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目的 :探讨核因子 NF- κB是否与柔红霉素 (DNR)在体外诱导 HL- 6 0细胞凋亡的过程有关。方法 :应用光镜、流式细胞技术 (FCM)检测 DNR对 HL- 6 0细胞的凋亡作用 ;并采用细胞免疫化学 (IC)、FCM、电泳运动转移分析 (EMSA)法分别检测对照细胞组、DNR诱导 HL- 6 0细胞凋亡组、PTDC或 FBI抑制组细胞核内 NF- κB的表达情况。结果 :1.0 μm ol/ L DNR对 HL- 6 0细胞作用 5 h时 ,有显著的凋亡现象发生 ,且细胞内 NF- κB的表达较对照细胞显著增强 ,PDTC可显著抑制 DNR作用 HL- 6 0后的凋亡率及 NF- κB的表达 ,而 FBI对此无明显作用。结论 :DNR诱导 HL- 6 0凋亡的过程与细胞核因子 NF- κB有关 ,ROS参与了此凋亡过程。
Objective: To investigate whether nuclear factor NF-κB is involved in daunorubicin (DNR) induced apoptosis of HL-60 cells in vitro. Methods: The apoptotic effect of DNR on HL-60 cells was detected by light microscopy and flow cytometry (FCM). Cell apoptosis was detected by immunocytochemistry (IC), FCM and electrophoretic mobility shift assay (EMSA) , DNR induced NF-κB expression in HL-60 cell apoptosis group, PTDC or FBI inhibition group. Results: The apoptosis of HL-60 cells treated with 1.0 μmol / L DNR for 5 h resulted in significant apoptosis, and the expression of NF-κB was significantly increased in HL-60 cells. PDTC could significantly inhibit the effect of DNR on HL-6 0 after the apoptosis rate and NF-κB expression, while FBI had no significant effect. CONCLUSION: The apoptotic process of HL-60 induced by DNR is related to the nuclear factor NF-κB, and ROS is involved in this process.