Intracerebroventricular BDNF infusion may reduce cerebral ischemia/reperfusion injury by promoting autophagy and suppressing apoptosis

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dc.authoridTanbek, Kevser/0000-0003-2099-2273
dc.authoridYilmaz, Umit/0000-0003-0248-3483
dc.contributor.authorYilmaz, Umit
dc.contributor.authorTanbek, Kevser
dc.contributor.authorGul, Semir
dc.contributor.authorKoc, Ahmet
dc.contributor.authorGul, Mehmet
dc.contributor.authorSandal, Suleyman
dc.date.accessioned2024-09-29T16:04:40Z
dc.date.available2024-09-29T16:04:40Z
dc.date.issued2024
dc.departmentKarabük Üniversitesien_US
dc.description.abstractHere, it was aimed to investigate the effects of intracerebroventricular (ICV) Brain Derived Neurotrophic Factor (BDNF) infusion for 7 days following cerebral ischemia (CI) on autophagy in neurons in the penumbra. Focal CI was created by the occlusion of the right middle cerebral artery. A total of 60 rats were used and divided into 4 groups as Control, Sham CI, CI and CI + BDNF. During the 7-day reperfusion period, aCSF (vehicle) was infused to Sham CI and CI groups, and BDNF infusion was administered to the CI + BDNF group via an osmotic minipump. By the end of the 7th day of reperfusion, Beclin-1, LC3, p62 and cleaved caspase-3 protein levels in the penumbra area were evaluated using Western blot and immunofluorescence. BDNF treatment for 7 days reduced the infarct area after CI, induced the autophagic proteins Beclin-1, LC3 and p62 and suppressed the apoptotic protein cleaved caspase-3. Furthermore, rotarod and adhesive removal test times of BDNF treatment started to improve from the 4th day, and the neurological deficit score from the 5th day. ICV BDNF treatment following CI reduced the infarct area by inducing autophagic proteins Beclin-1, LC3 and p62 and inhibiting the apoptotic caspase-3 protein while its beneficial effects were apparent in neurological tests from the 4th day.en_US
dc.description.sponsorshipInn niversitesien_US
dc.description.sponsorshipNo Statement Availableen_US
dc.identifier.doi10.1111/jcmm.18246
dc.identifier.issn1582-1838
dc.identifier.issn1582-4934
dc.identifier.issue8en_US
dc.identifier.pmid38520223en_US
dc.identifier.scopus2-s2.0-85188538555en_US
dc.identifier.scopusqualityQ2en_US
dc.identifier.urihttps://doi.org/10.1111/jcmm.18246
dc.identifier.urihttps://hdl.handle.net/20.500.14619/6256
dc.identifier.volume28en_US
dc.identifier.wosWOS:001189338800001en_US
dc.identifier.wosqualityN/Aen_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherWileyen_US
dc.relation.ispartofJournal of Cellular and Molecular Medicineen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.subjectadhesive removal testen_US
dc.subjectautophagyen_US
dc.subjectbrain-derived neurotrophic factor (BDNF)en_US
dc.subjectcerebral ischemiaen_US
dc.subjectneurological deficit scoreen_US
dc.subjectrotarod testen_US
dc.titleIntracerebroventricular BDNF infusion may reduce cerebral ischemia/reperfusion injury by promoting autophagy and suppressing apoptosisen_US
dc.typeArticleen_US

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