GSH 耗竭介导5, 7- 二甲氧基黄酮诱导肺癌A 549 细胞凋亡

目的探讨5,7-二甲氧基黄酮（5,7-dimethoxyflavone,DMF）诱导人肺癌A549细胞凋亡作用是否涉及细胞内谷胱甘肽（glutathione,GSH）耗竭。方法体外培养A549细胞,分光光度法测定细胞内GSH含量;流式细胞术检测细胞凋亡率;琼脂糖凝胶电泳观察细胞DNA断裂。结果 DMF以浓度依赖方式诱导A549细胞凋亡率增高（P〈0.05）,并导致细胞DNA断裂。DMF显著降低A549细胞内GSH水平（P〈0.05）,呈浓度依赖性。500μmol·L-1GSH预孵育1h,能有效阻断DMF诱导细胞内GSH耗竭,并减弱DMF触发细胞凋亡作用（P〈0.05）。结论细胞内GSH耗竭是DMF诱导人肺癌A549细胞凋亡作用机制之一。

5, 7-dimethoxyflavone-induced apoptosis of lung cancer A540 cells is mediated by intracellular glutathione depletion

Objective To explore whether 5, 7-dimethoxyflavone（DMF） induces apoptosis through intracellular glutathione（GSH） depletion in human lung cancer A549 cell line in vitro. Method Human lung cancer A549 cells were cultured in vitro. The intracellular level of GSH was measured using spectrophotometer. The apoptotic rate was examined by flow cytometry （FCM） using propidium iodide staining. DNA fragmentation was examined using DNA agarose gel electrophoresis. Results DMF significantly induced increase of apoptotic rate and DNA fragmentation of A549 cells（P 0.05）, in a concentration-dependent manner. DMF significantly reduced the intracellular contents of GSH （P 0.05） in A549 cells, in a concentrationdependent manner. Pretreated with 500μmol·L-1 GSH for 1 h can effectively blocked the effects of DMF on induction of GSH depletion and apoptosis in A549 cells. Conclusion GSH depletion is one of the mechanisms underlying DMF induce apoptosis of human lung cancer A549 cell line.