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-PI3 K, 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/PI3 K 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.%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, G1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.
展开▼
