Gunal, Mehmet YalcinSakul, Ayse ArzuCaglayan, Ahmet BurakErten, FusunKursun, Oznur Ece DurmazKilic, ErtugrulSahin, Kazim2026-01-242026-01-2420211029-84281476-3524https://doi.org/10.1007/s12640-021-00385-3https://hdl.handle.net/20.500.12868/5596Previous 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.eninfo:eu-repo/semantics/closedAccessLutein/zeaxanthin isomersTraumatic brain injuryNF-kappa BNrf2BDNFArticle10.1007/s12640-021-00385-339515431550341291762-s2.0-85107985820Q1WOS:000661818000001Q2