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Abstract
Background Diabetic nephropathy, a serious complication ofdiabetes mellitus, is the most common cause of end stage renalfailure. Studies indicate that hydrogen sulfide(H2S) exerts its effect through the upregulation of SIRT1and increasing its activity. Aim of the work The aim of this study is to evaluate the protective role of H2S (using sodium hydrosulfide (NaHS) as an exogenous donor of H2S) against diabetic nephropathy (DN)through inhibition of apoptosis and reduction of oxidative stress in kidney, by activation of SIRT-1. Materials and Methods Sixty male rats were divided into four groups: control, DN, DN+ NaHS 30 omol/kg/day and DN+ NaHS100 omol/kg/day.Blood glucose,kidney function tests,SIRT1 activity, superoxide dismutase activity (SOD), malondialdehyde(MDA) andrelative gene expression of caspase 3and p53 by real time PCR in renal tissues were performed. Also, histopathological examination of renal tissue was done. Results DN rats had higher blood glucose levels, renal dysfunction as evidenced by increased serum creatinine,creatinine clearance, urinary albumin .They also had decreased SIRT1 activity levels, increased relative expression of caspase 3and p53,increased MDA and decreased SOD activity in renal tissues. NaHS decreased blood glucose, improved kidney functions, increased SIRT1 activity levels decreased relative expression of caspase 3and p53, decreased MDA and increased SOD activity in renal tissues with better results on administration of NaHS100 omol/kg/day.SIRT1 activity levels in renal tissues correlated negatively with the relative expression of caspase 3 and p53 in DN, DN+NaHS 30and DN+NaHS 100groups.Administration of NaHS alleviated renal histopathological changes in diabetic rats