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本研究通过观察抗CXCR4单克隆抗体12G5对Ara C杀伤HL-60细胞效应的影响,评价其在白血病骨髓 残留病变中的治疗价值。培养并共培养HL-60细胞,在共培养体系中采用12G5(10μg／ml)阻抑基质细胞SDF-1的 生物作用后,通过MTT法及细胞形态学观察检测不同浓度Ara c对HL-60细胞杀伤作用的变化。药物杀伤效应曲 线显示,在20μg／ml Ara C组,对照组中前2天A540值明显下降,但从3-4天开始出现上升,而加12G5实验组中 A540值虽然下降平缓,但持续下降,并于观察第5天后低于对照组,整个观察期中未出现反弹。在40μg／ml Ara C 组,对照组A540在0-3天明显下降,从第4天开始回升,于第5-6天与实验组曲线交叉,从7-12天时照组A540值 总体呈上升趋势,并明显高于实验组,而加12G5实验组曲线在整个观察期间虽然在7-9天有小幅度攀升,但总的 趋势是下降。细胞形态学观察显示,在两个浓度组,对照组HL-60细胞数量最初明显减少,随着培养时间延长,细 胞数量逐渐增多,实验组结果正相反。结论:12G5减弱Ara C对HL-60细胞的早期杀伤作用,但12G5增强Ara C 总体杀伤作用,同时,延缓HL-60细胞对Ara c的耐药性,因此12G5有助于白血病骨髓残留病变的治疗。
In this study, by observing the effect of anti-CXCR4 monoclonal antibody 12G5 on the Ara C cytotoxic effect on HL-60 cells, we evaluated its therapeutic value in residual leukemia bone marrow disease. HL-60 cells were cultured and co-cultured with 12G5 (10μg / ml) to inhibit the biological effects of stromal cells SDF-1 in the co-culture system. MTT assay and cell morphology were used to detect the effects of Ara c on HL-60 Changes in cell killing. The drug-killing effect curve showed that in the 20μg / ml Ara C group, the value of A540 in the first two days of the control group decreased significantly, but increased from 3-4 days, while the A540 value in the 12G5 experimental group decreased slowly but decreased , And was lower than the control group on the 5th day after the observation. There was no rebound in the whole observation period. In 40μg / ml Ara C group, the control group A540 decreased significantly from day 0-3 and rose from day 4, and crossed with the experimental group on day 5-6. The A540 value of control group increased from 7 to 12 days Trend, and was significantly higher than the experimental group, while the experimental group plus 12G5 throughout the observation period although a slight increase in 7-9 days, but the overall trend is declining. Morphological observation showed that the number of HL-60 cells in the control group initially decreased significantly at both concentrations, and the number of cells gradually increased with the prolongation of culture time. The results of the experimental group were opposite. CONCLUSIONS: 12G5 attenuates the early killing effect of Ara C on HL-60 cells, but 12G5 enhances the overall killing effect of Ara C and delays the resistance of Ara-c to HL-60 cells. Therefore, 12G5 contributes to the leukemia residual disease treatment.