Nitric oxide diminishes apoptosis and p53 gene expression after renal ischemia and reperfusion injury

Background. The role of nitric oxide in the ischemic injury of the kidney i s still controversial. The aim of this study was to reevaluate the benefici al effect of exogenous nitric oxide and define its effects as regulator of gene p53 expression and apoptosis in the ischemic renal injury, Methods. Sprague-Dawley rats mere subjected to 75 min of renal warm ischemi a and contralateral nephrectomy, The animals were divided into six groups ( n=6 per group): Two sham groups at 4 and 24 hr, two ischemic control (IC) a t same times and two treated groups (Na-NP), studied at same intervals, whe re sodium nitroprusside (5 mg/kg) was given 15 min before reperfusion. The parameters evaluated included: serum creatinine, blood urea nitrogen, neutr ophil infiltration determined by myeloperoxidase, gene p53 expression deter mined by reverse transcriptase polymerase chain reaction, apoptosis determi ned by peroxidase in situ technique and light histology. Results. There were significant improvements in serum creatinine and blood urea nitrogen at 24 hr in the NA-NP group when compared with the IC group ( P<0.05). Myeloperoxidase levels were higher in the IC when evaluated agains t the Na-NP groups. Na-NP exhibited a downregulating effect in the expressi on of gene p53 when compared to the IC group. Apoptosis was more evident in the IC group and had moderately increased histological damage when compare d to the Na-NP group. Conclusions. Nitric oxide demonstrated a protective effect in the ischemic injury of the kidney and exerted an antiapoptotic action dowregulating the expression of gene p53.