缺血后处理通过PI3K信号通路抑制脑缺血再灌注损伤  

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

作　　者：宫利 王志[3] 肖松华[2] 刘运林[4] 周海红[2] 邢诒刚[2] 

机构地区：[1]毓璜顶医院神经内科,烟台264000 [2]中山医科大学附属第二医院神经内科,广州510120 [3]中山医科大学附属第二医院麻醉科,广州510120 [4]山东省泰安市中心医院神经科,271000

出　　处：《中华神经医学杂志》2009年第4期344-346,共3页Chinese Journal of Neuromedicine

基　　金：广东省医学科研基金（A2008179）

摘　　要：目的研究缺血后处理（IP）对脑缺血再灌注损伤的影响及其机制。方法采用开颅机械闭塞法建立SD大鼠局灶性脑缺血模型，通过开放／夹闭双侧颈总动脉实现IP。24只大鼠按照随机数字表法分为IP组、非口组、LY294002＋IP组、DMSO＋IP组，每组6只，再灌注48h后测脑梗死面积；其中LY294002、DMSO于建模前1h侧脑室注入。结果各组左侧大脑皮层均可见清晰梗死灶，符合血管分布范围。其中IP组脑梗死面积（34．02％±7．17％）明显小于非IP组（57．05％±10．05％），差异有统计学意义（P〈0．05）；LY294002＋IP组脑梗死面积（73．41％±2．06％）明显大于DMSO＋IP组（35．76％±1．51％），差异有统计学意义（P〈0．05）；DMSO＋IP组与碑组脑梗死面积差异无统计学意义（P〉0．05）。结论碑可减轻局灶性脑缺血大鼠的脑缺血再灌注损伤，PI3K信号通路参与其作用机制。Objective To investigate the neuroprotective effect of ischemic postconditioning （IP） against cerebral ischemia-reperfusion injury and the role of phosphoinositide 3-kinase （PI3K） signaling pathway in the neuroprotection. Methods Focal cerebral ischemia was induced in 24 SD rats by permanent distal middle cerebral artery occlusion and transient bilateral common 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 injected into the ventricular space on the ischemic side 1 h before ischemia. The cerebral infarct sizes were measured in all the 4 groups at 48 h after the reperfusion. Results Cerebral infarcts were observed in all the groups on the ischemic side, all locating in the left neocortex and the middle cerebral artery territory. At 48 h 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 infarct size between DMSO＋IP group and IP group （P〉0.05）. Conclusion IP ameliorates cerebral reperfusion injury in rats, and the mechanism of this neuroprotective effect involves the preservation of PI3K activity.

关 键 词：缺血后处理 局灶性脑缺血 神经保护 PI3K信号通路 

分 类 号：R686[医药卫生—骨科学]