation of Fas and FasL prior to the processing and activation of pro-caspase-8 and cleavage of Bid, suggesting the involvement of a Fas-mediated pathway in acacetin-induced apoptosis.	acacetin	31-39	BH3 interacting domain death agonist	Homo sapiens	155-158
15686411-11	2005	On the other hand, the results showed that acacetin-induced apoptosis was accompanied by up-regulation of Bax and p53, down-regulation of Bcl-2, and cleavage of Bad.	acacetin	43-51	BCL2 associated X, apoptosis regulator	Homo sapiens	106-109
15686411-11	2005	On the other hand, the results showed that acacetin-induced apoptosis was accompanied by up-regulation of Bax and p53, down-regulation of Bcl-2, and cleavage of Bad.	acacetin	43-51	tumor protein p53	Homo sapiens	114-117
15686411-11	2005	On the other hand, the results showed that acacetin-induced apoptosis was accompanied by up-regulation of Bax and p53, down-regulation of Bcl-2, and cleavage of Bad.	acacetin	43-51	BCL2 apoptosis regulator	Homo sapiens	138-143
15563763-5	2004	The order of antioxidative activity was norwogonin > acacetin > icariin by the analysis of the relationship between the concentration of Chm-OHs and the prolongation percentage of the lag time of haemolysis (PP%).	acacetin	56-64	CHM Rab escort protein	Homo sapiens	143-146
15246561-3	2004	ELISA assay demonstrated that acacetin significantly increased the expression of p53 and p21/WAF1 protein, which caused cell cycle arrest.	acacetin	30-38	cyclin dependent kinase inhibitor 1A	Homo sapiens	89-92
15246561-3	2004	ELISA assay demonstrated that acacetin significantly increased the expression of p53 and p21/WAF1 protein, which caused cell cycle arrest.	acacetin	30-38	cyclin dependent kinase inhibitor 1A	Homo sapiens	93-97
15246561-4	2004	An enhancement in Fas and its two forms of ligands, membrane-bound Fas ligand (mFasL) and soluble Fas ligand (sFasL), might be responsible for the apoptotic effect induced by acacetin.	acacetin	175-183	Fas ligand	Homo sapiens	67-77
15246561-4	2004	An enhancement in Fas and its two forms of ligands, membrane-bound Fas ligand (mFasL) and soluble Fas ligand (sFasL), might be responsible for the apoptotic effect induced by acacetin.	acacetin	175-183	Fas ligand	Homo sapiens	98-108
15246561-5	2004	Taken together, p53 and Fas/FasL apoptotic system may participate in the antiproliferative activity of acacetin in A549 cells.	acacetin	103-111	tumor protein p53	Homo sapiens	16-19
15246561-5	2004	Taken together, p53 and Fas/FasL apoptotic system may participate in the antiproliferative activity of acacetin in A549 cells.	acacetin	103-111	Fas ligand	Homo sapiens	28-32
15104235-5	2004	Enzyme-linked immunosorbent assay showed that acacetin significantly increased the expression of p53 and p21/WAF1 protein, contributing to cell cycle arrest.	acacetin	46-54	tumor protein p53	Homo sapiens	97-100
15205350-4	2004	In this study, we show that phytoestrogens/flavonoids, such as genistein, naringenin, acacetin, and kaempferol, potentiated the cytotoxicity of SN-38 and mitoxantrone in BCRP-transduced K562 (K562/BCRP) cells.	acacetin	86-94	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	170-174
15205350-4	2004	In this study, we show that phytoestrogens/flavonoids, such as genistein, naringenin, acacetin, and kaempferol, potentiated the cytotoxicity of SN-38 and mitoxantrone in BCRP-transduced K562 (K562/BCRP) cells.	acacetin	86-94	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	197-201
15104235-5	2004	Enzyme-linked immunosorbent assay showed that acacetin significantly increased the expression of p53 and p21/WAF1 protein, contributing to cell cycle arrest.	acacetin	46-54	cyclin dependent kinase inhibitor 1A	Homo sapiens	105-108
15104235-5	2004	Enzyme-linked immunosorbent assay showed that acacetin significantly increased the expression of p53 and p21/WAF1 protein, contributing to cell cycle arrest.	acacetin	46-54	cyclin dependent kinase inhibitor 1A	Homo sapiens	109-113
15104235-6	2004	An enhancement in Fas/APO-1 and its two form ligands, membrane-bound Fas ligand and soluble Fas ligand, as well as Bax protein, was responsible for the apoptotic effect induced by acacetin.	acacetin	180-188	Fas cell surface death receptor	Homo sapiens	22-27
15104235-6	2004	An enhancement in Fas/APO-1 and its two form ligands, membrane-bound Fas ligand and soluble Fas ligand, as well as Bax protein, was responsible for the apoptotic effect induced by acacetin.	acacetin	180-188	Fas ligand	Homo sapiens	69-79
15104235-6	2004	An enhancement in Fas/APO-1 and its two form ligands, membrane-bound Fas ligand and soluble Fas ligand, as well as Bax protein, was responsible for the apoptotic effect induced by acacetin.	acacetin	180-188	Fas ligand	Homo sapiens	92-102
15104235-6	2004	An enhancement in Fas/APO-1 and its two form ligands, membrane-bound Fas ligand and soluble Fas ligand, as well as Bax protein, was responsible for the apoptotic effect induced by acacetin.	acacetin	180-188	BCL2 associated X, apoptosis regulator	Homo sapiens	115-118
15104235-7	2004	Taken together, our study suggests that the induction of p53 and activity of the Fas/Fas ligand apoptotic system may participate in the antiproliferative activity of acacetin in Hep G2 cells.	acacetin	166-174	tumor protein p53	Homo sapiens	57-60
15104235-7	2004	Taken together, our study suggests that the induction of p53 and activity of the Fas/Fas ligand apoptotic system may participate in the antiproliferative activity of acacetin in Hep G2 cells.	acacetin	166-174	Fas ligand	Homo sapiens	85-95
10781868-2	2000	The flavones acacetin and diosmetin were potent inhibitors of ethoxyresorufin O-dealkylase (EROD) activity of CYP1A and CYP1B1.	acacetin	13-21	cytochrome P450 family 1 subfamily B member 1	Homo sapiens	120-126
8825617-3	1996	By screening flavonoids from six different classes, three structurally related compounds (chrysin, acacetin, and apigenin) were identified that inhibited HIV expression in TNF-alpha-treated OM-10.1 cultures.	acacetin	99-107	tumor necrosis factor	Homo sapiens	172-181