Protective effects of baicalin on carbon tetrachloride induced liver injury by activating PPARγ and inhibiting TGFβ1

Traditional Chinese herbal medicines have attracted considerable attention in many countries with treatment of several end-stage liver diseases.The present study investigated the protective effects of baicalin on hepatotoxicity and hepatic fibrosis and explored the role of transforming growth factor β1 (TGFβ1) and peroxisome proliferator activated receptors γ (PPARγ) on the rat liver injury model.The rat liver injury model was introduced by subcutaneous injection of carbon tetrachloride (CCl(4)) for 8 weeks. At week 5, rats were treated with baicalin of different doses or silymarin. Detection of biochemical indicators, histological analysis, and enzyme-linked immunosorbent assays were employed to evaluate severity of liver inflammation, and western blotting and RT-PCR assay were performed to evaluate TGFβ1 and PPARγ pathway related proteins and gene expression.The administration of baicalin could significantly improve histological changes of CCl(4) treated rat livers and return biochemical indicators for liver injury to nearly baseline level. In addition, the increased expression of TGFβ1 was markedly suppressed by baicalin, and decreased expression of PPARγ was also dramatically elevated by baicalin as well. The hepatoprotective effects of baicalin may be conferred by elevating the level of PPARγ contributing to down-regulation of TGFβ1 signaling pathway and suppression of hepatic stellate cell activation.The studies demonstrated that baicalin is a potent and promising antifibrotic drug in the treatment of hepatic fibrosis.