一般认为青蒿琥酯(ART)引起细胞凋亡是因为产生了活性氧（ROS）,从而启动多种凋亡途径。利用荧光染料2′,7′-二氯荧光素二乙酸酯(DCFH-DA)和罗丹明(Rhodamine)123分别表征细胞中ROS的水平以及线粒体的膜电位，然后采用动态显微荧光成像技术在单个活细胞中实时监测ART诱导人类肺腺癌细胞（ASTC-a-1）凋亡过程中ROS的产生和线粒体膜电位的下降。结果显示0~50 μg/mL质量浓度的ART均能引起细胞活力的降低， 40 μg/mL质量浓度的ART能明显产生ROS，并且引起细胞线粒体膜电位的显著下降；CCK-8试剂对细胞活性的检测结果表明，ROS清除剂N-乙酰半胱氨酸(NAC)可以显著抑制ART诱导的细胞凋亡和线粒体膜电位下降，证明ART诱导了ROS依赖性的细胞凋亡和线粒体膜电位下降。

It is known that artesunate (ART) induced apoptosis is due to the reactive oxygen species (ROS) generation which triggers many apoptosis. DCFH-DA and Rhodamine 123 were used to probe the level of ROS and mitochondrial membrane potential. Time-lapse confocal fluorescence microscopy was used to monitor the dynamics of ROS generation and the loss of mitochondrial membrane potential during ART-induced human lung adenocarcinoma cells (ASTC-a-1) apoptosis. The data show that the cell ability can be reduced by ART of 0~50 μg/mL. ART of 40 μg/mL which be used to generate significantly ROS can induce notablely loss of mitochondrial membrane potential. Results show that N-acetylcysteine (NAC), a scavenger of ROS, can significantly inhibits the ART-induced apoptosis and the loss of mitochondrial membrane potential and ART induces ROS-mediated apoptosis and loss of mitochondrial membrane potential.