Nebivolol attenuates cerebral vasospasm both by increasing endothelial nitric oxide and by decreasing oxidative stress in an experimental subarachnoid haemorrhage

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dc.authoridAladag, M. Arif/0000-0003-3872-3741
dc.authoridTürköz, Yusuf/0000-0001-5401-0720
dc.authoridParlakpinar, Hakan/0000-0001-9497-3468
dc.authoridParlakpınar, Hakan/0000-0001-9497-3468
dc.authorwosidAladag, M. Arif/ABI-1182-2020
dc.authorwosidTürköz, Yusuf/ABG-7931-2020
dc.authorwosidParlakpinar, Hakan/V-6637-2019
dc.authorwosidParlakpınar, Hakan/T-6517-2018
dc.contributor.authorAladag, Mehmet Arif
dc.contributor.authorTurkoz, Yusuf
dc.contributor.authorParlakpinar, Hakan
dc.contributor.authorGul, Mehmet
dc.date.accessioned2024-08-04T20:43:03Z
dc.date.available2024-08-04T20:43:03Z
dc.date.issued2017
dc.departmentİnönü Üniversitesien_US
dc.description.abstractObjective: Evidence suggests that reduction of nitric oxide (NO) bioavailability due to oxidative stress plays a central role in the pathophysiology of cerebral vasospasm after subarachnoid haemorrhage (SAH). To prevent SAH-induced cerebral vasospasm, therefore we used nebivolol hydrochloride as a NO-mediated vasodilator and an antioxidant drug in an experimental rat model of SAH.Materials and methods: Forty female Wistar rats were divided into control, SAH, SAH plus placebo, and SAH plus nebivolol groups. Starting six hours after inducing SAH, 5mg/kg of nebivolol hydrochloride and of pharmaceutical excipients of nebivolol was given orally once daily for five days to SAH plus nebivolol and SAH plus placebo groups, respectively. The lumen diameter and vessel wall thickness of the basilar artery were measured in brain sections. The serum and brain supernatant levels of nitric oxide (NO) were analysed. The brain supernatant levels of intrinsic antioxidants superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) were measured as markers of the antioxidant status.Results: Nebivolol administration attenuated cerebral vasospasm both by increasing NO levels and by decreasing oxidative stress. Our study also demonstrated that nebivolol administration reverses SAH created imbalance between SOD and GSH-Px by increasing GSH-Px activity relative to SOD.Conclusions: Nebivolol attenuates the cerebral vasospasm after SAH both increasing NO levels and decreasing oxidative stress. Therefore, it may promise to prevent SAH-induced cerebral vasospasm as an anti-spasmodic and anti-oxidant agent.en_US
dc.description.sponsorshipScientific Research Projects Unit of Inonu University [2011/137]en_US
dc.description.sponsorshipThe authors thank The Scientific Research Projects Unit of Inonu University for financial support (Grant 2011/137).en_US
dc.identifier.doi10.1080/02688697.2017.1297367
dc.identifier.endpage445en_US
dc.identifier.issn0268-8697
dc.identifier.issn1360-046X
dc.identifier.issue4en_US
dc.identifier.pmid28335640en_US
dc.identifier.scopus2-s2.0-85016166765en_US
dc.identifier.scopusqualityQ3en_US
dc.identifier.startpage439en_US
dc.identifier.urihttps://doi.org/10.1080/02688697.2017.1297367
dc.identifier.urihttps://hdl.handle.net/11616/97758
dc.identifier.volume31en_US
dc.identifier.wosWOS:000415986300015en_US
dc.identifier.wosqualityQ3en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherTaylor & Francis Ltden_US
dc.relation.ispartofBritish Journal of Neurosurgeryen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectSAHen_US
dc.subjectcerebral vasospasmen_US
dc.subjectNOen_US
dc.subjectnebivololen_US
dc.subjectoxidative stressen_US
dc.titleNebivolol attenuates cerebral vasospasm both by increasing endothelial nitric oxide and by decreasing oxidative stress in an experimental subarachnoid haemorrhageen_US
dc.typeArticleen_US

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