三氧化二砷诱导多药耐药白血病细胞K562-n/VCR凋亡  

Apoptosis on multi-drug resistant leukemia cell line K562-n/VCR induced by arsenic trioxide

作　　者：许晓巍[1] 许小平[1] 陈少谊[1] 易克[1] 陈莉[1] 吕书晴[1] 贾新颜[1] 

机构地区：[1]第二军医大学附属长海医院血液科,上海200433

出　　处：《白血病．淋巴瘤》2005年第1期4-6,共3页Journal of Leukemia & Lymphoma

基　　金：国家自然科学基金资助项目(39770330)

摘　　要：目的研究三氧化二砷(As2O3)对裸鼠高成瘤性慢性粒细胞白血病(CML)急变细胞系K562蛳n及其表达mdr蛳1的多药耐药细胞系K562蛳n/VCR诱导凋亡作用的差异。方法采用WST法、细胞形态学、流式细胞术等多参数分析。结果As2O3对K562蛳n及K562蛳n/VCR的抑制作用无显著性差异。As2O3对K562蛳n及K562蛳n/VCR细胞的凋亡诱导作用呈作用时间和浓度依赖关系。结论As2O3对表达mdr蛳1的CML急变期细胞系K562蛳n/VCR具有抑制生长及较明显的诱导凋亡作用。Objective To investigate the efficacy of arsenic trioxide (As2O3) on K562- n and K562- n/VCR. Methods The apoptosis of the two cell lines induced by As2O3 solution of different concentrations were studied with WST, cell morphology and flow cytometry. Results It was found that there was no significant different of IC50 between K562- n and K562- n/VCR. As2O3 could induce the apoptosis of K562- n and K562- n/VCR cell lines, which dependent on its concentration and time in vitro. Conclusions As2O3 had a pronounced effect on K562- n/VCR cell line expressing mdr- 1 gene.

关 键 词：三氧化二砷 凋亡 白血病 多药耐药 

分 类 号：R733.7[医药卫生—肿瘤]