Apocynin restores endothelial dysfunction in streptozotocin diabetic rats through regulation of nitric oxide synthase and NADPH oxidase expressions

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dc.contributor.authorOlukman, Murat
dc.contributor.authorOrhan, Cahide Elif
dc.contributor.authorCelenk, Fatma Gul
dc.contributor.authorUlker, Sibel
dc.date.accessioned2019-10-27T21:14:09Z
dc.date.available2019-10-27T21:14:09Z
dc.date.issued2010
dc.departmentEge Üniversitesien_US
dc.description.abstractAim: Increased production of reactive oxygen species (ROS) in the diabetic vasculature results in the impairment of nitric oxide (NO)mediated relaxations leading to impaired endothelium-dependent vasodilation. An important source of ROS is nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, and the inhibition of this enzyme is an active area of interest. This study aimed to investigate the effects of apocynin, an NADPH oxidase inhibitor, on endothelial dysfunction and on the expression of NO synthase (NOS) and NADPH oxidase in thoracic aorta of diabetic rats. Method: Streptozotocin (STZ)-diabetic rats received apocynin (16 mg/kg per day) for 4 weeks. Endothelium-dependent and -independent relaxations were determined in thoracic aortic rings. Western blotting and RT-PCR analysis were performed for NOSs and NADPH oxidase in the aortic tissue. Results: Acetylcholine-induced relaxations and L-NAME-induced contractions were decreased in diabetic aorta. The decrease in acetylcholine and L-NAME responses were prevented by apocynin treatment without a significant change in plasma glucose levels. Endothelial NOS (eNOS) protein and mRNA expression exhibited significant decrease in diabetes, while protein and/or mRNA expressions of inducible NOS (iNOS) as well as p22(phox) and gp91(phox) subunits of NADPH oxidase were increased, and these alterations were markedly prevented by apocynin treatment. Conclusion: NADPH oxidase expression is increased in diabetic rat aorta. NADPH oxidase-mediated oxidative stress is accompanied by the decreased eNOS and increased iNOS expressions, contributing to endothelial dysfunction. Apocynin effectively prevents the increased NADPH oxidase expression in diabetic aorta and restores the alterations in NOS expression, blocking the vicious cycle leading to diabetes-associated endothelial dysfunction. (C) 2010 Elsevier Inc. All rights reserved.en_US
dc.description.sponsorshipTurkish Diabetes Foundation; Ege UniversityEge University [03-TIP-013]en_US
dc.description.sponsorshipThe study was supported by the Turkish Diabetes Foundation and the Research Fund of Ege University (Project no: 03-TIP-013).en_US
dc.identifier.doi10.1016/j.jdiacomp.2010.02.001en_US
dc.identifier.endpage423en_US
dc.identifier.issn1056-8727
dc.identifier.issn1873-460X
dc.identifier.issue6en_US
dc.identifier.pmid20226688en_US
dc.identifier.scopusqualityQ2en_US
dc.identifier.startpage415en_US
dc.identifier.urihttps://doi.org/10.1016/j.jdiacomp.2010.02.001
dc.identifier.urihttps://hdl.handle.net/11454/43338
dc.identifier.volume24en_US
dc.identifier.wosWOS:000283897800009en_US
dc.identifier.wosqualityQ3en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherElsevier Science Incen_US
dc.relation.ispartofJournal of Diabetes and Its Complicationsen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectApocyninen_US
dc.subjectDiabetic complicationsen_US
dc.subjectEndothelial dysfunctionen_US
dc.subjectNitric oxide synthaseen_US
dc.subjectNADPH oxidaseen_US
dc.titleApocynin restores endothelial dysfunction in streptozotocin diabetic rats through regulation of nitric oxide synthase and NADPH oxidase expressionsen_US
dc.typeArticleen_US

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