Biochanin A Regulates Key Steps of Inflammation Resolution in a Model of Antigen-Induced Arthritis via GPR30/PKA-Dependent Mechanism
Autor(a) principal: | |
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Data de Publicação: | 2021 |
Outros Autores: | , , , , , , , , , , , , , |
Tipo de documento: | Artigo |
Idioma: | por |
Título da fonte: | Repositório Institucional da UFMG |
Texto Completo: | https://doi.org/10.3389/fphar.2021.662308 http://hdl.handle.net/1843/56324 https://orcid.org/0000-0002-2372-2781 https://orcid.org/0000-0002-4473-3340 https://orcid.org/0000-0003-4720-6746 https://orcid.org/0000-0002-1042-9762 https://orcid.org/0000-0003-3644-7632 https://orcid.org/0000-0002-6944-3008 https://orcid.org/0000-0003-1038-2324 https://orcid.org/0000-0001-8188-3738 https://orcid.org/0000-0002-8666-6342 https://orcid.org/0000-0001-7853-3809 https://orcid.org/0000-0001-9434-8814 https://orcid.org/0000-0002-4178-0387 https://orcid.org/0000-0003-4041-6441 https://orcid.org/0000-0002-7884-7709 |
Resumo: | BiochaninA(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. |
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2023-07-14T22:29:41Z2023-07-14T22:29:41Z202112117https://doi.org/10.3389/fphar.2021.6623081663-9812http://hdl.handle.net/1843/56324https://orcid.org/0000-0002-2372-2781https://orcid.org/0000-0002-4473-3340https://orcid.org/0000-0003-4720-6746https://orcid.org/0000-0002-1042-9762https://orcid.org/0000-0003-3644-7632https://orcid.org/0000-0002-6944-3008https://orcid.org/0000-0003-1038-2324https://orcid.org/0000-0001-8188-3738https://orcid.org/0000-0002-8666-6342https://orcid.org/0000-0001-7853-3809https://orcid.org/0000-0001-9434-8814https://orcid.org/0000-0002-4178-0387https://orcid.org/0000-0003-4041-6441https://orcid.org/0000-0002-7884-7709BiochaninA(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.porUniversidade Federal de Minas GeraisUFMGBrasilFAR - DEPARTAMENTO DE ANÁLISES CLÍNICAS E TOXICOLÓGICASICB - DEPARTAMENTO DE BIOQUÍMICA E IMUNOLOGIAICB - DEPARTAMENTO DE FARMACOLOGIAICB - DEPARTAMENTO DE MORFOLOGIAFrontiers in PharmacologyArtriteApoptoseInflamaçãoBiochanin A (PubChem CID 5280373)ArthritisApoptosisEfferocytosisResolution of inflammationBiochanin A Regulates Key Steps of Inflammation Resolution in a Model of Antigen-Induced Arthritis via GPR30/PKA-Dependent Mechanisminfo:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/articlehttps://www.frontiersin.org/articles/10.3389/fphar.2021.662308/fullFranciel Batista FelixGabriel Henrique Campolina SilvaFrederico Marianetti SorianiLirlândia Pires SousaRenata GrespanMauro Martins TeixeiraVanessa PinhoJuliana Priscila VagoDébora de Oliveira FernandesDébora Gonzaga MartinsIsabella Zaidan MoreiraWalyson Coelho CostaJessica Maria Dantas AraújoCelso Martins Queiroz JuniorWilliam Antonio Gonçalvesinfo:eu-repo/semantics/openAccessreponame:Repositório Institucional da UFMGinstname:Universidade Federal de Minas Gerais (UFMG)instacron:UFMGORIGINALBiochanin A Regulates Key Steps of Inflammation Resolution in a Model of Antigen-Induced Arthritis via GPR30PKA-Dependent Mechanism.pdfBiochanin A Regulates Key Steps of Inflammation Resolution in a Model of Antigen-Induced Arthritis via GPR30PKA-Dependent Mechanism.pdfapplication/pdf56568066https://repositorio.ufmg.br/bitstream/1843/56324/2/Biochanin%20A%20Regulates%20Key%20Steps%20of%20Inflammation%20Resolution%20in%20a%20Model%20of%20Antigen-Induced%20Arthritis%20via%20GPR30PKA-Dependent%20Mechanism.pdf430e10e503f66df6120f6e46febc3cb1MD52LICENSELicense.txtLicense.txttext/plain; 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dc.title.pt_BR.fl_str_mv |
Biochanin A Regulates Key Steps of Inflammation Resolution in a Model of Antigen-Induced Arthritis via GPR30/PKA-Dependent Mechanism |
title |
Biochanin A Regulates Key Steps of Inflammation Resolution in a Model of Antigen-Induced Arthritis via GPR30/PKA-Dependent Mechanism |
spellingShingle |
Biochanin A Regulates Key Steps of Inflammation Resolution in a Model of Antigen-Induced Arthritis via GPR30/PKA-Dependent Mechanism Franciel Batista Felix Biochanin A (PubChem CID 5280373) Arthritis Apoptosis Efferocytosis Resolution of inflammation Artrite Apoptose Inflamação |
title_short |
Biochanin A Regulates Key Steps of Inflammation Resolution in a Model of Antigen-Induced Arthritis via GPR30/PKA-Dependent Mechanism |
title_full |
Biochanin A Regulates Key Steps of Inflammation Resolution in a Model of Antigen-Induced Arthritis via GPR30/PKA-Dependent Mechanism |
title_fullStr |
Biochanin A Regulates Key Steps of Inflammation Resolution in a Model of Antigen-Induced Arthritis via GPR30/PKA-Dependent Mechanism |
title_full_unstemmed |
Biochanin A Regulates Key Steps of Inflammation Resolution in a Model of Antigen-Induced Arthritis via GPR30/PKA-Dependent Mechanism |
title_sort |
Biochanin A Regulates Key Steps of Inflammation Resolution in a Model of Antigen-Induced Arthritis via GPR30/PKA-Dependent Mechanism |
author |
Franciel Batista Felix |
author_facet |
Franciel Batista Felix Gabriel Henrique Campolina Silva Frederico Marianetti Soriani Lirlândia Pires Sousa Renata Grespan Mauro Martins Teixeira Vanessa Pinho Juliana Priscila Vago Débora de Oliveira Fernandes Débora Gonzaga Martins Isabella Zaidan Moreira Walyson Coelho Costa Jessica Maria Dantas Araújo Celso Martins Queiroz Junior William Antonio Gonçalves |
author_role |
author |
author2 |
Gabriel Henrique Campolina Silva Frederico Marianetti Soriani Lirlândia Pires Sousa Renata Grespan Mauro Martins Teixeira Vanessa Pinho Juliana Priscila Vago Débora de Oliveira Fernandes Débora Gonzaga Martins Isabella Zaidan Moreira Walyson Coelho Costa Jessica Maria Dantas Araújo Celso Martins Queiroz Junior William Antonio Gonçalves |
author2_role |
author author author author author author author author author author author author author author |
dc.contributor.author.fl_str_mv |
Franciel Batista Felix Gabriel Henrique Campolina Silva Frederico Marianetti Soriani Lirlândia Pires Sousa Renata Grespan Mauro Martins Teixeira Vanessa Pinho Juliana Priscila Vago Débora de Oliveira Fernandes Débora Gonzaga Martins Isabella Zaidan Moreira Walyson Coelho Costa Jessica Maria Dantas Araújo Celso Martins Queiroz Junior William Antonio Gonçalves |
dc.subject.por.fl_str_mv |
Biochanin A (PubChem CID 5280373) Arthritis Apoptosis Efferocytosis Resolution of inflammation |
topic |
Biochanin A (PubChem CID 5280373) Arthritis Apoptosis Efferocytosis Resolution of inflammation Artrite Apoptose Inflamação |
dc.subject.other.pt_BR.fl_str_mv |
Artrite Apoptose Inflamação |
description |
BiochaninA(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. |
publishDate |
2021 |
dc.date.issued.fl_str_mv |
2021 |
dc.date.accessioned.fl_str_mv |
2023-07-14T22:29:41Z |
dc.date.available.fl_str_mv |
2023-07-14T22:29:41Z |
dc.type.status.fl_str_mv |
info:eu-repo/semantics/publishedVersion |
dc.type.driver.fl_str_mv |
info:eu-repo/semantics/article |
format |
article |
status_str |
publishedVersion |
dc.identifier.uri.fl_str_mv |
http://hdl.handle.net/1843/56324 |
dc.identifier.doi.pt_BR.fl_str_mv |
https://doi.org/10.3389/fphar.2021.662308 |
dc.identifier.issn.pt_BR.fl_str_mv |
1663-9812 |
dc.identifier.orcid.pt_BR.fl_str_mv |
https://orcid.org/0000-0002-2372-2781 https://orcid.org/0000-0002-4473-3340 https://orcid.org/0000-0003-4720-6746 https://orcid.org/0000-0002-1042-9762 https://orcid.org/0000-0003-3644-7632 https://orcid.org/0000-0002-6944-3008 https://orcid.org/0000-0003-1038-2324 https://orcid.org/0000-0001-8188-3738 https://orcid.org/0000-0002-8666-6342 https://orcid.org/0000-0001-7853-3809 https://orcid.org/0000-0001-9434-8814 https://orcid.org/0000-0002-4178-0387 https://orcid.org/0000-0003-4041-6441 https://orcid.org/0000-0002-7884-7709 |
url |
https://doi.org/10.3389/fphar.2021.662308 http://hdl.handle.net/1843/56324 https://orcid.org/0000-0002-2372-2781 https://orcid.org/0000-0002-4473-3340 https://orcid.org/0000-0003-4720-6746 https://orcid.org/0000-0002-1042-9762 https://orcid.org/0000-0003-3644-7632 https://orcid.org/0000-0002-6944-3008 https://orcid.org/0000-0003-1038-2324 https://orcid.org/0000-0001-8188-3738 https://orcid.org/0000-0002-8666-6342 https://orcid.org/0000-0001-7853-3809 https://orcid.org/0000-0001-9434-8814 https://orcid.org/0000-0002-4178-0387 https://orcid.org/0000-0003-4041-6441 https://orcid.org/0000-0002-7884-7709 |
identifier_str_mv |
1663-9812 |
dc.language.iso.fl_str_mv |
por |
language |
por |
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Frontiers in Pharmacology |
dc.rights.driver.fl_str_mv |
info:eu-repo/semantics/openAccess |
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openAccess |
dc.publisher.none.fl_str_mv |
Universidade Federal de Minas Gerais |
dc.publisher.initials.fl_str_mv |
UFMG |
dc.publisher.country.fl_str_mv |
Brasil |
dc.publisher.department.fl_str_mv |
FAR - DEPARTAMENTO DE ANÁLISES CLÍNICAS E TOXICOLÓGICAS ICB - DEPARTAMENTO DE BIOQUÍMICA E IMUNOLOGIA ICB - DEPARTAMENTO DE FARMACOLOGIA ICB - DEPARTAMENTO DE MORFOLOGIA |
publisher.none.fl_str_mv |
Universidade Federal de Minas Gerais |
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reponame:Repositório Institucional da UFMG instname:Universidade Federal de Minas Gerais (UFMG) instacron:UFMG |
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Universidade Federal de Minas Gerais (UFMG) |
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UFMG |
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UFMG |
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Repositório Institucional da UFMG |
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Repositório Institucional da UFMG |
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