Publication:
Aging protects rat cortical slices against to oxygen-glucose deprivation induced damage

dc.contributor.authorGul, Zulfiye
dc.contributor.authorBuyukuysal, Rifat Levent
dc.contributor.buuauthorDemircan, Celaleddin
dc.contributor.buuauthorDEMİRCAN, CELALEDDİN
dc.contributor.buuauthorBagdas, Deniz
dc.contributor.departmentBursa Uludağ Üniversitesi/Tıp Fakültesi/Farmakoloji Anabilim Dalı.
dc.contributor.researcheridHJZ-4470-2023
dc.date.accessioned2024-07-01T13:43:44Z
dc.date.available2024-07-01T13:43:44Z
dc.date.issued2020-02-22
dc.description.abstractObjective: In present study, we aimed to clarify effect of aging on the susceptibility of brain tissue to neurodegeneration induced by ischemia. Methods: Damage induced by oxygen-glucose deprivation (OGD) followed by reoxygenation (REO) were compared in cortical slices prepared from young (3 months of age) and aged (22-24 months of age) male Sprague Dawley rats. Results: After incubation of the slices in an oxygen and glucose containing control condition, 2,3,5-triphenyl tetrazolium chloride (TTC) staining intensity was found significantly high in aged cortical slices. Although thirty minutes incubation of the slices in OGD medium followed by REO (OGD-REO) caused similar decline in TTC staining in young and aged cortical slices, staining intensity was still significantly higher in the slices prepared from aged animals. Thirty minutes of OGD-REO, on the other hand, also caused more increase in lactate dehydrogenase (LDH) leakage from young slices. While water contents of the slices were almost equal under control condition, it was significantly high in young cortical slices after OGD-REO incubations. In contrary to these findings, OGD and REO caused more increases in S100B output from aged rat cortical slices. S100B levels in brain regions including the cerebral cortex were also found higher in aged rats. Conclusion: All these results indicate that, cortical slices prepared from aged male rats are significantly less responsive to in vitro OGD-REO induced alterations. Since protein S100B outputs were almost doubled from aged cortical slices, a possible involvement of this enhanced S100B output seems to be likely.
dc.identifier.doi10.1080/00207454.2020.1730830
dc.identifier.endpage1191
dc.identifier.issn0020-7454
dc.identifier.issue12
dc.identifier.startpage1183
dc.identifier.urihttps://doi.org/10.1080/00207454.2020.1730830
dc.identifier.urihttps://hdl.handle.net/11452/42672
dc.identifier.volume130
dc.identifier.wos000515749800001
dc.indexed.wosWOS.SCI
dc.language.isoen
dc.publisherTaylor & Francis
dc.relation.bapHDP(T)-2011/26
dc.relation.journalInternational Journal Of Neuroscience
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.subjectAge-related-changes
dc.subjectMessenger-rna
dc.subjectBrain-slices
dc.subjectExperimental stroke
dc.subjectOxidative stress
dc.subjectIschemic-stroke
dc.subjectS100 beta
dc.subjectGlutamate
dc.subjectNeurons
dc.subjectExpression
dc.subjectAging
dc.subjectEdema
dc.subjectLdh
dc.subjectOxygen-glucose deprivation
dc.subjectS100b
dc.subjectScience & technology
dc.subjectLife sciences & biomedicine
dc.subjectNeurosciences
dc.subjectNeurosciences & neurology
dc.titleAging protects rat cortical slices against to oxygen-glucose deprivation induced damage
dc.typeArticle
dspace.entity.typePublication
relation.isAuthorOfPublicatione221ff67-55ca-4800-98f0-eeecb4e2bdc0
relation.isAuthorOfPublication.latestForDiscoverye221ff67-55ca-4800-98f0-eeecb4e2bdc0

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