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目的:探讨三氧化二砷诱导急性早幼粒细胞株(HL60)凋亡机制。方法:以HL60为研究对象,通过丙二醛和谷胱甘肽含量的测量检测氧化应激反应;通过用单细胞凝胶电泳检测DNA损伤;通过共聚焦成像检测线粒体膜电位去极化和半胱氨酸蛋白酶-3的表达。结果:在HL60细胞中,亚砷酸显著(P<0.05)诱导氧化应激、DNA损伤以及半胱氨酸蛋白酶3活性的变化,并呈剂量依赖性。它也通过显著降低线粒体膜电位激活凋亡的内在途径。结论:亚砷酸通过线粒体途径诱导HL60凋亡。这个凋亡信号调节通过氧化应激、DNA损伤和线粒体膜电位变化导致细胞程序性死亡。
Objective: To investigate the mechanism of apoptosis induced by arsenic trioxide in acute promyelocytic cell line (HL60). METHODS: Oxidative stress was measured by measuring the content of malondialdehyde and glutathione in HL60. DNA damage was detected by single cell gel electrophoresis. Mitochondrial membrane potential depolarization and half Cystatin-3 expression. Results: In HL60 cells, arsenious acid significantly (P <0.05) induced oxidative stress, DNA damage and caspase 3 activity in a dose-dependent manner. It also activates the intrinsic pathway of apoptosis by significantly reducing mitochondrial membrane potential. Conclusion: Arsenious acid induces HL60 apoptosis through mitochondrial pathway. This apoptotic signal regulates programmed cell death through oxidative stress, DNA damage and changes in mitochondrial membrane potential.