Ameliorating the effects of Adalimumab on rabbits with experimental cerebral vasospasm after subarachnoid hemorrhage

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dc.contributor.authorToguslu, Gokhan
dc.contributor.authorErdi, Mehmet Fatih
dc.contributor.authorArac, Densel
dc.contributor.authorKeskin, Fatih
dc.contributor.authorKilinc, Ibrahim
dc.contributor.authorCuce, Gokhan
dc.date.accessioned2024-02-23T14:31:41Z
dc.date.available2024-02-23T14:31:41Z
dc.date.issued2020
dc.departmentNEÜen_US
dc.description.abstractBACKGROUND: Adalimumab (ADA), which is a new-generation recombinant human monoclonal antibody for tumor necrosis factor a (TNF alpha), has strong anti-inflammatory effects. The role of enhanced inflammation is well established for the development and progression of cerebral vasospasm. Investigated in the present study is the probable ameliorating and neuroprotective effects of ADA in rabbits using a cerebral vasospasm model with biochemical and histopathological methods. METHODS: Thirty male New-Zealand white rabbits were randomly divided into control, subarachnoid hemorrhage (SAH) only and SAH plus ADA treatment groups. SAH was established as a single cisterna magna autologous arterial blood injection. ADA treatment was started just after intracisternal blood injection and continued for 72 hours once a day. The animals were sacrificed 72 hours after the induction of SAH, serum and brainstem tissue obtained for investigations. RESULTS: Brainstem tissue and plasma levels of tumor necrosis factor-alpha and Interleukin-1 beta, brainstem tissue Matrix metalloproteinase-9 levels increased after SAH and partly decreased after treatment. Plasma levels of brain-derived neurotrophic factor decreased after SAH and partly restored after treatment. ADA treatment significantly increased the mean cross-sectional area of the vasospastic basilar arteries, reduced the basilar artery wall thickness and also ameliorates enhanced endothelial apoptosis. CONCLUSION: Findings obtained in this study suggest that ADA is an effective neuroprotective agent for ameliorating cerebral vasospasm in experimental rabbit vasospasm.en_US
dc.identifier.doi10.14744/tjtes.2019.52504
dc.identifier.endpage852en_US
dc.identifier.issn1306-696X
dc.identifier.issue6en_US
dc.identifier.pmid33107964en_US
dc.identifier.scopus2-s2.0-85094901902en_US
dc.identifier.scopusqualityQ2en_US
dc.identifier.startpage847en_US
dc.identifier.urihttps://doi.org/10.14744/tjtes.2019.52504
dc.identifier.urihttps://hdl.handle.net/20.500.12452/15307
dc.identifier.volume26en_US
dc.identifier.wosWOS:000582710000003en_US
dc.identifier.wosqualityQ4en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherTurkish Assoc Trauma Emergency Surgeryen_US
dc.relation.ispartofUlusal Travma Ve Acil Cerrahi Dergisi-Turkish Journal Of Trauma & Emergency Surgeryen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.subjectAdalimumaben_US
dc.subjectCerebral Vasospasmen_US
dc.subjectCytokineen_US
dc.subjectInflammationen_US
dc.subjectNeuroprotectionen_US
dc.subjectRabbiten_US
dc.subjectSubarachnoid Hemorrhageen_US
dc.titleAmeliorating the effects of Adalimumab on rabbits with experimental cerebral vasospasm after subarachnoid hemorrhageen_US
dc.typeArticleen_US

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