目的 探讨亚低温对大鼠全脑缺血再灌注损伤后神经元凋亡的影响.方法 选取成年雄性健康清洁级Wistar大鼠42只,随机分为假手术组、对照组及亚低温组.亚低温组和对照组采用大鼠4条血管阻断全脑缺血模型(Pulsinelli-4VO法)制备大鼠全脑缺血再灌注模型,假手术组仅切开颈部皮肤和肌层暴露双侧椎动脉和颈动脉,不行椎动脉凝闭和颈总动脉夹闭.假手术组和对照组置于室温下,亚低温组给予亚低温处理.采用流式细胞仪对海马神经元Bcl-2、Bax表达进行测定.结果 假手术组、对照组及亚低温组神经元凋亡百分率及增殖指数比较,差异均有统计学意义(F=142.869,P＜0.01;F=153.993,P＜0.01).假手术组Bcl-2、Bax表达(均道值)微弱,在此忽略;对照组Bcl-2、Bax表达(均道值)与亚低温组比较,差异均有统计学意义(t值分别为63.747、28.803,P＜0.01);两组Bcl/Bax比值比较,差异亦有统计学意义(t=9.601,P＜0.01).结论 全身亚低温可有效干预大鼠全脑缺血再灌注损伤后神经元凋亡,其机制与Bcl-2、Bax的表达有关,受到二者比值的调控.%Objective To investigate the intervention effect of mild hypothermia on neuronal apoptosis after global cerebral ischemic reperfusion injury in rats. Methods 42 Wistar male rats were divided into sham operation group, control group and mild hypothermia group. Global cerebral ischemic reperfusion model was established in mild hypothermia group and control group by Pulsinelli - 4VO method. While the sham operation group was only given neck skin and muscular layer incision to expose bilateral vertebral artery and carotid artery, but occlusion of vertebral artery and carotid artery was not performed. The sham operation group and control group were in room temperature and the mild hypothermia group was in mild hypothermia environment. Flow cytometry was used to detect the expression of Bel - 2 and Bax in hippocampus. Results The nerve cell apoptosis percentage and proliferation index between sham operation group, control group and mild hypothermia group showed statistically significant difference ( F = 142. 869, P < 0. 01; F = 153. 993 , P < 0. 01 ) .The expression of Bel - 2 and Bax in sham operation group was ignored due to its weakness. The expression of Bel - 2 and Bax between control group and mild hypothermia group showed statistically significant difference ( t =63. 747 and 28. 803 , P <0. 01 ) . The Bcl/Bax between the two groups also showed statistically significant difference ( t =9. 601, P <0. 01 ) . Conclusion Whole body mild hypothermia can effectively decrease nerve cells apoptosis after global cerebral ischemic reperfusion injury and its mechanism is related to the expression of Bel - 2 and Bax and is regulated by the value of Bcl/Bax.
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