Abstract
Myricetin is found in most berries, vegetables, and various medicinal herbs, which has been reported to possess various bio-activities. However, the role of myricetin on liver fibrosis remains to be elucidated. Hepatic stellate cell (HSC) line CFSC-8B was stimulated by transforming growth factor β1 (TGF-β1) or platelet-derived growth factor BB (PDGF-BB) to induce liver fibrosis in vitro. The results showed that myricetin significantly ameliorated TGF-β1- or PDGF-BB-induced HSCs activation, cell migration, and extracellular matrix production; blocked TGF-β1-induced phosphorylation of Smad2, P38, extracellular signal-regulated kinase (ERK), and protein kinase B (Akt); and downregulated PDGF-BB stimulated phosphorylation of extracellular signal-regulated kinase and Akt in HSCs in a dose-dependent manner. Meanwhile, the carbon tetrachloride (CCl4 ) induced mouse model has been used to study antifibrosis role of myricetin in vivo. Our data demonstrated that myricetin suppressed α-smooth muscle actin and collagen type I deposition and blocked phosphorylation of Smad2, mitogen-activated protein kinases, and Akt in CCl4 -treated mice. Myricetin inhibits the activation of HSCs and ameliorates CCl4 -induced liver fibrosis in mice and may serve as a potential therapeutic agent in the treatment of liver fibrosis.
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