Hydrogen sulfide protects retina from blue light-induced photodamage and degeneration via inhibiting ROS-mediated ER stress-CHOP apoptosis signal

Background: Hydrogen sulfide (H(2)S) is a small reducing gas molecule with various biological functions such as anti-oxidative, anti-apoptotic and anti-inflammatory activities. In this study, we investigated the therapeutic effects of exogenous H(2)S in the experimental models of retinal photodamage in vivo and in vitro. Methods: Rats with open eyelids were pretreated with H(2)S (80~120 μmol/kg) for 10 days and then continuously exposed to blue light (435~445nm, 11.2W/m2) for 8 h to establish in vivo experimental model. ARPE-19 cells were pretreated with H(2)S and then exposed to blue light to establish in vitro experimental model. Results: In vivo experiments, H(2)S significantly ameliorated blue light-induced retinal oxidative stress, apoptosis and degeneration. Moreover, H(2)S inhibited the activation of blue light-induced endoplasmic reticulum (ER) stress CHOP apoptotic signaling. In vitro experiments, H(2)S improved blue light-induced oxidative stress and oxidative damage. H(2)S inhibited ROS-mediated activation of ER stress CHOP apoptotic signaling. H(2)S alleviated blue light-induced apoptosis and increases cell viability. The ER stress inhibitor 4-PBA alleviated blue light-induced apoptosis and increases cell viability. Conclusion: Taken together, these results indicate that H(2)S can inhibit ROS-mediated ER stress-CHOP apoptosis signal, thereby alleviating blue light-triggered retinal apoptosis and degeneration.