Ascorbic acid ameliorates isoniazid-rifampicin-induced hepatocellular damage in rats.

Background: Phyto-constituents are widely recognized for hepatoprotective effects. Ascorbic acid is extensively studied for the radical scavenging effect. The objective of the present study was to evaluate the hepatoprotective effect of ascorbic acid against isoniazid and rifampicin-induced liver damage in rats. Methods: Wistar rats were used in the present study. Hepato-cellular damage was produced by the administration of isoniazid (100 mg/kg) and rifampicin (100 mg/kg) for 21 days. Ascorbic acid was administered in the dose of 50, 100, and 200 mg/kg body weight. At the end of the study, blood was collected and biochemical studies were performed to determine antioxidant status. Results: Ascorbic acid administration (50, 100, and 200 mg/kg body weight) caused restoration of serum glutamic oxaloacetic transaminase, serum glutamic-pyruvic transaminase, and serum alkaline phosphatase. The level of superoxide dismutase and catalase were also restored due to the administration of ascorbic acid. There was a decrement in the expression of tumor necrosis factor-α, interleukin-1β, interleukin-6, malondialdehyde and nitric oxide. Conclusion: The outcome of the study established ascorbic acid as a notable hepatoprotective effect. The radical scavenging and cytokine suppression effect is the possible mechanism associated with the hepatoprotective effect of ascorbic acid.