论文部分内容阅读
目的:探讨全反式维A酸(all-trans retinoic acid,ATRA)诱导U937细胞分化的可能机制。方法:以急性单核细胞性白血病细胞株U937细胞为体外模型,以细胞表面分化抗原CD11b、四唑氮蓝(nitro-blue tetrazolium,NBT)还原实验和形态学观察,评估细胞分化。应用蛋白印迹法,检测ATRA对C/EBPβ、C/EBPε和PU.1蛋白表达水平的影响。结果:MEK特异性抑制剂U0126预处理不影响ATRA诱导U937细胞分化。蛋白印迹检测显示,ATRA可提高PU.1、C/EBPβ和C/EBPε蛋白水平。结论 :ATRA诱导U937细胞分化可能与PU.1、C/EBPβ、C/EBPε的蛋白表达调控相关,而并不涉及MEK-ERK信号转导途径。
Objective: To investigate the possible mechanism of all-trans retinoic acid (ATRA) -induced U937 cell differentiation. Methods: The acute myeloid leukemia cell line U937 cells were used as an in vitro model to evaluate the cell differentiation by cell surface differentiation antigen CD11b and the reduction experiments of NB4 and morphological observation. The effect of ATRA on the expression of C / EBPβ, C / EBPε and PU.1 protein was detected by Western blotting. Results: Pretreatment with MEK specific inhibitor U0126 did not affect the differentiation of U937 cells induced by ATRA. Western blotting showed that ATRA increased PU.1, C / EBPβ and C / EBPε protein levels. CONCLUSION: ATRA-induced U937 cell differentiation may be related to the regulation of the protein expression of PU.1, C / EBPβ and C / EBPε, but not the MEK-ERK signal transduction pathway.