Ischemic postconditioning alleviates rat cerebral ischemia-reperfusion injury through the phosphoinositide 3-kinase signaling pathway
10.3760/cma.j.issn.1671-8925.2009.04.005
- VernacularTitle:缺血后处理通过PI3K信号通路抑制脑缺血再灌注损伤
- Author:
Li GONG
1
;
Zhi WANG
;
Song-Hua XIAO
;
Yun-Lin LIU
;
Hai-Hong ZHOU
;
Dai-Gang XING
Author Information
1. 烟台毓璜顶医院
- Keywords:
Ischemic postconditioning;
Focal cerebral isehemia;
Neuroprotection;
Phosphoinositide 3-kinase signaling pathway
- From:
Chinese Journal of Neuromedicine
2009;8(4):344-346
- CountryChina
- Language:Chinese
-
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.
