三氧化二砷通过线粒体途径诱导人白血病HL-60细胞凋亡  

Arsenic Trioxide Induces Apoptotic Cell Death through Mitochondrial Pathway in Human Leukemia HL-60 Cells

作　　者：冯品[1] 姚青林[2] 王晓光[3] 胡晓辉[4] 熊春雷[5] 

机构地区：[1]第四军医大学唐都医院心内科,陕西西安710038 [2]第四军医大学唐都医院消化内科,陕西西安710038 [3]第四军医大学唐都医院内分泌科,陕西西安710038 [4]第四军医大学唐都医院神经内科,陕西西安710038 [5]第四军医大学唐都医院血液科,陕西西安710038

出　　处：《现代生物医学进展》2017年第24期4621-4625,共5页Progress in Modern Biomedicine

基　　金：国家自然科学基金项目(31572344)

摘　　要：目的:研究三氧化二砷(Arsenic trioxide,ATO)对人白血病HL-60细胞凋亡的影响,并以线粒体通路为靶点探讨其可能的机制。方法:采用1μg/m L、5μg/m L及10μg/m LATO处理HL-60细胞24小时后,采用流式细胞术检测细胞凋亡情况,通过细胞内MDA与GSH含量检测反映氧化应激水平,采用免疫印迹法检测凋亡相关分子表达,并通过免疫荧光染色检测细胞线粒体膜电位(mitochondrial membrane potential,MMP)水平。结果:5μg/m L及10μg/m L ATO可显著诱导人白血病HL-60细胞凋亡,并显著增加其氧化应激水平,增加促凋亡分子Bax和Caspase-3的表达,而抑制抗凋亡分子Bcl-2的表达,降低HL-60细胞线粒体膜电位的水平。结论:一定剂量的ATO可诱导人白血病HL-60细胞凋亡,而这一作用可能是通过诱导线粒体相关性凋亡信号通路激活实现。Objective：To investigate the potential pro-apoptotic activity of arsenic trioxide （ATO） in human leukemia HL-60 cells,as well as the potential mechanism with focus on mitochondrial pathway.Methods：After treatment with different concentrations of ATO （1 μg/mL,5 μg/mL or 10 μg/mL） for 24 h,apoptotic cell death was detected by flow cytometry,oxidative stress was determined by measuring MDA and GSH levels,the expression of apoptotic factors was detected by western blot,and mitochondrial membrane potential （MMP） was determined by immunofluorescence staining.Results：ATO at the concentrations of 5 μg/mL or 10 μg/mL induces apoptotic cell death and increases oxidative stress in human leukemia HL-60 cells.ATO significantly increases the expression of pro-apoptotic factors （Bax and Caspase-3）,whereas decreases the expression of anti-apoptotic factor Bcl-2.Compared with the control group,ATO treatment significantly decreases the MMP level in HL-60 ceils.Conclusions：Arsenic trioxide induces apoptotic cell death through mitochondrial pathway in human leukemia HL-60 cells.

关 键 词：三氧化二砷 氧化应激 凋亡 线粒体 HL-60细胞 

分 类 号：R-33[医药卫生] R733.71