1型糖尿病模型大鼠Meynert基底核神经元凋亡及Bax与Bcl-2的蛋白表达  

Neuron apoptosis and Bax/Bcl-2 protein expression in the nucleus basalis of Meynert in rats with type 1 diabetes

作　　者：王薇[1] 赵健[1] 郭灵[2] 

机构地区：[1]皖南医学院解剖学教研室,安徽芜湖241002 [2]广西医科大学解剖学教研室,广西南宁530021

出　　处：《皖南医学院学报》2016年第1期1-4,共4页Journal of Wannan Medical College

基　　金：皖南医学院中青年科研基金项目(WK201108)

摘　　要：目的:观察1型糖尿病模型大鼠脑内Meynert基底核神经元凋亡以及凋亡相关因子Bax与Bcl-2的蛋白表达,探索1型糖尿病中枢神经系统功能障碍的发生机制。方法:将24只成年健康Wistar大鼠随机分为糖尿病组、载体组和正常组。腹腔注射溶于p H 4.4柠檬酸缓冲液的链脲佐菌素,建立1型糖尿病模型大鼠;载体组大鼠腹腔注射等体积的p H 4.4柠檬酸缓冲液;正常组不进行任何处理。应用TUNEL反应技术和免疫组织化学方法,检测各组大鼠脑Meynert基底核神经元凋亡及凋亡相关因子Bax与Bcl-2基因的蛋白表达情况。结果:1型糖尿病大鼠脑Meynert基底核的Bax、TUNEL阳性细胞数明显高于正常组和载体组(P<0.01),但Bcl-2阳性细胞数明显低于正常组和载体组(P<0.01)。结论:1型糖尿病能引起Meynert基底核中神经元的凋亡及凋亡因子Bax的蛋白表达增加,同时使抗凋亡因子Bcl-2的蛋白表达减少。Objective： To observe neuron apoptosis and Bax and Bcl-2 protein expression in the nucleus basalis of Meynert in rats with type 1 diabetes for exploring the mechanisms of central nervous system dysfunction in type 1 diabetes. Methods： Twenty-four Wistar rats were randomized into group of diabetes,vehicle and normal. Type 1 diabetic model rats were induced by intraperitoneal injection of streptozotocin dissolved in citrate buffer solution（ p H 4. 4）.Rats in vehicle group were given equal volume of the same buffer,and normal controls were free of any treatment. Terminal-deoxynucleotidyl-transferasemediated-d UTP nick and labeling（ TUNEL） technique and immunohistochemical methods were used to detect the neuron apoptosis in the nucleus basalis of Meynert in each group of rats. Results： The number of Bax immunereactive（ Bax-IR） neurons and TUNEL-positive neurons in the nucleus basalis of Meynert was significantly higher,yet the count of Bcl-2 IR neurons was markedly lower,in type 1 diabetic group than the vehicle and normal groups（ P〈0. 01）. Conclusion： Type 1 diabetic rats may be complicated with apoptosis of nucleus basalis of Meynert and up-regulated Bax expression,yet decrease of Bcl-2 protein expression.

关 键 词：1型糖尿病 细胞凋亡 BAX BCL-2 MEYNERT基底核 

分 类 号：R587.1[医药卫生—内分泌]