摘要
目的:研究地塞米松对K562细胞的增殖抑制作用及诱导细胞凋亡的机制。方法:用不同浓度的地塞米松对K562细胞进行处理,检测细胞增殖抑制率,观察细胞凋亡的形态学变化,测定细胞端粒酶活性,Fas表达及NO产生情况。结果:地塞米松能抑制K562细胞的增殖,降低端粒酶活性,使Fas表达上调,诱导细胞凋亡。但对NO的生成不具有显著性差异。结论:地塞米松可能通过抑制端粒酶的活性而诱导K562细胞的凋亡。同时,Fas也可能参与了凋亡的调节。
Objective：To investigate the effect of dexamethasone on the growth and the mechanism of apoptosis in K562 cells. Methods：Treat of different dosages of dexamethasone in K562 cell cultural to observe cell inhibitory rate and cell morphology variation. To detected telomerase activity,Fas expression and NO release. Results：Dexamethasone can inhibit the proliferation of K562 cell,decrease telomerase activity,increase Fas expression and induce apoptosis. But no significant effect on nitric oxide production. Conclusion：Inhibit telomerase activity and increase Fas expression maybe one of mechanism of apoptosis.
出处
《重庆医科大学学报》
CAS
CSCD
2008年第8期911-913,979,共4页
Journal of Chongqing Medical University
基金
国家自然科学基金(No.30300449)
国家中医药管理局(No.02-03ZP52)
重庆医科大学校级课题(No.XBYB2007104
No.XBYB2007108)
