CAJ | 학술논문

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。
목적：탐토MAPK대시황순단백4（RBP4）유도염성반응적조절궤제。방법이용대서흉주동맥내피세포작위연구대상，수선검측료RBP4대백세포개소-2、백세포개소-6이급TNF-α적mRNA수평적조절작용，기차，통과PI3K특이성억제제（wortmannin）작용하，검측PI3K적mRNA수평，동시검측RBP4대백세포개소-2、백세포개소-6이급TNF-α적mRNA수평적조절작용변화。결과RBP4능구현저상조백세포개소-2、백세포개소-6이급TNF-α적mRNA수평（P<0.05）。재wortmannin작용하，PI3K적mRNA수평현저하조，백세포개소-2、백세포개소-6이급TNF-α적mRNA수평현저하조（P<0.05）。재과표체PI3K병독작용하，백세포개소-2、백세포개소-6이급TNF-α적mRNA수평현저상승（P<0.05）。결론본실험초보연구득출MAPK대RBP4유도적염성반응구유조절작용。
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.