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目的 探讨氧化砷 (As2 O3)是否诱导多发性骨髓瘤细胞凋亡与其可能机制。方法 以两株多发性骨髓瘤细胞系RPMI82 2 6和U2 66为体外模型。以细胞形态学观察、流式细胞仪检测亚G1期细胞含量以及DNA凝胶电泳判定细胞凋亡。通过检测胞内Rhodamine12 3染色强度来判定线粒体跨膜电位。通过Western印迹分析蛋白表达。结果 0 1- 0 5μmol LAs2 O3抑制RPMI82 2 6与U2 66细胞系生长 ,2 0 μmol LAs2 O3 诱导两株细胞凋亡 ,而 1 0μmol LAs2 O3抑制细胞生长同时也诱导部分细胞凋亡。As2 O3诱导的细胞凋亡伴随线粒体跨膜电位下降与细胞凋亡 ,而二巯基苏糖醇 (二巯基还原剂 )则部分抑制以上效应。虽然全反式维甲酸 (ATRA)诱导RPMI82 2 6细胞凋亡 ,但是它与As2 O3无协同效应。结论 不同深度As2 O3可抑制多发性骨髓瘤细胞生长与诱导细胞凋亡。线粒体是As2 O3 诱导细胞凋亡的重要且共同的“靶子”。
Objective To investigate whether arsenic trioxide (As2O3) induces apoptosis of multiple myeloma cells and its possible mechanism. Methods Two multiple myeloma cell lines, RPMI82 26 and U2 66, were used as in vitro models. Cellular morphology was observed, flow cytometry was used to detect sub-G1 phase cell content, and DNA gel electrophoresis was used to determine cell apoptosis. Mitochondrial transmembrane potential was determined by measuring intracellular Rhodamine 12 3 staining intensity. Protein expression was analyzed by Western blot. Results 0 1- 05 μmol LAs2 O3 inhibited the growth of RPMI82 2 6 and U2 66 cell lines, and apoptosis was induced by 20 μmol LAs2 O3. While 10 μmol LAs2 O3 inhibited the cell growth and induced apoptosis. As2O3-induced apoptosis was accompanied by a decrease in mitochondrial transmembrane potential and apoptosis, while dithiothreitol (dithiol reductant) partially inhibited these effects. Although all-trans retinoic acid (ATRA) induced apoptosis in RPMI82 26 cells, it had no synergistic effect with As2O3. Conclusion Different levels of As2O3 can inhibit the growth of multiple myeloma cells and induce apoptosis. Mitochondria are important and common “targets” for apoptosis induced by As2O3.