Protective Effect of Lutein/Zeaxanthin Isomers in Traumatic Brain Injury in Mice

dc.authorid0000-0001-7702-2441
dc.authorid0000-0001-6494-8923
dc.authorid0000-0001-9542-5244
dc.authorid0000-0002-6242-3709
dc.authorid0000-0002-9354-0000
dc.authorid0000-0002-3400-7468
dc.contributor.authorGunal, Mehmet Yalcin
dc.contributor.authorSakul, Ayse Arzu
dc.contributor.authorCaglayan, Ahmet Burak
dc.contributor.authorErten, Fusun
dc.contributor.authorKursun, Oznur Ece Durmaz
dc.contributor.authorKilic, Ertugrul
dc.contributor.authorSahin, Kazim
dc.date.accessioned2026-01-24T12:31:01Z
dc.date.available2026-01-24T12:31:01Z
dc.date.issued2021
dc.departmentAlanya Alaaddin Keykubat Üniversitesi
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 Sciences (TUBA)
dc.description.sponsorshipThis research was supported by OmniActive Health Technologies, NJ, USA. This work was also supported in part by the Turkish Academy of Sciences (TUBA) (KS, EK).
dc.identifier.doi10.1007/s12640-021-00385-3
dc.identifier.endpage1550
dc.identifier.issn1029-8428
dc.identifier.issn1476-3524
dc.identifier.issue5
dc.identifier.pmid34129176
dc.identifier.scopus2-s2.0-85107985820
dc.identifier.scopusqualityQ1
dc.identifier.startpage1543
dc.identifier.urihttps://doi.org/10.1007/s12640-021-00385-3
dc.identifier.urihttps://hdl.handle.net/20.500.12868/5596
dc.identifier.volume39
dc.identifier.wosWOS:000661818000001
dc.identifier.wosqualityQ2
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoen
dc.publisherSpringer
dc.relation.ispartofNeurotoxicity Research
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.snmzKA_WoS_20260121
dc.subjectLutein/zeaxanthin isomers
dc.subjectTraumatic brain injury
dc.subjectNF-kappa B
dc.subjectNrf2
dc.subjectBDNF
dc.titleProtective Effect of Lutein/Zeaxanthin Isomers in Traumatic Brain Injury in Mice
dc.typeArticle

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