Ischemic postconditioningalleviates rat cerebral ischemia-reperfusion injury through the phosphoinositide 3-kinasesignaling pathway

：Objective To investigatethe neuroprotective effect of ischcmic posteonditioning (IP)against cerebralischemia-reperfusion injury and the role of phosphoinositide 3-kinase(P13K)signalingpathway in the neuroprotection. Methods Focal cerebral ischernia was induced in 24 SD ratsby permanent distal middle cerebral artery occlusion and transient bilateral comlllOncarotid artery occlusion.The rats were then randomized into 4 groups for treatment withIP,LY294002+IP,DMSO+IP,or without IP.In LY294002+IP and DMSO+IP groups,LY294002 or DMSOwas injcoted into the ventricular space on the ischemic side 1 h before ischemia.Thecerebral infarct sizes wgre measured in all the 4 groups at 48h after thereperfusion.Results Cerebral infarcts were observed in all the groups on theischemicside,all locating in the left neocortex and the middle cerebral artery territory.At48hafter reperfusion,the infarct size was significantly smaller in rats with IP(34.02%±7.17%)thanin those without IP(57.05%±10.05%)(P＜0.05),and significantly larger in LY294002+IP group(73.41%±2.06%)thanin DMSO+IP group(35.76%±1.51%)(P＜0.05).No significant difference was found in the infarctsizebetween DMSO+IP group and IP group(P＞0.05).Conclusion IP ameliorates cerebral reperfusion mjury inrats,and the mechanism of this neuroprotective effect involves the preservation of PI3Kactivity. Key words: Ischemic postconditioning; Focal cerebralisehemia; Neuroprotection; Phosphoinositide 3-kinase signaling pathway