Sürdürülebilir Kalkınma Amaçları

• 2

Yazarlar

• Erten, Fusun(2)
• Sahin, Kazim(2)
• Bilgic, Ahmet Alp(1)
• Caglayan, Ahmet Burak(1)
• Dhavan, Nanasaheb(1)
• Gunal, Mehmet Yalcin(1)
• Kilic, Ertugrul(1)
• Kursun, Oznur Ece Durmaz(1)
• Lal, Mohan(1)
• Morde, Abhijeet(1)
• Orhan, Cemal(1)
• Ozercan, Ibrahim Hanifi(1)
• Padigaru, Muralidhara(1)
• Sahin, Emre(1)
• Sahin, Nurhan(1)
• Sakul, Ayse Arzu(1)

• MakaleAçık Erişim2023Scopus SJRQ1/r/munzur/1979
  Lutein/Zeaxanthin Isomers and Quercetagetin Combination Safeguards the Retina from Photo-Oxidative Damage by Modulating Neuroplasticity Markers and the Nrf2 Pathway

  Sahin, Emre; Orhan, Cemal; Sahin, Nurhan; Padigaru, Muralidhara; Morde, Abhijeet; Lal, Mohan; Dhavan, Nanasaheb; Erten, Fusun; Bilgic, Ahmet Alp; Ozercan, Ibrahim Hanifi

  Exposure to light-emitting diode (LED) light is a primary cause of retinal damage, resulting in vision loss. Several plant-derived substances, such as lutein and quercetagetin (QCG), show promise in supporting eye health. In this study, the impact of lutein/zeaxanthin (L/Z, Lutemax 2020) and QCG were evaluated individually and together in a rat model of LED-induced retinal damage. A total of 63 Wistar rats were allocated into nine groups (n = 7). For 28 days, the rats received L/Z (10 or 20 mg/kg BW), quercetin (QC, 20 mg/kg BW), QCG (10 or 20 mg/kg BW), or a mixture of different lutein and QCG dosages, after which they were exposed to LED light for 48 h. LED exposure led to a spike in serum malondialdehyde (MDA) and inflammatory cytokines, as well as an increase in retinal NF-κB, ICAM, GFAP, and MCP-1 levels (p < 0.0001 for all). It also reduced serum antioxidant enzyme activities and retinal Nrf2, HO-1, GAP43, NCAM, and outer nuclear layer (ONL) thickness (p < 0.0001 for all). However, administering L/Z and QCG, particularly a 1:1 combination of L/Z and QCG at 20 mg/kg, effectively reversed these changes. The treatment suppressed NF-κB, ICAM, GFAP, and MCP-1 while enhancing Nrf2, HO-1, GAP43, and NCAM and preventing ONL thickness reduction in LED-induced retinal damage rats. In conclusion, while LED light exposure caused retinal damage, treatment with L/Z, QC, and QCG, particularly a combined L/Z and QCG regimen, exhibited protective effects on the retina. This is possibly due to the modulation of neuroplasticity markers and nuclear transcription factors in the rats’ retinal cells.

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  AtıfScopus22·OpenAlex22

  İncele
• MakaleAçık Erişim2021Scopus SJRQ2/r/munzur/2931
  Protective Effect of Lutein/Zeaxanthin Isomers in Traumatic Brain Injury in Mice

  Gunal, Mehmet Yalcin; Sakul, Ayse Arzu; Caglayan, Ahmet Burak; Erten, Fusun; Kursun, Oznur Ece Durmaz; Kilic, Ertugrul; Sahin, Kazim

  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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  AtıfScopus39·OpenAlex40

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