| Autor: |
Hsu MY; School of Medicine, Chung Shan Medical University, Taichung 40201, Taiwan.; Department of Ophthalmology, Chung Shan Medical University Hospital, Taichung 40201, Taiwan.; Biotechnology Center, National Chung Hsing University, Taichung 40227, Taiwan., Hsiao YP; School of Medicine, Chung Shan Medical University, Taichung 40201, Taiwan.; Department of Ophthalmology, Chung Shan Medical University Hospital, Taichung 40201, Taiwan., Lin YT; School of Medicine, Chung Shan Medical University, Taichung 40201, Taiwan.; Department of Ophthalmology, Chung Shan Medical University Hospital, Taichung 40201, Taiwan., Chen C; Department of Optometry, Chung Shan Medical University, Taichung 40201, Taiwan.; Institute of Optometry, Chung Shan Medical University, Taichung 40201, Taiwan., Lee CM; School of Medicine, Chung Shan Medical University, Taichung 40201, Taiwan.; Department of Ophthalmology, Chung Shan Medical University Hospital, Taichung 40201, Taiwan., Liao WC; Department of Optometry, Chung Shan Medical University, Taichung 40201, Taiwan.; Department of Anatomy, Faculty of Medicine, Chung Shan Medical University, Taichung 40201, Taiwan., Tsou SC; Department of Nutrition, Chung Shan Medical University, Taichung 40201, Taiwan., Lin HW; Department of Optometry, Asia University, Taichung 41354, Taiwan.; Department of Medical Research, China Medical University Hospital, China Medical University, Taichung 40447, Taiwan., Chang YY; School of Medicine, Chung Shan Medical University, Taichung 40201, Taiwan.; Department of Medical Education, Chung Shan Medical University Hospital, Taichung 40201, Taiwan. |
| Abstrakt: |
Oxidative damage of retinal pigment epithelium (RPE) cells plays an important role in the pathogenesis of blindness-related diseases, such as age-related macular degeneration (AMD). Quercetin, a bioactive flavonoid compound, has been shown to have a protective effect against oxidative stress-induced cell apoptosis and inflammation in RPE cells; however, the detailed mechanism underlying this protective effect is unclear. Therefore, the aim of this study was to investigate the regulatory mechanism of quercetin in a sodium iodate (NaIO 3 )-induced retinal damage. The clinical features of the mice, the production of oxidative stress, and the activity of autophagy and mitochondrial biogenesis were examined. In the mouse model, NaIO 3 treatment caused changes in the retinal structure and reduced pupil constriction, and quercetin treatment reversed the oxidative stress-related pathology by decreasing the level of superoxide dismutase 2 (SOD2) while enhancing the serum levels of catalase and glutathione. The increased level of reactive oxygen species in the NaIO 3 -treated ARPE19 cells was improved by treatment with quercetin, accompanied by a reduction in autophagy and mitochondrial biogenesis. Our findings indicated that the effects of quercetin on regulating the generation of mtROS were dependent on increased levels of deacetyl-SOD2 through the Nrf2-PGC-1α-Sirt1 signaling pathway. These results demonstrated that quercetin may have potential therapeutic efficacy for the treatment of AMD through the regulation of mtROS homeostasis. |
