1. Repositório Institucional da UFMG
  2. Publicações Científicas e Culturais
  3. Artigo de Periódico
Please use this identifier to cite or link to this item: http://hdl.handle.net/1843/61856
Full metadata record
DC FieldValueLanguage
dc.creatorPedro Henrique Villar-Delfinopt_BR
dc.creatorNathália Augusta Oliveira Gomespt_BR
dc.creatorPaulo Pereira Christopt_BR
dc.creatorJosé Augusto Nogueira-Machadopt_BR
dc.creatorCaroline Maria Oliveira Volpept_BR
dc.date.accessioned2023-12-07T21:39:07Z-
dc.date.available2023-12-07T21:39:07Z-
dc.date.issued2022-
dc.citation.volume14pt_BR
dc.citation.spage1pt_BR
dc.citation.epage7pt_BR
dc.identifier.doihttps://doi.org/10.1177/11795735221092524pt_BR
dc.identifier.issn1179-5735pt_BR
dc.identifier.urihttp://hdl.handle.net/1843/61856-
dc.description.resumoBACKGROUND: Oxidative stress is associated with the pathogenesis of MS. Edaravone (EDV) has been proposed as a therapeutic resource for central nervous system diseases, and it was effective in reducing oxidative stress. However, the antioxidant mechanisms of EDV are poorly studied. OBJECTIVE: This study aimed to evaluate the effects of EDV on resting, phagocytosis, and PKC-activated granulocytes derived from MS patients and a healthy control group. METHODS: The effects of EDV on ROS production in phagocytosis (ROS production in the presence of opsonized particles) and PKC-stimulated granulocytes were evaluated in a luminol-dependent chemiluminescence method. Calphostin C was used in some experiments to compare with those of EDV. RESULTS: EDV inhibited ROS production in phagocytosis of opsonized particles and PKC-stimulated granulocytes from MS patients and healthy control group. In the presence of calphostin C, the inhibition of ROS production was similar to that observed with EDV. CONCLUSION: These findings suggest the involvement of EDV on the ROS-PKC-NOX signaling pathways modulating oxidative stress in MS. EDV represents a promising treatment option to control oxidative innate immune response for MS. KEYWORDS: edaravone, multiple sclerosis, innate immunity, reactive oxygen species, phagocytosis, protein kinase C.pt_BR
dc.format.mimetypepdfpt_BR
dc.languageengpt_BR
dc.publisherUniversidade Federal de Minas Geraispt_BR
dc.publisher.countryBrasilpt_BR
dc.publisher.departmentMED - DEPARTAMENTO DE CLÍNICA MÉDICApt_BR
dc.publisher.initialsUFMGpt_BR
dc.relation.ispartofJournal of Central Nervous System Diseasept_BR
dc.rightsAcesso Abertopt_BR
dc.subjectMultiple Sclerosispt_BR
dc.subjectEdaravonept_BR
dc.subjectOxidative stress modulationpt_BR
dc.subject.otherEdaravonept_BR
dc.subject.otherEsclerose Múltiplapt_BR
dc.subject.otherEstresse Oxidativopt_BR
dc.titleEdaravone inhibits the production of reactive oxygen species in phagocytosis- and pkc-stimulated granulocytes from multiple sclerosis patients edaravone modulate oxidative stress in multiple sclerosispt_BR
dc.typeArtigo de Periódicopt_BR
dc.url.externahttps://journals.sagepub.com/doi/10.1177/11795735221092524pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0003-1224-5243pt_BR
Appears in Collections:Artigo de Periódico

Files in This Item:
File Description SizeFormat 
Edaravone inhibits the production of reactive oxygen species in phagocytosis- and pkc-stimulated granulocytes from multiple sclerosis patients edaravone modulate oxidative stress in multiple sclerosis.pdf229.38 kBAdobe PDFView/Open
Show simple item record


Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.