ROS在FTY720诱导U266细胞死亡中的作用机制研究

摘要

本研究探讨活性氧(ROS)在FTY720诱导多发性骨髓瘤U266细胞株凋亡及自噬中的作用.不同浓度FTY720处理U266细胞24 h后,应用流式细胞仪检测细胞凋亡,应用Western blot检测LC3B的表达.结果显示:应用FTY720可引起U266细胞发生凋亡及自噬,自噬的发生可促进细胞死亡.自噬抑制剂Bafilomycin A1可降低FTY720导致的细胞生存率下降.应用ROS抑制剂NAC或Tiron后,FTY720引起的细胞凋亡减轻,联合应用NAC或Tiron和FTY720后LC3B-Ⅱ表达较单用FTY720明显下降.结论:FTY720可诱导U266细胞发生凋亡及自噬,ROS是FTY720引起的多发性骨髓瘤细胞凋亡及自噬的共同调节剂.%This study was purposed to investigate the role of reactive oxygen species (ROS) in apoptosis and autophagy induced by FTY720 in multiple myeloma cell line U266.U266 cells were treated by different concentrations of FTY720 for 24 h,the apoptotic rates were detected by flow cytometry,and the expression of LC3B was detected by Western blot.The results indicated that apoptosis and autophagy were induced by FTY720 in U266 cells.Autophagy induced by FTY720 could lead to cell death.Bafilomycin A1,the inhibitor of autophagy,could enhance the cell viability in U266 cells treated with FTY720.NAC or Tiron,ROS scavenger,could decrease the FTY720 induced apoptosis and the expression of LC3B-Ⅱ was reduced in combination of FTY720 with NAC or Tiron as compared with treatment with FTY720 only.It is concluded that FTY720 can induce U266 cell apoptosis and autophagy.ROS is the mediator that regnlates both the apoptosis and autophagy in multiple myeloma cells.