Protective effect of lutein/zeaxanthin isomers in traumatic brain injury in mice

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dc.authorid0000-0001-7702-2441
dc.authorid0000-0002-9354-0000
dc.authorid0000-0002-6242-3709
dc.authorid0000-0001-6494-8923
dc.contributor.authorGünal, Mehmet Yalçın
dc.contributor.authorŞakul, Ayşe Arzu
dc.contributor.authorÇağlayan, Ahmet Burak
dc.contributor.authorErten, Füsun
dc.contributor.authorDurmaz Kurşun, Öznur Ece
dc.contributor.authorKılıç, Ertuğrul
dc.contributor.authorŞahin, Kazım
dc.date.accessioned2021-10-19T12:52:45Z
dc.date.available2021-10-19T12:52:45Z
dc.date.issued2021
dc.departmentİstanbul Medipol Üniversitesi, Rektörlük, Rejeneratif ve Restoratif Tıp Araştırmaları Merkezi (REMER)
dc.departmentİstanbul Medipol Üniversitesi, Tıp Fakültesi, Dahili Tıp Bilimleri Bölümü, Tıbbi Farmakoloji Ana Bilim Dalı
dc.departmentİstanbul Medipol Üniversitesi, Tıp Fakültesi, Temel Tıp Bilimleri Bölümü, Fizyoloji Ana Bilim Dalı
dc.description.abstractPrevious studies revealed that oxidative stress and inflammation are the main contributors to secondary injury after traumatic brain injury (TBI). In an earlier study, we reported that lutein/zeaxanthin isomers (L/Zi) exert antioxidative and anti-inflammatory effects by activating the nuclear factor-kappa B (NF-kappa B) and nuclear factor-erythroid 2-related factor 2 (Nrf2) pathways. However, its precise role and underlying mechanisms were largely unknown after TBI. This study was conducted to investigate the potential mechanism of L/Zi isomers in a TBI model induced by a cold injury model in mice. To investigate the effects of L/Zi, male C57BL/6j mice-induced brain injury using the cold trauma model was allocated into two groups (n = 7): (i) TBI + vehicle group and (ii) TBI + L/Zi group (20 mg/kg BW). Brain samples were collected 24 h later for analyses. L/Zi given immediately after the injury decreased infarct volume and blood-brain barrier (BBB) permeability; L/Zi treatment also significantly reduced proinflammatory cytokines, including interleukin1 beta (IL-1 beta), interleukin 6 (IL-6), and NF-kappa B levels and increased growth-associated protein 43 (GAP-43), neural cell adhesion molecule (NCAM), brain-derived neurotrophic factor (BDNF), and Nrf2 levels compared with vehicle control. These data suggest that L/Zi improves mitochondrial function in TBI models, possibly decreasing inflammation and activating the Nrf2 pathway.
dc.description.sponsorshipOmniActive Health Technologies, NJ, USA ; Turkish Academy of Sciencesen_US
dc.identifier.citationGünal, M. Y., Şakul, A. A., Çağlayan, A. B., Erten, F., Durmaz Kurşun, Ö. E., Kılıç, E. ... Şahin, K. (2021). Protective effect of lutein/zeaxanthin isomers in traumatic brain injury in mice. Neurotoxicity Research, 39(5), 1543-1550. https://dx.doi.org/10.1007/s12640-021-00385-3
dc.identifier.doi10.1007/s12640-021-00385-3
dc.identifier.endpage1550
dc.identifier.issn1029-8428
dc.identifier.issn1476-3524
dc.identifier.issue5
dc.identifier.scopusqualityQ2
dc.identifier.startpage1543
dc.identifier.urihttps://dx.doi.org/10.1007/s12640-021-00385-3
dc.identifier.urihttps://hdl.handle.net/20.500.12511/8472
dc.identifier.volume39
dc.identifier.wosqualityQ2
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoen
dc.publisherSpringer
dc.relation.ispartofNeurotoxicity Researchen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/embargoedAccess
dc.subjectBDNF
dc.subjectLutein/Zeaxanthin Isomers
dc.subjectNF-?B
dc.subjectNrf2
dc.subjectTraumatic Brain Injury
dc.titleProtective effect of lutein/zeaxanthin isomers in traumatic brain injury in mice
dc.typeArticle

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