Protective effect of tripterine on carbon tetrachloride-induced hepatic fibrosis in immature rats

This study was designed to investigate the hepatoprotective activity of Tripterine (Tri) against carbon tetrachloride (CCl4) induced hepatic fibrosis in rats by suppressing TGF-beta 1/Smad signaling. In this study, a total of forty healthy male Wistar rats were randomly divided into five groups, including normal control, CCl4-treated, Colchicine (Col)-treated (0.1 mg/kg, b.w.), Tri-treated (4, 8 mg/kg, b.w.). After a period of 6 weeks, liver and spleen indexes were calculated. The levels of liver biological activities such as alanine aminotransferase (ALT), aspartate aminotransferase (AST), hyaluronate (HA), laminin (LN), collagen type IV (COL4), and procollagen III (PCIII) were determined after Tri administration. Histopathological analysis of the liver tissues was also determined. Expression of hepatic gene TGF-beta Receptor I (T beta-RI), Smad3, Smad7, Collagen I and Collagen III, were detected using qRT-PCR. Tri was found to ameliorate liver injury, and hepatic fibrogenesis induced by CCl4 in rats. Tri could significantly decrease the contents of ALT and AST (P<0.01). Compared with the CCl4-treated group, levels of HA, LN, COL4 and PCIII were significantly increased, and Tri treatment significantly reduced the levels of four biomarkers in CCl4-induced rats (P<0.01). Liver morphological examination showed that Tri ameliorated CCl4-induced state of fibrotic septa, necrosis, and hepatic steatosis. The results of mRNA expressions studies displayed that Tri (8 mg/kg, b.w.) could inhibit T beta-RI, Smad3, Smad7, Collagen I and Collagen III expression in the liver tissues (P<0.01 or P<0.05). This study provides evidence of protective effects of Tri against CCl4-induced hepatic fibrosis by reducing inflammatory response in the liver.