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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和Bax表达的动态影响,探讨亚低温脑保护作用的机制。方法:实验于2002-01/12在江苏省麻醉医学研究所(省级重点实验室)完成。实验动物选择126只SD雄性大鼠随机分为假手术组、常温缺血组和亚低温缺血组。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,分别在再灌注后4,8,24,48,72,96h,7d,7个时间点取脑标本,进行Bcl-2和Bax免疫组织化学及苏木精-伊红染色。结果:与常温组相比,全身亚低温组海马CA1区死亡细胞数明显减少[常温比亚低温24h:(195±18)比(214±20)个/mm,P<0.05;48h:(185±17)比(215±21)个/mm,P<0.01;72h:(130±20)比(200±17)个/mm,P<0.01)];Bcl-2蛋白免疫反应强度峰值增高,持续时间延长[灰度值:常温比低温:24h(40±8比57±8,P<0.01);48h(42±6比55±8,P<0.01);72h(38±4比41±6,P<0.01)]。Bax蛋白免疫反应强度峰值减低,持续时间缩短[灰度值:常温比低温24h(32±4比24±5,P<0.05);48h(30±7比24±6,P<0.05);72h(26±4比22±5,P<0.05)]。结论:全身亚低温对缺血性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?
Objective: To investigate the protective effects of whole body hypothermia after cerebral ischemic reperfusion and its dynamic effects on the expression of Bcl-2 and Bax, and to explore the mechanism of hypothermic brain protection. METHODS: The experiment was performed at Jiangsu Provincial Institute of Anesthesiology (Provincial Key Laboratory) from January to December 2002. A total of 126 male SD rats were randomly divided into sham operation group, warm ischemia group and mild hypothermia ischemia group. The model of global cerebral ischemia-reperfusion was established by Pulsinelli four-vessel occlusion method. Immediate whole body mild hypothermia was performed for 4 hours. The brain samples were taken at 4, 8, 24, 48, 72, 96, 7 and 7 hours after reperfusion , Bcl-2 and Bax immunohistochemistry and hematoxylin-eosin staining. Results: Compared with normal temperature group, the number of dead cells in hippocampal CA1 area of the whole body hypothermia group decreased obviously (24h ± (195 ± 18) vs (214 ± 20) /mm, P <0.05; 48h: P <0.01; 72h: (130 ± 20) vs (200 ± 17) /mm, P <0.01). The peak intensity of Bcl-2 protein immunoreactivity increased, Duration of gray-scale: gray value at room temperature: 24h (40 ± 8 vs 57 ± 8, P <0.01); 48h (42 ± 6 vs 55 ± 8, P <0.01); 72 ± 38 6, P <0.01)]. The peak intensity of Bax immunoreactivity was decreased and the duration was shortened (gray value: normal temperature was lower than that of low temperature 24h (32 ± 4 vs 24 ± 5, P <0.05); 48h (30 ± 7 vs 24 ± 6, P < (26 ± 4 vs. 22 ± 5, P <0.05)]. Conclusion: Whole body hypothermia has a good protective effect on ischemic pyramidal cells. Can enhance the expression of anti-apoptotic Bcl-2 protein, prolong the duration of its expression, and decrease the expression of Bax with pro-apoptotic, and shorten the expression duration.