氯化镉诱导大鼠心肌细胞 H9c2 凋亡的作用机制

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。方法：将培养的大鼠心肌细胞H9c2分为阴性对照组和镉处理组，阴性对照组为DMEM培养液，镉处理组分别暴露于 5﹑10﹑30﹑50和80 μmol•L^-1 CdCl₂ 作用6、12和24 h，采用MTT法检测细胞存活率；Annexin Ⅴ-FITC/ propidium iodide (PI)流式细胞技术(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有显著性（P<0.05或P<0.01）；CdCl₂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（P>0.05）；AO/EB 染色镜下可见H9c2细胞呈典型早期凋亡形态学改变。结论：H9c2 细胞对CdCl₂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CdCl₂有一定耐受性。

Mechanism of apoptosis in rat H9c2 cells induced by cadmium chloride

Objective To study the apoptosis of H9c2 myocardial cell lines induced by different concentrations of cadmium chloride(CdCl2).Methods The H9c2 cells were exposed to 5,10,30,50 and 80 μmol·L-1 CdCl2 for 6,12 and 24 h,the survival rate was measured by MTT assay and the apoptotic rate was detected by Annexin Ⅴ-FITC/propidium iodide(PI)-flow cytometry(FCM) and acridine oringe/ethidium bromide(AO/EB) staining.Results The survival rates in the groups treated with CdCl2 decreased significantly compared with those in negative controls(P<0.05 or P<0.01).The apoptotic rates in the groups treated with CdCl2 increased significantly compared with those of negative controls(P<0.001),but there were no significant differences between various doses groups(P>0.05).The typical morphological changes of early apoptosis in H9c2 cells could be observed under fluorescent microscope by AO/EB staining.Conclusion The H9c2 cells are sensitive to toxicity of CdCl2,low dose and short time treatment with CdCl2 can induce apoptosis of H9c2 cells,but the H9c2 cells have certain toleration to the effect of cadmium.