3种化疗药物诱导HL-60细胞凋亡及Fas FasL的表达

目的:观察阿糖胞苷(Ara-c)、柔红霉素(DNR)及长春新碱(VCR)诱导HL-60细胞株凋亡的规律及细胞凋亡中Fas、FasL抗原的变化,探讨凋亡基因在细胞凋亡中的作用。方法:应用流式细胞仪及吖啶橙染色荧光显微镜观察3种化疗药物对HL-60细胞凋亡的影响,及细胞Fas、FasL的表达情况。结果:DNR和Ara-C能诱导HL-60细胞发生凋亡,荧光显微镜观察HL-60细胞可见凋亡小体、核染色质聚集、胞体出芽改变。流式细胞仪检测在G1期前出现sub-G1峰,随着化疗药物浓度的增加及共培养作用时间的延长,HL-60细胞凋亡率逐渐增加。每个实验组细胞凋亡率与对照组相比差异有显著性(P<0.01,P<0.05)。VCR每个实验组细胞凋亡率与对照组比较差异无显著性(P>0.05)。DNR作用HL-60细胞可使Fas、FasL表达增加;Ara-C可使FasL表达增加,而Fas表达无变化;VCR作用后Fas表达增加,而对FasL表达无影响。结论:DNR和Ara-C可诱导HL-60细胞凋亡,VCR诱导调亡作用不明显。DNR可上调HL-60细胞Fas/FasL表达,Fas/FasL系统参与DNR诱导的细胞凋亡过程。

APOPTOSIS AND THE EXPRESSION OF FAS, FasL INDUCED BY THREE CHEMOTHERA-HEMOTHERAPEUTIC DRUGS IN CELL LINE HL-60

Objective:It has been reported that Fas and FasL,a double death factors,play an impor-tant role in immunoregulation and immunopathogenesis.The patterns of apoptosis and the expression of Fas and FasL of HL-60cells induced by chemotherapeutic drugs were studied,and explore the effect of Fas and FasL on the process of apoptosis.Methods:The effect on apoptosis and the expression of Fas and FasL of HL-60cell induced by cytosine arabinoside(Ara-C),daunorubicin(DNR)and vincristine(VCR)were measured by flow cytometry analysis and fluorescence microscope.Results:DNR and Ara-C could in-duced apoptosis of HL-60cell.Morphological changes such as apoptosis bodies,chromatic condensation,cytoplasm blubbling were observed by fluorescence microscope.Sub-G 1 peaks was found by flow cytometry.They increased with the increase of planting concentration of chemotherapeutic drugs and co-culture time.There were significant difference between each test group of DNR and Ara-C and control(P<0.01,P<0.05).There were not significant difference between VCR test group and control(P>0.05).DNR could upregulate the expression of Fas and FasL.Ara-C upregulated FasL without any change of Fas.VCR did not affected the expression of FasL,the expression of Fas was increased.Conclusion:DNR and Ara-C could in-duced apoptosis of HL-60cell.DNR could induce the expression of Fas and FasL of HL-60cell.Fas-FasL system participated in the apoptosis induced by DNR.