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目的探讨Dickkopf(DKK1)对人类白血病细胞株U937细胞的凋亡调控机制。方法用DCFH-DA荧光探针法检测活性氧(ROS)水平;用JC-1染色法检测线粒体跨膜电位(ΔΧm)水平;Annex in V/PI双标法检测凋亡率;Western-blot检测凋亡相关蛋白水平。结果 Dickkopf(DKK1)处理后的人白血病细胞活性氧水平显著升高且NAC可以阻断DKK1对活性氧水平的升高;线粒体膜电位水平显著下降;并且上调了促凋亡蛋白BAX的表达,下调了抗凋亡蛋白Mcl-1、Bcl-2的蛋白表达水平。结论 Dickkopf(DKK1)通过升高活性氧水平并降低线粒体膜电位水平从而诱导人白血病细胞的凋亡。
Objective To investigate the regulatory mechanism of Dickkopf (DKK1) on the apoptosis of human leukemia cell line U937. Methods The level of reactive oxygen species (ROS) was detected by DCFH-DA fluorescent probe method. The level of mitochondrial transmembrane potential (ΔΧm) was detected by JC-1 staining. The apoptosis rate was detected by Annexin V / PI double- Apoptosis-related protein levels. Results The levels of reactive oxygen species in Dickkopf (DKK1) -treated human leukemia cells were significantly increased and NAC could block the elevation of reactive oxygen species (DKK1), the mitochondrial membrane potential (MVD) and the expression of pro-apoptotic protein BAX The anti-apoptotic protein Mcl-1, Bcl-2 protein expression levels. Conclusion Dickkopf (DKK1) induces apoptosis in human leukemia cells by elevating reactive oxygen species and decreasing mitochondrial membrane potential.