Anti-inflammatory mechanisms and pharmacological actions of phycocyanobilin in a mouse model of experimental autoimmune encephalomyelitis: a therapeutic promise for multiple sclerosis

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dc.creatorJavier Marín-Prida
dc.creatorJulio Raúl Fernández-Massó
dc.creatorIgnacio Hernández-González
dc.creatorGillian Martínez-Donato
dc.creatorGerardo Guillén-Nieto
dc.creatorEduardo Pentón-Arias
dc.creatorMauro Martins Teixeira
dc.creatorGiselle Pentón-Rol
dc.creatorNancy Pavón-Fuentes
dc.creatorNielsen Lagumersindez-Denis
dc.creatorHanlet Camacho-Rodríguez
dc.creatorAna Margarita García-Soca
dc.creatorRocío de la Caridad Sarduy-Chávez
dc.creatorÉrica Leandro Marciano Vieira
dc.creatorJuliana Carvalho Tavares
dc.creatorViviana Falcón-Cama
dc.date.accessioned2024-07-25T20:14:30Z
dc.date.accessioned2025-09-09T01:17:25Z
dc.date.available2024-07-25T20:14:30Z
dc.date.issued2022-11-03
dc.description.sponsorshipOutra Agência
dc.format.mimetypepdf
dc.identifier.doi10.3389/fimmu.2022.1036200
dc.identifier.issn1664-3224
dc.identifier.urihttps://hdl.handle.net/1843/71565
dc.languageeng
dc.publisherUniversidade Federal de Minas Gerais
dc.relation.ispartofFrontiers in Immunology
dc.rightsAcesso Aberto
dc.subjectCitocinas
dc.subjectEsclerose Múltipla
dc.subjectEncefalomielite Autoimune Experimental
dc.subjectRemielinização
dc.subjectInterferon beta
dc.titleAnti-inflammatory mechanisms and pharmacological actions of phycocyanobilin in a mouse model of experimental autoimmune encephalomyelitis: a therapeutic promise for multiple sclerosis
dc.typeArtigo de periódico
local.citation.epage18
local.citation.spage1
local.citation.volume13
local.description.resumoCytokines, demyelination and neuroaxonal degeneration in the central nervous system are pivotal elements implicated in the pathogenesis of multiple sclerosis (MS) and its nonclinical model of experimental autoimmune encephalomyelitis (EAE). Phycocyanobilin (PCB), a chromophore of the biliprotein C-Phycocyanin (C-PC) from Spirulina platensis, has antioxidant, immunoregulatory and anti-inflammatory effects in this disease, and it could complement the effect of other Disease Modifying Treatments (DMT), such as Interferon-β (IFN-β). Here, our main goal was to evaluate the potential PCB benefits and its mechanisms of action to counteract the chronic EAE in mice. MOG35-55-induced EAE was implemented in C57BL/6 female mice. Clinical signs, pro-inflammatory cytokines levels by ELISA, qPCR in the brain and immunohistochemistry using precursor/mature oligodendrocytes cells antibodies in the spinal cord, were assessed. PCB enhanced the neurological condition, and waned the brain concentrations of IL-17A and IL-6, pro-inflammatory cytokines, in a dose-dependent manner. A down- or up-regulating activity of PCB at 1 mg/kg was identified in the brain on three (LINGO1, NOTCH1, and TNF-α), and five genes (MAL, CXCL12, MOG, OLIG1, and NKX2-2), respectively. Interestingly, a reduction of demyelination, active microglia/macrophages density, and axonal damage was detected along with an increase in oligodendrocyte precursor cells and mature oligodendrocytes, when assessed the spinal cords of EAE mice that took up PCB. The studies in vitro in rodent encephalitogenic T cells and in vivo in the EAE mouse model with the PCB/IFN-β combination, showed an enhanced positive effect of this combined therapy. Overall, these results demonstrate the anti-inflammatory activity and the protective properties of PCB on the myelin and support its use with IFN-β as an improved DMT combination for MS.
local.publisher.countryBrasil
local.publisher.departmentICB - DEPARTAMENTO DE FISIOLOGIA E BIOFÍSICA
local.publisher.initialsUFMG
local.url.externahttps://www.frontiersin.org/journals/immunology/articles/10.3389/fimmu.2022.1036200/full

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