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目的 研究脑缺血再灌注后全身亚低温的脑保护作用及其对Bcl- 2、Bax表达的动态影响。方法 12 6只S -D雄性大鼠随机分为假手术组、常温组和亚低温组。采用Pulsinelli四血管阻断法制作大鼠全脑缺血再灌注模型 ,即刻全身亚低温 4h ,分别在 7个时间点取脑标本 ,进行Bcl- 2、Bax免疫组织化学及苏木精 -伊红染色。结果 与常温组相比 :亚低温组海马CA1区死亡细胞数明显减少 (P <0 .0 1) ;Bcl - 2蛋白免疫反应强度峰值增高持续时间延长 ;Bax蛋白免疫反应强度峰值减低 ,持续时间缩短。结论 全身亚低温对缺血再灌注锥体细胞损害有较好的保护作用。可增强具有抗凋亡的Bcl- 2蛋白的表达 ,延长其表达持续时间 ;而减弱具有促凋亡的Bax表达 ,同时缩短其表达持续时间。此可能是亚低温对缺血再灌注脑组织损害产生保护作用的分子机制之一。
Objective To investigate the protective effects of general mild hypothermia after cerebral ischemia and reperfusion and its dynamic effects on the expression of Bcl-2 and Bax. Methods Twelve S-D male rats were randomly divided into sham operation group, normal temperature group and mild hypothermia group. The model of global cerebral ischemia-reperfusion in rats was made by Pulsinelli four-vessel occlusion method. Immediate whole body mild hypothermia was performed for 4 hours. Brain samples were taken at 7 time points. Immunohistochemistry of Bcl-2, Bax and hematoxylin-eosin dyeing. Results Compared with the normal temperature group, the number of apoptotic cells in hippocampal CA1 subregion decreased significantly (P <0.01), the duration of peak increase of Bcl - 2 immunoreactivity increased, the peak of Bax protein immunoreactivity decreased, and the duration shorten. Conclusion The whole body mild hypothermia has a good protective effect on the damage of pyramidal cells after ischemia-reperfusion. Can increase the expression of anti-apoptotic Bcl-2 protein and prolong the expression duration of Bcl-2 protein, and decrease the expression of Bax with pro-apoptotic protein while shortening the expression duration of Bcl-2 protein. This may be one of the molecular mechanisms of hypothermia on the protection of brain tissue against ischemia-reperfusion injury.