【摘要】 为研究阿司匹林对人慢性粒细胞白血病细胞株K562生长的影响,采用光学显微镜和Hoechst 33258染色观察阿司匹林处理后细胞的形态和数目变化,显示阿司匹林促进K562细胞的凋亡.MTT法、细胞计数、软琼脂克隆形成实验、FACS和裸鼠成瘤实验在体外和体内检测阿司匹林对K562细胞增殖和存活的影响,发现阿司匹林明显抑制K562细胞的体外增殖和裸鼠体内成瘤能力.Western blot实验分析细胞信号通道下游基因的表达影响,显示β-catenin、STAT5A、PARP和NF-κB p65蛋白的表达量下调,而细胞周期抑制因子p21表达上调.这些结果提示阿司匹林从体外和体内抑制K562细胞的生长,其作用的机制复杂,可能影响β-catenin信号通道、JAK蛋白酪氨酸激酶/STAT5A信号通道、NF-κB信号传导通道和细胞周期的进程.更多还原

【Abstract】 To study the effects of aspirin on the growth of chronic myeloid leukemia(CML) K562 cells,an optical microscopy and Hoechst 33258 staining were used to analyze the morphology and numbers of K562 cells treated by aspirin,and aspirin was found to enhance the apoptosis of K562 cells. MTT assay,cell counting,soft agar colony formation assays,FACS and tumorigenicity in nude mice were carried out to examine the in vitro and in vivo proliferation of K562 cells induced by aspirin,and confirmed that aspirin markedly inhibited K562 cellular proliferation in vitro and reduced in vivo tumor growth in nude mice. Western blots were performed to detect the protein expression levels of some major signaling pathways,and showed that aspirin resulted in a dose-dependent reduction of β-catenin,STAT5A,PARP and NF-κB p65 expression,and enhanced the activation of cyclin-dependent kinase inhibitor p21. These data suggested that aspirin suppresses K562 cellular growth in vitro and in vivo,possibly affecting β-catenin signaling pathway,JAK/STAT5A signaling pathways,NF-κB signaling pathways and inducing the cell cycle arrest.更多还原