Inhibitors of tumor necrosis factor synthesis as a new approach for the treatment of rheumatoid arthritis

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dc.contributorLab. Farmacologiapt_BR
dc.contributor.authorMendes, Mariana Trivilinpt_BR
dc.contributor.authorVendrame, Rafaela Fadoni Alpontipt_BR
dc.contributor.authorAlves, Patrícia Lúciopt_BR
dc.contributor.authorTrevizan, Isabela Lopespt_BR
dc.contributor.authorMarkus, Regina Pekelmannpt_BR
dc.contributor.authorFernandes, Pedro Augustopt_BR
dc.contributor.authorSilveira, Paulo Fláviopt_BR
dc.date.accessioned2020-12-23T18:22:53Z-
dc.date.available2020-12-23T18:22:53Z-
dc.date.issued2020pt_BR
dc.identifier.citationMendes MT, Vendrame RFA, Alves PL, Trevizan IL, Markus RP, Fernandes PA, et al. Inhibitors of tumor necrosis factor synthesis as a new approach for the treatment of rheumatoid arthritis. J. Arthritis. 2020 July;9(4):001-007. doi:4.pt_BR
dc.identifier.urihttps://repositorio.butantan.gov.br/handle/butantan/3421-
dc.description.abstractObjective: The treatment of rheumatoid arthritis (RA) is based on the inhibition of TNF. Here we evaluated whether drugs that might inhibit TNF, such as pentoxifylline (PTX), rupatadine (RUP), rolipram (ROL) and thalidomide (THA), could be an alternative for RA treatment. Methods: In wistar male rats the changes in paw thickness, plasma TNF and by the activity of basic aminopeptidase (APB) in soluble fraction of synovial tissue and peripheral blood mononuclear cells (PBMC) evaluated after daily injection for 30 days were taken as anti-inflammatory outputs, while hepatotoxicity was assessed by measuring plasma alanine transaminase (ALT) and aspartate transaminase (AST) activity. The content of IL1-β, IL-6 in serum and synovial fluid and the histology of the injured tissue were determined only for ROL, THA and ROL+THA. Prednisolone was used as a standard drug. Results: Collagen treatment induced paw thickness, histological changes in the tibiotarsal joint, increase in synovial fluid of both cytokines and synovial tissue of APB activity. Furthermore, the APB activity in PBMC was reduced and ALT and AST activity were enhanced. The most effective drug schedule in reducing arthritis induced changes described above, as well as recovering from control levels TNF, IL1-β, APB in synovial tissue and AST activities were THA and the association of ROL and THA. However, only THA alone reduced the levels of ALT. Conclusion: The synthesis of TNF in RA models can be blocked by drugs acting at different targets. We show that THA and THA+ROL emerges as simple and effective therapeutic alternatives for RA.pt_BR
dc.description.sponsorship(FAPESP) Fundação de Amparo à Pesquisa do Estado de São Paulopt_BR
dc.description.sponsorship(CNPq) Conselho Nacional de Desenvolvimento Científico e Tecnológicopt_BR
dc.description.sponsorship(CAPES) Coordenação de Aperfeiçoamento de Pessoal de Nível Superiorpt_BR
dc.description.sponsorship(FUNED) Fundação Ezequiel Diaspt_BR
dc.format.extent001-007pt_BR
dc.language.isoEnglishpt_BR
dc.relation.ispartofJournal of Arthritispt_BR
dc.rightsOpen accesspt_BR
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/pt_BR
dc.titleInhibitors of tumor necrosis factor synthesis as a new approach for the treatment of rheumatoid arthritispt_BR
dc.typeArticlept_BR
dc.rights.licenseCC BYpt_BR
dc.identifier.urlhttps://www.iomcworld.org/open-access/inhibitors-of-tumor-necrosis-factor-synthesis-as-a-new-approach-for-thetreatment-of-rheumatoid-arthritis.pdfpt_BR
dc.contributor.external(USP) Universidade de São Paulopt_BR
dc.identifier.citationvolume9pt_BR
dc.identifier.citationissue4pt_BR
dc.subject.keywordRheumatoid Arthritispt_BR
dc.subject.keywordTNFpt_BR
dc.subject.keywordAnti-TNFpt_BR
dc.subject.keywordBasic Aminopeptidasept_BR
dc.subject.keywordThalidomidept_BR
dc.subject.keywordRoliprampt_BR
dc.subject.keywordDrug Repositioningpt_BR
dc.relation.ispartofabbreviatedJ Arthritispt_BR
dc.identifier.citationabntv. 9, n. 4, p. 001-007, jul. 2020pt_BR
dc.identifier.citationvancouver2020 July;9(4):001-007pt_BR
dc.contributor.butantanMendes, Mariana Trivilin|:Aluno|:Lab. Farmacologia|:PrimeiroAutor:Autor de correspondênciapt_BR
dc.contributor.butantanVendrame, Rafaela Fadoni Alponti|:Aluno:Docente colaborador PPGTOX|:Lab. Farmacologiapt_BR
dc.contributor.butantanAlves, Patrícia Lúcio|:Aluno|:Lab. Farmacologiapt_BR
dc.contributor.butantanSilveira, Paulo Flávio|:Pesquisador|:Lab. Farmacologiapt_BR
dc.sponsorship.butantan(FAPESP) Fundação de Amparo à Pesquisa do Estado de São Paulo¦¦12/12105-9pt_BR
dc.sponsorship.butantan(FAPESP) Fundação de Amparo à Pesquisa do Estado de São Paulo¦¦14/24634-1pt_BR
dc.sponsorship.butantan(FAPESP) Fundação de Amparo à Pesquisa do Estado de São Paulo¦¦13/13963-1pt_BR
dc.sponsorship.butantan(CNPq) Conselho Nacional de Desenvolvimento Científico e Tecnológico¦¦140163/2013-1pt_BR
dc.sponsorship.butantan(CAPES) Coordenação de Aperfeiçoamento de Pessoal de Nível Superior¦¦pt_BR
dc.sponsorship.butantanFundação Ezequiel Dias (FUNED)¦¦pt_BR
dc.identifier.bvsccBR78.1pt_BR
dc.identifier.bvsdbIBProdpt_BR
dc.description.dbindexedYespt_BR
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item.languageiso639-1English-
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