ObjectiveTo investigate the role of icaritin in delaying the progression of liver cirrhotic process in rats and the related mechanism.MethodsFor in vitro study, primary rat hepatocytes were obtained by perfusing the liver of male Wistar rats; the cultured cells were exposed to the fresh medium containing CCl4, and then treated with various concentrations of icaritin. The activities of alanine transaninase (ALT) and glutamic-oxaloacetic transaminase (AST) in culture medium were measured with an automatic biochemical analyzer. The intracellular contents of malondialdehyde (MDA) and superoxide dismutase (SOD) were determined by spectro-photometry; the apoptotic cells were detected by the TUNEL method. For in vivo study, CCl4-induced experimental rat hepatic fibrosis model was established and was treated with icaritin. Serum levels of ALT, AST, albumin(ALB), and globulin(GLB) were measured; the pathological changes and collagen Ⅰ expression in livers were observed by HE staining and immunohistochemistry, respectively.ResultsCCl4 significantly increased the activities of ALT, AST, and the contents of MDA in culture media of hepatocytes, and significantly decreased the SOD activity. More apoptotic cells were observed in CCl4 group than that in icaritin group. The ALT, AST activities in culture supernatant and the intracellular MDA contents in icaritin group were significantly lower than those in both model group and drug carrier group, while intracellular SOD activity was much higher than that in other two groups (P<0.05). Icaritin also reduced the apoptotic ratios of hepatocytes induced by CCl4 compared with model group ( P<0.05 or 0.01). In the in vivo experiment, icaritin treatment significantly reduced serum levels of ALT and AST compared with model group (P<0.05) and greatly improved CCl4-induced liver histopathological injuries and collagen Ⅰ deposition in the liver tissues.ConclusionIcaritin treatment can attenuate CCl4-induced cirrhosis in rats, at least in part, by protecting the hepatocytes from peroxidation product.