【摘要】 目的观察在神经酰胺(CM)通路中,大麻受体激动剂花生四烯酸乙醇胺(AEA)抑制人胶质瘤U251细胞增殖及在诱导细胞凋亡中的作用。方法采用噻唑蓝(MTT)法,分别测定不同浓度的CM(5~20μmol/L)和烟曲霉毒素(FB1)(10μmol/L)预处理24h后对AEA(1~10μmol/L)抑制人胶质瘤U251细胞增殖作用的影响;流式细胞仪Annexin-V/PI双染色法定量分析FB1(10μmol/L)预处理24h后对AEA(10μmol/L)促细胞早期凋亡作用的影响。结果不同浓度的AEA对人胶质瘤U251细胞增殖的抑制作用不同,且与CM具有协同作用;10μmol/L FB1预处理24h后可显著对抗AEA对人胶质瘤U251细胞增殖的抑制作用;AEA(10μmol/L)可诱导人胶质瘤U251细胞发生早期凋亡,而FB1(10μmol/L)预处理24h后凋亡发生率明显下降。结论 AEA可通过CM从头合成通路,与CM呈浓度依赖性协同,从而抑制人胶质瘤U251细胞的增殖并诱导其早期凋亡。更多还原

【Abstract】 Objective To investigate the role of ceramide pathway in cell proliferation and early apoptosis induction in U251 glioma cell after cannabinoid receptora agent anandmide(AEA)treatment.Methods U251 gliom cells were treated with AEA(1-10μmol/L),Ceramide(5-20μmol/L)and fumonisin B1(FB1)(10μmol/L)pretreatment.The growth inhibition rate of U251 was investigated by MTT assay.The early events of the apoptosis were measured by flow cytometry using annexin-V/propium iodide(PI)double staining method.Results Different concentrations of AEA inhibited the proliferation of human glioma U251 cells,and had synergistic effect with CM by FB1(10μmol/L)pretreatment for 24 h.After exposure to AEA(10μmol/L)for 24 h,U251glioma cells could undergo the early cell apoptosis which was affected by FB1(10μmol/L).Conclusion AEA through the CM de novo synthesis pathway,and CM concentration was lazy in collaboration,thus inhibiting human glioma U251 cell proliferation and induce early apoptosis.更多还原