【摘要】 目的:探讨丝裂原活化蛋白激酶(mitogen-acti-vated protein kinases,MAPKs)信号转导系统对依托泊苷(Vp-16)诱导K562细胞分化作用的影响。方法:采用四甲基偶氮唑盐(MTT)法测定细胞增殖活性;流式细胞仪解析细胞周期;硝基四氮唑蓝(NBT)还原实验检测细胞向单核/巨噬系统分化。结果:0·1~0·8μg/mL的Vp-16抑制K562细胞增殖,引起细胞G2/M期阻滞,诱导细胞向单核/巨噬系统分化;细胞外信号调节激酶(extracellular signal-regulated kinases,ERK)抑制剂PD98059降低Vp-16的诱导分化作用,P<0·05;p38丝裂原活化蛋白激酶(p38mitogen-activated protein kina-ses,p38MAPK)抑制剂SB203580增强Vp-16的作用,P<0·05;而C-JUN氨基末端激酶(c-jun N-terminal ki-nases,JNK)抑制剂SP600125对Vp-16的诱导分化作用无明显影响,P>0·05。结论:在Vp-16诱导K562细胞向单核/巨噬系统分化过程中,ERK正向,p38MAPK负向调节Vp-16的诱导分化作用。更多还原

【Abstract】 To explore the effects of Mitogen-activated Protein Kinases on etoposide-induced differentiation in K562 cells.METHODS:The growth inhibition was determined by MTT assay; cell cycle was analysed by the flow cytometry; cell differentiation was measured by nitro blue tetrazolium （NBT） reduction test. RESULTS:Etoposide inhibited the proliferation and induced G₂/M phrase arrest and differentiation toward monocyte/macrophage- like cells of K562 cells. Extracellular signal-regulated kinase （ERK） inhibitor PD98059 decreased the differentiation by Vp-16, P<0.05; p38 Mitogen-Activated Protein Kinase （p38MAPK ） inhibitor SB203580 increased the action of Vp-16, P<0.05;c-jun N-terminal kinase（JNK）inhibitor SP600125 did not affect the action of etoposide, P>0.05. CONCLUSIONS:In the process of etoposide- induced differentiation toward monocyte/macrophage- like cells in K562 cells, ERK pathway positively and p38MAPK pathway negatively regulates the action of etoposide.更多还原