The Protective Effect And Mechanism Of Hypothermia On Global Cerebral Ischemia-repefrusion Brain Injury Of Rat

Objectives: Study of hypothermia on global cerebral ischemia reperfusionbrain injury protective effect and its mechanism of rat.Methods: choice one hundred and fifty male wistar rats weighing280-320g and were randomly divided into three groups of fifty animals sham, tenminutes global cerebral I／R, hypethermia-global cerebral I／R. we are usedrats with global cerebral ischemia-reperfusion model In this study, the time ofglobal cerebral ischemia is ten minutes, and the time of reperfusion weredistributed to4h injury,24h injury,48h injury,72h injury, and one week injury.By formalin-fixed brain tissue slices，we observed global cerebral ischemia andreperfusion in rat hippocampal CA1neurons after24h by H&E staining andusing high-powered microscopes to compare each group of neurons in rathippocampal CA1number of surviving. When the reperfusion time arrived, wecan measure it’s Nerve function between the groups with modified neurologicalseverity score (NSS). We analyzed ASK1and ASK1phosphorylation status anddistribution of the binding protein blots by differential centrifugation with globalcerebral ischemia and reperfusion after24h in rats’ brain tissue cells.Results:1. Stained by H&E,from hypothermia treatment group can significantlydecrease the number of neuronal death in the hippocampal CA1,andhypothermia treatment have protective effect on neurons under cerebralischemia and reperfusion.2. Through the improved NSS neurological score, confirmed the NSS scorecan significantly reduce by hypothermia treatment and the Neurological severity also significantly reduced under the global cerebral ischemia and reperfusion inrats.3. By Western Blot after cerebral ischemia and reperfusion after24h ASK1is activated, we confirmed that the activation status of ASK1in the postsynapticmembrane was increase following cerebral ischemia and reperfusion.Weobtained the activation of ASK1expression in10min I/R and hypothermiatreatment group.With respect to the sham group,10min I/R group and thehypothermia treatment group was significantly ASK1activation (pASK1), itsexpression significantly enhanced, with difference, with statistical significance(p<0.05).Versus10min I/R group, the degree of expression of hypothermiatreatment group was significantly lower than the activation of ASK110min I/Rgroup activated ASK1, a difference, with statistical significance (p<0.05).Conclusion:1. Hypothermia treatment can protect nerve tissue and reduce the death ofnerve cells after cerebral ischemia reperfusion.2. Hypothermia treatment can significantly reduce the damage of thenervous system function after cerebral ischemia and reperfusion.3. After cerebral ischemia reperfusion injury, protective effect ofhypothermia treatment may be through inhibiting the activation of ASK1,thereby inhibiting nerve cell death.