Effect of Acacia nilotica Against Nephrotoxicity Induced by Gentamicin in Rat: Role of Antioxidants, Anti-Inflammatory and Antiapoptotic Markers
Effect of Acacia nilotica Against Nephrotoxicity Induced by Gentamicin in Rat: Role of Antioxidants, Anti-Inflammatory and Antiapoptotic Markers
Saed A. Althobaiti1, Safa H. Qahl2, Layaly Elsigar1, Lobna M.A. Gurafi1, Zeinab Kanani1, Mohamed Mohamed Soliman3* and Omaima Nasir1
ABSTRACT
The generation of reactive oxygen species appears to be responsible for gentamicin nephrotoxicity. Recent research has shown that Acacia nilotica extract (AN) retains antioxidant and anti-inflammatory activity. This study assessed AN’s inhibitory impact on rat nephrotoxicity induced by gentamicin. Twenty-four male Wister rats have sub-divided into 4 groups, the control one received saline; the second group was administered with AN extraction (5%) for fifteen days; group-3 rats were daily injected intraperitoneally with gentamicin (100 mg/kg) for fifteen days, and groups 4 include rats injected with gentamicin and with AN extraction (5%) for fifteen days as stated in groups 2 and 3. An identical normal saline volume was administered to control and gentamycin-treated rats. Serum was extracted for chemistry analysis. The tissue samples were taken for both histopathological and immunohistochemistry studies and the renal gene expression. Gentamicin significantly increased serum creatinine, urea, and uric acid. It decreased the levels SOD, catalase and GSH, with significant increases of the malondialdehyde (MDA). Co-treatment of gentamicin and AN significantly improved the aforementioned parameters through increased considerably antioxidant activity as well as up-regulation in the expression of HO-1 and Nrf2. Moreover, it showed antiapoptotic activity and down-regulation of the cox2, NF-kB, and TGF-β expression that induced by the gentamycin. Co-treatment of gentamicin and AN normalized renal injuries induced by the gentamycin administration at cellular levels. AN treatment induced ameliorative impacts against gentamycin induced nephrotoxicity at the histological, biochemical indices and the molecular levels.
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