三氧化二砷对NB4及Jurkat细胞系端粒酶活性的抑制效应  

Inhibiting Effect of Arsenic Trioxide on Telomerase Activity of NB4 and Jurkat Cell Lines

作　　者：王韫芳[1] 孙红琰[1] 李昕权[2] 王全立[1] 

机构地区：[1]军事医学科学院野战输血研究所 [2]军事医学科学院附属医院肿瘤科,北京100039

出　　处：《中国实验血液学杂志》2003年第4期359-362,共4页Journal of Experimental Hematology

摘　　要：为了探讨三氧化二砷 (As2 O3 )对白血病细胞系NB4及Jurkat细胞端粒酶活性的调节作用和机制 ,采用MTT、基因组DNA电泳、蛋白 /DNA双参数流式细胞术 ,端粒重复扩增 (TRAP) SYBRGreenⅠ染色及RT PCR等方法研究了As2 O3 对两种细胞的增殖及端粒酶活性的影响。研究发现 ,随着As2 O3 作用时间的延长 ,NB4及Jurkat细胞增殖明显受到抑制 ,DNA电泳出现“梯状”条带 ;流式细胞术检出亚G1峰 ,细胞周期阻滞于G1和G2 /M期 ,端粒酶活性显著降低 ,部分细胞周期及凋亡相关的调控蛋白的表达发生变化。结论 :As2 O3 在抑制NB4及Jurkat细胞增殖和诱导其凋亡过程中导致端粒酶的活性下调 ,细胞周期及凋亡相关蛋白的表达改变可能参与了部分作用机制。To investigate the inhibiting effect of arsenic trioxide (As 2O 3) on the telomerase activity of leukemia cell lines NB4 and Jurkat cells, MTT assay, electrophoresis of genomic DNA, protein/DNA dual parameter flow cytometry as well as a semi quantitative telomeric repeat amplification protocol (TRAP) assay and RT PCR were used to examine the effect of As 2O 3 on cell proliferation, telomerase activity and expression of cell cycle regulatory proteins. The results showed that cell proliferation and telomerase activity were significantly inhibited and apoptosis was induced in these cells after exposure to As 2O 3. Furthermore, the expression of some cell cycle and apoptosis related proteins, such as Bcl 2, Rb, P16, caspase 3, cyclin A and cyclin E, was altered in As 2O 3 treated NB4 cells. Cell cycle was arrested at G 1 and G 2/M phases in both cells. It is concluded that the change of cell cycle regulatory proteins plays an important role in decline of the telomerase activity during the proliferation inhibition and apoptosis of NB4 and Jurkat cells induced by As 2O 3.

关 键 词：三氧化二砷 NB4细胞系 Jurkat细胞系 端粒酶 细胞周期 

分 类 号：R733.7[医药卫生—肿瘤] R979.1[医药卫生—临床医学]