FFA对巨噬细胞解偶联的影响.DOCVIP

巨噬细胞解耦联与炎症的关系 冯晓朋1，刘雪芳1，王铁鹏2，张君2，徐文静2，谢建新2 （450000河南，郑州市中心医院检验科1；832000新疆，石河子大学医学院/新疆地方病与民族高发病教育部重点实验室2） 【摘要】 目的 探讨肥胖状态下巨噬细胞解耦连蛋白2（UCP2）对免疫炎症信号通路关键因子NF-κB及下游炎症因子（IL-6、TNF-α）的影响。方法 体外培养RAW264.7巨噬细胞，分别用FFA和UCP2抑制剂胰岛素处理。Western blot检测NF-кBp65和UCP2水平。酶联免疫法检测细胞培养液中炎症因子IL-6与TNF-a水平。结果 与空白对照组比较，FFA组UCP2及p-NF-κB蛋白表达水平明显升高，胰岛素组UCP2及p-NF-κB蛋白表达水平明显降低， P均0.05。与空白对照组比较，FFA组IL-6、TNF-α表达水平明显升高,胰岛素组IL-6、TNF-α表达水平明显降低，P均0.05。结论 肥胖状态下，FFA通过增强UCP2的活性，作用于炎症信号通路的关键因子NF-кB，启动炎症反应；UCP2蛋白抑制剂能够抑制上述炎症反应。 【关键词】 巨噬细胞；解偶联蛋白2； NF-κB; 炎症因子 Macrophage uncoupling and the relationship between inflammation Feng Xiaopeng1,Liu xuefang1,Wang Tiepeng2,Zhang Jun2,et al. Clinical laboratory of Zhengzhou Central Hospital,Zhengzhou,4500001;Ministry of Education Key Laboratory of Xinjiang Endemic and Ethnic Diseases,Shihezi,Xinjiang 832000,China 【Abstract】 Objective To Study the affect of obesity to macrophage immune and inflammatory signaling pathways of NF-κB and inflammatory cytokines (IL-6, TNF-α). Method Cultured RAW264.7 macrophages in vitro,FFA and UCP2 inhibitor insulin treatment.Western Blot detection the NF-κBp65 and UCP2 levels.Enzyme-linked immunosorbent assay in cell culture medium of inflammatory cytokines IL-6 and TNF-α levels.Result Compared with blank control group the express levels of UCP2 and p-NF-κB in FFA group was significantly higher,in insulin group was significantly reduced; the express levels of IL-6 and TNF-α in FFA group was significantly higher,in insulin group was significantly reduced .Conclusion Obese state, the FFA role in inflammatory signaling pathways critical factor NF-kappa B by enhancing the activity of UCP2, which could initiates inflammation; the UCP2 protein inhibitors can inhibit the inflammatory response. 【Key words】 Macrophages; Uncoupling protein-2 ; NF-κB; Inflammatory cytokines 肥胖是一个严重的世界性健康问题。研究资料显示，肥胖使机体处于一种慢性低炎症状态，各种炎症 因子诱导机体各组织器官发生胰岛素抵抗，导致糖尿病的发生[1]。最近的研究提示，脂肪组织是机体这种慢性低炎症状态的始发部位[2]。 研究发现，脂肪细胞即是能量储存细胞，又是内分泌细胞。脂肪细胞分泌的MCP-1使巨噬细胞向脂肪 组织趋化，