dc.creatorSilva, KC
dc.creatorRosales, MAB
dc.creatorde Faria, JBL
dc.creatorde Faria, JML
dc.date2010
dc.dateJUN
dc.date2014-11-15T03:42:57Z
dc.date2015-11-26T16:30:42Z
dc.date2014-11-15T03:42:57Z
dc.date2015-11-26T16:30:42Z
dc.date.accessioned2018-03-28T23:11:44Z
dc.date.available2018-03-28T23:11:44Z
dc.identifierCurrent Eye Research. Taylor & Francis Inc, v. 35, n. 6, n. 519, n. 528, 2010.
dc.identifier0271-3683
dc.identifierWOS:000282896300012
dc.identifier10.3109/02713681003664923
dc.identifierhttp://www.repositorio.unicamp.br/jspui/handle/REPOSIP/80336
dc.identifierhttp://www.repositorio.unicamp.br/handle/REPOSIP/80336
dc.identifierhttp://repositorio.unicamp.br/jspui/handle/REPOSIP/80336
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/1270025
dc.descriptionFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.descriptionCoordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
dc.descriptionPurpose: To investigate if nitric oxide (NO) system contributes to the beneficial effect of angiotensin II type 1 receptor (AT 1) blocker losartan in the retina of diabetic spontaneously hypertensive rats (SHR). Methods: Diabetic SHR were randomized to receive oral treatment with losartan (DM-SHRLos). After 20 days, the rats were euthanized and the retinas collected. Results: Diabetic SHR rats exhibited a significant increase in glial fibrillary acidic protein (GFAP) and decrease in occludin, markers of early diabetic retinopathy (DR). The oxidative status, evaluated by NO end-products (NO(x)(-)) levels along with the antioxidative system superoxide dismutase, revealed an accentuated imbalance in favor to oxidants in DM-SHR leading to a higher tyrosine nitration and DNA damage. The inducible NO synthase (iNOS) was also elevated in DM-SHR rats. The treatment with losartan ameliorated all of the above alterations. Conclusions: Oral treatment with losartan reduces iNOS expression and reestablishes the redox status, thus ameliorating the early markers of DR in a model of diabetes and hypertension.
dc.description35
dc.description6
dc.description519
dc.description528
dc.descriptionFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.descriptionCoordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
dc.descriptionFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.descriptionCoordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
dc.descriptionFAPESP [05/58189-5, 08/54068-7]
dc.languageen
dc.publisherTaylor & Francis Inc
dc.publisherPhiladelphia
dc.publisherEUA
dc.relationCurrent Eye Research
dc.relationCurr. Eye Res.
dc.rightsfechado
dc.rightshttp://journalauthors.tandf.co.uk/permissions/reusingOwnWork.asp
dc.sourceWeb of Science
dc.subjectAngiotension II type 1 receptor blocker
dc.subjectDiabetic retinopathy
dc.subjectInducible nitric oxide synthase
dc.subjectNitric oxide end products
dc.subjectOxidative stress
dc.subjectEndothelial Growth-factor
dc.subjectIntercellular-adhesion Molecule-1
dc.subjectFactor-kappa-b
dc.subjectPoly(adp-ribose) Polymerase
dc.subjectAt(1) Receptor
dc.subjectCerebral-ischemia
dc.subjectIn-vivo
dc.subjectRetinopathy
dc.subjectStress
dc.subjectExpression
dc.titleReduction of Inducible Nitric Oxide Synthase via Angiotensin Receptor Blocker Prevents the Oxidative Retinal Damage in Diabetic Hypertensive Rats
dc.typeArtículos de revistas


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