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The present study aimed to investigate the biological actions of tricin on hepatic stellate cells (HSCs) in vitro, exploring its potential as a treatment of liver fibrosis, since HSC proliferation is closely related to the progression of hepatic fibrogenesis in chronic liver diseases leading to irreversible liver cirrhosis and hepatocellular carcinoma. Tricin inhibited platelet\u2010derived growth factor (PDGF)\u2010BB\u2010induced cell proliferation by blocking cell cycle progression and cell migration in the human HSC line LI90 and culture\u2010activated HSCs. It also reduced the phosphorylation of PDGF receptor \u03b2 and the downstream signaling molecules ERK1\/2 and Akt, which might be due to its tyrosine kinase inhibitor properties rather than inhibition of the direct binding between PDGF\u2010BB and its receptor. Our findings suggest that tricin might be beneficial in HSC\u2010targeting therapeutic or chemopreventive applications for hepatic fibrosis. J. Cell. Biochem. 113: 2346\u20132355, 2012. \u00a9 2012 Wiley Periodicals, Inc.<\/jats:p>","DOI":"10.1002\/jcb.24107","type":"journal-article","created":{"date-parts":[[2012,2,22]],"date-time":"2012-02-22T17:56:15Z","timestamp":1329933375000},"page":"2346-2355","source":"Crossref","is-referenced-by-count":28,"title":["Tricin inhibits proliferation of human hepatic stellate cells in vitro by blocking tyrosine phosphorylation of PDGF receptor and its signaling 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