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首页> 美国卫生研究院文献>Evidence-based Complementary and Alternative Medicine : eCAM >Effect of Corilagin on the Proliferation and NF-κB in U251 Glioblastoma Cells and U251 Glioblastoma Stem-Like Cells
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Effect of Corilagin on the Proliferation and NF-κB in U251 Glioblastoma Cells and U251 Glioblastoma Stem-Like Cells

机译：胶原蛋白对U251胶质母细胞瘤细胞和U251胶质母细胞瘤干细胞增殖和NF-κB的影响

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Background. This study is to explore the effect of corilagin on the proliferation and NF-κB signaling pathway in U251 glioblastoma cells and U251 glioblastoma stem-like cells. Methods. CD133 positive U251 glioblastoma cells were separated by immunomagnetic beads to isolate glioblastoma stem-like cells. U251 cells and stem-like cells were intervened by different corilagin concentrations (0, 25, 50, and 100 μg/mL) for 48 h, respectively. Cell morphology, cell counting kit-8 assay, flow cytometry, dual luciferase reporter assay, and a western blot were used to detect and analyze the cell proliferation and cell cycle and investigate the expression of IKBα protein in cytoplasm and NF-κB/p65 in nucleus. Results. Corilagin inhibited the cell proliferation of U251 cells and their stem-like cells and the inhibition role was stronger in U251 stem-like cells (P < 0.05). The cell cycle was arrested at G2/M phase in the U251 cells following corilagin intervention; the proportion of cells in G2/M phase increased as the concentration of corilagin increased (P < 0.05). The U251 stem-like cells were arrested at the S phase following treatment with corilagin; the proportion of cells in the S phase increased as the concentration of corilagin increased (P < 0.05). The ratio of dual luciferase activities of U251 stem-like cells was lower than that of U251 cells in the same corilagin concentration. With increasing concentrations of corilagin, the IKBα expression in cytoplasm of U251 cells and U251 stem-like cells was increased, but the p65 expression in nucleus of U251 cells and U251 stem-like cells was decreased (P < 0.05). Conclusion. Corilagin can inhibit the proliferation of glioblastoma cells and glioblastoma stem-like cells; the inhibition on glioblastoma stem-like cell proliferation is stronger than glioblastoma cells. This different result indicates that the effect of corilagin on U251 cells and U251 stem-like cells may have close relationships with mechanism of cell cycle and NF-κB signaling pathway; however, the real antitumor mechanism of corilagin is not yet clear and requires further study.
机译：背景。本研究旨在探讨可乐菌素对U251胶质母细胞瘤细胞和U251胶质母细胞瘤干细胞增殖和NF-κB信号通路的影响。方法。通过免疫磁珠分离CD133阳性U251胶质母细胞瘤细胞，以分离胶质母细胞瘤干样细胞。 U251细胞和干细胞样细胞分别以不同浓度的胶原蛋白（0、25、50和100μg/ mL）干预48 h。用细胞形态学，细胞计数试剂盒8检测，流式细胞仪，双重荧光素酶报告基因检测和Western blot来检测和分析细胞增殖和细胞周期，并研究IKBα蛋白在细胞质和NF-κB/ p65中的表达。核。结果。 Corilagin抑制U251细胞及其干样细胞的细胞增殖，并且在U251干样细胞中的抑制作用更强（P <0.05）。胶原蛋白干预后，U251细胞的细胞周期停滞在G2 / M期。 G2 / M期细胞比例随可乐宁浓度的增加而增加（P <0.05）。用可乐宁处理后，U251干细胞样细胞被阻滞在S期。随胶原蛋白浓度的增加，S期细胞比例增加（P <0.05）。在相同浓度的尿素中，U251干样细胞的双重荧光素酶活性比率低于U251细胞。随着胶原蛋白浓度的增加，U251细胞和U251干细胞样细胞中IKBα的表达增加，而U251细胞和U251干细胞样细胞核中的p65表达降低（P <0.05）。结论。角蛋白可抑制胶质母细胞瘤细胞和胶质母细胞瘤干细胞的增殖；对胶质母细胞瘤干样细胞增殖的抑制作用比胶质母细胞瘤细胞强。这个不同的结果表明，corilagin对U251细胞和U251干样细胞的作用可能与细胞周期机制和NF-κB信号通路密切相关。然而，corilagin的真正抗肿瘤机制尚不清楚，需要进一步研究。

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