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目的 研究二烯丙基二硫化物 (DADS)诱导CNE2细胞凋亡及 p38MAPK信号转导通路对此过程的作用。 方法 DADS处理CNE2细胞 2 4h后 ,荧光显微镜下观察形态学变化及凋亡细胞计数 ,MTT法测定细胞活性 ,流式细胞仪检测凋亡细胞 ,蛋白质印迹法检测磷酸化p38MAPK表达。结果 在培养的CNE2细胞中 ,DADS(50～ 1 50 μmol·L- 1 )作用 2 4h后 ,DADS诱导CNE2细胞产生典型的凋亡细胞形态学变化 (核浓染 ,核碎裂 ) ,流式细胞仪结果显示 ,随着DADS给药剂量增加 ,细胞周期中各期细胞所占百分率的变化无规律 ,细胞凋亡呈剂量依赖性 ,DADS(50～ 1 50 μmol·L- 1 )浓度依赖性刺激磷酸化p38MAPK的表达 ,p38MAPK抑制剂SB2 0 3580明显增强DADS致凋亡作用。结论 DADS诱导CNE2细胞凋亡时激活磷酸化 p38MAPK表达 ,磷酸化p38MAPK抑制剂增强DADS诱导CNE2细胞凋亡效应
Objective To study the effect of diallyl disulfide (DADS) on the apoptosis of CNE2 cells and the role of p38MAPK signal transduction pathway in this process. Methods DADS was used to treat CNE2 cells for 24 hours. Morphological changes and apoptotic cell counts were observed under fluorescence microscope. Cell viability was measured by MTT assay, apoptotic cells were detected by flow cytometry, and phosphorylated p38MAPK expression was detected by Western blotting. Results In cultured CNE2 cells, DADS induced CNE2 cells to produce typical apoptotic cell morphology changes (nuclear staining, nuclear fragmentation) after 24 h DADS (50-150 μmol·L-1) for 24 h. Cytometry results showed that with the increase of DADS dose, the percentage of cells in each phase of the cell cycle changed irregularly, apoptosis was dose-dependent, DADS (50 ~ 1 50 μmol · L - 1) concentration-dependent Stimulated phosphorylation of p38MAPK expression, p38MAPK inhibitor SB2 0 3580 significantly enhanced DADS apoptosis. Conclusion DADS induces phosphorylated p38MAPK expression in CNE2 cells. Phosphorylated p38MAPK inhibitors enhance DADS-induced apoptosis in CNE2 cells.