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目的探讨氟西汀的抗胶质瘤作用及相关机制。方法培养人源性胶质瘤U251、SHG-44细胞株;MTT法测定细胞活力;Hoechst 33342荧光染色测定细胞凋亡;提取U251细胞质蛋白,Western blot法测定NF-κB的亚基p65的表达水平及磷酸化p65(p-p65)水平。结果 MTT法显示氟西汀呈浓度依赖性地降低SHG-44、U251细胞的活力(P<0.05)。Hoechst 33342染色法显示氟西汀能够诱导SHG-44、U251细胞发生凋亡(P<0.05)。Western blot法显示氟西汀作用0.5h后引起U251细胞NF-κB的激活。结论氟西汀通过诱导胶质瘤细胞凋亡发挥抗胶质细胞瘤的作用,其作用机制与激活NF-κB有关。
Objective To investigate the anti-glioma effect of fluoxetine and its related mechanism. Methods The human glioma cell line U251 and SHG-44 were cultured and the cell viability was determined by MTT assay. The apoptosis of U251 cells was detected by Hoechst 33342 staining. The expression of NF-κB subunit p65 was detected by Western blot And phosphorylated p65 (p-p65) levels. Results MTT assay showed fluoxetine reduced the viability of SHG-44 and U251 cells in a concentration-dependent manner (P <0.05). Hoechst 33342 staining showed that fluoxetine could induce apoptosis of SHG-44 and U251 cells (P <0.05). Western blot analysis showed that fluoxetine induced NF-κB activation in U251 cells after 0.5 h treatment. Conclusion Fluoxetine can induce glioblastoma cells apoptosis by anti-glioblastoma. Its mechanism is related to the activation of NF-κB.