Biochanin A Regulates Key Steps of Inflammation Resolution in a Model of Antigen-Induced Arthritis via GPR30/PKA-Dependent Mechanism

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dc.creatorFranciel Batista Felix
dc.creatorGabriel Henrique Campolina Silva
dc.creatorFrederico Marianetti Soriani
dc.creatorLirlândia Pires Sousa
dc.creatorRenata Grespan
dc.creatorMauro Martins Teixeira
dc.creatorVanessa Pinho
dc.creatorJuliana Priscila Vago
dc.creatorDébora de Oliveira Fernandes
dc.creatorDébora Gonzaga Martins
dc.creatorIsabella Zaidan Moreira
dc.creatorWalyson Coelho Costa
dc.creatorJessica Maria Dantas Araújo
dc.creatorCelso Martins Queiroz Junior
dc.creatorWilliam Antonio Gonçalves
dc.date.accessioned2023-07-14T22:29:41Z
dc.date.accessioned2025-09-08T23:24:28Z
dc.date.available2023-07-14T22:29:41Z
dc.date.issued2021
dc.identifier.doihttps://doi.org/10.3389/fphar.2021.662308
dc.identifier.issn1663-9812
dc.identifier.urihttps://hdl.handle.net/1843/56324
dc.languagepor
dc.publisherUniversidade Federal de Minas Gerais
dc.relation.ispartofFrontiers in Pharmacology
dc.rightsAcesso Aberto
dc.subjectArtrite
dc.subjectApoptose
dc.subjectInflamação
dc.subject.otherBiochanin A (PubChem CID 5280373)
dc.subject.otherArthritis
dc.subject.otherApoptosis
dc.subject.otherEfferocytosis
dc.subject.otherResolution of inflammation
dc.titleBiochanin A Regulates Key Steps of Inflammation Resolution in a Model of Antigen-Induced Arthritis via GPR30/PKA-Dependent Mechanism
dc.typeArtigo de periódico
local.citation.epage17
local.citation.spage1
local.citation.volume12
local.description.resumoBiochaninA(BCA)isanaturalorganiccompoundoftheclassofphytochemicalsknownas flavonoidsandisoflavonesubclasspredominantlyfoundinredclover(Trifoliumpratense).It has anti-inflammatory activity and some pro-resolving actions, such as neutrophil apoptosis. However, the effect of BCA in the resolution of inflammation is still poorly understood. In this study, we investigated the effects of BCA on the neutrophilic inflammatory response and its resolution in a model of antigen-induced arthritis. Male wild-type BALB/c mice were treated with BCA at the peak of the inflammatory process (12h). BCA decreased the accumulation of migrated neutrophils, and this effect was associated with reduction of myeloperoxidase activity, IL-1β and CXCL1 levels, and the histological score in periarticular tissues. Joint dysfunction, as seen by mechanical hypernociception, was improved by treatment with BCA. The resolution interval (Ri) was also quantified, defining profiles of acute inflammatory parameters that include the amplitude and duration of the inflammatory response monitored by the neutrophil infiltration. BCA treatment shortened Ri from ∼23h observed in vehicle-treated mice to ∼5.5h, associated with an increase in apoptotic events and efferocytosis, both key steps for the resolution of inflammation. These effects of BCA were prevented by H89, an inhibitor of protein kinase A (PKA) and G15, a selective G protein–coupled receptor 30 (GPR30)antagonist.Inlinewiththeinvivodata,BCAalsoincreasedtheefferocyticabilityof murine bone marrow–derived macrophages. Collectively, these data indicate for the first time that BCA resolves neutrophilic inflammation acting in key steps of the resolution of inflammation, requiring activation of GPR30 and via stimulation of cAMP-dependent signaling.
local.identifier.orcidhttps://orcid.org/0000-0002-2372-2781
local.identifier.orcidhttps://orcid.org/0000-0002-4473-3340
local.identifier.orcidhttps://orcid.org/0000-0003-4720-6746
local.identifier.orcidhttps://orcid.org/0000-0002-1042-9762
local.identifier.orcidhttps://orcid.org/0000-0003-3644-7632
local.identifier.orcidhttps://orcid.org/0000-0002-6944-3008
local.identifier.orcidhttps://orcid.org/0000-0003-1038-2324
local.identifier.orcidhttps://orcid.org/0000-0001-8188-3738
local.identifier.orcidhttps://orcid.org/0000-0002-8666-6342
local.identifier.orcidhttps://orcid.org/0000-0001-7853-3809
local.identifier.orcidhttps://orcid.org/0000-0001-9434-8814
local.identifier.orcidhttps://orcid.org/0000-0002-4178-0387
local.identifier.orcidhttps://orcid.org/0000-0003-4041-6441
local.identifier.orcidhttps://orcid.org/0000-0002-7884-7709
local.publisher.countryBrasil
local.publisher.departmentFAR - DEPARTAMENTO DE ANÁLISES CLÍNICAS E TOXICOLÓGICAS
local.publisher.departmentICB - DEPARTAMENTO DE BIOQUÍMICA E IMUNOLOGIA
local.publisher.departmentICB - DEPARTAMENTO DE FARMACOLOGIA
local.publisher.departmentICB - DEPARTAMENTO DE MORFOLOGIA
local.publisher.initialsUFMG
local.url.externahttps://www.frontiersin.org/articles/10.3389/fphar.2021.662308/full

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