Publication:

Ascorbic acid attenuates ethanol induced apoptotic and oxidative response by blocking the Bax, Bcl2 and Caspase signaling pathways

Background Research evidence has demonstrated that oxidative stress plays important etiological role in pathogenesis of alcoholic liver disease. The agents having antioxidant property plays a promising therapeutic intervention in ALD. In our present study we investigate the effect of ascorbic acid on ethanol induced liver injury and molecular mechanism of ethanol induced apoptosis.

Methods Wistar albino rats were randomly divided into 4 groups with 6 animals in each group control, ethanol treatment 40% (2ml/100gm), ethanol+ascorbic acid 100mg/kg b.w. intra-gastric gavage, ethanol+silymarin 100mg/kg b.w. intra-gastric gavage for 21 days. Statistical analysis was carried out using one-way ANOVA followed by Tukey multiple comparision test.

Results Ethanol induced hepatotoxicity is evidenced by increased level of liver marker enzymes (AST, ALT, ALP and LDH) and lipid peroxidation whereas the level of antioxidants (SOD, CAT, GSH, VIT C and E) was significantly decreased. Our results are further supported by histopathological examination which shows drastic changes in liver architecture. Hepatic Bax, Bcl-2, Caspase 3 and Caspase 9 proteins expressions were altered. On contrary treatment with ascorbic acid ameliorated the changes induced by ethanol and improved liver architecture.

Conclusions Ascorbic acid as an antioxidant protect the liver from ethanol induced oxidative damage and apoptosis.