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目的探讨磷脂酰肌醇3激酶(PI3K)抑制剂BKM120对U251神经胶质瘤细胞凋亡的诱导作用。方法用(1、5、20)μmol/L BKM120处理U251细胞48 h后,采用CCK-8法检测BKM120对U251细胞增殖的影响,用异硫氰酸荧光素标记的膜联素Ⅴ/碘化丙啶(annexinⅤ-FITC/PI)双染法标记结合流式细胞术检测细胞凋亡,Western blot法检测Bax和Bcl-2的蛋白水平。结果 BKM120能抑制U251神经胶质瘤细胞的增殖并呈一定的浓度依赖性,最大抑制率为78.3%。BKM120处理可引起U251细胞凋亡。Western blot结果显示BKM120处理可引起Bax蛋白水平增加,同时Bcl-2蛋白水平降低。结论BKM120能抑制U251细胞的增殖并促进细胞凋亡。
Objective To investigate the induction of apoptosis of U251 glioma cells by phosphatidylinositol 3 - kinase (PI3K) inhibitor BKM120. Methods U251 cells were treated with (1,5,20) μmol / L BKM120 for 48 h. The effects of BKM120 on the proliferation of U251 cells were detected by CCK-8 assay. Fluorescein isothiocyanate labeled Melatonin Ⅴ / Annexin V-FITC / PI double staining and flow cytometry were used to detect the apoptosis. Western blot was used to detect the protein levels of Bax and Bcl-2. Results BKM120 inhibited the proliferation of U251 glioma cells in a concentration-dependent manner with the maximum inhibitory rate of 78.3%. BKM120 treatment can cause apoptosis in U251 cells. Western blot results showed that BKM120 treatment resulted in an increase of Bax protein and a decrease of Bcl-2 protein. Conclusion BKM120 can inhibit the proliferation of U251 cells and promote apoptosis.