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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、凋亡的作用及其机制。方法:分别以不同浓度的2-ME处理白血病细胞K562,通过MTT法检测K562细胞活力,应用Annexin V和PI双染的流式细胞术检测K562细胞凋亡率,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:随着2-ME浓度的升高,各项指标与对照组相比较的差异均有统计学意义(P<0.01);K562细胞增殖明显受到抑制;细胞凋亡率明显增加,且当2-ME浓度为8μmol·L~(-1)时,细胞凋亡率达64.3%;同时K562细胞核内NF-kappa B的DNA结合活性明显降低。结论:2-ME可显著抑制人白血病细胞K562增殖并诱导其凋亡;2-ME诱导K562细胞凋亡的机制与NF-kappa B蛋白信号通路有关。
Objective: To investigate the effect and mechanism of dimethoxyestradiol (2-ME) on the proliferation and apoptosis of human leukemia K562 cells. Methods: K562 leukemia cells were treated with different concentrations of 2-ME. The viability of K562 cells was detected by MTT assay. The apoptosis rate of K562 cells was detected by flow cytometry with Annexin V and PI double staining. The electrophoretic mobility shift assay EMSA detection of K562 cells in the nuclear NF-KB protein binding activity changes. Results: With the increase of 2-ME concentration, there was significant difference between each index and the control group (P <0.01); the proliferation of K562 cells was obviously inhibited; the apoptosis rate of K562 cells increased obviously, When the concentration of -ME was 8μmol·L -1, the apoptosis rate was 64.3%, and the DNA binding activity of NF-kappa B in K562 cells was significantly decreased. CONCLUSION: 2-ME can significantly inhibit the proliferation and induce apoptosis of K562 leukemia cells. The mechanism of 2-ME-induced apoptosis in K562 cells is related to NF-kappa B signaling pathway.