Abstract
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 (NaIO3)-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, NaIO3 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 NaIO3-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.
Highlights
Age-related macular degeneration (AMD) is a leading cause of progressive central vision loss and irreversible blindness in people older than 65 years in developed countries [1]
Combined with increasing reports in the NaIO3 -induced retinal pigment epithelium (RPE) cells and mice, retinal degeneration is often accompanied by the change of autophagy [37,38], these results indicated that quercetin may reduce the autophagy induced by NaIO3 treatment
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Summary
Age-related macular degeneration (AMD) is a leading cause of progressive central vision loss and irreversible blindness in people older than 65 years in developed countries [1]. Nonexudative (dry) AMD is the most common subtype (approximately 90%) of Antioxidants 2021, 10, 1125. The widespread drusen formation and RPE degeneration are the clinical features of dry AMD. The progression of AMD is attributed to a variety of risk factors, such as genetic factors, inflammatory responses, and oxidative stress [3,4]. Excessive exposure to oxidative stress caused by reactive oxygen species (ROS) of RPE cells is considered to be the leading reason in the pathophysiology of AMD [5,6,7]. Overproduction of ROS may cause a series of devastating results, including organelle damage, toxic lipoprotein debris, and extracellular drusen deposits, which eventually lead to RPE functional impairment, cell death, or dysregulated autophagy [8]
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