MAPK对RBP4诱导炎性反应的调节机制及研究  

The Regulation of MAPK on the Inflammatory Response induced by RBP4

作　　者：吴桂平[1] 付鑫[1] 张彦红[1] 邹慕蔚[1] 邓会明[1] 晏宁[1] 

机构地区：[1]沈阳医学院附属第二医院心内科,辽宁沈阳110035

出　　处：《中国医药指南》2014年第7期9-10,共2页Guide of China Medicine

基　　金：沈阳市科技计划项目(计划文号:沈科发[2011]21号;项目编号:F11-262-9-41;合同编号:11318)

摘　　要：目的探讨MAPK对视黄醇蛋白4(RBP4)诱导炎性反应的调节机制。方法利用大鼠胸主动脉内皮细胞作为研究对象,首先检测了RBP4对白细胞介素-2、白细胞介素-6以及TNF-α的mRNA水平的调节作用,其次,通过PI3K特异性抑制剂(wortmannin)作用下,检测PI3K的mRNA水平,同时检测RBP4对白细胞介素-2、白细胞介素-6以及TNF-α的mRNA水平的调节作用变化。结果 RBP4能够显著上调白细胞介素-2、白细胞介素-6以及TNF-α的mRNA水平(P<0.05)。在wortmannin作用下,PI3K的mRNA水平显著下调,白细胞介素-2、白细胞介素-6以及TNF-α的mRNA水平显著下调(P<0.05)。在过表达PI3K病毒作用下,白细胞介素-2、白细胞介素-6以及TNF-α的mRNA水平显著上升(P<0.05)。结论本实验初步研究得出MAPK对RBP4诱导的炎性反应具有调节作用。Objective To explore the mechanisms of regulation of MAPK on the inlfammatory response induced by retinol protein 4 （RBP4）. Methods The rat aortic endothelial cells as an object of study, ifrst detected RBP4 dialogue interleukin-2, the regulatory role of interleukin-6, and TNF-α mRNA levels, and secondly, the role of PI3K speciifc inhibitor （wortmannin） , the detection of mRNA levels of PI3K simultaneous detection of the changes of the regulatory role of RBP4 interleukin-2, interleukin-6 and of TNF-α mRNA levels. Results RBP4 signiifcant upregulation of interleukin-2, interleukin-6, as well as of TNF-α mRNA levels （P〈0.05）. Wortmannin role of PI3K mRNA level signiifcantly lowered, interleukin-2, interleukin-6 as well as of TNF-α the mRNA level signiifcantly signiifcantly lowered （P〈0.05） in the over-expression of PI3K virus, interleukin-2, interleukin prime -6, and TNF-α mRNA levels increased signiifcantly （P〈0.05）. Conclusions In this study, preliminary studies MAPK-induced inlfammatory response of RBP4 has a regulatory role.

关 键 词：视黄醇蛋白4 炎性反应 RBP4 

分 类 号：R541.4[医药卫生—心血管疾病]