Modulatory effect of Mangifera indica against carbon tetrachloride induced kidney damage in rats

Author:

Awodele Olufunsho1,Adeneye Adejuwon Adewale2,Aiyeola Sheriff Aboyade1,Benebo Adokiye Senibo3

Affiliation:

1. Department of Pharmacology, Therapeutics and Toxicology, Faculty of Basic Medical Science, College of Medicine, University of Lagos, Idi-Araba, Surulere, Lagos State, Nigeria

2. Department of Pharmacology, Faculty of Basic Medical Science, Lagos State University College of Medicine, Ikeja G.R.A., Lagos State, Nigeria

3. Department of Pathology and Forensic Medicine, Faculty of Basic Medical Science, Lagos State University College of Medicine, Ikeja G.R.A., Lagos State, Nigeria

Abstract

Abstract There is little scientific evidence on the local use of Mangifera indica in kidney diseases. This study investigated the reno-modulatory roles of the aqueous stem bark extract of Mangifera indica (MIASE) against CCl4-induced renal damage. Rats were treated intragastrically with 125, 250 and 500 mg/kg/day MIASE for 7 days before and after the administration of CCl4 (3 ml/kg of 30% CCl4, i.p.). Serum levels of electrolytes (Na+, K+, Cl, HCO3 ), urea and creatinine were determined. Renal tissue reduced glutathione (GSH), malondialdehyde (MDA), catalase (CAT), superoxide (SOD) activities were also assessed. The histopathological changes in kidneys were determined using standard methods. In CCl4 treated rats the results showed significant (p<0.05) increases in serum Na+, K+, Cl, urea and creatinine. CCl4 also caused significant (p<0.05) decreases in renal tissue SOD, CAT and GSH and significant (p<0.05) increases in MDA. The oral MIASE treatment (125–500 mg/kg) was found to significantly (p<0.05) attenuate the increase in serum electrolytes, urea and creatinine. Similarly, MIASE significantly (p<0.05) attenuated the decrease in SOD, CAT and GSH levels and correspondingly attenuated increases in MAD. Mangifera indica may present a great prospect for drug development in the management of kidney disease with lipid peroxidation as its etiology.

Publisher

Walter de Gruyter GmbH

Subject

Health, Toxicology and Mutagenesis,Pharmacology,Toxicology

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