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Endothelial. dysfunction in rats with ligature-induced periodontitis: Participation of nitric oxide and cycloxygenase-2-derived products

dc.contributor.authorCampi, Paula
dc.contributor.authorHerrera, Bruno Schneider [UNESP]
dc.contributor.authorJesus, Flavia Neto de
dc.contributor.authorNapolitano, Mauro
dc.contributor.authorTeixeira, Simone Aparecida
dc.contributor.authorMaia-Dantas, Aline
dc.contributor.authorSpolidorio, Luis Carlos [UNESP]
dc.contributor.authorAkamine, Eliana Hiromi
dc.contributor.authorAlves Mayer, Marcia Pinto
dc.contributor.authorCatelli de Carvalho, Maria Helena
dc.contributor.authorPereira Costa, Soraia Katia
dc.contributor.authorMuscara, Marcelo Nicolas
dc.contributor.institutionUniversidade de São Paulo (USP)
dc.contributor.institutionUniversidade Estadual Paulista (Unesp)
dc.contributor.institutionUniv N Carolina
dc.date.accessioned2018-11-26T16:27:43Z
dc.date.available2018-11-26T16:27:43Z
dc.date.issued2016-03-01
dc.description.abstractObjectives: Considering the evident relationship between periodontitis and cardiovascular diseases in humans, we aimed to study the in vitro vascular reactivity of aorta rings prepared from rats with ligature induced periodontitis. Methods: Seven days after the induction of unilateral periodontitis, the animals were euthanised; rings were prepared from the descending abdominal aortas and mounted in tissue baths for the in vitro measurement of the isometric force responses to norepinephrine (NE) and acetylcholine (ACh), as well as in the presence of inhibitors of nitric oxide synthase (NOS) and cycloxygenase (COX) isoenzymes. Aortic COX and NOS gene expressions were analysed by RT-PCR, as well as protein COX-2 expression by Western blot. Results: Periodontitis resulted in significant alveolar bone loss and did not affect arterial pressure. However, both NE-induced contraction and ACh-induced relaxation were significantly decreased and related to the presence of endothelium. Diminished eNOS and augmented COX-2 and iNOS expressions were found in the aortas from rats with periodontitis, and the pharmacological inhibition of COX-2 or iNOS improved the observed vasomotor deficiencies. Conclusions: We can thus conclude that periodontitis induces significant endothelial dysfunction in rat aorta which is characterized by decreased eNOS expression and mediated by upregulated iNOS and COX 2 products. (C) 2015 Elsevier Ltd. All rights reserved.en
dc.description.affiliationUniv Sao Paulo, Inst Biomed Sci, Dept Pharmacol, BR-05508000 Sao Paulo, SP, Brazil
dc.description.affiliationSao Paulo State Univ, Araraquara Sch Dent, Dept Physiol & Pathol, Araraquara, SP, Brazil
dc.description.affiliationUniv Sao Paulo, Inst Biomed Sci, Dept Microbiol, BR-05508000 Sao Paulo, SP, Brazil
dc.description.affiliationUniv N Carolina, Sch Dent, Dept Periodontol, Chapel Hill, NC 27599 USA
dc.description.affiliationUnespSao Paulo State Univ, Araraquara Sch Dent, Dept Physiol & Pathol, Araraquara, SP, Brazil
dc.description.sponsorshipFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.format.extent66-74
dc.identifierhttp://dx.doi.org/10.1016/j.archoralbio.2015.11.022
dc.identifier.citationArchives Of Oral Biology. Oxford: Pergamon-elsevier Science Ltd, v. 63, p. 66-74, 2016.
dc.identifier.doi10.1016/j.archoralbio.2015.11.022
dc.identifier.fileWOS000370833500009.pdf
dc.identifier.issn0003-9969
dc.identifier.lattes2640929291808415
dc.identifier.urihttp://hdl.handle.net/11449/161241
dc.identifier.wosWOS:000370833500009
dc.language.isoeng
dc.publisherElsevier B.V.
dc.relation.ispartofArchives Of Oral Biology
dc.relation.ispartofsjr0,752
dc.rights.accessRightsAcesso aberto
dc.sourceWeb of Science
dc.subjectPeriodontitis
dc.subjectEndothelium
dc.subjectVascular
dc.subjectAorta
dc.subjectNitric oxide
dc.subjectCyclooxygenase 2
dc.subjectInflammation
dc.titleEndothelial. dysfunction in rats with ligature-induced periodontitis: Participation of nitric oxide and cycloxygenase-2-derived productsen
dc.typeArtigo
dcterms.licensehttp://www.elsevier.com/about/open-access/open-access-policies/article-posting-policy
dcterms.rightsHolderElsevier B.V.
dspace.entity.typePublication
unesp.author.lattes2640929291808415
unesp.author.orcid0000-0001-7399-7276[4]
unesp.author.orcid0000-0002-0592-542X[7]
unesp.campusUniversidade Estadual Paulista (UNESP), Faculdade de Odontologia, Araraquarapt
unesp.departmentFisiologia e Patologia - FOARpt

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