Autor: |
Sahin E; Department of Animal Nutrition, Faculty of Veterinary Medicine, Bingol University, Bingol 12000, Turkey., Orhan C; Department of Animal Nutrition, Faculty of Veterinary Medicine, Firat University, Elazig 23119, Turkey., Sahin N; Department of Animal Nutrition, Faculty of Veterinary Medicine, Firat University, Elazig 23119, Turkey., Padigaru M; OmniActive Health Technologies Co., Ltd., Mumbai 400013, India., Morde A; OmniActive Health Technologies Co., Ltd., Mumbai 400013, India., Lal M; OmniActive Health Technologies Co., Ltd., Mumbai 400013, India., Dhavan N; OmniActive Health Technologies Co., Ltd., Mumbai 400013, India., Erten F; Department of Veterinary Medicine, Pertek Sakine Genc Vocational School, Munzur University, Tunceli 62500, Turkey., Bilgic AA; Department of Ophtalmology, Ankara Dışkapı Yıldırım Beyazıt Training and Research Hospital, University of Health Sciences, Ankara 06110, Turkey., Ozercan IH; Department of Pathology, Faculty of Medicine, Firat University, Elazig 23119, Turkey., Sahin K; Department of Animal Nutrition, Faculty of Veterinary Medicine, Firat University, Elazig 23119, Turkey. |
Abstrakt: |
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. |