Full metadata record
DC Field | Value | Language |
---|---|---|
dc.contributor.author | 최윤희 | * |
dc.date.accessioned | 2016-08-28T10:08:24Z | - |
dc.date.available | 2016-08-28T10:08:24Z | - |
dc.date.issued | 2013 | * |
dc.identifier.issn | 0014-4835 | * |
dc.identifier.other | OAK-10367 | * |
dc.identifier.uri | https://dspace.ewha.ac.kr/handle/2015.oak/223967 | - |
dc.description.abstract | The aim of this study was to determine the effect of pirfenidone on interleukin (IL)-1β-induced cyclooxygenase (COX)-2 and prostaglandin (PG)E2 expression in orbital fibroblasts from patients with thyroid-associated ophthalmopathy (TAO). Primary cultures of orbital fibroblasts from patients with TAO (n = 4) and non-TAO subjects (n = 4) were prepared. The level of PGE2 in orbital fibroblasts treated with IL-1β in the presence or absence of pirfenidone was measured using an enzyme-linked immunosorbent assay. The effect of pirfenidone on IL-1β-induced COX-2 expression in orbital fibroblasts from patients with TAO was evaluated by reverse transcription-polymerase chain reaction (PCR) and quantitative real-time PCR analyses, and verified by Western blot. Activation of nuclear factor-K{hooktop}B (NF-K{hooktop}B) was evaluated by immunoblotting for inhibitor of K{hooktop}B (IK{hooktop}B)α and phosphorylated IK{hooktop}Bα, and DNA-binding activity of p50/p65 NF-K{hooktop}B was analyzed by electrophoretic mobility shift assay. In addition, IL-1 receptor type 1 (IL-1R1) expression was assessed by RT-PCR in IL-1β-treated cells with or without pirfenidone. Pirfenidone significantly attenuated IL-1β-induced PGE2 release in both TAO and non-TAO cells. IL-1β-induced COX-2 mRNA and protein expression decreased significantly following co-treatment with pirfenidone. IL-1β-induced IK{hooktop}Bα phosphorylation and degradation decreased in the presence of pirfenidone and led to decreased nuclear translocation and DNA binding of the active NF-K{hooktop}B complex. In our system, neither IL-1? nor pirfenidone co-treatment influenced IL-1R1 expression. Our results suggest that pirfenidone attenuates the IL-1β-induced PGE2/COX-2 production in TAO orbital fibroblasts, which is related with suppression of the NF-K{hooktop}B activation. © 2013 Elsevier Ltd. | * |
dc.language | English | * |
dc.title | Pirfenidone attenuates IL-1β-induced COX-2 and PGE2 production in orbital fibroblasts through suppression of NF-K{hooktop}B activity | * |
dc.type | Article | * |
dc.relation.volume | 113 | * |
dc.relation.index | SCI | * |
dc.relation.index | SCIE | * |
dc.relation.index | SCOPUS | * |
dc.relation.startpage | 1 | * |
dc.relation.lastpage | 8 | * |
dc.relation.journaltitle | Experimental Eye Research | * |
dc.identifier.doi | 10.1016/j.exer.2013.05.001 | * |
dc.identifier.wosid | WOS:000322931700001 | * |
dc.identifier.scopusid | 2-s2.0-84878883756 | * |
dc.author.google | Choi Y.-H. | * |
dc.author.google | Back K.O. | * |
dc.author.google | Kim H.J. | * |
dc.author.google | Lee S.Y. | * |
dc.author.google | Kook K.H. | * |
dc.contributor.scopusid | 최윤희(7404776849) | * |
dc.date.modifydate | 20240123124738 | * |