Publications by authors named "Oznur Ece Durmaz Kursun"

2 Publications

  • Page 1 of 1

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

Neurotox Res 2021 Jun 15. Epub 2021 Jun 15.

Department of Animal Nutrition, Faculty of Veterinary Medicine, Firat University, Elazig, Turkey.

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.
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June 2021

Lutein/zeaxanthin isomers regulate neurotrophic factors and synaptic plasticity in trained rats.

Turk J Med Sci 2021 Apr 12. Epub 2021 Apr 12.

Background/aim: This study was conducted to elucidate the effects of lutein/zeaxanthin isomers (L/Zi) on lipid metabolism on lipid metabolism, oxidative stress, NF-?B/Nrf2 pathways, and synaptic plasticity proteins in trained rats.

Materials And Methods: Wistar rats were distributed into four groups: 1) Control; 2) L/Zi: Rats received L/Zi at the dose of 100 mg/kg by oral gavage; 3) Exercise: 4) Exercise+L/Zi: Rats exercised and received L/Zi (100 mg/kg) by oral gavage. The duration of the study was eight weeks.

Results: Exercise combined with L/Zi reduced lipid peroxidation and improved antioxidant enzyme activities of muscle and cerebral cortex in rats (P < 0.001). In the Exercise + L/ Zi group, muscle and cerebral cortex Nrf2 and HO-1 levels increased, while NF-?B levels decreased (P <0.001). Also, L/Zi improved BDNF, synapsin I, SYP, and GAP-43 levels of the cerebral cortex of trained rats (P < 0.001). The highest levels of BDNF, synapsin SYP, and GAP-43 in the cerebral cortex were determined in the Exercise+L/Zi group.

Conclusion: These results suggested that exercise combined with L/Zi supplementation might be effective to reduce neurodegeneration via improving neurotrophic factors and synaptic proteins, and oxidative capacity in the cerebral cortex.
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April 2021