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dc.contributor.authorGualtero, Diego Fernando
dc.contributor.authorViafara-García, Sergio Marino
dc.contributor.authorMorantes Medina, Sandra Johanna
dc.contributor.authorBuitrago Ramirez, Diana Marcela
dc.contributor.authorGonzaléz, Octavio A.
dc.contributor.authorLafaurie, Gloria Ines
dc.date.accessioned2020-07-09T19:42:21Z
dc.date.available2020-07-09T19:42:21Z
dc.identifier.issn1943-3670spa
dc.identifier.urihttp://hdl.handle.net/20.500.12495/3390
dc.format.mimetypeapplication/pdfspa
dc.language.isoengspa
dc.publisherWiley-Blackwellspa
dc.relation.ispartofseriesJournal of periodontology, 1943-3670, Vol. 88, Nro. 2, 2017, p. 225-235spa
dc.relation.urihttps://aap.onlinelibrary.wiley.com/doi/abs/10.1902/jop.2016.160288spa
dc.titleRosuvastatin inhibits interleukin (IL)-8 and IL-6 production in human coronary artery endothelial cells stimulated with Aggregatibacter actinomycetemcomitans serotype bspa
dc.type.localArtículo de revista
dc.subject.decsLipopolisacáridosspa
dc.subject.decsPeriodontitisspa
dc.subject.decsReacción en cadena de la polimerasaspa
dc.subject.keywordsAtherosclerosisspa
dc.subject.keywordsImmunityspa
dc.subject.keywordsInnatespa
dc.identifier.doihttps://doi.org/10.1902/jop.2016.160288spa
dc.type.hasversioninfo:eu-repo/semantics/publishedVersion
dc.publisher.journalJournal of periodontologyspa
dc.type.coarhttp://purl.org/coar/resource_type/c_6501
dc.type.driverinfo:eu-repo/semantics/article
dc.identifier.instnameinstname:Universidad El Bosque
dc.identifier.reponamereponame:Repositorio Institucional Universidad El Bosque
dc.identifier.repourlhttps://repositorio.unbosque.edu.co
dc.title.translatedRosuvastatin inhibits interleukin (IL)-8 and IL-6 production in human coronary artery endothelial cells stimulated with Aggregatibacter actinomycetemcomitans serotype bspa
dc.description.abstractenglishBackground:Rosuvastatin exhibits anti-inflammatory effects and reduces periodontal diseases andatherosclerosis; however, its role in regulating periodontopathogen-induced endothelial proinflammatoryresponses remains unclear. The purpose of this study is to determine whether rosuvastatin can reduce theproinflammatory response induced byAggregatibacter actinomycetemcomitans(Aa) in human coronaryartery endothelial cells (HCAECs).Methods:HCAECs were stimulated with purifiedAaserotype b lipopolysaccharide (LPS) (Aa-LPS),heat-killed (HK) bacteria (Aa-HK), or live bacteria. Expression of Toll-like receptors and cellular adhesionmolecules were evaluated by fluorometric enzyme-linked immunosorbent assay. Endothelial cell activationwas evaluated by quantifying nuclear factor (NF)-kappa B-p65 and cytokine expression levels by quan-titative polymerase chain reaction and flow cytometry. Effect of rosuvastatin in expression of the athero-protective factor Kru ̈ppel-like factor 2 (KLF2) and cytokines were also studied using similar approaches.Results:HCAECs showed increased interleukin (IL)-6, IL-8, intercellular adhesion molecule 1, and plateletendothelial cell adhesion molecule 1 expression when stimulated withAa-LPS orAa-HK. NF-kB-p65 activa-tion was induced by all antigens.Aa-induced IL-6 and IL-8 production was inhibited by rosuvastatin, partic-ularly at higher doses. Interestingly, reduced IL-6 and IL-8 levels were observed in HCAECs stimulated withAain the presence of higher concentrations of rosuvastatin. This anti-inflammatory effect correlated witha significant increase of rosuvastatin-inducedKLF2.Conclusions:These results suggestAa-induced proinflammatory endothelial responses are regulatedby rosuvastatin in a mechanism that appears to involveKLF2activation. Use of rosuvastatin to preventcardiovascular disease may reduce risk of endothelial activation by bacterial antigensspa
dc.rights.accessrightshttp://purl.org/coar/access_right/c_abf2
dc.rights.accessrightsinfo:eu-repo/semantics/openAccess
dc.rights.accessrightsAcceso abiertospa
dc.date.issued2016-10-14


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