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Ischemic postconditioning alleviates rat cerebral ischemia-reperfusion injury through the phosphoinositide 3-kinase signaling pathway

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Author:
No author available
Journal Title:
CHINESE JOURNAL OF NEUROMEDICINE
Issue:
4
DOI:
10.3760/cma.j.issn.1671-8925.2009.04.005
Key Word:
缺血后处理;局灶性脑缺血;神经保护;PI3K信号通路;Ischemic postconditioning;Focal cerebral isehemia;Neuroprotection;Phosphoinositide 3-kinase signaling pathway

Abstract: Objective To investigate the neuroprotective effect of ischcmic posteonditioning (IP)against cerebral ischemia-reperfusion injury and the role of phosphoinositide 3-kinase(P13K)signaling pathway in the neuroprotection. Methods Focal cerebral ischernia was induced in 24 SD rats by permanent distal middle cerebral artery occlusion and transient bilateral comlllOn carotid artery occlusion.The rats were then randomized into 4 groups for treatment with IP,LY294002+IP,DMSO+IP,or without IP.In LY294002+IP and DMSO+IP groups,LY294002 or DMSO was injcoted into the ventricular space on the ischemic side 1 h before ischemia.The cerebral infarct sizes wgre measured in all the 4 groups at 48h after the reperfusion.Results Cerebral infarcts were observed in all the groups on theischemic side,all locating in the left neocortex and the middle cerebral artery territory.At48h after reperfusion,the infarct size was significantly smaller in rats with IP(34.02%±7.17%)than in those without IP(57.05%±10.05%)(P<0.05),and significantly larger in LY294002+IP group(73.41%±2.06%)than in DMSO+IP group(35.76%±1.51%)(P<0.05).No significant difference was found in the infarctsize between DMSO+IP group and IP group(P>0.05).Conclusion IP ameliorates cerebral reperfusion mjury in rats,and the mechanism of this neuroprotective effect involves the preservation of PI3K activity.

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