氯化镉诱导大鼠心肌细胞 H9c2 凋亡的作用机制
he effect on apoptosis in H9c2 cells induced by cadmium chloride
目的：研究不同浓度氯化镉（CdCl2）引起大鼠心肌细胞 H9c2 凋亡及机制探讨。方法：阴性对照组为DMEM培养液，镉处理组分别暴露于 5﹑10﹑30﹑50﹑80 μmol·L-1 CdCl2 作用 6 h﹑12 h﹑24 h 后，采用MTT法检测细胞存活率；Annexin Ⅴ-FITC/ propidium iodide (PI)流式细胞技术(flowcytometric，FCM)、丫啶橙（AO）/ 溴化乙啶（EB）双荧光染色法检测细胞凋亡情况。结果：镉处理组细胞存活率随着剂量的加大及时间延长明显下降，与阴性对照比较差异显著（P ＜0.05或P ＜0.01）；镉可引起H9c2细胞凋亡，各剂量组凋亡率明显高于阴性对照组（P ＜0.001），各剂量组之间凋亡率差异无显著性；AO/EB 染色镜下可见H9c2细胞典型早期凋亡形态学改变。结论：H9c2 细胞对氯化镉的作用较敏感，低剂量﹑短时间作用即可引起细胞凋亡，但 H9c2 细胞对镉有一定耐受性。
Objective To study apoptosis of H9c2 cadiomyocyte cell line induced by different concentrations of cadmium .Method The H9c2 cells were exposed to 5﹑10﹑30﹑50﹑80μmol·L-1 Cadmium chloride after 6 h﹑12 h﹑24h.The rate of survival was measured by MTT assay and the rate of apoptosis was detected by Annexin Ⅴ/propidium iodide (PI)-FCM (flowcytometric,FCM) and acridine oringe/ethidium bromide(AO/EB) staining.Result The survival rate of the groups treated with Cadmium chloride decreased significantly compared with those of negative controls (P ＜0.05 or P ＜0.01); the rate of apoptosis detected by FCM increased significantly compared with those of negative controls(P ＜0.001) . The typical morphological changes of early apoptosis could be observed under fluorescent microscope by AO/EB staining. Conclusion The H9c2 cells are sensitive to toxicity of cadmium chloride ,low dose and short time can induce apoptosis,but the H9c2 cells cells have certain toleration to the effect of cadmium .
郭彩霞、王华、王雯、孙磊、黄渭、孙志伟、刘晓梅、金明华
基础医学细胞生物学生理学
氯化镉心肌细胞H9c2凋亡
dmium chloridecardiomyocytesH9c2apoptosis
郭彩霞,王华,王雯,孙磊,黄渭,孙志伟,刘晓梅,金明华.氯化镉诱导大鼠心肌细胞 H9c2 凋亡的作用机制[EB/OL].(2006-11-22)[2025-08-02].http://www.paper.edu.cn/releasepaper/content/200611-626.点此复制
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