芪苈强心对缺氧诱导的大鼠心脏微血管内皮细胞凋亡的作用及机制研究  

Investigation of Qiliqiangxin on Hypoxia Induced Cardiac Microvascular Endothelial Cells Apoptosis

作　　者：韩雪婷[1,2] 付明强[1] 李志明[2] 王艳艳[1] 汪菁峰[1] 王时俊[1] 陈丽[2] 邹云增[1] 周京敏[1] 

机构地区：[1]复旦大学附属中山医院,上海市心血管病研究所,上海市200032 [2]川北医学院附属医院,四川省南充市637000

出　　处：《中国分子心脏病学杂志》2016年第1期1593-1596,共4页Molecular Cardiology of China

基　　金：国家973项目子课题(2012CB518605)

摘　　要：目的探讨芪苈强心对缺氧诱导心脏微血管内皮细胞(CMVECs)凋亡的影响及可能机制。方法植块法培养大鼠CMVECs,传代至P2后随机分为对照组、缺氧组(采用低氧发生装置模拟缺氧刺激)、缺氧+芪苈强心(0.5mg/ml)干预组。采用电镜观察CMVECs形态;Caspase3活性检测试剂盒检测细胞Caspase3活性;原位末端标记法(TUNEL)检测细胞凋亡;Western Blot检测细胞Bcl-2,Bax蛋白表达水平。结果与对照组比较,缺氧组CMVECs细胞浆内可见大量凋亡小体,Caspase3活性明显升高(p<0.01),凋亡率增加(p<0.01),抗凋亡蛋白Bcl-2表达减少,促凋亡蛋白Bax表达增加(p<0.05);与缺氧组相比,芪苈强心干预组细胞形态接近正常;Caspase3活性下调(p<0.01),凋亡率下降(p<0.01);Bcl-2表达增加,Bax表达受抑(p<0.05)。结论芪苈强心可以减少缺氧刺激下CMVECs凋亡,上调抗凋亡蛋白Bcl-2表达,下调促凋亡蛋白Bax表达。Objective To investigate the mechanism of Qiliqiangxin（QL） against hypoxia induced cardiac microvascular endothelial cells（CMVECs） apoptosis. Methods CMVECs were cultured by the method of planting myocardium tissues. Cells were passaged to P2 and randomly divided into three groups： control group, hypoxia group and hypoxia ＋ QL treatment group. Hypoxia circumstance was induced in a hypoxia generator filled with 95% N2 and 5% CO2, and the intervention concentration of QL was selected at 0.5mg/ml. Mor phological changes of CMVECs were observed by electron microscopy. Caspase 3 activity was detected by caspase 3 activity kit. Cell apoptosis was measured by terminal deoxynucleotide transferase d UTP nick end labeling（TUNEL）. Protein expressions of Bcl-2 and Bax were determined by Western Blot. Results Compared to control group, CMVECs undergoing hypoxia exhibited significant apoptosis as evidenced by increased apoptosis bodies, elevated activity of caspase 3, increased expression of proapoptotic protein Bax as well as decreased antiapoptotic protein Bcl-2（all p〈0.05）, which were all effectively suppressed or retained by the treatment of QL（all p〈0.05）. Conclusions QL suppressed CMVECs apoptosis under hypoxia by upregulation of Bcl-2 and downregulation of Bax.

关 键 词：芪苈强心 心脏微血管内皮细胞 缺氧 凋亡 

分 类 号：R285.5[医药卫生—中药学]