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目的探讨亚低温对脑缺血/再灌注大鼠细胞骨架蛋白血影蛋白αⅡ(spectrinαⅡ)及卡配因(calpain)、胱冬酶-3(caspase-3)等相关蛋白酶的影响。方法采用线栓法建立大鼠大脑中动脉阻塞(MCAO)及再通模型,将其随机分为假手术组、常温缺血再灌注组(常温组)及亚低温缺血再灌注组(亚低温组),分别于再灌注后不同时间点采用免疫组化法检测各组大鼠血影蛋白αⅡ、卡配因Ⅰ及胱冬酶-3的表达。结果脑缺血再灌注组大鼠梗死灶中心区血影蛋白αⅡ染色消失;梗死灶周围缺血区血影蛋白αⅡ阳性细胞数量呈动态变化过程:再灌注2 h时,脑缺血区血影蛋白αⅡ阳性细胞数量较假手术组开始减少,随着再灌注时间延长,其阳性细胞数量进一步减少,于24 h时达到峰值;与相应常温组相比,亚低温组大鼠血影蛋白αⅡ阳性细胞数量明显大于前者,而卡配因Ⅰ及胱冬酶-3阳性细胞数量则较常温组明显减少。结论亚低温可以抑制局灶性脑缺血再灌注大鼠蛋白酶卡配因Ⅰ、胱冬酶-3的表达,减缓细胞骨架蛋白血影蛋白αⅡ的降解,从而发挥一定程度的脑保护效应。
Objective To investigate the effects of mild hypothermia on the cytoskeleton proteins spectrin α Ⅱ and calpain, caspase-3 and other related proteases in rats with cerebral ischemia / reperfusion. Methods The middle cerebral artery occlusion (MCAO) and recanalization models were established by thread occlusion. The rats were randomly divided into sham operation group, normal temperature ischemia reperfusion group (normal temperature group) and mild hypothermia ischemia reperfusion group (mild hypothermia Group) were used to detect the expression of spectrin αⅡ, Caspase Ⅰ and caspase-3 in each group by immunohistochemistry at different time points after reperfusion. Results Cerebral ischemia-reperfusion group in the infarct center of the spectrin α Ⅱ staining disappeared; ischemia zone ischemic area spectrin α Ⅱ positive cells showed a dynamic process: 2 h after reperfusion, blood in the ischemic area Compared with the sham-operation group, the number of αII-positive cells in the hypothermia group began to decrease. With the prolongation of reperfusion time, the number of positive cells decreased further and reached the peak at 24 h. Compared with the normal temperature group, The number of cells was significantly larger than the former, and the number of card-fitting factor I and caspase-3 positive cells was significantly reduced compared with the normal temperature group. Conclusion Mild hypothermia can inhibit the expression of protease card factor I and caspase-3 in focal cerebral ischemia-reperfusion rats and slow down the degradation of cytoskeletal protein spectrin αⅡ, which can exert a protective effect on brain.