Publication:
The effect of high mobility group box-1 protein on cerebral edema, blood-brain barrier, oxidative stress and apoptosis in an experimental traumatic brain injury model

dc.contributor.coauthorEvran, Şevket
dc.contributor.coauthorÇalış, Fatih
dc.contributor.coauthorAkkaya, Enes
dc.contributor.coauthorBaran, Oğuz
dc.contributor.coauthorKatar, Salim
dc.contributor.coauthorGürevin, Ebru Gürel
dc.contributor.coauthorHatiboğlu, Mustafa Aziz
dc.contributor.coauthorArmutak, Elif İlkay
dc.contributor.coauthorKarataş, Ersin
dc.contributor.coauthorKoçyiğit, Abdurrahim
dc.contributor.departmentKUH (Koç University Hospital)
dc.contributor.kuauthorÇevik, Serdar
dc.contributor.kuauthorHanımoğlu, Hakan
dc.contributor.kuauthorKaynar, Mehmet Yaşar
dc.contributor.schoolcollegeinstituteKUH (KOÇ UNIVERSITY HOSPITAL)
dc.date.accessioned2024-11-09T23:20:17Z
dc.date.issued2020
dc.description.abstractTraumatic brain injury (TBI) is one of the important reason of morbidity and mortality. While the primary injury due to mechanical impact is unavoidable, the secondary injury which is formed as a result of primary injury and thought to occur due to neurointlammation in the forefront can be prevented and by this way mortality and morbidity can be reduced. High mobility group box-1 (HMGB1) is a protein that triggers the neuroinflammatory process by being released from the nucleus of necrotic tissues after primary injury. The aim of this study is to investigate the effects of HMGB1 on its receptors TLR4 and RAGE, cerebral edema, blood-brain barrier, oxidative stress and apoptosis causing secondary damage in an experimental traumatic brain injury model. Weighing between 280-320 g, 10 to 12 weeks-old, a total of 30 adult male Sprague-Dawley rats were used for the experiments. The rats were randomly assigned to 3 groups: 1) Control, 2) TBI and 3) TBI + ethyl pyruvate group (n = 10 per group). Right parietal cortical contusion was made by using a weight-dropping TBI method. Brain samples were harvested from pericontusional area at 24 h after TBI. HMGB1, TLR4, RAGE, occludin, claudin-5, ZO-1 levels are investigated by western blot analyses and immunohistochemistry examinations. HMGB-1, TLR4 and RAGE expressions increased after TBI. Major tight junction proteins in the blood-brain barrier: occludin, claudin-5 and ZO-1 expressions decreased after TBI. Brain edema increased after TBI. Also, proapoptotic bax and active caspase 3 expressions increased, antiapoptotic bcl-2 levels decreased after TBI. Total oxidant status and oxidative stress increased, total antioxidant status decreased after TBI. HMGB-1 protein plays a key role in the pathophysiology of traumatic brain injury.
dc.description.indexedbyWOS
dc.description.indexedbyScopus
dc.description.openaccessNO
dc.description.publisherscopeInternational
dc.description.sponsoredbyTubitakEuN/A
dc.description.volume154
dc.identifier.doi10.1016/j.brainresbull.2019.10.013
dc.identifier.eissn1873-2747
dc.identifier.issn0361-9230
dc.identifier.quartileQ3
dc.identifier.scopus2-s2.0-85074896381
dc.identifier.urihttps://doi.org/10.1016/j.brainresbull.2019.10.013
dc.identifier.urihttps://hdl.handle.net/20.500.14288/10672
dc.identifier.wos508750400008
dc.keywordsHMGB-1
dc.keywordsOcdudin
dc.keywordsTraumatic brain injury
dc.keywordsBax
dc.keywordsbcl-2
dc.keywordsBrain edema
dc.language.isoeng
dc.publisherElsevier
dc.relation.ispartofBrain Research Bulletin
dc.subjectNeurosciences
dc.titleThe effect of high mobility group box-1 protein on cerebral edema, blood-brain barrier, oxidative stress and apoptosis in an experimental traumatic brain injury model
dc.typeJournal Article
dspace.entity.typePublication
local.contributor.kuauthorÇevik, Serdar
local.contributor.kuauthorKaynar, Mehmet Yaşar
local.contributor.kuauthorHanımoğlu, Hakan
local.publication.orgunit1KUH (KOÇ UNIVERSITY HOSPITAL)
local.publication.orgunit2KUH (Koç University Hospital)
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relation.isParentOrgUnitOfPublication055775c9-9efe-43ec-814f-f6d771fa6dee
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