<?xml version="1.0" encoding="UTF-8"?><OAI-PMH xmlns="http://www.openarchives.org/OAI/2.0/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/ http://www.openarchives.org/OAI/2.0/OAI-PMH.xsd"><responseDate>2026-10-29T20:44:41Z</responseDate><request verb="GetRecord" identifier="oai:munzur-rdlopen.rawdatalibrary.net:munzur/2931" metadataPrefix="oai_dc">https://munzur-rdlopen.rawdatalibrary.net/oai/request</request><GetRecord><record><header><identifier>oai:munzur-rdlopen.rawdatalibrary.net:munzur/2931</identifier><datestamp>2026-10-28T15:30:12Z</datestamp><setSpec>openaire</setSpec><setSpec>driver</setSpec><setSpec>com_munzur_1</setSpec><setSpec>col_munzur_2</setSpec><setSpec>com_munzur_11</setSpec><setSpec>col_munzur_164</setSpec></header><metadata><oai_dc:dc xmlns:oai_dc="http://www.openarchives.org/OAI/2.0/oai_dc/" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/oai_dc/ http://www.openarchives.org/OAI/2.0/oai_dc.xsd"><dc:title>Protective Effect of Lutein/Zeaxanthin Isomers in Traumatic Brain Injury in Mice</dc:title><dc:creator>Gunal, Mehmet Yalcin</dc:creator><dc:creator>Sakul, Ayse Arzu</dc:creator><dc:creator>Caglayan, Ahmet Burak</dc:creator><dc:creator>Erten, Fusun</dc:creator><dc:creator>Kursun, Oznur Ece Durmaz</dc:creator><dc:creator>Kilic, Ertugrul</dc:creator><dc:creator>Sahin, Kazim</dc:creator><dc:subject>BDNF</dc:subject><dc:subject>Lutein/zeaxanthin isomers</dc:subject><dc:subject>NF-κB</dc:subject><dc:subject>Nrf2</dc:subject><dc:subject>Traumatic brain injury</dc:subject><dc:description>Previous 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-κB) 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-1β), interleukin 6 (IL-6), and NF-κB 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><dc:publisher>Springer</dc:publisher><dc:date>2021</dc:date><dc:type>Article</dc:type><dc:identifier>https://rdlopen.rawdatalibrary.net/r/munzur/2931</dc:identifier><dc:identifier>https://doi.org/10.1007/s12640-021-00385-3</dc:identifier><dc:identifier>1029-8428</dc:identifier><dc:language>en</dc:language><dc:relation>Neurotoxicity Research</dc:relation><dc:rights>info:eu-repo/semantics/openAccess</dc:rights><dc:type>info:eu-repo/semantics/article</dc:type><dc:identifier>https://munzur-rdlopen.rawdatalibrary.net/tr/items/munzur/2931</dc:identifier></oai_dc:dc></metadata></record></GetRecord></OAI-PMH>