Melatonin Attenuates Cerebral Ischemia/Reperfusion Injury Through Inducing Autophagy

dc.authoridTanbek, Kevser/0000-0003-2099-2273
dc.authoridYilmaz, Umit/0000-0003-0248-3483
dc.authoridSandal, Suleyman/0000-0002-8916-3329
dc.authorwosidTanbek, Kevser/ABI-1174-2020
dc.authorwosidYilmaz, Umit/JFA-5784-2023
dc.authorwosidSandal, Suleyman/AAA-6388-2021
dc.contributor.authorYilmaz, Umit
dc.contributor.authorTanbek, Kevser
dc.contributor.authorGul, Semir
dc.contributor.authorGul, Mehmet
dc.contributor.authorKoc, Ahmet
dc.contributor.authorSandal, Suleyman
dc.date.accessioned2024-08-04T20:54:47Z
dc.date.available2024-08-04T20:54:47Z
dc.date.issued2023
dc.departmentİnönü Üniversitesien_US
dc.description.abstractIntroduction: The aim of this study was to investigate how melatonin administration for 3 days or 7 days following cerebral ischemia injury (CI/R) would affect autophagy, and therefore, survival in neurons of the penumbra region. Moreover, it was also aimed to determine how this melatonin treatment would affect the neurological deficit score and rotarod and adhesive removal test durations.Methods: Focal CI (90 min) was achieved in a total of 105 rats utilizing a middle cerebral artery occlusion model. After the start of reperfusion, the groups were treated with melatonin (10 mg/kg/day) for 3-days or 7-days. On all groups, neurological deficit scoring, rotarod and adhesive removal test were executed during reperfusion. Infarct areas were determined by TTC (2,3,5-triphenyltetrazolium chloride) staining at the end of the 3rd and 7th days of reperfusion. Beclin-1, LC3, p62 and caspase-3 protein levels were assessed using Western blot and immunofluorescence methods in the brain tissues. Moreover, penumbra areas were evaluated by transmission electron microscopy (TEM).Results: Following CI, it was observed that melatonin treatment improved the rotarod and adhesive removal test durations from day 5 and reduced the infarct area after CI. It also induced autophagic proteins Beclin-1, LC3 and p62 and suppressed the apoptotic protein cleaved caspase-3. According to TEM findings, melatonin treatment partially reduced the damage in neurons after CI.Conclusion: Melatonin treatment following CI reduced the infarct area and induced the autophagic proteins Beclin-1, LC3 and p62 via inhibiting the apoptotic caspase-3 protein. The functional reflection of melatonin treatment on neurological tests scores was became significant from the 5th day onward.en_US
dc.description.sponsorshipInonu University [TDK-2019-1970]en_US
dc.description.sponsorshipThe present work was supported by the Research Fund of Inonu University [Project No: TDK-2019-1970].en_US
dc.identifier.doi10.1159/000531567
dc.identifier.endpage1050en_US
dc.identifier.issn0028-3835
dc.identifier.issn1423-0194
dc.identifier.issue10en_US
dc.identifier.pmid37321200en_US
dc.identifier.scopus2-s2.0-85174752512en_US
dc.identifier.scopusqualityQ1en_US
dc.identifier.startpage1035en_US
dc.identifier.urihttps://doi.org/10.1159/000531567
dc.identifier.urihttps://hdl.handle.net/11616/101631
dc.identifier.volume113en_US
dc.identifier.wosWOS:001014327200001en_US
dc.identifier.wosqualityQ2en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherKargeren_US
dc.relation.ispartofNeuroendocrinologyen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectIschemia-Reperfusion Injuryen_US
dc.subjectLong-Term Potentiationen_US
dc.subjectArtery Occlusionen_US
dc.subjectFunctional Recoveryen_US
dc.subjectProtective Roleen_US
dc.subjectBrain-Damageen_US
dc.subjectModelen_US
dc.subjectExpressionen_US
dc.subjectApoptosisen_US
dc.subjectStrokeen_US
dc.titleMelatonin Attenuates Cerebral Ischemia/Reperfusion Injury Through Inducing Autophagyen_US
dc.typeArticleen_US

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