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作 者:尹文杰[1] 刘小鹏[1] 黄有章[1] 杨平地[1]
机构地区:[1]海军总医院血液科,北京100048
出 处:《中国实验血液学杂志》2012年第1期62-65,共4页Journal of Experimental Hematology
摘 要:本研究探讨骨髓间充质干细胞(MSC)对HL-60细胞增殖的影响及相关的分子机制。将单独培养的HL-60细胞作为对照组,与MSC共培养的HL-60细胞作为实验组。在不同时间计数两组HL-60细胞,描绘其时间-数量曲线;流式细胞仪检测2组HL-60细胞的细胞周期、凋亡细胞比例及Survivin和Bcl-2蛋白的表达。结果表明,实验组HL-60细胞的增殖明显受抑,在第5-7天差异显著(P<0.01),实验组HL-60细胞分布于G0/G1期的比例增加〔对照组(47.0±9.0)%vs实验组(70.0±16.0)%,P=0.003)〕,并且出现凋亡峰。实验组HL-60细胞Survivin和Bcl-2蛋白表达同时下调。Bcl-2表达率在对照组为(63.0±9.1)%,实验组为(50.0±14.1)%(P=0.045);Survivin表达率在对照组为(94.0±9.3)%,实验组为(77.0±11.8)%(P=0.006)。结论:骨髓MSC对HL-60细胞的增殖有抑制作用,并促进HL-60细胞凋亡。The objective of this study was to explore the effect of mesenchymal stem cells (MSC) on HL-60 proliferation and its molecular mechanism. HL-60 ceils co-cultivated with MSC were used as experiment group, and the cells cultivated solely were taken as control group. HL-60 cells in the two groups were counted at different time. The time-quantity curve was drawn. The cell cycle and apoptosis ratio of HL-60 cells were compared between the two groups and expressions of Survivin and Bcl-2 protein were detected by flow cytometry. The results showed that HL-60 cells cultivated with MSC were obviously inhibited, especially on day 5 and 7 ( P 〈 0.01 ). HL-60 cells were distributed on the phase of G0/G1 [ control group (47.0 ± 9.0) % vs experiment group (70.0 ±16.0) %, P = 0.0033, and apoptotic peak appeared. Both of Survivin and Bcl-2 protein expressions in HL-60 cells decreased [ Bcl-2 protein in control group (63.0 ±9.1)% vs experiment group (50.0± 14. 1)%, P =0.045; Survivin in control group (94.0±9.3)% vs experiment group (77.0± 11.8 ) %, P = 0.0063. It is concluded that the MSC can inhibite HL-60 cell proliferation, and promote HL-60 cell apoptosis.
分 类 号:R329.28[医药卫生—人体解剖和组织胚胎学] R733.7[医药卫生—基础医学]
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