PKB/AKT与脑缺血神经细胞凋亡的研究  

Research of Mild Hypothermia on Expression of AKT after Hypoxia-Ischemia Brain Damage

作　　者：王志敏[1] 杨玉欣[1] 孙丽红[1] 李雪娟[1] 石永丽[1] 郭庆章[1] 

机构地区：[1]黑龙江省大庆油田总医院门诊部,163001

出　　处：《医学研究杂志》2008年第7期68-70,共3页Journal of Medical Research

摘　　要：目的研究AKT在脑缺血再灌注后损伤神经元中的表达情况。方法采用大鼠局灶性脑缺血再灌注损伤模型,大脑中动脉阻塞2h。共分为常温对照、亚低温处理两大组,每组分别12例,再灌注时间段分别为2h、12h、24h、72h,每时间段各3例,共24例,进行免疫组化染色,检测AKT的表达情况。结果常温对照组模型再灌注2h后AKT即有表达,72h达高峰。亚低温处理组AKT表达阳性细胞数与常温对照组相应时间点相比,表达有所增高。结论脑缺血再灌注可诱导AKT表达,亚低温预处理可促进AKT表达,AKT表达可能是脑缺血再灌注保护途径之一。Objective To study the effect of local mild hypothermia on AKT protein expression after rats focal cerebral ischemia - reperfusion injury. Methods By using the model of rat focal cerebral ischemia - reperfusion injury , the middle cerebral arteries （MCA） of SD rats were occluded for 2 h , and reperfused for2h, 12h,24h,72h. Immunohistochemical analysis was used to detect expression of AKT. Results AKT expressed after ischemia 2h,the expression was significantly increased after ischemia reperfusion with peak expression at 72h in model group on normal temperature. In mild hypothermia group, the AKT expression was higher than that in normal temperature group when at the same time point. Conclusion Brain hypoxia - ischemia could induce the expression of AKT. Mild hypothermia could promote the expression of AKT. The expression of AKT could be one of the protected way of brain hypoxia - ischemia.

关 键 词：AKT 亚低温 脑缺血再灌注 

分 类 号：R743.31[医药卫生—神经病学与精神病学] R163[医药卫生—临床医学]