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Journal of Pharmaceutical and Biomedical Analysis 2018-Oct

Restorative activity of aqueous extract Mangifera indica leaves against CCl4 induced hepatic damage in rats.

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Hanaa Salem Saleh Gazwi
Magda Ewis Mahmoud

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Abstract

Hepatic diseases remain problematic throughout the world. There are no drugs that completely restore hepatic capacity and help to regenerate liver cells. Therefore, the present examination was intended to investigate the hepatoprotective impacts of Mangifera indica (M. indica) leaf aqueous extract at two doses (200 and 400 mg/kg body weight (b w) for 6 weeks. Liver damage was induced by CCl4 and the extent of damage was measured by body weight gain, feed efficiency, and liver index, and by assessing hematological, biochemical parameters, and liver histology. Results show that phytochemical analysis revealed the presence of important phytochemicals like flavonoids, phenols, steroids, glycosides, saponins and terpenoids. Also, aqueous extract of M. indica showed that the total phenolic contents (86.20 ± 2.6 μg GEA/mg),flavonoid contents (42.64 ± 3.1 μg QE/mg) and antioxidant activities (DPPH) were 92.58 ± 4.1. The 50% inhibitory concentration (IC50) was 0.467 μg ml-1. CCl4 caused a significant decrease in food intake, weight gain, feed efficiency ratio, and liver index, and also in the serum protein, albumin, globulin, high-density lipoprotein (HDLc), and CAT levels. CCl4 also caused an increase in serum AST, ALT, total cholesterol (TC), triglyceride (TG), low-density lipoprotein (LDLc), very low-density lipoprotein (VLDLc), and MAD. However, treatment with M. indica revealed attenuation of liver function, serum biomarker levels that had been increased by chronic CCl4 intoxication. M. indica (400 mg/kg of b w) showed a greater reduction in the biomarker levels compared with M. indica (200 mg/kg of b w) and silymarin. These results were supported by histopathological examination of liver sections. Collectively, this study indicates that M. indica leaf aqueous extract alleviates the harmful effect of CCl4-induced hepatic damage.

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