摘要
目的:探讨去甲基化制剂地西他滨和全反式维甲酸对MDS-RAEB细胞株SKM-1的体外影响及其机制。方法:SKM-1细胞经药物处理后,用台酚蓝拒染法观察SKM-1细胞生长曲线的变化;用硝基四氮唑蓝还原试验和流式细胞术观察药物对SKM-1细胞的诱导分化作用;用Annexin Ⅴ-FITC标记了解细胞的早期凋亡;用RT-PCR研究细胞DNMT3A和P15INK4B基因表达的变化。结果:地西他滨和ATRA抑制SKM-1细胞生长,增强SKM-1细胞的还原能力,增加细胞表面CD14、CD11b表达,促进细胞凋亡,两药联合应用具有协同作用;地西他滨可使SKM-1细胞P15INK4B mRNA表达增加,DNMT3A mRNA表达减少。结论:地西他滨和ATRA均可以促进SKM-1细胞凋亡和分化,二者有协同作用;地西他滨的作用可能与DNMT3A和P15INK4B基因表达有关。
Objective ：To explore the effects and the mechanisms of demethylating agent Decitabine and/or ATRA on SKM-1 cells in vitro. Method：The proliferation of SKM-lcells was assessed by trypan blue exclusion staining;the differentiation of SKM-lcells was tested by nitro-blue tetrazolium （NBT） reduction and flow cytometry; the early apoptosis of the cells was detected by Annexin V-FITC double staining; the mRNA expressions of DNMT3A and P15~4B in the cells were assayed by reverse transcription-polymerase chain reaction （RT-PCR）. Result：Decitabine and ATRA inhibited SKM-1cells＇ growth enhanced the cells＇ reducing power, increased the expressions of CD14 and CD1 lb, and induced apoptosis of the cells, Combination of Decitabine and ATRA had synergistic effect. Decitabine could up-regulate P15INK4B mRNA expression, and down-regulate DNMT3A mRNA expression. Conclusion：Both Decitabine and ATRA can induce the apoptosis and differentiation of SKM-1 cells, and their combination has synergistic effect. The effects of Decitabine may be linked to the expressions of DNMT3A and P15INK4B.
出处
《交通医学》
2009年第2期125-128,131,共5页
Medical Journal of Communications
