摘要目的 观察局灶性缺血预处理对小胶质细胞活化的影响,探讨小胶质细胞在内源性神经保护机制中的作用.方法 48只SD大鼠按随机数字表法分为空白对照组(SS+SS)、缺血预处理组(IPC+SS)、假手术+缺血组(SS+MCAO)、缺血预处理+再缺血组(IPC+MCAO),每组各12只.运用TTC染色、组织化学染色、透射电镜和图像方法分析比较各组大鼠梗死灶体积、超微结构及小胶质细胞活化的变化.结果 与SS+MCAO组相比,IPC+MCAO组脑梗死灶体积明显缩小,比较差异有统计学意义(P＜0.05),超微结构改变较轻.IPC+MCAO组及SS+MCAO组的小胶质细胞活化水平均较IPC+SS组增高,但二者相比,IPC+MCAO组明显低于SS+MCAO组,比较差异有统计学意义(P＜0.05).结论 小胶质细胞活化在脑缺血耐受中具有双重作用,其介导的轻微炎性过程可能是局灶性缺血预处理启动内源性神经保护的重要分子机制.

abstractsObjective To investigate the effect of focal cerebral ischemic preconditioning (IPC)on the activation of microglias to explore the endogenous neuroprotection of microglias. Methods SD rats were divided into 4 groups, in which the IPC (10 minutes)+MCAO group and SS (without IPC)+MCAO group received middle cerebral artery occlusion (MCAO, 2 h) followed by reperfusion (22 h),and the other 2 groups received SS+SS (blank controls) or IPC+SS (without MCAO). The infarct volume,ultrastructure and activation changes of microglias were evaluated in each group by riphenyltetrazolium chloride (TTC) staining, electron microscope and immunohistochemical staining, respectively. Results Compared with SS+MCAO group, the further reduction of infarct volume and slight ultrastructure changes were observed in the IPC+MCAO group. More severe pathological changes in the SS+MCAO group were observed than those in the IPC+MCAO group. In contrast with that in the IPC+SS group, the activation of microglias further increased in the SS+MCAO and IPC+MCAO group; while that in the SS+MCAO was significantly higher than that in the IPC+MCAO group (P＜0.05). Conclusion Microglias play a dual role in the induction of ischemic tolerance, and inflammation mediated by activation of microglias might be a key event in the mechanism of endogenous neuroprotection induced by focal IPC.