Neuroprotective effects of Caffeic acid phenethyl ester on experimental traumatic brain injury in rats

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dc.contributor.authorKerman, Memduh
dc.contributor.authorKanter, Mehmet
dc.contributor.authorCoskun, Kerim Kenan
dc.contributor.authorErboga, Mustafa
dc.contributor.authorGurel, Ahmet
dc.date.accessioned2024-06-12T11:16:41Z
dc.date.available2024-06-12T11:16:41Z
dc.date.issued2012
dc.departmentTrakya Üniversitesien_US
dc.description.abstractThe aim of this study was to evaluate the therapeutic efficacy of caffeic acid phenethyl ester (CAPE) with an experimental traumatic brain injury (TBI) model in rats. Twenty-four adult male Sprague-Dawley rats were randomly divided into three groups of 8 rats each: control, TBI, and TBI + CAPE treatment. In TBI and TBI + CAPE treatment groups, a cranial impact was delivered to the skull from a height of 7 cm at a point just in front of the coronal suture and over the right hemisphere. Rats were sacrificed at 4 h after the onset of injury. Brain tissues were removed for biochemical and histopathological investigation. To date, no biochemical and histopathological changes of neurodegeneration in the frontal cortex after TBI in rats by CAPE treatment have been reported. The TBI significantly increased tissue malondialdehyde (MDA) levels, and significantly decreased tissue superoxide dismutase (SOD) and glutathione peroxidase (GPx) activities, but not tissue catalase (CAT) activity, when compared with controls. The administration of a single dose of CAPE (10 mu mol/kg) 15 min after the trauma has shown protective effect via decreasing significantly the elevated MDA levels and also significantly increasing the reduced antioxidant enzyme (SOD and GPx) activities, except CAT activity. In the TBI group, severe degenerative changes, shrunken cytoplasma and extensively dark picnotic nuclei in neurons, as well as vacuolization indicating tissue edema formation. The morphology of neurons in the CAPE treatment group was well protected. The number of neurons in the trauma alone group was significantly less than that of both the control and TBI +CAPE treatment groups. The caspase 3 immunopositivity was increased in degenerating neurons of the traumatic brain tissue. Treatment of CAPE markedly reduced the immunoreactivity of degenerating neurons. TBI caused severe degenerative changes, shrunken cytoplasma, severely dilated cisternae of endoplasmic reticulum, markedly swollen mitochondria with degenerated cristae and nuclear membrane breakdown with chromatin disorganization in neurons of the frontal cortex. In conclusion, the CAPE treatment might be beneficial in preventing trauma-induced oxidative brain tissue damage, thus showing potential for clinical implications. We believe that further preclinical research into the utility of CAPE may indicate its usefulness as a potential treatment on neurodegeneration after TBI in rats.en_US
dc.identifier.doi10.1007/s10735-011-9376-9
dc.identifier.endpage57en_US
dc.identifier.issn1567-2379
dc.identifier.issn1567-2387
dc.identifier.issue1en_US
dc.identifier.pmid22124729en_US
dc.identifier.scopus2-s2.0-84856540774en_US
dc.identifier.scopusqualityQ2en_US
dc.identifier.startpage49en_US
dc.identifier.urihttps://doi.org/10.1007/s10735-011-9376-9
dc.identifier.urihttps://hdl.handle.net/20.500.14551/24396
dc.identifier.volume43en_US
dc.identifier.wosWOS:000299376400006en_US
dc.identifier.wosqualityQ4en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherSpringeren_US
dc.relation.ispartofJournal Of Molecular Histologyen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectTraumatic Brain Injuryen_US
dc.subjectCAPEen_US
dc.subjectOxidative Stressen_US
dc.subjectApoptosisen_US
dc.subjectRatsen_US
dc.subjectClosed-Head Traumaen_US
dc.subjectLipid-Peroxidationen_US
dc.subjectReperfusion Injuryen_US
dc.subjectN-Acetylcysteineen_US
dc.subjectMechanismsen_US
dc.subjectCaspase-3en_US
dc.subjectIschemiaen_US
dc.subjectDysfunctionen_US
dc.subjectStressen_US
dc.subjectImpacten_US
dc.titleNeuroprotective effects of Caffeic acid phenethyl ester on experimental traumatic brain injury in ratsen_US
dc.typeArticleen_US

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