摘要
目的研究2-甲氧基雌二醇(2-ME)对K562/AO2细胞耐药性逆转作用及其可能机制。方法利用不同浓度的2-ME作用于K562及K562/AO2细胞,MTT法检测细胞对阿霉素的耐药性,计算耐药倍数及逆转倍数;利用AnnexinV/PI双染色法检测K562/AO2细胞的凋亡效应。结果与K562细胞相比,K562/AO2细胞的耐药倍数为50倍;2-ME可显著降低阿霉素对K562/AO2细胞的IC50,逆转倍数为5.9倍。AnnexinV/PI双染色法检测显示,1、4、16μmol/L的2-ME处理K562/AO2细胞后细胞凋亡率分别为10.32%、21.56%和16.45%,而对照组凋亡率仅为6.68%。结论 2-ME能够逆转K562/AO2阿霉素耐药,其机制可能与诱导K562/AO2细胞凋亡有关。
Objective To investigate the possible mechanism of 2-methoxyestradiol reversing multidrug resistance of K562/AO2 cells.Methods The inhibitory effects of 2-methoxyestradiol on the proliferation of K562 and K562/AO2 cells were observed by MTT assay.Annexin V-FITC /PI staining was used to detect apoptosis.Results The resistance of K562/AO2 cells to ADR was 50 folds compared with K562 cells.The IC50 of ADR was evidently reduced by 2-methoxyestradiol.The reversal folds of 2-methoxyestradiol for K562/AO2 cells were 5.9.The result of Annexin-V /PI staining showed that rates of the apoptotic cells were 10.32%,21.56% and 16.45% respectively,which were remarkably higher than that of control(6.68%).Conclusion 2-methoxyestradiol has reverse effect on K562/AO2 cells,its possible mechanism might be related with apoptosis of K562/AO2 cells.
出处
《肿瘤防治研究》
CAS
CSCD
北大核心
2011年第11期1257-1259,共3页
Cancer Research on Prevention and Treatment
基金
西安交通大学医学院第一附属医院院基金资助项目(2007-YK-10)