Hepatoprotective effects of Ginkgo biloba against carbon tetrachloride induced hepatic injury in rats

Objectives: To assess the protective activity of Ginkgo biloba (GB) against CCl4 induced hepatotoxicity in rats and probe into its mechanism of action. Methods: Liver damage was induced in Wistar rats by administering (150-250 g) CCl4 (0.5 ml/kg, i.p.) once daily for 7 days. GB (50 mg/kg, i.p.) was given for one week. Silymarin (200 mg/kg, p.o.) was given as a reference drug. Levels of marker enzymes (AST, ALT, ALP) and total proteins (TP), albumin (Alb) were estimated in serum. A probe into the mechanism of action was attempted by estimating thiobarbituric acid reactive substances (TBARS) and glutathione (GSH) levels in liver homogenates in order to evaluate the degree of lipid peroxidation. Histopathological studies were also done to confirm the biochemical changes. Results: The mean ± SEM serum AST, ALT, ALP levels in control animals were 66.8 ± 4.2, 31.1 ± 2.0 and 445.3 ± 23.1 IU/L respectively whereas in CCl₄ treated rats, the level rose to 319.6 ± 22.7, 192.8 ± 16.0 and 809.3 ± 65.3 IU/L respectively. GB reduced the AST, ALT and ALP levels to 55.5 ± 5.3, 36.5 ± 3.6 and 489.6 ± 43.9 IU/L respectively. Silymarin reduced AST, ALT and ALP levels to 51.8 ± 5.2, 30.8 ± 3.4 and 437.8 ± 35.7 IU/L respectively. There was a significant decrease in serum TP and Alb levels after CCl₄, which was reversed by GB and silymarin. The tissue mean ± SEM values of TBARS and GSH in control animals were 3.1 ± 0.1 nmol of malondialdehyde/g of wet tissue and 1.9 ± 0.1 mg/g of wet tissue respectively. In CCl₄ treated animals, the TBARS and GSH levels were 3.91 ± 0.41 and 1.97 ± 0.11 respectively. GB reduced TBARS to 2.4 ± 0.09 nmol of MDA/g of wet tissue and increased GSH level to 2.4 ± 0.1 mg/g of wet tissue. Silymarin reduced TBARS to 2.1 ± 0.2 nmol of MDA/g of wet tissue and increased GSH level to 2.5 ± 0.17 mg/g of wet tissue. Conclusion: GB has protected the liver from CCl₄ damage. Probable mechanism of action is by protection against oxidative damage produced by CCl₄.