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Neuroprotective effect of ebselen against intracerebroventricular streptozotocin-induced neuronal apoptosis and oxidative stress in rats

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dc.contributor.authorYANARTAŞ, ÖMER
dc.contributor.authorsUnsal, Cuneyt; Oran, Mustafa; Albayrak, Yakup; Aktas, Cevat; Erboga, Mustafa; Topcu, Birol; Uygur, Ramazan; Tulubas, Feti; Yanartas, Omer; Ates, Ozkan; Ozen, Oguz Aslan
dc.date.accessioned2022-03-12T20:28:44Z
dc.date.available2022-03-12T20:28:44Z
dc.date.issued2016
dc.description.abstractThe goal of this study was to examine the neuroprotective effect of ebselen against intracerebroventricular streptozotocin (ICV-STZ)-induced oxidative stress and neuronal apoptosis in rat brain. A total of 30 adult male Sprague-Dawley rats were randomly divided into 3 groups of 10 animals each: control, ICV-STZ, and ICV-STZ treated with ebselen. The ICV-STZ group rats were injected bilaterally with ICV-STZ (3 mg/kg) on days 1 and 3, and ebselen (10 mg/kg/day) was administered for 14 days starting from 1st day of ICV-STZ injection to day 14. Rats were killed at the end of the study and brain tissues were removed for biochemical and histopathological investigation. Our results demonstrated, for the first time, the neuroprotective effect of ebselen on Alzheimer's disease (AD) model in rats. Our present study, in ICV-STZ group, showed significant increase in tissue malondialdehyde levels and significant decrease in enzymatic antioxidants superoxide dismutase and glutathione peroxidase in the frontal cortex tissue. The histopathological studies in the brain of rats also supported that ebselen markedly reduced the ICV-STZ-induced histopathological changes and well preserved the normal histological architecture of the frontal cortex tissue. The number of apoptotic neurons was increased in frontal cortex tissue after ICV-STZ administration. Treatment of ebselen markedly reduced the number of degenerating apoptotic neurons. The study demonstrates the effectiveness of ebselen, as a powerful antioxidant, in preventing the oxidative damage and morphological changes caused by ICV-STZ in rats. Thus, ebselen may have a therapeutic value for the treatment of AD.
dc.identifier.doi10.1177/0748233713509429
dc.identifier.eissn1477-0393
dc.identifier.issn0748-2337
dc.identifier.pubmed24231787
dc.identifier.urihttps://hdl.handle.net/11424/233967
dc.identifier.wosWOS:000373605800015
dc.language.isoeng
dc.publisherSAGE PUBLICATIONS INC
dc.relation.ispartofTOXICOLOGY AND INDUSTRIAL HEALTH
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.subjectIntracerebroventricular streptozotocin
dc.subjectebselen
dc.subjectoxidative stress
dc.subjectneuronal damage
dc.subjectneuronal apoptosis
dc.subjectrats
dc.subjectMILD COGNITIVE IMPAIRMENT
dc.subjectFREE-RADICAL THEORY
dc.subjectALZHEIMERS-DISEASE
dc.subjectGLUTATHIONE-PEROXIDASE
dc.subjectCEREBRAL-ISCHEMIA
dc.subjectNEURODEGENERATIVE DISEASES
dc.subjectBRAIN CORTEX
dc.subjectADULT RATS
dc.subjectANTIOXIDANT
dc.subjectMETABOLISM
dc.titleNeuroprotective effect of ebselen against intracerebroventricular streptozotocin-induced neuronal apoptosis and oxidative stress in rats
dc.typearticle
dspace.entity.typePublication
local.avesis.idc3582a24-e5f0-46ba-8ee8-892b74427787
local.import.packageSS17
local.indexed.atWOS
local.indexed.atSCOPUS
local.indexed.atPUBMED
local.journal.numberofpages11
local.journal.quartileQ3
oaire.citation.endPage740
oaire.citation.issue4
oaire.citation.startPage730
oaire.citation.titleTOXICOLOGY AND INDUSTRIAL HEALTH
oaire.citation.volume32
relation.isAuthorOfPublication354b8f95-e1bd-4035-8ee6-9e1551100f30
relation.isAuthorOfPublication.latestForDiscovery354b8f95-e1bd-4035-8ee6-9e1551100f30

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