Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P05412 (c-Jun)
 11,453 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Artemisia asiatica Nakai has been used frequently in traditional Asian medicine for the treatment of inflammation and cancer. Eupatilin (5,7-dihydroxy-3',4', 6-trimethoxy-flavone) was shown to be a pharmacologically active ingredient of A. asiatica. In the present study, we found that expression of cyclin D1, a key protein that regulates G1/S progression, was decreased in MCF-10A-ras cells treated with eupatilin. Downregulation of cyclin D1 expression by eupatilin was accompanied by a reduced expression of c-Jun and the DNA binding activity of the transcription factor AP-l. The expression of p21waf1/Cip1 was also decreased by eupatilin treatment in both protein and the mRNA levels. We concluded that the inhibitory effect of eupatilin on p21waf1/Cip1 expression is likely to be associated with the downregulation of cyclin D1 expression and AP-1 activation, which play an important role in the cell cycle arrest of ras-transformed breast epithelial cells.
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PMID:Eupatilin inhibits proliferation of ras-transformed human breast epithelial (MCF-10A-ras) cells. 1639 19

Eupatilin (5,7-dihydroxy-3',4',6-trimethoxyflavone), an extract from Artemisia asiatica Nakai, is a flavonoid of pharmacologically active ingredients. Eupatilin is known to possess anti-cancer, anti-inflammatory, and anti-oxidative activity. Recently, eupatilin has been reported to be effective in producing gastric mucosal as an anti-gastritis agents. However, the mechanism of protective action is still unknown. We studied cytoprotective actions of eupatilin on H(2)O(2)-induced cell death and its possible mechanisms of action in human gastric (AGS) cells. Eupatilin dose-dependently inhibited H(2)O(2)-induced apoptosis as indicated by co-staining with Annexin V and propidium iodide. Hydrogen peroxide provoked phosphorylation of extracellular regulated kinase (ERK) and c-Jun NH(2)-terminal kinase (JNK), and activation of nuclear factor-kappaB (NF-kappaB). On the contrary, eupatilin decreased H(2)O(2)-induced activation of ERK, JNK and NF-kappaB. In addition, treatment of specific inhibitors for ERK, JNK, and NF-kappaB attenuated H(2)O(2)-induced apoptosis. Co-treatment of inhibitors and eupatilin was more effective in decreasing H(2)O(2)-induced apoptosis. Taken together, we suggest that eupatilin inhibits H(2)O(2)-induced apoptosis through the inhibition ERK, JNK, and NF-kappaB.
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PMID:Eupatilin inhibits H(2)O(2)-induced apoptotic cell death through inhibition of mitogen-activated protein kinases and nuclear factor-kappaB. 1860 43