贵州医科大学学报

2010, v.35;No.144(03) 233-235+239

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慢性应激对心肌梗死大鼠心肌细胞凋亡和bax、bcl-2表达的影响
The Effect of Chronic Stress on Cardiac Myocyte Apoptosis and Expression of Proteins bax and bcl-2 in Rats with Myocardial Infarction

张东风;王艺明;刘兴德;
ZHANG Dongfeng1,WANG Yiming1,LIU Xingde2(1.Department of Psychology,the Affiliated Hospital of Guiyang Medical College,Guiyang 550004,Guizhou,China; 2.Department of Cardiology,the Affiliated Hospital of Guiyang Medical College,Guiyang 550004,Guizhou,China)

摘要(Abstract):

目的:探讨慢性应激对心肌梗死模型大鼠心肌细胞凋亡及bax、bcl-2表达的影响。方法:大鼠随机分为4组(每组12只),正常对照组(A组),假手术组(B组),心肌梗死模型组(C组),心肌梗死后慢性应激组(C组);用TUNEL法检测心肌细胞凋亡,免疫组织化学法检测bax和bcl-2蛋白表达。结果:(1)与A、B组比较,C、D组心肌细胞凋亡指数明显增加,P<0.01;与C组比较,D组心肌细胞凋亡指数明显增加,P<0.01;A和B组心肌细胞凋亡指数比较无统计学差别;(2)与A、B组比较,C、D组心肌细胞bax和bcl-2蛋白表达均明显增加,P<0.01;与C组比较,D组心肌细胞bax蛋白表达明显增加,P<0.01,而bcl-2蛋白表达明显减少,P<0.01。结论:慢性应激可促进心肌梗死后大鼠心肌细胞凋亡,其机制可能与上调bax蛋白表达和下调bcl-2的蛋白表达有关。
Objective:To observe the effect of chronic stress on cardiac myocyte apoptosis and expression of proteins bax and bcl-2 in rats with myocardial infarction. Methods:Rats were divided randomly into four groups (12 in each):control group (group A) ,sham-operation group (group B),myocardial infarction model rat group (group C),group in which rats suffered myocardial infarction and received chronic stress intervention (group D). Cardiac myocyte apoptosis was detected with TUNEL method,and expression of proteins bax and bcl-2 detected with immunohistochemistry methods. Results:(1) Apoptosis indexes (AI) in groups C and D were significantly higher than those in groups A and B(P<0.01); AI in group D was obviously higher than that in group C(P<0.01); There was no significant difference of AI between groups A and B; (2)Expression of proteins bax and bcl-2 in groups C and D was significantly higher than those in groups A and B(P<0.01); expression of protein bax was significantly higher and expression of protein bcl-2 was significantly lower in group D than in group C(P<0.01,P<0.01). Conclusions:Chronic stress could promote cardiac myocyte apoptosis in rats with myocardial infarction. Its mechanism might relate to up-regulating of protein bax expression and down-regulating of protein bcl-2 expression.

关键词(KeyWords): 应激;心肌梗塞;细胞凋亡;基因,bcl-2;基因,bax
stress; myocardial infardtion; apoptosis; gene,bcl-2; gene,bax

Abstract:

Keywords:

基金项目(Foundation): 贵州省优秀科技教育人才省长资金项目(2005)306号

作者(Author): 张东风;王艺明;刘兴德;
ZHANG Dongfeng1,WANG Yiming1,LIU Xingde2(1.Department of Psychology,the Affiliated Hospital of Guiyang Medical College,Guiyang 550004,Guizhou,China; 2.Department of Cardiology,the Affiliated Hospital of Guiyang Medical College,Guiyang 550004,Guizhou,China)

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DOI: 10.19367/j.cnki.1000-2707.2010.03.007

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