Abstract
Age-related macular degeneration (AMD) is a major cause of visual impairment and blindness among the elderly. AMD is characterized by retinal pigment epithelial (RPE) cell dysfunction. However, the pathogenesis of AMD is still unclear, and there is currently no effective treatment. Accumulated evidence indicates that oxidative stress and autophagy play a crucial role in the development of AMD. H2S is an antioxidant that can directly remove intracellular superoxide anions and hydrogen peroxide. The purpose of this study is to investigate the antioxidative effect of H2S in RPE cells and its role in autophagy. The results show that exogenous H2S (NaHS) pretreatment effectively reduces H2O2-induced oxidative stress, oxidative damage, apoptosis, and inflammation in ARPE-19 cells. NaHS pretreatment also decreased autophagy levels raised by H2O2, increased cell viability, and ameliorated cell morphological damage. Interestingly, the suppression of autophagy by its inhibitor 3-MA showed an increase of cell viability, amelioration of morphology, and a decrease of apoptosis. In summary, oxidative stress causes ARPE-19 cell injury by inducing cell autophagy. However exogenous H2S is shown to attenuate ARPE-19 cell injury, decrease apoptosis, and reduce the occurrence of autophagy-mediated by oxidative stress. These findings suggest that autophagy might play a crucial role in the development of AMD, and exogenous H2S has a potential value in the treatment of AMD.
Highlights
Age-related macular degeneration (AMD) is the leading cause of irreversible vision loss in the elderly people around the world, and the prevalence of AMD is increasing [1]
The results showed that H2O2 treatment induced the increase of MDA, which was dramatically inhibited by the NaHS pretreatment (Figure 1(d)), demonstrating the protective effect of H2S on oxidative damage
H2S significantly attenuated the morphological damage of cells induced by H2O2. These results demonstrate that exogenous H2S protected ARPE-19 cells against H2O2-induced oxidative injury
Summary
Age-related macular degeneration (AMD) is the leading cause of irreversible vision loss in the elderly people around the world, and the prevalence of AMD is increasing [1]. The retina is one of the most oxygen-consuming tissues in the human body, and RPE cells are vulnerable to oxidative stress caused by reactive oxygen species (ROS). Intracellular enzymes, such as catalase, superoxide dismutase (SOD), and glutathione peroxidase (GPx), protect RPE cells against oxidative stress through scavenging ROS and attenuating oxidative damage. Further research reveals that several antioxidants could inhibit AMD progression [1,2,3]. Inhibiting oxidative stress-induced RPE cell damage might represent an effective approach to slow down the progress of AMD in patients [1, 3]
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