Phellinus rimosus Protects Carbon Tetrachloride-Induced Chronic Hepatotoxicity In Rats: Antioxidant Defense Mechanism

Abstract The capacity of a chemical to produce liver damage in vivo. often results from interaction of a series of complex cellular processes that are involved in the uptake, biotransformation, and elimination of potentially toxic compounds. Reactive oxygen species (ROS) are involved in the pathophysiology of a number of human ailments including carbon tetrachloride-induced hepatotoxicity. Several phytochemicals found in natural products associated with pharmacological attributes have been reported to scavenge free radicals. Chronic hepatotoxicity was induced by intraperitoneal injection of CCl4 (1.5 ml/kg body wt.) in paraffin oil. Administration of ethyl acetate extract of Phellinus rimosus. (Berk) Pilat (Hymenochaetaceae) 25 and 50 mg/kg body wt. orally prior to CCl4 injection significantly and dose-dependently protected the CCl4-mediated elevation of serum transaminases such as glutamate pyruvate transaminase (GPT) and glutamate oxaloacetate transaminase (GOT), and of serum alkaline phosphatase (ALP). The hepatic antioxidant status, superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) activities and the reduced glutathione (GSH) level was reduced in the CCl4 alone treated animals. Administration of extract prior to CCl4 challenge restored the hepatic antioxidant status. The antioxidant status in the blood of CCl4 alone treated animals also decreased compared with the normal as well as extract plus CCl4 treated animals. The activity of a phase I enzyme, aniline hydroxylase, showed profound increase in the CCl4 alone treated animals that was reduced in the extract plus CCl4 treated group. The activity of phase II enzyme glutathione S.-transferase (GST) was also elevated in the liver and blood of animals treated with the extract compared with the CCl4 alone treated group. The serum and liver lipid peroxidation levels were elevated in the CCl4-treated animals compared with the normal or extract plus CCl4 treated animals. The findings thus suggested ethyl acetate extract of P. rimosus. protects CCl4-induced chronic hepatotoxicity in rat by restoring the liver antioxidant status, inhibiting phase I and enhancing phase II enzyme activities.