氧化砷诱导维甲酸耐药早幼粒细胞白血病细胞(MR-2)凋亡的体外研究  

In vitro study on arsenic trioxideinduced apoptosis of retinoic acid resistant acute promyelocytic leukemia cell line(MR-2)

作　　者：蔡循[1,2] 贾培敏[1,2] 石学耕 史桂英[1,2] 朱新华[1,2] 王龙[1,2] 陈赛娟[1,2] 王振义[1,2] 陈竺 陈国强[1,2] 

机构地区：[1]上海第二医科大学附属瑞金医院 [2]上海第二医科大学生物物理教研室

出　　处：《中华血液学杂志》1998年第7期339-341,共3页Chinese Journal of Hematology

基　　金：国家自然科学基金;杰出青年科学基金;上海市青年启明星计划;上海血液学研究所胡应洲基金

摘　　要：目的：深入了解氧化砷（Ａｓ２Ｏ３）治疗急性早幼粒细胞白血病（ＡＰＬ）的机制。方法：以对全反式维甲酸耐药的ＡＰＬ细胞株ＭＲ２为模型，用细胞生长、活力测定、形态学观察和流式细胞仪分析、四氮唑蓝还原反应及免疫荧光等指标观察Ａｓ２Ｏ３治疗ＡＰＬ的效应途径。结果：１．０μｍｏｌ／ＬＡｓ２Ｏ３可诱导ＭＲ２细胞凋亡，并能降解ＡＰＬ特异蛋白ＰＭＬＲＡＲα融合蛋白。结论：Ａｓ２Ｏ３治疗ＡＰＬ的效应途径可能不同于ＡＴＲＡ。Objective:To study the possible mechanisms of arsenic trioxide (As_2O_3)in the treatment of acute promyelocytic leukemia (APL). Methods:Retinoic acid resistant APL cell line MR-2 was used as in vitro model. The effect of As_2O_3 on MR-2 cell line was observed by cell viability,cell growth,cell morphology,flow cytometry assay,NBT reduction test and immunofluorescence analysis. Results:1.0μmol/L of As_2O_3 could induce apoptosis of MR-2 cells and it correlated with the degradation of PML-RARα fusion protein. Conclusions: The therapeutic effect of As_2O_3 for APL possibly differs from that of ATRA, however, PML-RARα fusion protein may be the target of both the therapy.

关 键 词：白血病 APL 药物疗法 氧化砷 维甲酸 细胞凋亡 

分 类 号：R733.710.5[医药卫生—肿瘤]