Oleanolic acid acetate inhibits rheumatoid arthritis by modulating T cell immune responses and matrix-degrading enzymes

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dc.contributor.authorJ K Choi-
dc.contributor.authorS W Kim-
dc.contributor.authorD S Kim-
dc.contributor.authorJ Y Lee-
dc.contributor.authorSoyoung Lee-
dc.contributor.authorHyun-Mee Oh-
dc.contributor.authorY S Ha-
dc.contributor.authorJ Yoo-
dc.contributor.authorP H Park-
dc.contributor.authorT Y Shin-
dc.contributor.authorT K Kwon-
dc.contributor.authorMun Chual Rho-
dc.contributor.authorS H Kim-
dc.date.accessioned2017-04-19T10:14:43Z-
dc.date.available2017-04-19T10:14:43Z-
dc.date.issued2016-
dc.identifier.issn0041008X-
dc.identifier.uri10.1016/j.taap.2015.11.005ko
dc.identifier.urihttps://oak.kribb.re.kr/handle/201005/13005-
dc.description.abstractRheumatoid arthritis (RA) is a chronic autoimmune disease associated with a combination of synovium joint inflammation, synovium hyperplasia, and destruction of cartilage and bone. Oleanolic acid acetate (OAA), a compound isolated from Vigna angularis, has been known to possess pharmacological activities, including anti-inflammation and anti-bone destruction. In this study, we investigated the effects of OAA on RA and the underlying mechanisms of action by using a type-II collagen-induced arthritis (CIA) mouse model and tumor necrosis factor (TNF)-α-stimulated RA synovial fibroblasts. Oral administration of OAA decreased the clinical arthritis symptoms, paw thickness, histologic and radiologic changes, and serum total and anti-type II collagen IgG, IgG1, and IgG2a levels. OAA administration reduced Th1/Th17 phenotype CD4+ T lymphocyte expansions and inflammatory cytokine productions in T cell activated draining lymph nodes and spleen. OAA reduced the expression and production of inflammatory mediators, such as cytokines and matrix metalloproteinase (MMP)-1/3, in the ankle joint tissue and RA synovial fibroblasts by down-regulating Akt, mitogen-activated protein kinases, and nuclear factor-κB. Our results clearly support that OAA plays a therapeutic role in RA pathogenesis by modulating helper T cell immune responses and matrix-degrading enzymes. The immunosuppressive effects of OAA were comparable to dexamethasone and ketoprofen. We provide evidences that OAA could be a potential therapeutic candidate for RA.-
dc.publisherElsevier-
dc.titleOleanolic acid acetate inhibits rheumatoid arthritis by modulating T cell immune responses and matrix-degrading enzymes-
dc.title.alternativeOleanolic acid acetate inhibits rheumatoid arthritis by modulating T cell immune responses and matrix-degrading enzymes-
dc.typeArticle-
dc.citation.titleToxicology and Applied Pharmacology-
dc.citation.number0-
dc.citation.endPage9-
dc.citation.startPage1-
dc.citation.volume290-
dc.contributor.affiliatedAuthorSoyoung Lee-
dc.contributor.affiliatedAuthorMun Chual Rho-
dc.contributor.alternativeName최진경-
dc.contributor.alternativeName김성완-
dc.contributor.alternativeName김덕실-
dc.contributor.alternativeName이종영-
dc.contributor.alternativeName이소영-
dc.contributor.alternativeName오현미-
dc.contributor.alternativeName하영수-
dc.contributor.alternativeName유정수-
dc.contributor.alternativeName박필훈-
dc.contributor.alternativeName신태용-
dc.contributor.alternativeName권택규-
dc.contributor.alternativeName노문철-
dc.contributor.alternativeName김상현-
dc.identifier.bibliographicCitationToxicology and Applied Pharmacology, vol. 290, pp. 1-9-
dc.identifier.doi10.1016/j.taap.2015.11.005-
dc.subject.keywordCollagen-induced arthritis-
dc.subject.keywordInflammatory cytokine-
dc.subject.keywordLymph nodes-
dc.subject.keywordMatrix metalloproteinase-
dc.subject.keywordOleanolic acid acetate-
dc.subject.keywordSynovial fibroblasts-
dc.subject.localCollagen-induced arthritis-
dc.subject.localInflammatory cytokine-
dc.subject.localLymph nodes-
dc.subject.localLymph node-
dc.subject.localMatrix metalloproteinase-
dc.subject.localOleanolic acid acetate-
dc.subject.localSynovial fibroblasts-
dc.subject.localSynovial fibroblast-
dc.description.journalClassY-
Appears in Collections:
Jeonbuk Branch Institute > Immunoregulatory materials Research Center > 1. Journal Articles
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