Overexpression of heat-shock protein 20 in rat heart myogenic cells confers protection against simulated ischemia/reperfusion injury

作     者：Yan-hui ZHU Xian WANG~2 Department of Physiology and Pathophysiology,Basic Medical College,Key Laboratory of Molecular Cardiovascular Biology,Ministry of Education,Peking University,Beijing 100083,China 

作者机构：Department of Physiology and Pathophysiology Basic Medical College Key Laboratory of Molecular Cardiovascular Biology Ministry of Education Peking University Beijing China 

出 版 物：《Acta Pharmacologica Sinica》 (中国药理学报(英文版))

年 卷 期：2005年第26卷第9期

页      面：1076-1080页

核心收录：

学科分类：1007[医学-药学(可授医学、理学学位)] 1006[医学-中西医结合] 100706[医学-药理学] 1002[医学-临床医学] 100602[医学-中西医结合临床] 10[医学] 

基　　金：the National Basic Research Program of China(No G2000056908)awardet to Xian WANG 

主　　题：reperfusion injury adenovirus apoptosis necrosis heat-shock proteins 

摘      要：Aim:To explore whether overexpression of the small heat shock protein HSP20 inrat cardiomyocytes protects against simulated ischemia/reperfusion(SI/R)***:Recombinant adenovirus expressing HSP20 was used to infect rat H9c2cardiomyocytes at high efficiency,as assessed by green fluorescent protein.H9c2cells were subjected to SI/R stress;survival was estimated through assessment oflactate dehydrogenase and cell apoptosis through caspase-3 ***:Overexpression of HSP20 decreased lactate dehydrogenase release by 21.5% andcaspase-3 activity by 58.8%.Pretreatment with the protein kinase C inhibitor Ro-31-8220(0.1 μmol/L)for 30 min before SI/R canceled the protective effect of *** selective mitochondrial K+awP channel inhibitor 5-hydroxydecanoate(100 μmol/L)had a similar ***,the non-selective K~+ATPchannel inhibitorglibenclamide(100 μmol/L)had no significant ***:These dataindicate that the protective effect of HSP20 in vitro is primarily due to reducednecrotic and apoptotic death of cardiomyocytes,possibly via the protein kinaseC/mitochondrial K~+ATP pathway.