The effects of ozone oxidative preconditioning on subarachnoid hemorrhage via rat cerebral vasospasm model

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dc.authoridAVSAR, TIMUCIN/0000-0001-8841-4811;en_US
dc.contributor.authorSüslü, Hikmet Turan
dc.contributor.authorTatarli, Necati
dc.contributor.authorCeylan, Davut
dc.contributor.authorSuslu, Husnu
dc.contributor.authorBozkurt, Suheyla Uyar
dc.contributor.authorAvsar, Timucin
dc.contributor.authorGuclu, Bülent
dc.date.accessioned2024-07-12T21:37:20Z
dc.date.available2024-07-12T21:37:20Z
dc.date.issued2021en_US
dc.department[Belirlenecek]en_US
dc.description.abstractObjective: Cerebral vasospasm after subarachnoid hemorrhage (SAH) is a major cause of morbidity and mortality. Inflammation is the major molecular mechanism observed in vasospastic SAH. Özone (O3) has been used as a therapeutic agent in the treatment of various conditions and diseases for years. The aim of this study was to evaluate the anti-inflammatory effect of ozone oxidative preconditioning (OOP) in a rat model of SAH in order to assess the therapeutic potential of O3 in SAH therapy. Materials and Methods: In the presented study, an experimental in vivo SAH rat model that provided constriction of large cerebral arteries was used. The inflammatory response of cerebral vasospasm after SAH and the effects of OOP were evaluated by comparing the mRNA levels of inflammatory molecules (tumor necrosis factor-alpha, interleukin-1 beta, and intercellular adhesion molecule-1) in the serum samples of rats. Results: The level of inflammatory molecules increased in vasospasm at 12 h, 24 h, and 48 h in the posttreatment groups. However, intraperitoneal OOP decreased the level of inflammatory molecules dramatically. Conclusions: Our study indicated that O3 treatment has potential in the management of inflammation created in a rat SAH model. These findings may inform further studies investigating possible uses of O3 in the treatment of vasospasm.en_US
dc.identifier.doi10.4103/NSN.NSN_74_20
dc.identifier.endpage66en_US
dc.identifier.issn2636-865X
dc.identifier.issue1en_US
dc.identifier.scopus2-s2.0-85104044262en_US
dc.identifier.scopusqualityQ4en_US
dc.identifier.startpage60en_US
dc.identifier.trdizinid505369en_US
dc.identifier.urihttps://doi.org/10.4103/NSN.NSN_74_20
dc.identifier.urihttps://search.trdizin.gov.tr/yayin/detay/505369
dc.identifier.urihttps://hdl.handle.net/20.500.12415/6752
dc.identifier.volume38en_US
dc.identifier.wosWOS:000635873000010en_US
dc.identifier.wosqualityQ4en_US
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakTR-Dizin
dc.language.isoenen_US
dc.publisherWolters Kluwer Medknow Publicationsen_US
dc.relation.ispartofNeurological Sciences And Neurophysiologyen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.snmzKY04094
dc.subjectCerebral Aneurysmen_US
dc.subjectInflammationen_US
dc.subjectÖzone Oxidative Preconditioningen_US
dc.subjectSubarachnoid Hemorrhageen_US
dc.subjectVasospasm Modelen_US
dc.titleThe effects of ozone oxidative preconditioning on subarachnoid hemorrhage via rat cerebral vasospasm modelen_US
dc.typeArticle
dspace.entity.typePublication

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