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机构地区:[1]青岛大学医学院附属烟台毓璜顶医院血液科,山东烟台264000 [2]青岛大学医学院附属医院血液科,山东青岛266003
出 处:《中华肿瘤防治杂志》2008年第14期1073-1075,共3页Chinese Journal of Cancer Prevention and Treatment
摘 要:目的:探讨三氧化二砷(As2O3)治疗白血病的作用机制。方法:1)用流式细胞仪检测细胞膜上的CD11b的表达和细胞凋亡率。2)用RT-PCR方法检测c-myc基因在mRNA水平上的表达。结果:2.5μmol/LAs2O3处理HL-60细胞90h后,细胞分化的标志性细胞膜抗原CD11b表达明显升高,由(14.5±2.1)%升高到(35.4±5.7)%,P<0.05;NBT阳性细胞由(10.0±2.1)%升高到(31.2±3.4)%(P<0.05),同时c-myc基因在mRNA水平也明显降低。结论:As2O3通过降低c-myc基因表达及上调细胞分化抗原CD11b表达,从而促进HL-60细胞分化。OBJECTIVE: To explore the mechanism of arsenic trioxide (As203)in the treatment of leukemia. METHODS: 1)The expression of CDllh, cell cycle and apoptosis were investi gated by flow cytometry. 2)The mRNA expression of c-myc was showed by RT PCR. RESULTS: Arsenic trioxide significantly increased CDllh in HL-60 cells, and the expression rate of CDllh increased from (14.5±2.1)% to (35.4±5.7)% after treated by 2.5 μmol/L arsenic trioxide for 90 hours (P(0. 05), and the percentage of NBT positive cells increased from ( 10. 0±2. 1 )% to (31.2±3.4) % (P〈0. 05),and mRNA expression of c-myc was reduced significantly. CONCLUSION: Arsenic trioxide increases the cell differentiation in HL-60 cells by reducing mRNA expression of c-myc and increasing the expression of CDllb.
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