三氧化二砷对K562/A02细胞的凋亡及细胞周期的影响  

Effect of Arsenic Trioxide on Cell Cycle and Apoptosis of Multidrug Resistant K562/A02 Cell Line

作　　者：陆跃武[1] 耿华云[1] 张峰[1] 盖灿[1] 韩慧杰[1] 孙海英[2] 

机构地区：[1]淮北市人民医院内二科,安徽淮北235000 [2]徐州医学院附属医院血液科,江苏徐州221006

出　　处：《现代生物医学进展》2012年第15期2852-2854,2875,共4页Progress in Modern Biomedicine

摘　　要：目的:研究三氧化二砷对多药耐药急性白血病细胞株K562/A02凋亡与细胞周期的影响及可能机制。方法:取阿霉素(Adr)的耐药白血病细胞株分为未加药的对照组及加入不同浓度的三氧化二砷(其终浓度为4.0μmol/L、5.0μmol/L)组,流式细胞仪检测细胞凋亡及细胞周期分布,Western blot方法检测不同浓度三氧化二砷对K562/A02细胞核NF-κBp65蛋白水平。结果:与对照组比较,三氧化二砷可显著增加Adr对K562/A02细胞凋亡率,阻滞细胞于G0/G1期,降低K562/A02细胞胞核中NF-kB p65的表达(P均<0.05)。结论:三氧化二砷可能是通过抑制NF-kB的胞内活化转位,从而促进K562/A02细胞凋亡及抑制细胞增殖。Objective： To explore the effect of arsenic trioxide on cell cycle and apoptosis of K562/A02 cells and its possible mechanism.Methods： Adriamycin（Adr） resistant K562/A02 were treated with arsenic trioxide（non-cytotoxic concentration at 4.0υmol/L,5.0υmol/L） or without arsenic trioxide（control）,flow cytometry was used to evaluate apoptosis and cell cycle distribution,and change of the expression level of NF-κBp65 protein in nucleus was detected by western blot.Results： As compared with control arsenic trioxide significantly increased the rate of apoptosis,arrested cells in G0/G1phase and reduced the levels of NF-κBp65 protein in nucleus（allP〈0.05）.Conclusion： The underlying mechanism for arsenic trioxide to promote apoptosis of K562/A02 and suppress cell proliferation lies in its impact on NF-κBp65 protein expression.

关 键 词：三氧化二砷 多药耐药 K562/A02 细胞凋亡 细胞周期 

分 类 号：R733.7[医药卫生—肿瘤]