他汀类药物对心肌缺血再灌注损伤心肌细胞凋亡作用机制的研究进展  

Advances in Study of Mechanism of Statins on Cardiomyocyte Apoptosis Induced by Myocardial Ischemia Reperfusion

作　　者：苏强[1] 李浪[1] 

机构地区：[1]广西医科大学第一附属医院心内科广西心血管病研究所,广西南宁530021

出　　处：《心血管病学进展》2010年第1期134-137,共4页Advances in Cardiovascular Diseases

基　　金：国家自然科学基金资助项目(C030313)

摘　　要：近年研究表明,细胞凋亡在心肌缺血再灌注损伤(MIRI)中占有重要地位,细胞凋亡与MIRI之间有着密切关系。实验证实他汀类药物具有除调脂以外的心肌保护效应。现主要从他汀类药物的抗氧化作用和激活磷脂酰肌醇-3-激酶丝氨酸-苏氨酸激酶/一氧化氮合酶(PI3K/Akt/eNOS)信号通路两个方面阐述在心肌缺血再灌注过程中他汀类药物抑制心肌细胞凋亡的主要机制。Recent research indicates that apoptosis plays an important role in myocardial ischemia-reperfusion injury. There is an intimate relationship between apoptosis and myocardial ischemia-reperfusion injury. Some experiments have reported that statins exert cardio-pm- tection independent of lipid lowering. This article reviews the main mechanism of inhibiting cardiomyocyte apoptosis in myocardial ischemia- reperfusion injury through inhibiting oxidative stress and activating PI3K/Akt/eNOS signal pathway.

关 键 词：他汀类药物 心肌细胞 凋亡 缺血再灌注损伤 

分 类 号：R965.1[医药卫生—药理学]