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

The role of nitric oxide in the ischemic injury of the kidney is still controversial. The aim of this study was to reevaluate the beneficial effect of exogenous nitric oxide and define its effects as regulator of gene p53 expression and apoptosis in the ischemic renal injury.

Sprague-Dawley rats were subjected to 75 min of renal warm ischemia 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) at same times and two treated groups (Na-NP), studied at same intervals, where sodium nitroprusside (5 mg/kg) was given 15 min before reperfusion. The parameters evaluated included: serum creatinine, blood urea nitrogen, neutrophil infiltration determined by myeloperoxidase, gene p53 expression determined by reverse transcriptase polymerase chain reaction, apoptosis determined by peroxidase in situ technique and light histology.

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 against the Na-NP groups. Na-NP exhibited a downregulating effect in the expression of gene p53 when compared to the IC group. Apoptosis was more evident in the IC group and had moderately increased histological damage when compared to the Na-NP group.

Nitric oxide demonstrated a protective effect in the ischemic injury of the kidney and exerted an antiapoptotic action dowregulating the expression of gene p53.