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目的探讨地西他滨对伊马替尼耐药细胞株KBM5-T315I的增殖抑制及诱导凋亡作用。方法应用细胞增殖及毒性检测法(新型四唑单钠盐法)观察不同浓度(0～40μmol/L)地西他滨作用于KBM5-T315I细胞24、48及72h后的细胞增殖活力变化,采用Annexin V-FITC/PI双染流式细胞术观察不同浓度地西他滨对KBM5-T315I处理24h后的细胞凋亡率,JC-1法检测细胞线粒体膜电位的变化,Western blot检测cleaved PARP的变化。结果地西他滨可显著抑制KBM5-T315I细胞生长,显示出明显的量-效与时-效关系。随着地西他滨药物浓度增加,KBM5-T315I细胞株凋亡率逐渐升高,线粒体膜电位逐渐下降,cleaved PARP表达水平显著上升。结论地西他滨能抑制KBM5-T315I细胞的生长及诱导其凋亡,从而为治疗伊马替尼耐药慢性粒细胞白血病提供实验依据。
Objective To investigate the inhibitory and apoptosis-inducing effects of decitabine on the proliferation of imatinib-resistant KBM5-T315I cells. Methods Cell proliferation and cytotoxicity assay (the new tetrazolium monosodium salt method) were used to observe the changes of cell proliferation after 24, 48 and 72 h treatment of different concentration (0-40 μmol / L) of decitabine on KBM5-T315I cells. Annexin V-FITC / PI double staining flow cytometry cells treated with different concentrations of decitabine KBM5-T315I treatment 24h after apoptosis, JC-1 method to detect changes in mitochondrial membrane potential, Western blot detection of cleaved PARP Variety. Results Decitabine can significantly inhibit the growth of KBM5-T315I cells, showing a significant dose-effect and time-effect relationship. With the increase of drug concentration of decitabine, the apoptotic rate of KBM5-T315I cells gradually increased, the mitochondrial membrane potential decreased gradually, cleaved PARP expression increased significantly. Conclusion Decitabine can inhibit the growth of KBM5-T315I cells and induce their apoptosis, so as to provide experimental evidence for the treatment of Imatinib-resistant CML.