CAJ | 학술논문

目的研究二甲氧雌二醇(2-ME)对人白血病细胞K562细胞的增殖、凋亡作用及其机制.方法分别以不同浓度的2-ME处理白血病细胞K562,应用Annexin Ⅴ和PI双染的流式细胞术检测K562细胞凋亡率,应用比色法测定caspase-3及caspase-9的活性变化,应用凝胶蛋白电泳迁移率分析法EMSA检测K562细胞核内NF-KB蛋白的结合活性变化情况.结果 2-ME浓度升高,细胞凋亡率明显增加(P＜0.01)；当2-ME浓度为8μmol/L时,细胞凋亡率达64.3％；4μmol/L,2-ME作用K562细胞24h、36h、48 h后Caspase-3、Caspase-9活性明显升高.同时K562细胞核内NF-kappa B的DNA结合活性明显降低(P＜0.05).结论 2 -ME可显著抑制人白血病细胞K562增殖并诱导其凋亡,其机制与Caspase-3、-9活化及NF-kappa B蛋白信号通路有关.
목적 연구이갑양자이순(2-ME)대인백혈병세포K562세포적증식、조망작용급기궤제.방법 분별이불동농도적2-ME처리백혈병세포K562,응용Annexin Ⅴ화PI쌍염적류식세포술검측K562세포조망솔,응용비색법측정caspase-3급caspase-9적활성변화,응용응효단백전영천이솔분석법EMSA검측K562세포핵내NF-KB단백적결합활성변화정황.결과 2-ME농도승고,세포조망솔명현증가(P＜0.01)；당2-ME농도위8μmol/L시,세포조망솔체64.3％；4μmol/L,2-ME작용K562세포24h、36h、48 h후Caspase-3、Caspase-9활성명현승고.동시K562세포핵내NF-kappa B적DNA결합활성명현강저(P＜0.05).결론 2 -ME가현저억제인백혈병세포K562증식병유도기조망,기궤제여Caspase-3、-9활화급NF-kappa B단백신호통로유관.
Objective To study the effect of 2-methoxyestradiol (2-ME) on proliferation,apoptosis and its mechanism.Methods K562 cells were treated with 2-ME of different concentrations and time in vitro.Cell apoptosis rate was measured by flow cytometry(FCM).Activity of NF-Kappa B in nucleus was detected by electrophoretic molility shift assay(EMSA).Results After treatment with 2-ME,K562 cells apoptotic rate increased significantly.After treatment with 4μmol/L 2-ME for 24h、36h、48h,the activity of Caspase-3 and Caspase-9 were significantly higher and activity of NF-Kappa B in nucleus was significantly lower.Conclusion The present study showed that 2-ME induced apoptosis of K562 cells via active Caspase-3 and Caspase-9 and inhibit the activity of NF-kappa B in nucleus.This study provided useful experimental data for clinical application of 2-ME.