缺氧前激活α_1受体对心肌细胞凋亡的影响及机制  

Mechanism by which activation of α_1-adrenoceptor before is chemia controls myocardial apoptosis

作　　者：方宏[1] 冯义柏[2] 方盈[2] 

机构地区：[1]上海同济大学附属同济医院心内科,上海200065 [2]武汉华中科技大学同济医学院附属协和医院心导管室,湖北武汉430022

出　　处：《中国病理生理杂志》2005年第4期714-717,共4页Chinese Journal of Pathophysiology

摘　　要：目的:从影响心肌细胞凋亡的分子学机制,了解α1受体发挥生物学效应的机制。方法:采用免疫组化和分子生物技术测定Bcl - 2、Bax、cytochromeC、caspase - 3的表达量。结果:缺血前使用苯肾上腺素(phenylen phrine) ,缺血时凋亡细胞数减少,Bcl- 2明显增加,cytochromeC、caspase - 3降低。结论:α1受体可影响Bcl- 2表达,改变线粒体膜的通透性,调节凋亡蛋白的表达,从而可能决定心肌细胞的凋亡。AIM: To study the mechanism for biological effect of α 1-adrenoceptors by inves tigating the molecular mechanism involving in the apoptotic processi on in myocardium. METHODS: The expressions of Bcl-2, Bax, cytochrome C, caspase-3 were determined by means of immunohistochemistry and molecular technique. RESULTS: Bcl-2 was increased but apoptosis, Bax, cytochrome C, caspase-3 were decreased when phenylephrine was used before ischemia. CONCLUSION: α 1 -adrenoceptors may influence the expression of Bcl-2 ,change the permeabil ity of mitochondrion and adjust the expression of apoptotic protein to control apoptosis.

关 键 词：受体 肾上腺素能α1 心肌 细胞凋亡 

分 类 号：R363[医药卫生—病理学]