Hydrogen Sulfide Protects Retinal Pigment Epithelial Cells from Oxidative Stress-Induced Apoptosis and Affects Autophagy

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.

Lycium Barbarum polysaccharide protects HaCaT cells from PM2.5-induced apoptosis via inhibiting oxidative stress, ER stress and autophagy

“…One percent of PMSF was added into lysate to prevent protein degradation. Further operation is consistent with our previous research [ 23 ].…”

“…The viability of HaCaT cells was detected by MTT method, consistent with our previous research [ 23 ]. In addition, lactate dehydrogenase (LDH) release was also used to analyze the cytotoxicity, according to the manufacturer's instructions (Nanjing Jiancheng Bioengineering Institute, Nanjing, China).…”

“…Autophagy is another cell self-protection mechanism that can clean up damaged organelles and recycle metabolites to maintain cell function and homeostasis [ 39 ]. However, a lot of evidence has confirmed that autophagy does not necessarily protect cells, on the contrary, it may cause negative effects and induce cell apoptosis, including our previous study on oxidative stress-mediated autophagy in ARPE-19 cells [ 23 ]. In this study, the results have shown that the autophagy inhibitor 3-MA pretreatment can reduce PM2.5-induced apoptosis and cytotoxicity ( Figure 6 ), indicating that autophagy may be involved in inducing cell apoptosis and aggravating cytotoxicity.…”

Protective effect of H2S on LPS‑induced AKI by promoting autophagy

“…2021101119; Changsha, China). Both our preliminary experiments and literature reports showed that 3-MA alone did not increase damage, therefore our experiment did not set up a 3-MA group alone ( 30 ).…”

TRAP1 in Oxidative Stress and Neurodegeneration

“…Hu et al synthesized a series of TPP-conjugated SMTIN-P01 analogues, substituting the C6 linker with carbon chains of different lengths. From these, the compound with a 10-carbon linker (SMTIN-C10) presented stronger inhibition of TRAP1 than SMTIN-P01 [ 106 ].…”