sCD40L对白血病K562细胞的影响及机制

Effect of Soluble CD40L on Leukemia K562 Cells and Its Mechanism

目的:观察s CD40L对白血病K562细胞系生物学行为的影响并探讨其机制。方法:用不同浓度s CD40L处理K562细胞,通过检测细胞增殖抑制率筛选最佳s CD40L浓度;用最佳浓度s CD40L处理K562细胞,用流式细胞术检测K562细胞凋亡率、凋亡相关因子P53、BCL-2表达水平;ELISA法检测s CD40L处理后K562细胞Caspase8、Caspase 3表达水平。结果:最佳s CD40L实验浓度为4μg/ml;经s CD40L处理后K562细胞凋亡率明显增高,凋亡相关因子P53的表达明显上调,BCL-2的表达显著下调;经s CD40L处理的K562细胞上清液中Caspase 8、Caspase3水平明显增高。结论:4μg/ml s CD40L可显著抑制K562细胞增殖并可促进其凋亡,其机制可能与线粒体和P53途径通路有关。

Objective:To investigate the effect of sCD40 L on biological behavior of leukemia cell line K562 and the possible mechanism.Methods:The different concentration of sCD40 L was used to treat K562 cells,and the optimum concentration of sCD40 L was screened by detecting the proliferation inhibition rate of K562 cells.The optimum concentration of sCD40 L was used to treat K562 cells,the cell apoptosis rate and expression level of P53 and BCL-2were detected by flow cytometry and the expression levels of Caspase 8 and Caspase 3 were detected by ELISA.Results:The optimum concentration of sCD40 L was 4 μg/ml.After treated with sCD40 L,the cell apoptosis rate,the expression of apoptosis-related factor P53 and the expression of Caspase 8 and Caspase 3 were significantly up-regulated in K562 cells,but the expression of BCL-2 was significantly down-regulated.Conclusion:4 μg/ml sCD40 L can inhibit the cell proliferation and promote the apoptosis of K562 cells,its mechanism may be related with mitochondrial and P53 pathway.