阿糖胞苷对HL60细胞凋亡及其Bcl-2蛋白表达的影响

Effect of Ara-C on Apoptosis and bcl-2 Protein Expressions in HL60

目的 探讨阿糖胞苷对白血病细胞的作用及其机制。方法 以人急性早幼粒白血病细胞HL6 0为淋巴细胞 ,分别应用HE染色和透射电镜观察Ara C对HL6 0细胞形态学的影响及其超微结构的变化 ;应用流式细胞术及免疫细胞化学研究Ara C对细胞凋亡和Bcl 2蛋白表达的变化。结果 细胞形态不规则 ,核深染 ,染色质聚边等多种形态改变。电镜下可见典型的凋亡特征。流式细胞仪分析结果显示 ,细胞凋亡率随药物浓度增加和作用时间延长而增加 ,Bcl 2蛋白的表达则下降。结论 Ara C能诱导HL6 0细胞凋亡 ;下调Bcl 2蛋白的表达 ,这可能是Ara C诱导细胞凋亡的机制之一。

Objective To investigate the effects and mechanisms of Ara-C on HL60.Methods HL60 cells were incubated for 24、48h.Morphologic changes were observed by HE stain and electron microscopy.Apoptosis and level of bcl-2 protein were assessed by flow cytometry(FCM) and immunocytochemistry,respectively.Results After incubated with Ara-C for 48 hours,HL60 cells exhibited characteristic morphologic changes of apoptosis,including irregular cell morphology,cytoplasm membrane blebbing,chromatin condensation,crescents formation and nuclear fragmentation.The apoptosis rate of protein expressions of HL60 cells were significantly augmented and bcl-2 decreased with concentration and time of Ara-C increasing(P<0.05)respectively.Conclusion Ara-C induces HL60 apoptosis,and the down-regulation of bcl-2 protein expressions may be one of the mechanisms of this apoptosis-promoting effect.