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Modulatory effect of Mangifera indica against carbon tetrachloride induced kidney damage in rats
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 CCl(4)-induced renal damage. Rats were treated intragastrically with 125, 250 and 500 mg...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Slovak Toxicology Society SETOX
2015
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4961916/ https://www.ncbi.nlm.nih.gov/pubmed/27486379 http://dx.doi.org/10.1515/intox-2015-0027 |
Sumario: | 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 CCl(4)-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 CCl(4) (3 ml/kg of 30% CCl(4), 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 CCl(4) treated rats the results showed significant (p<0.05) increases in serum Na+, K+, Cl(−), urea and creatinine. CCl(4) 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 MDA. Mangifera indica may present a great prospect for drug development in the management of kidney disease with lipid peroxidation as its etiology. |
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