The common dietary flavonoid myricetin attenuates liver fibrosis in carbon tetrachloride treated mice

Scope 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. Methods and results 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 (CCl 4 ) 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 CCl 4 ‐treated mice. Conclusion Myricetin inhibits the activation of HSCs and ameliorates CCl 4 ‐induced liver fibrosis in mice and may serve as a potential therapeutic agent in the treatment of liver fibrosis.