局灶性脑缺血预处理上调大鼠梗死区周围巢蛋白的表达

Focal cerebral ischemic preconditioning promotes the expressionof NESTIN around infarct area in rat brain

目的观察局灶性脑缺血预处理(IP)对巢蛋白(NESTIN)表达的影响,探讨NESTIN与脑缺血耐受(BIT)的关系及可能的内源性神经保护机制。方法 45只SD雄性大鼠随机分为脑缺血预处理(CIP)组、大脑中动脉阻塞(MCAO)组、假手术(sham)组。采用TTC染色测定脑梗死体积,光镜下观察脑组织病理改变,免疫组织化学染色和图像分析评价各组NESTIN的表达。结果再灌注24及72 h,CIP组脑梗死体积比分别为12.4%±3.2%、9.8%±1.9%,较MCAO组的18.5%±3.7%、15.8%±3.5%明显减小(P<0.05),免疫组化NESTIN阳性细胞数及Western blot测定缺血侧脑组织的NESTIN蛋白表达水平,均高于同时间段的MCAO组(P<0.05)。结论 CIP可有效减小局灶性脑缺血再灌注后的脑梗死体积,并促进梗死区周围脑组织表达敏感的胚性蛋白NESTIN,后者可能与BIT的脑保护机制有关。

Objective To investigate the expression of NESTIN in the ischemic tolerance induced by focal cerebral ischemic preconditioning. Methods Cerebral ischemic preconditioning （CIP） was induced by intraluminal filament middle cerebral artery for 20 rain. Middle cerebral artery occlusion （MCAO） was induced by intraluminal filament for 2, 72 h after IP. Forty five male SD rats were randomly divided into 3 groups （5 in each group） ： sham opera- tion group did not receive any treatment, MCAO group only received sham surgery and 2 h MCAO followed by 6, 24,72 h reperfusion respectively, and CIP group received simple 20 min ischemic preconditioning and the same sec- ond procedure. At end of reperfusion the infarct volume was measured by TTC staining, and the expression of NESTIN was detected by immunohistochemistry in each group. Results At 24, 72 h after reperfusion, the infarct volumes of CIP group were 12.4% ±3.2% and 9.8% ± 1.9% , significantly less than those （ 18.5% ±3.7% and 15.8% ±3.5% ）of MCAO grouprespectively（P 〈0. 05）. The rate of NESTIN positive cells in the brain of MCAO group was significantly lower than that in the CIP group at 24, 72 h after reperfusion （P 〈 0. 05 ）, meanwhile, theduce the infarct brain volume following focal cerebral ischemia and promote the expression of sensitive embryogenic protein （ NESTIN）, which might be associated with the mechanism of BIT.