摘要
目的研究不同程度亚低温对大鼠心肺复苏(CPR)后脑组织凋亡的影响。方法利用窒息法制作心肺复苏模型,SD大鼠15只,随机分为对照组(正常体温)、34℃低温组、32℃低温组,每组各5只。对照组在CPR后置于室温25℃下常规治疗;34℃低温组(34+/-0.2℃)和32℃低温组(32+/-0.2℃)在CPR 0.5 h后分别给予亚低温治疗。各组大鼠均于CPR后12 h取脑组织,免疫组化法测定大脑皮层caspase-3蛋白表达,Western blotting测定Bcl-2、Bax表达,同时观察各组脑组织病理变化。结果与常温组相比,低温组神经元caspase-3表达均明显减弱(P<0.05),其中32℃低温组caspase-3表达减弱更加明显(P<0.05);低温组Bcl-2表达明显增强(P<0.05),32℃低温组的Bcl-2蛋白表达比34℃低温组表达更强;3组大鼠神经元凋亡蛋白bax的表达无明显差异。结论亚低温可能通过降低caspase-3蛋白的表达、增强Bcl-2的表达,从而抑制脑细胞凋亡减轻脑损伤,32℃亚低温治疗比34℃更能起到脑保护的作用。
Objective To explore the effect of mild to moderate hypothermia on the expressions of apoptosis-related genes in the brain tissue of rats after cardiopulmonary resuscitation （CPR）. Methods CPR models were established by asphyxia in 15 male SD rats, which were randomized equally into normal temperature group, 34℃ hypothermia group and 32℃ hypothermia group. The brain tissues of the rats were obtained after treatment for 12 h to observe the pathological changes. The expression of caspase-3 in cerebral cortex neurons was determined with immunohistochemistry. and the expressions of Bcl-2 and Bax were detected by Western blotting. Results Compared with normal temperature group, the two hypothermia groups （especially 32℃ group） showed significantly decreased expression of caspase-3 in the cortical neurons （P〈0.05）. Bcl-2 protein expression was significantly increased in the hypothermia groups, especially in 32 % hypothermia group （P〈0.05）. There was no significant difference in Bax protein expression among the 3 groups. Conclusion Mild hypothermia can relieve brain injury by down-regulating caspase-3 expression and up-regulating Bcl-2 protein expression to inhibit apoptosis of the brain neurons. Hypothermia at 32℃ offers better protection of the brain tissue than hypothermia at 34℃.
出处
《南方医科大学学报》
CAS
CSCD
北大核心
2013年第10期1489-1493,共5页
Journal of Southern Medical University
基金
湖南省科技厅项目(2011FJ3009)
