应激对大鼠心肌细胞线粒体膜通透性转换孔开放的影响及其分子基础的研究  

Mitochondrial membrane mechanism of rat heart injury induced by stress

作　　者：任会荣[1] 王新兴[1] 弓景波[1] 钱令嘉[1] 任崇余[1] 

机构地区：[1]卫生学环境医学研究所,天津300050

出　　处：《中国病理生理杂志》2004年第4期537-540,共4页Chinese Journal of Pathophysiology

基　　金：国家自然科学基金资助项目 (No .39970 6 35 )

摘　　要：目的 :观察应激对大鼠心肌线粒体膜通透性转换孔 (PTP)开放的影响 ,探讨PTP开放的分子基础。方法 :建立应激动物模型 ,分别束缚不同时间后处死所有大鼠 ,分光光度法检测线粒体PTP开放程度、Westernblot方法检测线粒体Bcl- 2、Bax蛋白表达水平。结果 :应激可导致大鼠心肌线粒体膜PTP开放 ,Bcl- 2表达水平降低、Bax水平增高。结论 :PTP开放为应激性心肌损伤的重要线粒体机制 ;Bcl- 2表达降低、Bax水平上调则为PTP开放的重要分子基础。AIM: To investigate the effects of stress on the opening of mitochondrial membrane permeability pore (PTP) in rat heart and explore the possible molecular mechanism underlying PTP opening. METHODS: Stress animal model was established. After strained for differnet time, all rats were killed and PTP opening degree were examined by spectrophotometer. Bcl-2, Bax expression levels were determined by Western blot. RESULTS: Stress induced PTP opning, Bcl-2 expression inhibition and Bax level elevation in myocardial mitochondria. CONCLUSION: PTP opening was the important mitochondrial mechanism of stress-induced heart injury. Decrease in Bcl-2 expression and increase of Bax level may be an important molecular basis for PTP opening.

关 键 词：应激 心脏损伤 线粒体 心脏 细胞膜通透性 

分 类 号：R363[医药卫生—病理学]