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目的探讨自噬在顺铂心脏毒性损伤中的调控作用。方法采用顺铂处理心肌细胞,通过检测LC3、P62观察自噬的变化;通过阻断自噬,观察心肌细胞经顺铂处理后细胞活力的变化,并通过TUNEL染色检测细胞凋亡情况。结果采用顺铂分别处理原代新生大鼠心肌细胞(Neonatal rat cardiomyocyte,NRCM)和H9c2细胞系,观察到LC3-II的增加和P62蛋白的下调,表明顺铂可显著诱导心肌细胞自噬。采用自噬抑制剂氯喹或3-MA联合顺铂处理细胞后,发现细胞活力较单纯顺铂处理组显著下调。TUNEL染色结果显示,联合处理组细胞凋亡率较单纯顺铂处理组显著上调。结论顺铂诱导心肌细胞自噬,阻断自噬增强顺铂对心肌细胞的损伤作用。
Objective To investigate the regulatory role of autophagy in cisplatin cardiotoxicity injury. Methods Cardiomyocytes were treated with cisplatin, and the changes of autophagy were detected by detecting LC3 and P62. By blocking autophagy, the changes of cell viability after cisplatin treatment were observed. The cell apoptosis was detected by TUNEL staining. Results The primary cultured neonatal rat cardiomyocytes (NRCM) and H9c2 cells were treated with cisplatin. The increase of LC3-II and the down-regulation of P62 protein were observed, indicating that cisplatin could induce cardiomyocyte autophagy. After using autophagy inhibitor chloroquine or 3-MA combined with cisplatin cells, cell viability was significantly lower than the cisplatin alone treatment group. The results of TUNEL staining showed that the apoptosis rate of the combined treatment group was significantly up-regulated compared with the cisplatin-treated group. Conclusion Cisplatin induces cardiomyocyte autophagy and blocks autophagy and enhances the effect of cisplatin on cardiomyocyte injury.