自噬在顺铂诱导的心肌细胞凋亡中的调控作用  

The Role of Autophagy in the Regulation of Cisplatin-induced Cardiomyocytes Apoptosis

作　　者：仇炜[1] 林俊[1] 张磊[1] 朱一辰[1] 张健[1] 孙雯[1] 马麟麟[1] 田野[1] 

机构地区：[1]首都医科大学附属北京友谊医院泌尿外科,北京市100050

出　　处：《中国分子心脏病学杂志》2017年第2期2044-2046,共3页Molecular Cardiology of China

基　　金：国家自然科学基金面上项目(81372737)

摘　　要：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 LC3-11 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.

关 键 词：顺铂 心肌细胞 自噬 

分 类 号：R54[医药卫生—心血管疾病]