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目的:研究放线菌素D对沙尔威辛诱导K562细胞凋亡和细胞毒性的影响。方法:采用四氮唑盐(MTT)还原法测定药物对K562细胞的生长抑制作用;凋亡诱导作用采用荧光显微镜术、DNA琼脂糖凝胶电泳和流式细胞术进行评价。结果:药物处理K562细胞24h后检测发现,放线菌素D能在一定程度上增强沙尔威辛6.25μmol/L的细胞毒性作用,平均生长抑制率由沙尔威辛单独应用时8％上升到联合应用放线菌素D 0.04、0.4和4μmol/L时的69％、71％和70％。在沙尔威辛浓度大于6.25μmol/L时,未见同样的增强作用,却也不减弱其抑制细胞生长的作用。这显示放线菌素D可以增强或至少不减弱沙尔威辛的细胞毒性作用。但荧光显微镜 术、DNA琼脂糖凝胶电泳和流式细胞术却表明,在同等条件下,放线菌素D抑制沙尔威辛诱导K562细胞凋亡。结论:放线菌素D可增强沙尔威辛适当浓度范围内的细胞毒性作用,但却抑制其诱导的白血病细胞凋亡,提示该过程中存在着除凋亡以外的其它细胞死亡方式。
Objective: To study the effects of actinomycin D on apoptosis and cytotoxicity of K562 cells induced by sharmazine. Methods: MTT assay was used to determine the growth inhibition of K562 cells. The induction of apoptosis was evaluated by fluorescence microscopy, DNA agarose gel electrophoresis and flow cytometry. Results: After treatment with K562 cells for 24 h, it was found that actinomycin D could enhance the cytotoxicity of 6.25 μmol / L of salbutamol to a certain extent. The average growth inhibition rate was increased by 8% when Salbutamol alone To 69%, 71% and 70% at the combined application of actinomycin D 0.04, 0.4 and 4 [mu] mol / L. At concentrations of more than 6.25 μmol / L, the same enhancement was not observed in Salbutamol, but did not diminish its inhibitory effects on cell growth. This shows that dactinomycin D may enhance, or at least not diminish, the cytotoxic effect of chardzin. However, fluorescence microscopy, DNA agarose gel electrophoresis and flow cytometry showed that actinomycin D inhibited the apoptosis of K562 cells induced by salbutamol under the same conditions. Conclusion: Actinomycin D can enhance the cytotoxicity of Salbutamol in the proper concentration range, but inhibit the apoptosis of Leukemia cells induced by it, suggesting that there are other cell death modes besides apoptosis in this process.