糖尿病大鼠脑缺血再灌注后脑组织细胞凋亡与Bax、Bcl-2及p53基因表达  

Apoptosis and expression of Bax,Bcl-2 and p53 in a rat of diabetes mellitus with cerebral ischemic reperfusion

作　　者：杨小艳 何玲[2] 范瑞明[2] 余昌胤[2] 

机构地区：[1]贵州省航天医院,贵州遵义563003 [2]遵义医学院附属医院

出　　处：《山东医药》2008年第42期1-3,共3页Shandong Medical Journal

基　　金：贵州省教育厅科研基金资助项目(2002320);贵州省卫生厅优秀医学青年人才基金资助项目(D-202)

摘　　要：目的观察糖尿病性高血糖大鼠脑缺血再灌注后脑组织细胞凋亡与Bax、Bcl-2和p53表达情况。方法将Wistar大鼠随机分成正常对照组、假手术组、正常血糖脑缺血再灌注组(NIR)和糖尿病性高血糖脑缺血再灌注组(DIR),采用链脲佐菌素腹腔注射制作糖尿病模型、线栓法制作大脑中动脉缺血再灌注模型,应用TUNEL法和免疫组化法分别检测细胞凋亡和Bax、Bcl-2及p53表达。结果与假手术组和正常对照组比较,NIR组凋亡细胞百分率和Bax、Bcl-2、p53表达明显增加(P均<0.01);与NIR组比较,DIR组凋亡细胞百分率和Bax、p53表达明显增加,Bcl-2表达明显降低(P均<0.01)。结论糖尿病性高血糖大鼠脑缺血再灌注后梗死周边区细胞凋亡增加是高血糖加重缺血性脑损伤的机制之一;Bax和p53表达上调、Bcl-2表达下调参与了糖尿病大鼠脑缺血再灌注后细胞凋亡的调控。Objective To observe the apoptosis and expression of Bax, Bc1-2 and p53 in a rat of diabetes mellitus with cerebral ischemic reperfusion. Methods Wistar rats were randomly divided into four groups ： control group, sham op- eration group, isehemic reprfusion in hyperglycemia group（DIR） and normoglycemia group（NIR）. Hyperglycemia modal was made by injection of streptozocin through abdomen and model of cerebral ischemia reperfusion was developed by thread embolism method in rats. The apoptosis of cell and expression of Bax, Bcl-2 and p.53 were detected by TUNEL and immunohistochemistry ,respectively. Results Compared with sham operated and control group, expression of Bax, Bc1-2, p53 and percent of apoptosis were ignificanfly higher in NIR group （P〈0.01） ; Compared with NIR group, expression of Bax, p53 and percent of apoptosis were significantly higher and expression of Bcl-2 were significantly lower in DIR group （P〈0.01）. Conclusion Apoptosis which result from the change of Bax, p53 and Bel-2 may play an important role in ischemic injury in diabetes rats with focal cerebral ischemia reperfusion.

关 键 词：糖尿病 再灌注损伤 细胞凋亡 基因 Bc1-2 基因 Bax 基因 p53 

分 类 号：R743.3[医药卫生—神经病学与精神病学] R587.1[医药卫生—临床医学]