内脂素对巨噬细胞凋亡的影响及其机制研究  

Visfatin Enhanced Macrophages Apoptosis through Insulin Receptor Signaling Pathway

作　　者：张高峰[1] 许澎[1] 乔祺[1] 

机构地区：[1]复旦大学附属上海市第五人民医院心内科,上海200240

出　　处：《中国临床医学》2011年第5期617-620,共4页Chinese Journal of Clinical Medicine

摘　　要：目的:探讨内脂素对巨噬细胞凋亡的影响及其机制。方法:血清饥饿法诱导THP-1细胞凋亡,加入不同浓度的内脂素(0～100 ng/mL5个浓度组),每组分别孵育24～48 h。同时设立2-羟基萘甲基磷酸三乙酸甲基酯(HNMPA)组。用Annex-inⅤ-碘化丙啶流式细胞仪检测及末端脱氧核苷酸转移酶介导的dUTP缺口末端标记(TUNEL)检测细胞凋亡情况,并检测caspase-3活性及细胞色素C的释放。结果:内脂素增加THP-1细胞凋亡百分比,呈浓度依赖(P<0.05);增加caspase-3活性及细胞色素C的释放(P<0.05)。HNMPA能完全抵消内脂素的促进凋亡作用。结论:内脂素促进巨噬细胞凋亡,凋亡过程涉及增加线粒体内细胞色素C的释放;其机制可能通过胰岛素受体信号途径发挥作用。Objective：To investigate the effect of visfatin on macrophages apoptosis and possible mechanism. Methods： Apoptosis was induced in macrophages derived from THP-1 cell line by serum starvation. Visfatin administration enhanced macrophage apoptosis by means of annexin V binding assay,TUNEL assay and caspase activity in a dose-dependent manner within the range of 12.5 to 100ng/mL. Results： Visfatin also increased release of cytochrome C. In the exploration of the signaling pathway involved in these pro-apoptotic effects of visfatin, pretreatment of cells with a specific insulin receptor antagonist-HNMPA significantly suppressed visfatin-mediated cell apoptosis and caspase activity in macrophages. Conclusions： Visfatin enhance macrophages apoptosis, and it is mediated through insulin receptor signaling pathway.

关 键 词：内脂素 巨噬细胞 细胞凋亡 动脉粥样硬化 

分 类 号：Q255[生物学—细胞生物学]