Hepatoprotective effects of total saponins isolated from Taraphochlamys affinis against carbon tetrachloride induced liver injury in rats.

In this study, rats were orally treated with the total saponins of Taraphochlamys affinis (TSTA) daily with administration of CCl4 twice a week for 8 weeks. Compared to the normal control, CCl4 induced liver damage significantly increased the activities of alanine aminotransferase (ALT), aspartate aminotransferase (AST) and alkaline phosphatase (ALP) in serum and decreased the activities of superoxide dismutase (SOD), catalase, glutathione peroxidase (GSH-Px), and glutathione reductase (GSH-Rd) in liver. Meanwhile content of hepatic malondialdehyde (MDA), which was oxidative stress marker, was increased. Histological finding also confirmed the hepatotoxic characterization in rats. Furthermore, proinflammatory mediators including tumor necrosis factor-α(TNF-α) in serum, prostaglandin E2 (PGE2), inducible enitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) in liver were detected with elevated contents, while expression of xenobiotic metabolizing enzyme--cytochrome P4502E1 (CYP2E1) was inhibited. The results revealed that TSTA not only significantly reversed CCl4 originated changes in serum toxicity and hepatotoxic characterization, but also altered expression of hepatic oxidative stress markers and proinflammatory mediators, combined with restoring liver CYP2E1 level. The results indicated that protective effect of TSTA against CCl4-induced hepatic injury may rely on its effect on reducing oxidative stress, suppressing inflammatory responses and improving drug-metabolizing enzyme activity in liver.