不同低温对大鼠永久性大脑中动脉闭塞后NF-кB、Bcl-2、Bax蛋白表达的影响  

The effects of different hypothermia on expression of NF-κB、Bcl-2、Bax following permanent middle cerebral artery occlusion in rats

作　　者：兰晶[1,2] 张其梅[1,2] 张强[1,2] 胡萌[1,2] 李耀彩[1,2] 

机构地区：[1]三峡大学第一临床医学院 [2]湖北省宜昌市中心人民医院神经内科,宜昌443003

出　　处：《陕西医学杂志》2010年第12期1584-1586,1600,共4页Shaanxi Medical Journal

摘　　要：目的:探讨不同低温对大鼠永久性大脑中动脉闭塞后NF-κB、Bcl-2、Bax表达的影响。方法:84只雄性SD大鼠随机分为三组:常温组(37℃),轻度低温组(34℃),中度低温组(32℃),每组分缺血2,4,6,12h共四个亚组。采用栓线法制作永久性大脑中动脉闭塞(MCAO)模型,各组大鼠分别于缺血2,4,6,12h后置于常温操作台和冰毯机上,分别保持肛温为37±0.5℃,34±0.5℃和32±0.5℃12h。在各自规定时间点处死大鼠,作免疫组织化学染色。结果:与常温组相比,除轻度低温组缺血4h外,其余各时间点两低温组的NF-κB蛋白水平均显著低于常温组(P<0.01)。除轻度低温组缺血2h、4h、12h外,其余各时间点两低温组的Bcl-2蛋白水平较常温组有统计学差异(P<0.05或P<0.01)。除中度低温组缺血4h,轻度低温组缺血4h、12h外,其余各时间点两低温组的Bax蛋白水平较常温组有统计学差异(P<0.05或P<0.01)。结论:低温治疗显著抑制NF-κB的蛋白表达,使NF-κB蛋白表达高峰前移;显著降低了Bax蛋白水平。这些改变可增强缺血后神经元对凋亡的耐受。Objective：To investigate the effects of different hypothermia on expression of NF-κB、Bcl-2 and Bax following permanent middle cerebral artery occlusion in rats. Methods： 84 male Sprague-Dawley rats were divided randomly into 3 groups： normothermia group（37℃）, mild hypothermia group（34℃）, moderate hypothermia group（32℃）, and every group were divided 4 subsets： ischemia 2h, 4h, 6h and 12h. Permanent middle cerebral artery occlusion models were established by using the intraluminal suture method. The rats were placed on consple and ice blanket machine after ischemia 2h, 4h, 6h and 12h, respectively. Meanwhile, the rectal temperature were maintained 37±0.5℃,34±0.5℃and 32±0.5℃12h, respectively. The rats were sacrificed in prescript time point, which were used in measuring the expression of NF-κB、Bcl-2 and Bax with immunohistochemical staining. Results： Excepting after ischemia 4h of mild hypothermia group, protein level of NF-κB descended significantly in mild hypothermia group and moderate hypothermia group in every ischemia time point （P0.01）. Compared to normothermic group, there were statistics disparation in protein level of Bcl-2 of those hypothermia group in every ischemia time point （P0.05 P0.01） excepting after ischemia 2h、4h and 12h of mild hypothermia group. Compared to normothermic group, there were statistics disparation in protein level of Bax of those hypothermia group in every ischemia time point （P0.05 P0.01） excepting after ischemia 4h of moderate hypothermia group, after ischemia 4h and 12h of mild hypothermia group. Conclusions： It is significant that by hypothermia treatment, the protein expression of NF-κB is repressed. The protein level of Bax descends significantly, too. It is assumed that the inhibition of NF-κB and Bax expression, up-regulation proportion of Bcl-2/Bax and enhancement of neuron’s tolerance on apoptosis may be one of the mechanism of hypothermic neuroprotection.

关 键 词：脑缺血/病理生理学 核因子 @Bcl-2 @Bax 动物 实验 大鼠 

分 类 号：R-332[医药卫生]