活性氧介导5,7-二甲氧基黄酮增敏TRAIL诱导肺癌细胞凋亡

Sensitization of 5,7-dimethoxyflavone on TRAIL-induced Apoptosis Mediated by ROS in Human Lung Cancer A549 Cells

目的研究5,7-二甲氧基黄酮(5,7-DMF)是否能增强肿瘤坏死因子相关凋亡诱导配体(TRAIL)诱导的人肺癌细胞凋亡及其作用机制。方法体外培养人肺癌A549细胞。MTT法测定细胞增殖活性;碘化丙啶(PI)染色流式细胞术(FCM)和ELISA试剂盒检测细胞凋亡;DCFH-DA荧光标记FCM检测细胞内活性氧(ROS)水平。结果 5,7-DMF能增强TRAIL诱导的A549细胞凋亡和ROS生成。N-乙酰半胱氨酸能有效阻断5,7-DMF与TRAIL所诱导的A549细胞凋亡及ROS生成。结论 5,7-DMF通过促进A549细胞内活性氧生成从而增强TRAIL诱导的凋亡。

Objective To examine whether 5,7-dimethoxyflavone（5,7-DMF） sensitizes human lung cancer A549 cells to tumor necrosis factor-related apoptosis inducing ligand（TRAIL）-mediated apoptosis and its mechanism.Method Human lung cancer A549 cells were cultured in vitro.The cell proliferation capability was detected using MTT assay.The apoptotic cell death was examined by ELISA detection kit and Flow cytometry with PI staining.Reactive oxygen species（ROS） level was examined by Flow cytometry with DCFH-DA labeling.Results 5,7-DMF sensitized A549 cells to TRAIL-induced apoptosis and significantly promoted the intracellular ROS generation of A549 cells.N-L-acetylcysteine can effectively block the ROS generation and apoptosis of A549 cells induced by combination of 5,7-DMF and TRAIL.Conclusion 5,7-DMF enhances TRAIL-induced apoptosis by promoting ROS generation.