nNOS expression in the brain of rats after burn and the effect of the ACE inhibitor captopril

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dc.authorid0000-0003-1005-5526en_US
dc.authorid0000-0003-4968-9761en_US
dc.authorid0000-0002-0021-8400en_US
dc.contributor.authorDemiralay, Ebru
dc.contributor.authorSaglam, Ibrahim Yaman
dc.contributor.authorOzdamar, Emine Nur
dc.contributor.authorSehirli, Ahmet Ozer
dc.contributor.authorSener, Goksel
dc.contributor.authorSaglam, Esra
dc.date.accessioned2024-07-12T21:45:22Z
dc.date.available2024-07-12T21:45:22Z
dc.date.issued2013en_US
dc.departmentMaltepe Üniversitesien_US
dc.description.abstractObjective: To investigate the role of endogenous neuronal nitric oxide synthase (nNOS) on brain injury after burn and the effects of the captopril. Methods: Wistar albino rats (200-250 g) were exposed on the dorsal surface to 90 degrees C (burn) or 25 degrees C (sham) water for 10 s. The ACE group was treated with intraperitoneal 10 mg/kg captopril immediately after burn and this treatment was repeated twice daily. At the end of the 24 h brain samples were taken. nNOS was studied in brain areas by immunohistochemistry. Results: There was no difference between the cerebellar and hypothalamic areas the nNOS expression of all groups. nNOS expression increased in the frontal cortex, striatum and midbrain in the burn group compared to the control group. In the frontal cortex, nNOS expression significantly decreased after ACE inhibitor treatment (p < 0.05). The striatal nNOS of the ACE group significantly increased when compared to the control group (p = 0.001). In the midbrain of the animals, nNOS decreased in the ACE group. Hippocampal nNOS expression did not change after burn and significantly increased after ACE inhibitor therapy (p < 0.05). Conclusions: Our data showed that the pathophysiological events following burn appear to be related to an acute inflammatory reaction which is associated with nNOS in the frontal cortex, striatum and midbrain, and captopril treatment abrogates the nNOS response in the frontal cortex and midbrain. (C) 2012 Elsevier Ltd and ISBI. All rights reserved.en_US
dc.identifier.doi10.1016/j.burns.2012.10.008
dc.identifier.endpage904en_US
dc.identifier.issn0305-4179
dc.identifier.issue5en_US
dc.identifier.pmid23137627en_US
dc.identifier.scopus2-s2.0-84879005488en_US
dc.identifier.scopusqualityQ1en_US
dc.identifier.startpage897en_US
dc.identifier.urihttps://dx.doi.org/10.1016/j.burns.2012.10.008
dc.identifier.urihttps://hdl.handle.net/20.500.12415/7827
dc.identifier.volume39en_US
dc.identifier.wosWOS:000321602800010en_US
dc.identifier.wosqualityQ2en_US
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoenen_US
dc.publisherELSEVIER SCI LTDen_US
dc.relation.ispartofBURNSen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.snmzKY00458
dc.subjectnNOSen_US
dc.subjectBurnen_US
dc.subjectACE inhibitoren_US
dc.subjectBrainen_US
dc.subjectRaten_US
dc.titlenNOS expression in the brain of rats after burn and the effect of the ACE inhibitor captoprilen_US
dc.typeArticle
dspace.entity.typePublication

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