心力衰竭心肌凋亡基因蛋白研究  

Expression of bcl-2 and Bax protein in the failing human heart —an inhibitor or accelerator of apoptosis?

作　　者：陈忆九[1] 黄晓华[1] 陈龙[2] 

机构地区：[1]司法部司法鉴定科学技术研究所,上海200063 [2]上海医科大学法医学系,上海200032

出　　处：《法医学杂志》2000年第1期10-11,共2页Journal of Forensic Medicine

摘　　要：心肌梗死致心力衰竭猝死者 ,心肌细胞存在凋亡现象。基因蛋白bcl-2和Bax对心肌凋亡具有调控作用。急性肌梗死灶周围有bcl-2 表达 。In general, myocyte death in myocardial infarctions (MI) is attributed to necrosis, but recently the involvement of apoptosis has been suggested. Loss of myocytes is an important mechanism in the development of cardiac failure of either ischemic or nonischemic origin. The expression of two proto-oncogenes influence apoptosis. Myocytes with positive bcl-2 immunoreactivity were seen in the heart of acute MI, localized only in the salvaged areas surrounding the infarcted tissues. Myocytes with overexpressed positive Bax immunoreactivity were observed in the salvaged areas of old MI.

关 键 词：心肌细胞凋亡 BCL-2 BAX 心力衰竭 

分 类 号：R541.6[医药卫生—心血管疾病]