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目的 :研究柔红霉素 (DNR)诱导白血病细胞凋亡的机制 ,进一步探讨Fas/FasL途径在DNR诱导白血病细胞凋亡中的作用 ,并评价sFasL与DNR联用的致凋亡效应。方法 :将DNR作用于白血病细胞系HL 6 0、K5 6 2、U937细胞 ,并用流式细胞术 (FCM)检测其Fas抗原表达的改变。sFasL、DNR诱导白血病细胞凋亡 ,以抗Fas单抗 (IgG1)阻断Fas/FasL途径 ,借助原位末端标记法 (TUNEL)和FCM检测白血病细胞凋亡率。结果 :DNR处理HL 6 0、K5 6 2、U937细胞 18h后 ,Fas表达阳性率无明显变化 (P >0 .0 5 ) ,与sFasL联合作用后显示出协同效应。IgG1不能阻断DNR致白血病细胞凋亡的作用 ,但可阻断sFasL致白血病细胞凋亡的作用。结论 :DNR致白血病细胞株U937、HL 6 0凋亡的作用不依赖于Fas/FasL途径 ,但sFasL与DNR联合应用可协同增强抗肿瘤效应。
Objective: To study the mechanism of daunorubicin (DNR)-induced apoptosis of leukemia cells, further investigate the role of Fas/FasL pathway in DNR-induced apoptosis of leukemia cells, and evaluate the apoptotic effects of sFasL and DNR. METHODS: DNR was applied to leukemic cell lines HL 60, K562, and U937, and the expression of Fas antigen was detected by flow cytometry (FCM). sFasL and DNR induced apoptosis of leukemia cells, and Fas/FasL pathway was blocked by anti-Fas monoclonal antibody (IgG1). The apoptosis rate of leukemia cells was detected by TUNEL and FCM. RESULTS: After treatment with HL 60, K562, and U937 cells for 18 h, DNR had no significant change in the positive rate of Fas expression (P > 0.05). Synergistic effects were observed with sFasL. IgG1 can not block the effect of DNR-induced apoptosis of leukemia cells, but it can block the effect of sFasL-induced apoptosis of leukemia cells. Conclusion : The effect of DNR-induced apoptosis of leukemic cell lines U937 and HL 60 is not dependent on the Fas/FasL pathway, but the combination of sFasL and DNR can synergistically enhance the anti-tumor effect.