Phytomedicinal Role of Pithecellobium dulce against CCl(4)-mediated Hepatic Oxidative Impairments and Necrotic Cell Death.

Present study investigates the beneficial role of the aqueous extract of the fruits of Pithecellobium dulce (AEPD) against carbon tetrachloride (CCl(4))-induced hepatic injury using a murine model. AEPD has been found to possess free radical (DPPH, hydroxyl and superoxide) scavenging activity in cell-free system. CCl(4) exposure increased the activities of various serum maker enzymes and intracellular reactive oxygen species (ROS) production. In line with these findings, we also observed that CCl(4) intoxication increased the lipid peroxidation and protein carbonylation accompanied by decreased intracellular antioxidant defense, activity of cytochrome P450 and CYP2E1 expression. DNA fragmentation and flow cytometric analyses revealed that CCl(4) exposure caused hepatic cell death mainly via the necrotic pathway. Treatment with AEPD both pre- and post-toxin exposure protected the organ from CCl(4)-induced hepatic damage. Histological findings also support our results. A well-known antioxidant vitamin C was included in this study to compare the antioxidant potency of AEPD. Combining all, results suggest that AEPD protects murine liver against CCl(4)-induced oxidative impairments probably via its antioxidative property.