Protective Effect of Lutein/Zeaxanthin Isomers in Traumatic Brain Injury in Mice
| Autor: | Ahmet Burak Çağlayan, Mehmet Yalçın Günal, Fusun Erten, Kazim Sahin, Ayşe Arzu Şakul, Ertugrul Kilic, Oznur Ece Durmaz Kursun |
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| Rok vydání: | 2021 |
| Předmět: |
0301 basic medicine
Male medicine.medical_specialty Lutein Traumatic Brain Injury Traumatic brain injury Inflammation Toxicology medicine.disease_cause NF-κB Nrf2 Antioxidants Proinflammatory cytokine 03 medical and health sciences chemistry.chemical_compound Mice 0302 clinical medicine Isomerism Neurotrophic factors Zeaxanthins Internal medicine Brain Injuries Traumatic medicine Animals Interleukin 6 biology General Neuroscience Lutein/Zeaxanthin Isomers medicine.disease Zeaxanthin Mice Inbred C57BL Oxidative Stress BDNF 030104 developmental biology Endocrinology Neuroprotective Agents chemistry biology.protein medicine.symptom 030217 neurology & neurosurgery Oxidative stress |
| Zdroj: | Neurotoxicity research. 39(5) |
| ISSN: | 1476-3524 |
| Popis: | 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-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. OmniActive Health Technologies, NJ, USA ; Turkish Academy of Sciences |
| Databáze: | OpenAIRE |
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