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Xanthohumol and 8-prenylnaringenin reduce type 2 diabetes–associated oxidative stress by downregulating galectin-3

dc.contributor.authorLuís, Carla
dc.contributor.authorCosta, Raquel
dc.contributor.authorRodrigues, Ilda
dc.contributor.authorCastela, Ângela
dc.contributor.authorCoelho, Pedro
dc.contributor.authorGuerreiro, Susana
dc.contributor.authorGomes, Joana
dc.contributor.authorReis, Celso
dc.contributor.authorSoares, Raquel
dc.date.accessioned2024-05-20T13:36:49Z
dc.date.available2024-05-20T13:36:49Z
dc.date.issued2019
dc.description.abstractGalectin-3 (Gal3) expression is associated with accumulation of Advanced Glycation End products (AGE), a common feature in diabetes mellitus (DM). The role of Gal3 in oxidative stress is, however, controversial, being considered in the literature to play either a protective role or exacerbating disease. :Herein, we examined the interplay between Gal3 and oxidative stress in a high-fat diet -induced type 2 DMC57Bl/6 mice model. Because natural polyphenols are known to play antioxidant and anti-inflammatory roles and to modulate metabolic activity, we further evaluated the effect of xanthohumol and 8-prenylnaringenin polyphenols in this crosstalk. Gal3 expression was accompanied by 3-nitrotyrosine and AGE production in liver and kidney of diabetic mice compared to healthy animals (fed with standard diet). Oral supplementation with polyphenols decreased the levels of these oxidative biomarkers as evaluated by immunohistochemistry and western blotting. Interestingly, blocking Gal3 by incubating human microvascular endothelial cells with modified citrus pectin increased 3-nitrotyrosine protein expression. These findings imply that Gal3 overexpression is probably controlling oxidative stress in endothelial cells. In conclusion, our results indicate that supplementation with 8-prenylnaringenin or xanthohumol reverses diabetes-associated oxidation in liver and kidney, and consequently decreases this diabetic biomarker that predispose to cardiovascular complications.pt_PT
dc.description.versioninfo:eu-repo/semantics/publishedVersionpt_PT
dc.identifier.citationLuís, C., Costa, R., Rodrigues, I., Castela, Â., Coelho, P., Guerreiro, S., Gomes, J., Reis, C., & Soares, R. (2019). Xanthohumol and 8-prenylnaringenin reduce type 2 diabetes–associated oxidative stress by downregulating galectin-3. Porto Biomedical Journal, 4(1), e23. https://doi.org/10.1016/j.pbj.0000000000000023pt_PT
dc.identifier.doi10.1016/j.pbj.0000000000000023pt_PT
dc.identifier.urihttp://hdl.handle.net/10400.22/25535
dc.language.isoengpt_PT
dc.peerreviewedyespt_PT
dc.publisherWolters Kluwer Healthpt_PT
dc.relationFCT (UID/ BIM/04293/2013), FEDER—Fundo Europeu de Desenvolvimento Regional funds through the COMPETE 2020—Operacional Programme for Competitiveness and Internationalization (POCI), Portugal 2020, and by Portuguese funds through FCT—Fundação para a Ciência e a Tecnologia/ Ministério da Ciência, Tecnologia e Inovação in the framework of the project “Institute for Research and Innovation in Health Sciences” (POCI-01-0145-FEDER-007274).pt_PT
dc.relation.publisherversionhttps://journals.lww.com/pbj/fulltext/2019/02000/xanthohumol_and_8_prenylnaringenin_reduce_type_2.1.aspxpt_PT
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/pt_PT
dc.subjectAdvanced glycation end productspt_PT
dc.subjectDiet polyphenolspt_PT
dc.subjectMicrovascular endothelial cellspt_PT
dc.subject3-nitrotyrosinept_PT
dc.subjectOxidative stress biomarkerpt_PT
dc.titleXanthohumol and 8-prenylnaringenin reduce type 2 diabetes–associated oxidative stress by downregulating galectin-3pt_PT
dc.typejournal article
dspace.entity.typePublication
oaire.citation.endPage7pt_PT
oaire.citation.startPage1pt_PT
oaire.citation.titlePorto Biomedical Journalpt_PT
oaire.citation.volume4(1)pt_PT
person.familyNameCoelho
person.givenNamePedro
person.identifier.ciencia-idBE18-3DB2-8D79
person.identifier.orcid0000-0002-2343-1108
person.identifier.ridAAZ-9239-2020
person.identifier.scopus-author-id57214054449
rcaap.rightsopenAccesspt_PT
rcaap.typearticlept_PT
relation.isAuthorOfPublicationeb030614-4140-437b-8ac3-f59c52566ecf
relation.isAuthorOfPublication.latestForDiscoveryeb030614-4140-437b-8ac3-f59c52566ecf

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