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目的 目前研究发现 ,骨髓基质细胞分泌的基质衍生因子 1(stromalcellderivedfactor 1,SDF 1)及其受体CXCR4可能参与髓内残留病变的形成。因此 ,本研究着重探讨了阻抑SDF 1活性对与正常骨髓基质细胞共培养的HL 60细胞增殖、生存的影响。方法 培养并共培养HL 60细胞。实验分为两组 ,实验组采用抗CXCR4单克隆抗体 12G5( 2 0ug/ml)阻断SDF 1生物作用 ,孵育 2 4小时后采用免疫组化染色检测HL 60细胞Bcl 2、PCNA、Fas蛋白表达。 结果 免疫组化染色显示 ,实验组中Bcl 2、PCNA及Fas阳性率分别为 ( 15 .7± 4.9) %、( 4 2 .1± 3 .9) %及 ( 3 9.7± 7 5 ) % ,而对照组分别为 ( 3 1.6± 5 .2 ) %、( 67.4± 8.5 ) %和 ( 2 4.1± 6.7) % ,t检验显示 12G5下调HL 60细胞Bcl 2及PCNA蛋白表达 ,上调Fas蛋白表达。结论 12G5可在一定程度抑制HL 60细胞增殖 ,促进凋亡 ,影响其生存。
OBJECTIVE: The present study found that stromalcell-induced factor 1 (SDF-1) and its receptor CXCR4 secreted by bone marrow stromal cells may participate in the formation of residual intramedullary lesions. Therefore, this study focused on the inhibition of SDF 1 activity on proliferation and survival of HL 60 cells co-cultured with normal bone marrow stromal cells. Methods HL 60 cells were cultured and co-cultured. The experiment was divided into two groups. In the experimental group, the anti-CXCR4 monoclonal antibody 12G5 (20ug / ml) was used to block the biological effect of SDF1. The expression of Bcl2, PCNA and Fas protein in HL-60 cells was detected by immunohistochemistry 24 hours after incubation . Results Immunohistochemical staining showed that the positive rates of Bcl-2, PCNA and Fas in the experimental group were (15.7 ± 4.9)%, (42.1 ± 3.9%) and (37.77 ± 7.5)%, respectively While the control group was (31.6 ± 5.2)%, (67.4 ± 8.5)% and (2.41 ± 6.7)%, respectively. T test showed that 12G5 down-regulated the expression of Bcl-2 and PCNA, and up-regulated the expression of Fas protein in HL-60 cells. Conclusion 12G5 can inhibit HL 60 cell proliferation, promote apoptosis and affect its survival.