首页> 外文期刊>Tropical Journal of Pharmaceutical Research >Luteoloside Inhibits Proliferation of Human Chronic Myeloid Leukemia K562 Cells by Inducing G2/M Phase Cell Cycle Arrest and Apoptosis
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Luteoloside Inhibits Proliferation of Human Chronic Myeloid Leukemia K562 Cells by Inducing G2/M Phase Cell Cycle Arrest and Apoptosis

机译:黄体苷通过诱导G2 / M期细胞周期阻滞和凋亡抑制人慢性粒细胞白血病K562细胞的增殖。

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Purpose: To investigate the effects of luteoloside on the proliferation of human chronic myeloid leukemia K562 cells and whether luteoloside induces cell cycle arrest and apoptosis in K562 cells. Methods: Luteoloside’s cytotoxicity was assessed using a cell counting kit. Cell cycle distribution was analysed by flow cytometry after propidium iodide (PI) staining. Cell apoptosis was assayed with apoptosis detection kit and Hoechst staining followed by observation under a fluorescence microscope. The expression of cell cycle- and apoptosis-related proteins was examined by Western blot analysis. Results: Luteoloside inhibited the proliferation of K562 cells in a dose- and time- dependent manner (IC50 = 30.7 μM) with less toxicity in a normal human cell line (IC50 = 91.8 μM). Moreover, antiproliferative effect of luteoloside was accompanied with G2/M phase arrest(p < 0.05 or p<0.01) and apoptosis(p < 0.01 or p < 0.001). Further studies revealed that the expression level of cyclinB1 was down-regulated by luteoloside treatment. Furthermore, luteoloside treatment also increased proapoptotic protein Bax expression and decreased anti-apoptotic protein Bcl-2 expression. Conclusion: These results suggest that the inhibitory effect of luteoloside on K562 cell proliferation is associated with inducing G2/M phase arrest and apoptosis, and that luteoloside is worth further studying for anticancer potential.
机译:目的:研究黄体甙对人慢性粒细胞白血病K562细胞增殖的影响,以及黄体甙是否诱导K562细胞周期阻滞和凋亡。方法:使用细胞计数试剂盒评估黄体甙的细胞毒性。碘化丙锭(PI)染色后,通过流式细胞仪分析细胞周期分布。用凋亡检测试剂盒和Hoechst染色测定细胞凋亡,然后在荧光显微镜下观察。通过蛋白质印迹分析检查细胞周期和凋亡相关蛋白的表达。结果:黄体苷以剂量和时间依赖性(IC 50 = 30.7μM)抑制K562细胞的增殖,对正常人细胞株(IC 50 = 91.8μM)。此外,黄体苷的抗增殖作用还伴有G2 / M期阻滞(p <0.05或p <0.01)和细胞凋亡(p <0.01或p <0.001)。进一步的研究表明,黄体甙处理后下调了cyclinB1的表达水平。此外,黄体苷处理还增加了促凋亡蛋白Bax表达并降低了抗凋亡蛋白Bcl-2表达。结论:这些结果表明,黄体甙对K562细胞增殖的抑制作用与诱导G2 / M期阻滞和凋亡有关,黄体甙具有进一步的抗癌潜力。

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