论文部分内容阅读
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 role of autophagy in the regulation of cisplatin-induced cardiac injury.Methods Autophagy was evaluated with the expression of LC3 and P62.The cell viability was detected by using CCK-8 assay,and apoptosis was detected using TUNEL assay.Results The neonatal rat cardiomyocytes and H9c2 cells were treated with cisplatin.We observed that the LC3-Ⅱ was upregulate and the P62 was down-regulated.We then treated the cells with cisplatin combined with chloroquine or 3-MA.We observed a decreased viability and increased apoptosis in the co-treatment group compared with the single cisplatin treated group.Conclusion Cisplatin could activate autophagy in cardiomyocytes.Blocking autophagy in cardiomyocytes increased cisplatin-induced injury of cardiomyocytes.