Ischemic postconditioning modified renal oxidative stress and lipid peroxidation caused by ischemic reperfusion injury in rats.

Several recent studies have shown that ischemic postconditioning (IPostC) protects hears from ischemic reperfusion insults in various animal models. However, the mechanism of IPostC remains unclear. In the present study, we investigated the hypothesis that PostC protected kidneys against ischemic reperfusion injury by modifying renal oxidative stress and lipid peroxidation. Rats underwent 45 minutes of renal pedicle ligature followed by reperfusion for 1, 3, 6, 12, or 24 hours. IPostC was performed using 6, 10 second cycles of reperfusion and 10 seconds of renal pedicle occlusion at the end of the ischemia. Our data showed that IPostC attenuated renal dysfunction, significantly increasing the activity of antioxidases, including superoxide dismutase (SOD), catalase (CAT), and glutathione perokidase (GSH-Px) in renal homogenates, and concentrations of GSH and SOD expression. The level of malondialdehyde (MDA) and the activity of myeloperoxidase (MPO) were significantly decreased in IPostC rats. These results indicated that the protective effects of IPosC may be related to modification of renal oxidative stress and lipid peroxidation caused by ischemic reperfusion injury in rats.