TNF-α通过死亡受体途径促进IFN-γ诱导NIT-1细胞凋亡  

TNF-α enhances IFN-γ-induced NIT-1 cells apoptosis via death receptor pathway

作　　者：董世访[1] 李桂清[1] 江伟凡[1] 杨菲[1] 曹朝晖[1] 许桂莲[1] 

机构地区：[1]第三军医大学基础部免疫学教研室,重庆400038

出　　处：《中国免疫学杂志》2014年第11期1448-1451,共4页Chinese Journal of Immunology

基　　金：国家自然科学基金面上项目(30971394);湖南省教育厅项目(12A118;12C0359);湖南省科技厅项目(2013SK3121);衡阳市科技局项目(2013KS22)

摘　　要：目的:探讨TNF-α和IFN-γ对小鼠胰岛β细胞株NIT-1细胞凋亡的影响及其可能的分子机制。方法:用MTT法检测TNF-α和IFN-γ单独或联合作用对NIT-1细胞活力的影响,倒置显微镜观察NIT-1细胞形态变化,Hoechst 33258荧光染色后激光共聚焦显微镜观察细胞核形态的变化,Western blot技术检测凋亡相关蛋白Caspase-8,-3和PARP的活化。结果:TNF-α联合IFN-γ处理明显抑制了NIT-1细胞的活力,诱导了细胞的凋亡,促进了凋亡蛋白Caspase-8,-3和PARP的活性。结论:TNF-α通过细胞凋亡的死亡受体途径信号传递促进了IFN-γ诱导的NIT-1细胞凋亡。Objective： To investigate the effect of TNF-α and IFN-γ on NIT-1 cells apoptosis and the apoptosis mechanism. Methods： NIT-1 cells were exposed to a combination of TNF-α and IFN-γ treatment. The viability of NIT-1 cells was assessed via MTT assay. The morphological changes of the cells and nuclei were observed under the inverted or confocal laser scanning microscope with Hoechst 33258 staining. The activation of Caspase-8,-3 and PARP was detected by Western blot. Results： TNF-α and IFN-γ significantly inhibited NIT-1 cells viability,promoted cells apoptosis,induced the activation of Caspase-8,-3 and PARP cleavage. Conclusion： TNF-α combined with IFN-γ treatment induced the apoptosis of NIT-1 cells through death receptor pathway.

关 键 词：TNF-Α IFN-Γ 胰岛Β细胞 T1DM 

分 类 号：R329.2[医药卫生—人体解剖和组织胚胎学]