ischemic postconditioning attenuates bilateral renal ischemia-induced cognitive impairments

Introduction: acute kidney injury (aki) is a frequent complication of kidney failure withhigh mortality, leading to brain dysfunction. this study aimed to investigate the possibleprotective effect of ischemic postconditioning (ipo) against brain dysfunction induced bybilateral renal ischemia (bri).methods: male wistar rats underwent bri, sham, or ipo surgery 24h and 1w after reperfusion.the rats’ explorative behaviors and motor function were evaluated by an open field, rotarod,and wire grip tests. the cognitive function was assessed by passive avoidance learning andmorris water maze tests. western blotting was performed to evaluate hippocampal brain-derived neurotrophic factor (bdnf) expression.results: the impairment of balance function induced by bri was not reversed; however,passive avoidance learning impairment was reversed by postconditioning 24h after reperfusion.ipo increased muscle strength compared to the bri group; however, explorative behaviors andbalance function had no difference 1w after reperfusion. bri significantly decreased the bdnfprotein expression in the hippocampus, and postconditioning increased 24h after reperfusion.conclusion: the obtained results demonstrated the deleterious effect of bri on cognitiveand balance function 24h after reperfusion. ipo indicated a curative effect against cognitivedysfunction probably by enhancing bdnf protein expression in the hippocampus.