镉致大鼠心肌细胞H9c2凋亡作用  

Study on apoptosis of rats H9c2 cells induced by cadmium chloride

作　　者：黄渭[1] 王华[1] 郭彩霞[1] 金明华[1] 孙磊[1] 杜海英[1] 刘晓梅[1] 孙志伟[1] 

机构地区：[1]吉林大学公共卫生学院卫生毒理教研室,长春130021

出　　处：《中国公共卫生》2009年第1期96-98,共3页Chinese Journal of Public Health

基　　金：教育部高等学校博士学科点专项科研基金(20030183006)

摘　　要：目的研究不同浓度氯化镉(CdCl2)引起大鼠心肌细胞H9c2凋亡作用。方法采用姬姆萨染色法观察氯化镉对细胞毒作用的形态学改变;采用Annexin V-FITC/propidium iodide(PI)流式细胞技术(flowcytometric,FCM)检测氯化镉对H9c2细胞凋亡的影响;采用流式细胞术法检测线粒体膜电位(MMP)的变化;采用免疫细胞化学法检测细胞色素C表达。结果5,10,30,50,80μmol/L的氯化镉分别作用H9c2细胞6,12,24 h可以诱导细胞凋亡;随着镉剂量的加大及作用时间的延长,线粒体膜电位明显下降,与阴性对照比较,差异有统计学意义(P<0.05);随着镉剂量增加,CytC表达增强。结论镉可以通过线粒体途径诱导H9c2细胞凋亡。Objective To study the apoptosis of H9c2 cardiomyocyte cell line induced by different concentrations of cadmium chloride. Methods Giemsa staining was applied to observe the morphological changes of H9c2 cells and the rate of apoptosis was detected by annexin V/propidium iodide（PI） -flowcytometric （FCM）. Rhodamine 123 as a fluorescent probe combined with FCM was applied to determine mitochondrial membrane potential. cal method was applied to detect the expression levels of Cyt C. Results The results showed that 5,10,30,50,80 μ mol/L cadmium chloride could induce apoptosis, decrease mitochondrial membrane potential and change the expression levels of related apoptosis proteins. A statistics difference between cadmium chloride groups and negative control group was observed. Conclusion Cadmium can induce H9c2 cells apoptosis through mitochondrial pathway.

关 键 词：氯化镉 H9C2 细胞凋亡 细胞色素C 

分 类 号：R994.6[医药卫生—毒理学]