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Citral impairs intestinal changes caused by ulcerative colitis through modulation of antioxidant, anti-inflammatory and healing activities

dc.contributor.authorSilva, Maycon Tavares Emílio
dc.contributor.authorRodrigues, Vinícius Peixoto
dc.contributor.authorRuiz-Malagon, Antonio J.
dc.contributor.authorGuidolin, Isabela Galende
dc.contributor.authorDario, Felipe Lima
dc.contributor.authorFioravanti, Mariana Moraes
dc.contributor.authorRodriguez-Nogales, Alba
dc.contributor.authorGálvez, Julio
dc.contributor.authorLima, Clelia Akiko Hiruma
dc.date.accessioned2026-04-22T16:48:57Z
dc.date.issued2025-12-03
dc.description.abstractIntroductionUlcerative colitis (UC) is the main representative of inflammatory bowel diseases (IBD) are chronic conditions characterized by intestinal inflammation, caused by the overproduction of pro-oxidant species and an immune response that damages the gut mucosa.ObjectiveTo evaluate the anti-inflammatory and protective effect of Citral, a monoterpene, on in vitro and in vivo models of UC.MethodologyMale C57BL/6J mice were used for DSS 3%-induced UC for 5 days in drinking water. Concomitantly, daily oral citral (25, 100, and 300 mg/kg, p.o.) or vehicle was administered. Colonic segments were collected to evaluate neutrophil infiltration, lipid peroxidation, and the expression of antioxidant markers. NCM-356 and RAW-294 cells were stimulated with LPS (10 and 100 ng/mL, respectively). Cell viability, nitrite levels, scratch wound healing assay, and gene expression of inflammatory and growth factors were assessed.ResultsAcute treatment with citral (100 and 300 mg/kg) exhibited an anti-colitis effect by reducing the disease activity index (DAI) score compared to that in the DSS-vehicle group. This response was mediated by a significant reduction in myeloperoxidase activity and thiobarbituric acid reactive species levels, associated with an increase in superoxide dismutase activity, indicating anti-inflammatory and antioxidant activities (p < 0.05). The monoterpene reversed LPS-induced intestinal epithelial disturbance in the scratch wound healing process under different conditions and possibly reduced inos expression.ConclusionCitral treatment prevents the development of UC via anti-inflammatory, antioxidant, and healing effects.
dc.description.affiliationDepartment of Structural and Functional Biology, Physiology Sector, Institute of Bioscience, São Paulo State University, Botucatu, São Paulo, Brazil
dc.description.affiliationDepartment of Pharmacology, Center for Biomedical Research (CIBM), University of Granada, Granada, Spain
dc.description.affiliationInstituto de Investigación Biosanitaria de Granada, (ibs.GRANADA), 18012, Granada, Spain
dc.description.affiliationCIBER de Enfermedades Hepáticas y Digestivas (CIBER-EHD), Instituto de Salud Carlos III, Madrid, Spain
dc.description.affiliationUnespDepartment of Structural and Functional Biology, Physiology Sector, Institute of Bioscience, São Paulo State University, Botucatu, São Paulo, Brazil
dc.identifierhttps://app.dimensions.ai/details/publication/pub.1195688583
dc.identifier.dimensionspub.1195688583
dc.identifier.doi10.1007/s10787-025-02067-4
dc.identifier.issn0925-4692
dc.identifier.issn1568-5608
dc.identifier.orcid0000-0003-1927-0628
dc.identifier.orcid0000-0002-1957-6152
dc.identifier.orcid0000-0003-4323-650X
dc.identifier.orcid0000-0001-5466-3414
dc.identifier.orcid0000-0002-9312-2431
dc.identifier.orcid0000-0001-6876-3782
dc.identifier.orcid0000-0002-8645-3777
dc.identifier.pmid41335164
dc.identifier.urihttps://hdl.handle.net/11449/322365
dc.publisherSpringer Nature
dc.relation.ispartofInflammopharmacology; p. 1-15
dc.rights.accessRightsAcesso restritopt
dc.rights.sourceRightsclosed
dc.sourceDimensions
dc.titleCitral impairs intestinal changes caused by ulcerative colitis through modulation of antioxidant, anti-inflammatory and healing activities
dc.typeArtigopt
dspace.entity.typePublication
relation.isAuthorOfPublication07dc8178-994d-49f4-bc92-a68c781d3334
relation.isAuthorOfPublication.latestForDiscovery07dc8178-994d-49f4-bc92-a68c781d3334
relation.isOrgUnitOfPublicationab63624f-c491-4ac7-bd2c-767f17ac838d
relation.isOrgUnitOfPublication.latestForDiscoveryab63624f-c491-4ac7-bd2c-767f17ac838d
unesp.campusUniversidade Estadual Paulista (UNESP), Instituto de Biociências, Botucatupt

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