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作 者:林琦[1] 吴丽贤[1] 许建华[2] 黄秀旺[1] 张昆仲[1] 温彩霞[1] 陈元仲
机构地区:[1]福建医科大学药理系,福建福州350004 [2]福建医科大学临床药理研究所,福建福州350004 [3]福建省血液研究所,福建福州350004
出 处:《世界肿瘤杂志》2008年第1期9-12,共4页Tumour Journal of the World
基 金:国家自然科学基金(No30171158,30472187)资助:福建省资助省属高校项目(N02005K048)资助
摘 要:目的研究姜黄素(Cur)对K562细胞和HL-60细胞的细胞周期阻断与细胞周期蛋白的关系。方法用流式细胞光度术对K562细胞和HL-60细胞进行细胞周期检测,用蛋白免疫印迹检测细胞周期蛋白水平。结果姜黄素0—10mg/L作用24h可将K562细胞和HL-60细胞阻滞于G0/G1期,该期细胞比例增加;阻断细胞从S期向G2/M期转化,G2/M期细胞比例减少;姜黄素作用24h减少K562细胞和HL-60细胞Cyclin D1、Cyclin B1的蛋白水平,但几乎不影响K562细胞和HL-60细胞Cyclin A的蛋白水平。结论姜黄素扰乱K562细胞和HL-60细胞的细胞周期进程与Cyclin D1和Cyclin B1的蛋白水平减少有一定关系。AIM To study the effects of curcumin on cell cycle progression in k562 and HL-60 cell lines and determine the relationship of the effect to cyclins. Methods Flow cytometry was used to examine curcumin-induced cell cycle arrest, and western blot was used to analyze the levels of cyclins in curcumin-treating cells. Results An exposure of k562 and HL-60 cells to Cur 0-10μg/ml for 24h produced a dose dependent increase in G0/G1 phase cells from 32.6% and 36.8% to 47.6 % and 57.9%, respectively; G2/M phase cells were decreased from 11.6% and 2.8% to 0% and 0%, respectively. Consistent with this effects, the abundance of Cyclin D1, Cyclin B1 was deregulated in a dose dependent way, while the levels of Cyclin A were not changed. Conclusions The cell cycle arrest induced in k562 and HL-60 cells by curcumin was correlated with deregulation of the abundance of Cyclin D1 and Cyclin B1.
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