Background
The chemoprevention of chemically-induced hepatotoxicity is a crucial means of minimizing susceptibility to hepatic carcinogenesis and plants remain a rich source of anti-hepatotoxicants with antioxidant properties.
Conclusion
These findings suggest that the mechanism of hepatoprotection elicited by MECF and EF, involve its antioxidative properties and regulation of Ca(2+) homeostasis.
Methods
Adult male Wistar rats were orally administered MECF or EF (125 - 500 mg/kg bwt/5mL) or silymarin (25 mg/kg bwt/5 mL) separately for three days before intervention with an intraperitoneal dose of CCl4. Biomarkers of liver and kidney toxicity as well as Ca(2+) regulation were evaluated.
Objective
The protective role of defatted-methanol (MECF) and ethyl acetate fractions (EF), obtained from Leaves of Cnestis ferruginea in rats induced with carbon tetrachloride (CCl4) toxicity was investigated. Materials and
Results
Pre-treatment with MECF and EF significantly (P < 0.05) decreased the activities of serum alanine and aspartate aminotransferases, levels of urea, creatinine and cholesterol. A significantly (P < 0.05) enhanced Ca(2+) -ATPase activity and lowered levels of membrane cholesterol: Phospholipid ratio were observed in liver microsomes of pre-treated as compared to CCl4 -only treated rats. Rat liver superoxide dismutase activity was enhanced by 125 mg/kg and 250 mg/kg of EF and MECF, while decreases were observed at 500 mg/kg. MECF and EF, like silymarin, attenuated CCl4 -induced hepatotoxicity, microsomal membrane Ca(2+) -ATPase inactivation and renal dysfunction. Phytochemistry of MECF revealed the presence of anthraquinones, cardiac and flavone glycosides, tannins and trihydroxyl phenol.