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机构地区:[1]西安交通大学第一医院血液科,西安710061 [2]第四军医大学免疫学教研室
出 处:《山西医科大学学报》2009年第10期884-887,共4页Journal of Shanxi Medical University
基 金:陕西省自然科学基金资助项目(2005C237)
摘 要:目的观察IFN-α对慢性粒细胞白血病细胞株K562端粒酶活性和凋亡的作用和机制。方法将IFN-α按100,1000,10000U/ml三种不同浓度作用于K562细胞72h,采用PCR-ELISA法测定端粒酶活性;流式细胞仪分析细胞周期和细胞凋亡及CD11b表达。结果100,1000,10000U/ml的IFN-α(72h)可以引起K562细胞S期阻滞,同时诱导细胞凋亡,但细胞粒酶活性和CD11b表达无明显改变。结论IFN-α诱导K562细胞凋亡可能不通过端粒酶活性的调控;细胞S期阻滞可能与IFN-α作用K562细胞的机制有一定相关性。Objective To investigate the effect of IFN-α on telomerase activity and apoptosis in CML cell line K562 and its mechanism. Methods The different concentrations of IFN-α( 100,1 000,10 000 U/ml)were used on K562 cells for 72 h. Telomerase activity was determined by PCR-ELISA. Flow cytometry was used to analyze the cell cycle, apoptosis and CD11 b expression in K562 ceils. Results After cultured with 100,1 000,10 000 U/ml IFN-α for 72 h, K562 cell was arrested in S phase and cell apoptosis was induced,but the telomerase activity and the expression of CD1 lb had no significant changes. Conclusion The apoptosis of K562 cell induced by IFN-α may not be regulated by telomerase. S phase arrest may be correlated with the mechanism of IFN-α affecting K562 cell.
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