Antioxidant and neuroprotective effects of dexpanthenol in rats induced with traumatic brain injury

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dc.authoridKoyuncuoğlu, Türkan/0000-0003-4749-9470
dc.authoridÇelikoğlu, Erhan/0000-0002-2064-9072
dc.authoridYegen, Berrak/0000-0003-0791-0165
dc.authoridKuru Bektasoglu, Pinar/0000-0001-9889-9955
dc.authorwosidKoyuncuoğlu, Türkan/AAD-3962-2021
dc.authorwosidGürer, Bora/K-1177-2012
dc.authorwosidÇelikoğlu, Erhan/IZE-8796-2023
dc.authorwosidYegen, Berrak/O-6652-2017
dc.authorwosidBangir AKAKIN, Dilek/JMR-1536-2023
dc.authorwosidKuru Bektasoglu, Pinar/K-8612-2013
dc.contributor.authorBektasoglu, Pinar Kuru
dc.contributor.authorKoyuncuoglu, Turkan
dc.contributor.authorOzaydin, Dilan
dc.contributor.authorKandemir, Cansu
dc.contributor.authorAkakin, Dilek
dc.contributor.authorYuksel, Meral
dc.contributor.authorGurer, Bora
dc.date.accessioned2024-05-19T14:39:02Z
dc.date.available2024-05-19T14:39:02Z
dc.date.issued2023
dc.departmentİstinye Üniversitesien_US
dc.description.abstractTrauma-induced primary damage is followed by secondary damage, exacerbating traumatic brain injury (TBI). Dexpanthenol has been shown to protect tissues against oxidative damage in various inflammation models. This study aimed to investigate possible antioxidant and neuroprotective effects of dexpanthenol in TBI. Wistar albino male rats were randomly assigned to control ( n = 16), trauma ( n = 16) and dexpan-thenol (500 mg/kg; n = 14) groups. TBI was induced under anesthesia by dropping a 300 g weight from 70-cm height onto the skulls of the rats. Twenty-four hours after the trauma, the rats were decapitated and myeloperoxidase (MPO) levels, luminol-and lucigenin-enhanced chemiluminescence (CL), malondi-aldehyde (MDA) levels, superoxide dismutase (SOD) levels, and catalase (CAT) and caspase-3 activities were measured in brain tissues. Following transcardiac paraformaldehyde perfusion, histopathological damage was graded on hematoxylin-eosin-stained brain tissues. In the trauma group, MPO level, caspase-3 activity and luminol-lucigenin CL levels were elevated ( p < 0.05-0.001) when compared to controls; meanwhile in the dexpanthenol group these increases were not seen ( p < 0.05-0.001) and MDA levels were decreased ( p < 0.05). Decreased SOD and CAT activities ( p < 0.01) in the vehicle-treated TBI group were increased above control levels in the dexpanthenol group ( p < 0.05-0.001). in the dexpanthenol group there was relatively less neuronal damage observed micro-scopically in the cortices after TBI. Dexpanthenol reduced oxidative damage, suppressed apoptosis by stimulating antioxidant systems and alleviated brain damage caused by TBI. Further experimental and clinical investigations are needed to confirm that dexpanthenol can be administered in the early stages of TBI. (c) 2023 Elsevier Ltd. All rights reserved.en_US
dc.identifier.doi10.1016/j.injury.2023.02.025
dc.identifier.endpage1070en_US
dc.identifier.issn0020-1383
dc.identifier.issn1879-0267
dc.identifier.issue4en_US
dc.identifier.pmid36841697en_US
dc.identifier.scopus2-s2.0-85149895500en_US
dc.identifier.scopusqualityQ1en_US
dc.identifier.startpage1065en_US
dc.identifier.urihttps://doi.org10.1016/j.injury.2023.02.025
dc.identifier.urihttps://hdl.handle.net/20.500.12713/4682
dc.identifier.volume54en_US
dc.identifier.wosWOS:000955252600001en_US
dc.identifier.wosqualityN/Aen_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.language.isoenen_US
dc.publisherElsevier Sci Ltden_US
dc.relation.ispartofInjury-International Journal of the Care of the Injureden_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.snmz20240519_kaen_US
dc.subjectAntiapoptoticen_US
dc.subjectAnti-Inflammatoryen_US
dc.subjectAntioxidanten_US
dc.subjectDexpanthenolen_US
dc.subjectNeuroprotectionen_US
dc.subjectTraumatic Brain Injuryen_US
dc.titleAntioxidant and neuroprotective effects of dexpanthenol in rats induced with traumatic brain injuryen_US
dc.typeArticleen_US

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