Please use this identifier to cite or link to this item: http://hdl.handle.net/11452/22654
Full metadata record
DC FieldValueLanguage
dc.date.accessioned2021-11-15T11:05:16Z-
dc.date.available2021-11-15T11:05:16Z-
dc.date.issued2010-01-
dc.identifier.citationAbaş, F. vd. (2010). "Neuroprotective effects of postconditioning on lipid peroxidation and apoptosis after focal cerebral ischemia/reperfusion injury in rats". Turkish Neurosurgery, 20(1), 1-8.en_US
dc.identifier.issn1019-5149-
dc.identifier.urihttp://turkishneurosurgery.org.tr/pdf/pdf_JTN_712.pdf-
dc.identifier.urihttp://turkishneurosurgery.org.tr/abstract.php?id=712-
dc.identifier.urihttp://hdl.handle.net/11452/22654-
dc.description.abstractAIM: Apoptosis after cerebral ischemia/reperfusion (I/R) injury leads to the process of cell death. The deal therapeutic approach would target the apoptosis after I/R. Ischemic postconditioning is a recently discovered neuroprotective strategy that involves the application of brief mechanical reperfusion with a specific algorithm at the onset of reperfusion following an ischemic period. MATERIAL and METHODS: Transient MCAo was performed on male SD (275 +/- 25g) rats with intraluminal thread insertion for 2hrs. Rats (n:36) were treated with postconditioning after 60 minutes of occlusion. The postconditioning algorithm was 30 secs of brief reperfusion followed by 30 secs of MCAo and this cycle was repeated 3 times at the onset of reperfusion. RESULTS: After I/R injury, % change of the malonyldialdehyde (MDA) levels in the cortex, which is an index of lipid peroxidation, was found significantly higher in the I/R group. On the other hand postconditioning upregulated Bcl-2 and Bax translocation to the mitochondria, and caspase-3 activity and also reduced oxidative stress levels. CONCLUSION: These findings indicated this neuroprotective effect is most likely achieved by antiapoptotic mechanisms through caspase pathways.en_US
dc.language.isoenen_US
dc.publisherTürkiye Nöroşirürji Derneğitr_TR
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.rightsAtıf Gayri Ticari Türetilemez 4.0 Uluslararasıtr_TR
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/*
dc.subjectAntioxidant enzymesen_US
dc.subjectIschemia reperfusion injuryen_US
dc.subjectLipid peroxidationen_US
dc.subjectNeuroprotectionen_US
dc.subjectPostconditioningen_US
dc.subjectReduces infarct sizeen_US
dc.subjectArtery occlusionen_US
dc.subjectCytochrome-cen_US
dc.subjectBrain-injuryen_US
dc.subjectReperfusionen_US
dc.subjectIschemiaen_US
dc.subjectProtectsen_US
dc.subjectStrokeen_US
dc.subjectMitochondriaen_US
dc.subjectTransitionen_US
dc.subjectNeurosciences & neurologyen_US
dc.subjectSurgeryen_US
dc.subject.meshAnimalsen_US
dc.subject.meshApoptosisen_US
dc.subject.meshBcl-2-associated X proteinen_US
dc.subject.meshBrainen_US
dc.subject.meshBrain ischemiaen_US
dc.subject.meshCaspase 3en_US
dc.subject.meshFunctional lateralityen_US
dc.subject.meshIschemic preconditioningen_US
dc.subject.meshLipid peroxidationen_US
dc.subject.meshMaleen_US
dc.subject.meshMitochondriaen_US
dc.subject.meshNeuroprotective agentsen_US
dc.subject.meshOxidative stressen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, sprague-dawleyen_US
dc.subject.meshReperfusion injuryen_US
dc.subject.meshUp-regulationen_US
dc.titleNeuroprotective effects of postconditioning on lipid peroxidation and apoptosis after focal cerebral ischemia/reperfusion injury in ratsen_US
dc.typeArticleen_US
dc.identifier.wos000274702500001tr_TR
dc.identifier.scopus2-s2.0-77951635024tr_TR
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergitr_TR
dc.contributor.departmentUludağ Üniversitesi/Tıp Fakültesi/Beyin ve Sinir Cerrahisi Anabilim Dalı.tr_TR
dc.contributor.departmentUludağ Üniversitesi/Tıp Fakültesi/Fizyoloji Anabilim Dalı.tr_TR
dc.contributor.departmentUludağ Üniversitesi/Tıp Fakültesi/Biyokimya Anabilim Dalı.tr_TR
dc.contributor.departmentUludağ Üniversitesi/Tıp Fakültesi/Tıbbi Patoloji Anabilim Dalı.tr_TR
dc.contributor.orcid0000-0002-2593-7196tr_TR
dc.identifier.startpage1tr_TR
dc.identifier.endpage8tr_TR
dc.identifier.volume20tr_TR
dc.identifier.issue1tr_TR
dc.relation.journalTurkish Neurosurgeryen_US
dc.contributor.buuauthorAbaş, Faruk-
dc.contributor.buuauthorAlkan, Tülin-
dc.contributor.buuauthorGören, Bülent-
dc.contributor.buuauthorTaşkapılıoğlu, Özgür-
dc.contributor.buuauthorSarandöl, Emre-
dc.contributor.buuauthorTolunay, Şahsine-
dc.contributor.researcheridABE-1716-2020tr_TR
dc.contributor.researcheridAAH-1718-2021tr_TR
dc.contributor.researcheridABB-8161-2020tr_TR
dc.contributor.researcheridAAH-1792-2021tr_TR
dc.indexed.trdizinTrDizintr_TR
dc.identifier.pubmed20066614tr_TR
dc.subject.wosClinical neurologyen_US
dc.subject.wosSurgeryen_US
dc.indexed.wosSCIEen_US
dc.indexed.scopusScopusen_US
dc.indexed.pubmedPubmeden_US
dc.wos.quartileQ4en_US
dc.contributor.scopusid8546184300tr_TR
dc.contributor.scopusid6601953747tr_TR
dc.contributor.scopusid6602543716tr_TR
dc.contributor.scopusid6506852772tr_TR
dc.contributor.scopusid55943324800tr_TR
dc.contributor.scopusid6602604390tr_TR
dc.subject.scopusIschemic Postconditioning; Reperfusion Injury; Mitochondrial Permeability Transition Poreen_US
dc.subject.emtreeCaspase 3en_US
dc.subject.emtreeNeuroprotective agenten_US
dc.subject.emtreeProtein baxen_US
dc.subject.emtreeAnimalen_US
dc.subject.emtreeApoptosisen_US
dc.subject.emtreeArticleen_US
dc.subject.emtreeBrainen_US
dc.subject.emtreeBrain ischemiaen_US
dc.subject.emtreeHemispheric dominanceen_US
dc.subject.emtreeIschemic preconditioningen_US
dc.subject.emtreeLipid peroxidationen_US
dc.subject.emtreeMaleen_US
dc.subject.emtreeMetabolismen_US
dc.subject.emtreeMitochondrionen_US
dc.subject.emtreeOxidative stressen_US
dc.subject.emtreePathologyen_US
dc.subject.emtreePathophysiologyen_US
dc.subject.emtreePhysiologyen_US
dc.subject.emtreeRaten_US
dc.subject.emtreeReperfusion injuryen_US
dc.subject.emtreeSprague dawley raten_US
dc.subject.emtreeUpregulationen_US
Appears in Collections:Scopus
Web of Science

Files in This Item:
File Description SizeFormat 
Abaş_vd_2010.pdf127.05 kBAdobe PDFThumbnail
View/Open


This item is licensed under a Creative Commons License Creative Commons