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机构地区:[1]卫生部北京医院卫生部北京老年医学研究所,北京市100730
出 处:《医学分子生物学杂志》2011年第3期189-193,共5页Journal of Medical Molecular Biology
基 金:国家自然科学基金(No.81070634,30801218)
摘 要:目的 探讨炎性因子IL-6是否通过Sirt1/p53/caspase-3通路介导胰岛β细胞凋亡.方法 Western 印迹检测Sirt1在小鼠各组织器官和胰岛β细胞系NIT-1细胞中的表达,免疫荧光法检测Sirt1在细胞中的定位.IL-6(10 ng/ml)处理NIT-1细胞48 h,Hoechst3334染色及流式细胞仪检测细胞凋亡,Western印迹检测细胞内Sirt1、P53、乙酰化P53(acety-P53)、caspase-3和cleaved caspase-3的水平变化.结果 Sirt1在小鼠各组织器官和胰岛β细胞中均有表达,主要定位于细胞核.IL-6处理NIT-1细胞后,伴随Sirt1表达的显著减少,acety-P53明显上调,p53/caspase-3通路活化,NIT-1细胞凋亡增加.结论 IL-6通过下调Sirt1进而激活p53/caspase-3信号通路引起胰岛β细胞凋亡.Objective To investigate whether IL-6 induces pancreatic β cell apoptosis through down-regulation of Sirtl and activation of p53/caspase-3 pathway. Methods Sirtl expression in di- verse mouse organs and pancreatic β cell line NIT-1 was detected by Western blot. The location of Sirtl in NIT-1 cells was observed by immunofluorescence. After treated with 10ng/ml IL-6 for 48 h, apoptosis of NIT-1 cells was detected by Hoechst3334 staining and flow cytometry. Western blot was used to analyze the levels of Sirtl, p53, acety-p53, caspase-3 and cleaved caspase-3, respectively. Results Sirtl was expressed in diverse mouse organs and pancreatic β cell line NIT-1, and mainly located in the nucleus. Treatment of NIT-1 cells with 10ng/ml IL-6 for 48 h induced apoptosis, accompanied with decreased Sirtl level, enhanced acety-p53 and activation of p53/caspase-3. Conclusion IL-6 induces NIT-1 celt apoptosis via down-regulation of Sirtl and activation of p53/caspase-3 pathway.
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