Experimental and Mathematical Model for the Hepatoprotective Effect of Methanolic Extract of Moringa oleifera Leaf against CCl4- induced Hepatotoxicity in Sprague Dawley Male Albino Rats

摘要

Background: To evaluate the in-vivo antioxidant potential of methanolic extract of Moringa oleifera leaf against CCl_4- induced toxicity in rats. Methods: The phytochemicals present in the plant were determined using standard methods. Male albino rats were made hepatotoxic by orally administered with CCl₄ (20% CCl₄ in olive oil) twice per week for a period of four weeks. They were orally treated with Moringa oleifera leaf extract (250 and 500 mg/kg body weight) and silymarin (200 mg/kg body weight) once a day for 28 days. Biochemical assays such as: plasma levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), gamma glutamyl transferase (GGT), total cholesterol (TC), triglyceride (TG), total protein (TP), lipid peroxidation, catalase, reduced glutathione, superoxide dismutase, glutathione peroxidise and histopathology were used to assess damage caused by CCl₄ and the protective effects of the extract on the liver tissues. The mathematical model was analysed using Maple 18.0 software Results: Phytochemical screening of Moringa oleifera shows the presence of secondary metabolites like tannin, anthocyanine, steroid, anthraquinones, terpenoids and saponin. The extract does not have any effect on the hematological parameters. The results showed that oral administration of M. oleifera significantly reduced (P4. Treatment with the extract was also found to significantly increase (P4. Mathematical model analysis shows that treating the rats with Moringa oleifera leaf extract gives an optimal result just like the standard drug which is in conformity with the experimental result of the bench work. Conclusion : The result suggested that M. oleifera exhibits potent hepatoprotective effects on CCl₄-induced liver damage in rats due to the increase of antioxidant-defence system activity and the inhibition of lipid peroxidation.