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机构地区:[1]镇江医学院附属医院,江苏省镇江市212001 [2]上海第二医科大学瑞金医院
出 处:《白血病》1998年第3期136-139,共4页
摘 要:为了探讨砷剂治疗白血病的作用机制,我们采用形态学、细胞生长曲线、祖细胞培养、DNA电泳、荧光染色法流式细胞仪分析、P53蛋白和bcl-2蛋白表达等多参数研究,结果显示三氧化二砷和硫化砷作用相似,均能抑制NB4细胞增殖,对NB4细胞CFU-L和对正常人骨CFU-GM、BFU-E也有抑制作用。抑制作用强度三氧化二砷优于流化砷。二种砷剂均能诱导NB4细胞程序化死亡.其机制可能与P53蛋白和bci-2蛋白表达水平下降有关。Cell morphology, cell growth curve, CFU-L.CFU-GM.BFU-E culture in intro, DNA electrophoresis, flow cytometry, p53 and Bcl-2 protein expression were used to study the mechanisms of the arsenicals treatment for leukemia. The results indicate that arsenic trioxide (As,O, )and arsenic disulfide (As2S2) can show a significant cytolytic effect on NB4. Arsenicals might also appear inhibitive activity for CFU-L of NB4.CFU-GM of BFU-E of bone marrow in normal human. Inhibitive activity of As2O3 is higher than that of As2S2.Programmed cell death in NB4 can be induced by both of the arsenicals. The mechanisms of the induction of programmed cell death may be associated with overexpression of p53 and Bcl-2 protein.
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