Arsenic Trioxide Induces Apoptotic Cell Death through Mitochondrial Pathway in Human Leukemia HL-60 Cells
10.13241/j.cnki.pmb.2017.24.005
- VernacularTitle:三氧化二砷通过线粒体途径诱导人白血病HL-60细胞凋亡
- Author:
Pin FENG
;
Qinglin YAO
;
Xiaoguang WANG
;
Xiaohui HU
;
Chunlei XIONG
- Keywords:
Arsenic trioxide;
Oxidative stress;
Apoptosis;
Mitochondria;
HL-60 cells
- From:
Progress in Modern Biomedicine
2017;17(24):4621-4625
- CountryChina
- Language:Chinese
-
Abstract:
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.
