【摘要】 本研究探讨不同浓度的三氧化二砷(As2O3)对人淋巴瘤细胞株Raji细胞凋亡诱导的作用特点及其机制,并探讨其与mcl-1基因表达的关系。应用琼脂糖凝胶电泳检测不同浓度As2O3作用于Raji细胞后的典型DNA-Ladder凋亡条带,激光共聚胶显微镜检测Raji细胞线粒体膜电位的变化,实时荧光定量PCR技术检测As2O3对mcl-1基因表达的影响。结果表明:1μmol/LAs2O3作用于Raji细胞时其凋亡不明显,2-8μmol/LAs2O3可以诱导Raji细胞凋亡。随着药物浓度的增加,Raji细胞线粒体的呼吸功能和跨膜电位明显减低,同时mcl-1基因表达量明显下调。结论:As2O3降低Raji细胞线粒体的呼吸功能和跨膜电位、下调mcl-1基因表达,而这些可能是导致细胞凋亡的机制。更多还原

【Abstract】 The aim of this study was to investigate the effect of different concentrations of arsenic trioxide (As2O3) on apoptosis of lymphoblastoid Raji cell line and its possible mechanisms,as well as its relation to the expression of mcl-1 gene. The Raji cells were treated with different concentrations of As2O3,the classical DNA ladder of cell apoptosis was detected by agar gel electrophoresis,the changes of mitochondrial membrane potential in Raji cells were assayed by confocal laser scanning microscopy,the changes of mcl-1 gene expression after exposure of cells to As2O3 was detected by real-time quantitative fluorescence PCR. The results indicated that 1 μ mol/L As2O3 did not lead to significant apoptosis of Raji cells,2-8 μmol/L As2O3 induced Raji cell apoptosis. Along with increase of drug concentration,the metochondrial respiratory function and membrane potential of Raji cells obviously decreased. At same time,the expression level of mcl-1 gene were significantly down-regulated. It is concluded that As2O3 can markedly decrease mitochondrial respiratory function and membrane potential of Raji cells,and down-regulate expression of mcl-1 gene,which may be the mechanisms resulting in cell apoptosis.更多还原