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Decrease of CD68 synovial macrophages in celastrol treated arthritic rats

2015Artigo científico Acesso aberto
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dc.contributor.authorCascao, Rita
dc.contributor.authorVidal, Bruno
dc.contributor.authorLopes, Inês
dc.contributor.authorPaisana, Eunice
dc.contributor.authorRino, José
dc.contributor.authorMoita, Luis
dc.contributor.authorFonseca, João Eurico
dc.date.accessioned2022-06-21T15:31:38Z
dc.date.available2022-06-21T15:31:38Z
dc.date.issued2015
dc.descriptionCopyright: © 2015 Cascão et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are creditedpt_PT
dc.description.abstractBackground: Rheumatoid arthritis (RA) is a chronic immune-mediated inflammatory disease characterized by cellular infiltration into the joints, hyperproliferation of synovial cells and bone damage. Available treatments for RA only induce remission in around 30% of the patients, have important adverse effects and its use is limited by their high cost. Therefore, compounds that can control arthritis, with an acceptable safety profile and low production costs are still an unmet need. We have shown, in vitro, that celastrol inhibits both IL-1β and TNF, which play an important role in RA, and, in vivo, that celastrol has significant anti-inflammatory properties. Our main goal in this work was to test the effect of celastrol in the number of sublining CD68 macrophages (a biomarker of therapeutic response for novel RA treatments) and on the overall synovial tissue cellularity and joint structure in the adjuvant-induced rat model of arthritis (AIA). Methods: Celastrol was administered to AIA rats both in the early (4 days after disease induction) and late (11 days after disease induction) phases of arthritis development. The inflammatory score, ankle perimeter and body weight were evaluated during treatment period. Rats were sacrificed after 22 days of disease progression and blood, internal organs and paw samples were collected for toxicological blood parameters and serum proinflammatory cytokine quantification, as well as histopathological and immunohistochemical evaluation, respectively. Results: Here we report that celastrol significantly decreases the number of sublining CD68 macrophages and the overall synovial inflammatory cellularity, and halted joint destruction without side effects. Conclusions: Our results validate celastrol as a promising compound for the treatment of arthritis.pt_PT
dc.description.sponsorshipRC was supported with a fellowship from Fundação para a Ciência e a Tecnologia (FCT, SFRH/BPD/92860/2013).pt_PT
dc.description.versioninfo:eu-repo/semantics/publishedVersionpt_PT
dc.identifier.citationPLoS One. 2015 Dec 11;10(12):e0142448pt_PT
dc.identifier.doi10.1371/journal.pone.0142448pt_PT
dc.identifier.eissn1932-6203
dc.identifier.urihttp://hdl.handle.net/10451/53427
dc.language.isoengpt_PT
dc.peerreviewedyespt_PT
dc.publisherPLoSpt_PT
dc.relationEvaluation of celastrol as a candidate for the treatment of rheumatoid arthritis
dc.relation.publisherversionhttps://journals.plos.org/plosone/pt_PT
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/pt_PT
dc.titleDecrease of CD68 synovial macrophages in celastrol treated arthritic ratspt_PT
dc.typejournal article
dspace.entity.typePublication
oaire.awardTitleEvaluation of celastrol as a candidate for the treatment of rheumatoid arthritis
oaire.awardURIinfo:eu-repo/grantAgreement/FCT//SFRH%2FBPD%2F92860%2F2013/PT
oaire.citation.issue12pt_PT
oaire.citation.titlePLOS ONEpt_PT
oaire.citation.volume10pt_PT
person.familyNameCascão
person.familyNameCosta Vidal
person.familyNameLopes
person.familyNameRibeiro João Silva Paisana
person.familyNameRino Henriques
person.familyNameMoita
person.familyNameFonseca
person.givenNameRita
person.givenNameBruno Miguel
person.givenNameInês
person.givenNameEunice
person.givenNameJosé Miguel
person.givenNameLuis
person.givenNameJoão
person.identifier335918
person.identifier.ciencia-idB616-D8BB-3CF2
person.identifier.ciencia-id251C-3CD5-FB69
person.identifier.ciencia-idC91E-84E5-4636
person.identifier.ciencia-idA117-FBDB-A27B
person.identifier.ciencia-idCA1C-AE28-33FE
person.identifier.ciencia-idF310-B85D-57C7
person.identifier.orcid0000-0001-5533-9413
person.identifier.orcid0000-0003-2906-4705
person.identifier.orcid0000-0002-2109-6203
person.identifier.orcid0000-0001-5915-8556
person.identifier.orcid0000-0002-0637-4527
person.identifier.orcid0000-0003-0707-315X
person.identifier.orcid0000-0003-1432-3671
person.identifier.ridN-6675-2013
person.identifier.ridL-1296-2013
person.identifier.scopus-author-id35728434100
person.identifier.scopus-author-id24554088300
person.identifier.scopus-author-id7101983519
project.funder.identifierhttp://doi.org/10.13039/501100001871
project.funder.nameFundação para a Ciência e a Tecnologia
rcaap.rightsopenAccesspt_PT
rcaap.typearticlept_PT
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