尼莫地平对局灶性脑缺血再灌注损伤大鼠脑神经元的保护作用及其机制

目的： 探讨尼莫地平对局灶性脑缺血再灌注损伤大鼠脑神经元的保护作用及其对Bax和Bcl-2蛋白表达的影响并阐明其作用机制。方法：30只雄性Wistar大鼠随机分
为假手术组、模型组和尼莫地平组，每组10只。采用线栓法堵塞大鼠大脑中动脉制作脑缺血再灌注损伤模型。缺血2 h再灌注2 h后进行神经功能学评分。之后断头取脑，应用TUNEL染色及SP免疫组织化学方法观察脑组织梗死情况并检测Bax和Bcl-2蛋白的表达水平。结果：与模型组比较，尼莫地平组大鼠脑组织凋亡细胞数明显减少(P<0.05)，Bax蛋白表达水平减少(P<0.05)，Bcl-2蛋白表达水平增加(P<0.05)。形态学观察，模型组大鼠脑细胞坏死严重，水肿明显；尼莫地平组大鼠脑组织坏死细胞数减少，水肿情况有所改善。结论：尼莫地平对局灶性脑缺血再灌注损伤大鼠脑组织具有保护作用，其作用可能是通过下调Bax和上调Bcl-2相关蛋白表达从而抑制
脑神经元凋亡实现的。

Protective effect of nimodipine on neuron of rats with focal cerebral ischemia-reperfusion injury and its mechanism

Objective To investigate the protective effect of nimodipine on neuron of the rats with focal cerebral ischemia-reperfusion injury and the expressions of Bax and Bcl-2,and to clarify their mechanisms.Methods The focal cerebral-ischemia reperfusion model was induced by the middle cerebral artery occlusion(MCAO)method. 30male Wistar rats were randomly divided into sham operation,model,and nimodipine groups(n=10).The neurological deficit score was performed after 2hischemia following 2hreperfusion.The infarction was observed by TUNEL staining and the expressions of Bax and Bcl-2 were detected by SP immunohistochemistry method. Results Compared with model group,the number of apoptotic cells of the rats in nimodipine group was significantly decreased(P<0.05),the expression of Bax was significantly decreased(P<0.05),and the Bcl-2 expression was increased significantly(P<0.05).The morphological examination showed that the neurons of the rats in model group had serious necrosis and edema while the number of dead cells in nimodipine treatment group was reduced and the edema was improved.Conclusion Nimodipine has a protective effect on brain tissue of the rats with focal cerebral ischemia-reperfusion injury,which is closely related to the down-regulation of Bax and upregulation of Bcl-2and inhibition of the apoptosis of neuron.