Hepatoprotective activity of Thunbergia laurifolia Linn extract in rats treated with ethanol: In vitro and in vivo studies

Primary cultures of rat hepatocyte and rats were used as the in vitro and in vivo models to evaluate the hepatoprotective activity of aqueous extract from Thunbergia laurifolia (TLE). Ethanol was selected as hepatotoxin. Silymarin (SL) was the reference hepatoprotective agent. In the in vitro study, MTT reduction assay and release of transaminases (ALT and AST) were the criteria for cell viability. Primary cultures of rat hepatocyte (24 h culturing) were treated with ethanol (96 μl/ml) and various concentrations of TLE (2.5, 5.0, 7.5 and 10.0 mg/ml) or SL (1, 2 and 3 mg/ml) for 2 h. Ethanol decreased MTT (%) nearly by half. Both TLE and SL increased MTT reduction and brought MTT (%) back to normal. Ethanol induced release of ALT and AST was also reduced by TLE (2.5 and 5.0 mg/ml) and SL (1 mg/ml). In the in vivo study, serum transaminases, serum triglyceride (STg) together with hepatic triglyceride (HTg) and histopathological examination were the criteria for evidences of liver injury. Ethanol (4 g/(kg day), po for 14 days) caused the increase in ALT, AST, HTg and centrilobular hydropic degeneration of hepatocytes. TLE at 25 mg/(kg day), po, or SL at 5 mg/(kg day), po, for 7 days after ethanol enhanced liver cell recovery by bringing HTg, ALT and/or AST back to normal. These results suggest that TLE and SL possess the hepatoprotective activity against ethanol induced liver injury in both primary cultures of rat hepatocyte and rats.