摘要
目的 研究三氧化二砷 (AS2 O3 )体外对K5 6 2细胞凋亡的诱导作用 ,探讨AS2 O3 促进慢性粒细胞系K5 6 2细胞凋亡机制。方法 采用不同浓度AS2 O3 处理慢性粒细胞系K5 6 2细胞 ,观察细胞形态改变 ,细胞生长抑制检测 (MTT)分析方法检测AS2 O3 对K5 6 2细胞增殖抑制作用 ;流式细胞仪检测细胞周期变化。结果 (1~8)× 10 -6mol/LAS2 O3 能明显诱导K5 6 2细胞凋亡。流式细胞检测表明 ,随AS2 O3 浓度增加和处理时间延长 ,S期细胞比例渐下降 ,细胞凋亡率上升 ,其作用呈浓度 时间依赖性 (P <0 .0 1)。结论 AS2 O3 可诱导K5 6 2细胞凋亡 ,其作用机制可能是使细胞受阻于S期前的某个时期 ,从而诱导细胞凋亡 ,其作用呈剂量
Objective To investigate the apoptosis induced function of arsenic trioxide(AS 2O 3) in leukemia cell line K562 in vitro and elucidate the possible cellular mechanisms.Methods K562 cells were treated with AS 2O 3 in different concentrations. Morphological changes of apoptosis were observed with invert fluorescence microscope and cell proliferation was determined by MTT assay. Cell cycle was examined by PI fluorescence flow cytometry (FCM).Results AS 2O 3 (1~8)×10 -6mol/L could induce obviously K562 cell line apoptosis. Flow cytometry analysis showed that the number of S phase cells decreased gradually and cell apoptosis rates increased with raised concentrations and prolonged treatment of AS 2O 3. The relationship between cell apoptosis rates and the concentrations of AS 2O 3 showed a dose-and-time-dependent effect (P<0.01 ).Conclusions AS 2O 3 might induce K562 cell line apoptosis. The mechanism is probably through blocking the cell cycle before S phase to induce K562 apoptosis in a dose-and-time-dependent manner.
出处
《实用儿科临床杂志》
CAS
CSCD
北大核心
2004年第5期353-354,共2页
Journal of Applied Clinical Pediatrics
基金
湖南省卫生厅基金资助项目 (2 0 0 1 -Y1 7)