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dc.contributor.authorCatalán Santos, Úrsula
dc.contributor.authorLópez de las Hazas Mingo, María del Carmen
dc.contributor.authorRubió Piqué, Laura
dc.contributor.authorFernández Castillejo, Sara
dc.contributor.authorPedret, Anna
dc.contributor.authorDe la Torre, Rafael
dc.contributor.authorMotilva Casado, Mª José
dc.contributor.authorSolà, Rosa
dc.date.accessioned2017-04-20T12:01:36Z
dc.date.available2017-04-20T12:01:36Z
dc.date.issued2015
dc.identifier.issn1613-4125
dc.identifier.urihttp://hdl.handle.net/10459.1/59520
dc.description.abstractScope Hydroxytyrosol (HT) is the major phenolic compound in virgin olive oil (VOO) in free and conjugated forms that may exert health benefits against atherosclerosis. The native form of HT is undetectable in plasma due to an extensive first pass phase II metabolism. Therefore, it is necessary to find strategies to obtain HT metabolites and to demonstrate their protective role against the endothelial dysfunction. Methods and results Biosynthesis of the main plasmatic HT metabolites was performed through Caco-2 cells. The bioactivity of HT and the mixture of metabolites was tested at physiological concentrations (1, 2, 5, and 10 μM) in human aortic endothelial cells (HAEC) co-incubated with TNF-α (10 ng/mL) for 18 and 24 h. After the incubations, cells and media were analyzed to test possible deconjugation of metabolites or conjugation of HT. Both HT and metabolites significantly reduced the secretion of E-selectin, P-selectin, ICAM-1, and VCAM-1, but only HT metabolites further reduced MCP-1 at 24 h. HT underwent a conjugation process after incubation leading to its main metabolites in a dose-dependent manner. Conclusion Physiological HT metabolites, synthetized for the first time by using an intestinal cell model, might be responsible in part for the protection against endothelial dysfunction.ca_ES
dc.description.sponsorshipThis studywas supported by the Spanish Ministry of Education and Science, The MEFOPC Project (AGL2012-40144-C03-03, AGL2012-40144-C03-02 and AGL2012-40144-C03-01) and by the University of Lleida through the M-C. L´opez de las Hazas grant.ca_ES
dc.language.isoengca_ES
dc.publisherWileyca_ES
dc.relationMICINN/PN2008-2011/AGL2012-40114-C03-01ca_ES
dc.relationMICINN/PN2008-2011/AGL2012-40114-C03-02ca_ES
dc.relationMICINN/PN2008-2011/AGL2012-40114-C03-03ca_ES
dc.relation.isformatofVersió postprint del document publicat a https://doi.org/10.1002/mnfr.201500361ca_ES
dc.relation.ispartofMolecular Nutrition & Food Research, 2015, vol. 59, núm. 12, p. 2523–2536ca_ES
dc.rights(c) Wiley-VCH Verlag, 2015ca_ES
dc.subjectAtherosclerosisca_ES
dc.subjectCaco-2ca_ES
dc.subjectHuman aortic endothelial cellsca_ES
dc.subjectHydroxytyrosolca_ES
dc.subjectHydroxytyrosol metabolitesca_ES
dc.titleProtective effect of hydroxytyrosol and its predominant plasmatic human metabolites against endothelial dysfunction in human aortic endothelial cellsca_ES
dc.typearticleca_ES
dc.identifier.idgrec023570
dc.type.versionacceptedVersionca_ES
dc.rights.accessRightsinfo:eu-repo/semantics/openAccessca_ES
dc.identifier.doihttps://doi.org/10.1002/mnfr.201500361


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