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，但ＰＭＬＲＡＲα可能是二者的共同作用靶点 Objective: To understand the mechanism of arsenic trioxide (As2O3) in the treatment of acute promyelocytic leukemia (APL). METHODS: MR  2 APL cell line resistant to all-trans retinoic acid was used as a model, observed by cell growth, viability assay, morphological observation and flow cytometry analysis, tetrazolium blue reduction reaction and immunofluorescence. The effect of As2O3 in the treatment of APL. RESULTS: 1.0 μmol/L A 2 O 3 could induce apoptosis of MR 2 cells and degrade APL-specific protein PMLRARα fusion protein. Conclusion: As2O3 may be different from ATRA in the treatment of APL, but PMLRARα may be the target of both