摘要
目的:研究过氧化氢(H2O2)诱导的内皮细胞凋亡及罗格列酮(rosiglitazone,RSG)的保护作用和可能机制。方法:将体外培养的猪髂动脉内皮细胞(PIECs)随机分为:不加干预的对照组(A组);加入500μmol/LH2O2组(B组);分别加入0.1(C组)、1.0(D组)、10.0(E组)μmol/LRSG组;分别予0.1(F组)、1.0(G组)、10.0(H组)μmol/L的RSG预处理1h后,再加入500μmol/LH2O2,孵育18h的RSG加H2O2组。倒置显微镜下观察各组细胞生长状况,MTT法检测PIECs存活率,流式细胞术(FCM)检测细胞凋亡状况和细胞内活性氧(ROS)水平。结果:与A组相比,B组显著增加了细胞凋亡率及细胞内ROS水平(P<0.01),降低细胞存活率(P<0.01)。RSG则明显降低细胞凋亡率及细胞内ROS水平,增加细胞存活率(P<0.01)。结论:RSG可以抑制H2O2诱导的内皮细胞凋亡,该作用与降低细胞内ROS生成有关。
Objective： To investigate the protective effect of rosiglitazone （RSG） on hydrogen peroxide （H2O2）-induced pig＇s Iliae artery （PIECs） apoptosis. Method： PIECs were randomly divided into 4 groups ： control, H2O2, RSG, RSG＋ H2O2. The PIECs were observed under inverted microscope and the cell viability was measured by MTT assay. Flow cytometry was used to evaluate the percentage of PIECs apoptosis and intracellular level of reactive oxygen species （ROS）. Result： The 500 μmol/L H2O2 significantly increased the percentage of PIECs apoptosis and intracellular ROS compared to control （P〈0.01 for both）, which was inhibited by RSG （P 〈0.01）. In the H2O2 group, the PIECs viability was markly decreased （P〈0.01） ; RSG significantly increased cell viability compared to the H2O2 group （P〈0.01）. Conclusion： RSG can inhibit the PIECs apoptosis induced by Ha O2, and the decrease of intracellular ROS level may contribute to the protective effects of RSG.
出处
《临床心血管病杂志》
CAS
CSCD
北大核心
2009年第5期374-377,共4页
Journal of Clinical Cardiology
基金
湖北省科技计划项目(No:2008BCZ001)
关键词
过氧化氢
罗格列酮
内皮细胞
氧化应激
凋亡
hydrogen peroxide
rosiglitazone
endothelial cell
oxidative stress
apoptosis
