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扁塑藤素抑制人胶质母细胞瘤U251细胞增殖的机制探讨
引用本文:徐高峰,鲍 钢,白晓斌,祁 磊,谢万福,李瑞春. 扁塑藤素抑制人胶质母细胞瘤U251细胞增殖的机制探讨[J]. 现代肿瘤医学, 2019, 0(3): 363-366. DOI: 10.3969/j.issn.1672-4992.2019.03.001
作者姓名:徐高峰  鲍 钢  白晓斌  祁 磊  谢万福  李瑞春
作者单位:西安交通大学医学院第一附属医院神经外科,陕西 西安 710061
基金项目:陕西省科技研究发展(攻关)计划项目(编号:2014K11-01-01-03)
摘    要:目的:探讨扁塑藤素对人胶质母细胞瘤U251细胞增殖的影响及其机制。方法:2、4和8μmol/L的扁塑藤素作用U251细胞24 h后,使用四甲基偶氮唑蓝(MTT)法检测U251细胞活力; Cell cycle staining Kit检测U251细胞周期;免疫印迹法检测增殖细胞核抗原(PCNA)蛋白和p-PI3K、PI3K、p-AKT以及AKT蛋白表达。结果:2、4和8μmol/L的扁塑藤素显著降低U251细胞的活力,且具有浓度依赖性。扁塑藤素可下调U251细胞PCNA蛋白的表达。扁塑藤素处理U251细胞后,G_1期细胞数明显增加,S期细胞数明显减少。扁塑藤素处理可明显降低U251细胞p-PI3K/PI3K、p-AKT/AKT的比值。结论:扁塑藤素可能通过抑制PI3K/AKT信号通路的活化抑制人胶质母细胞瘤的细胞增殖。

关 键 词:扁塑藤素  胶质母细胞瘤  细胞增殖  PI3K/AKT信号通路

The mechanism of pristimerin inhibits proliferation of human glioblastoma U251 cells
Xu Gaofeng,Bao Gang,Bai Xiaobin,Qi Lei,Xie Wanfu,Li Ruichun. The mechanism of pristimerin inhibits proliferation of human glioblastoma U251 cells[J]. Journal of Modern Oncology, 2019, 0(3): 363-366. DOI: 10.3969/j.issn.1672-4992.2019.03.001
Authors:Xu Gaofeng  Bao Gang  Bai Xiaobin  Qi Lei  Xie Wanfu  Li Ruichun
Affiliation:Department of Neurosurgery,the First Affiliated Hospital of Xi'an Jiaotong University,Shaanxi Xi'an 710061,China.
Abstract:Objective:To explore the impact of pristimerin on cell proliferation of U251 cells.Methods:After treating with different concentrations of pristimerin(2,4,8 μmol/L) for 24 h,the viability of U251 cells was measured using MTT assay.Cell cycle was detected by cell cycle staining Kit.The expression levels of PCNA(proliferating cell nuclear antigen),p-PI3K,PI3K,p-AKT and AKT were determined by Western blot.Results:Compared with the control group,pristimerin markedly reduced the cell viability of U251 in a dose dependent way.Additionally,the expression levels of PCNA protein were obviously downregulated in pristimerin-treated U251 cells.We also found that the cell numbers in G1 period were obviously increased while the cell numbers in S period were markedly decreased in U251 cells treated by pristimerin.Eventually,the ratios of p-PI3K/PI3K and p-AKT/AKT were markedly reduced in pristimerin-treated U251 cells.Conclusion:Pristimerin can inhibit cell proliferation of human glioblastoma by inhibiting the activation of PI3K/AKT signalling.
Keywords:pristimerin   human glioblastoma   cell proliferation   PI3K/AKT signalling
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