凋亡调控因子XIAP对缺氧诱导大鼠心肌细胞凋亡的影响  

Effects of Apoptosis-Regulative Gene XIAP on Cultured Rat Cardiomyocytes Apoptosis Induced by Hypoxia

作　　者：秦瑶[1] 郑洪[2] 杨永福[2] 刘华庆[2] 

机构地区：[1]遵义医学院附属医院心内科,贵州遵义563000 [2]遵义医学院附属医院病理科,贵州遵义563000

出　　处：《遵义医学院学报》2011年第5期477-479,共3页Journal of Zunyi Medical University

摘　　要：目的建立体外培养新生大鼠心肌细胞缺氧模型,用XIAP进行干预,以探讨XIAP能否抑制细胞凋亡。方法培养新生SD大鼠(1～3天龄)心肌细胞至第4天,脂质体介导转染pDsRed2-XIAP、pDsRed2-N1质粒和不转染的心肌细胞分别设为模型组、对照组和空白组。以物理性缺氧(95%N2+5%CO2)方式培养,在6h、12h用流式细胞仪AnnexinVFITC及原位末端标记法(TUNEL)检测细胞调亡,结果采用统计学SPSS11.5软件包进行单项方差分析。<0.05,有显著差异。结果①缺氧后经TUNEL检测,各组均有心肌细胞凋亡;②流式细胞仪检测心肌细胞凋亡随缺氧时间延长而增多;③模型组心肌细胞凋亡率较对照组与空白组明显减少(<0.01)。结论缺氧能诱导心肌细胞凋亡。XIAP能明显减少缺氧诱导鼠心肌细胞的凋亡。Objective The study was designed to establish myocardial cell hypoxia model of newly born rat in vitro culture,to study whether XIAP could suppress cadiomyocytes apoptosis after XIAP intervention with the model.Methods Cultured cardiomyocytes of one to three days SD rat for four days.To set up study group,pDsRed2-XIAP plasmid was transfected into cadiomyocytes by liposomes;pDsRed2-N1 plasmid transfected into cadiomyocytes was control group,and there was blank group transfected nothing into.Apoptosis rate was detected by Flow cytometry with Annexin V FITC and TUNEL after hypoxia（95%N2€？%CO2） for 6h and 12h.The software package spss11.5 carryed out One-way ANOVA.P0.05 was considered statistically significant.Results ① Cadiomyocytes apoptosis was present in each group showed by TUNEL;② By using Annexin V FITC,we found the longer the hypoxia,the more the apoptosis number;③ Compared with the control group and the blank group,cadiomyocytes apoptosis rate in study group obviously decreased（P〈0.01）.Conclusion Cadiomyocytes,apoptosis could be induced by hypoxia.XIAP can obviously attenuate cadiocyte apoptosis induced by hypoxia.

关 键 词：XIAP 心肌细胞凋亡 凋亡抑制 

分 类 号：R363[医药卫生—病理学]