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目的探讨亚低温对局灶性脑缺血再灌注后生存素(Survivin)及半胱氨酸天冬氨酸蛋白酶-3(Caspase-3)表达的影响。方法用线拴法制作大鼠大脑中动脉闭塞(MCAO)局灶脑缺血再灌注模型,随机将168只SD大鼠分为假手术组、常温组和亚低温组,两个缺血组各分为缺血2、3、6、8 h后再灌注4 h、24 h、72 h、1周、2周然后处死。亚低温组于缺血后30 min,实施病灶侧亚低温持续4 h,经免疫组化测定Survivin、Caspase-3阳性细胞数。结果 与常温组各时间点相比,亚低温组各时间点缺血侧Survivin表达水平显著增高,Caspase-3表达明显降低(P<0.05,P<0.01)。结论 局灶性脑缺血后30 min,应用局部亚低温能够减少梗塞面积,促进脑缺血后神经功能恢复,这种保护作用的产生与亚低温促进梗塞灶周围半暗带Survivin表达,抑制Caspase-3的表达从而抑制神经元凋亡有关。
Objective To investigate the effects of mild hypothermia on the expression of Survivin and Caspase-3 after focal cerebral ischemia-reperfusion. Methods The focal cerebral ischemia-reperfusion model of middle cerebral artery occlusion (MCAO) in rats was made by tethering method. 168 SD rats were randomly divided into sham operation group, normal temperature group and mild hypothermia group. Ischemia 2, 3, 6, 8 h after reperfusion 4 h, 24 h, 72 h, 1 week, 2 weeks and then sacrificed. Mild hypothermia group 30 min after ischemia, the implementation of hypocalocal lesions on the side continued for 4 h, Survivin, Caspase-3 positive cells by immunohistochemistry. Results Compared with normal temperature group, the expressions of Survivin and Caspase-3 in ischemia group were significantly increased at each time point (P <0.05, P <0.01). Conclusion Local hypothermia at 30 min after focal cerebral ischemia can reduce infarct size and promote neurological recovery after cerebral ischemia. This protective effect and hypothermia promote the expression of Survivin in the penumbra around the infarct and inhibit Caspase -3 expression and thereby inhibit neuronal apoptosis.