Blue light induces skin apoptosis and degeneration through activation of the endoplasmic reticulum stress-autophagy apoptosis axis: Protective role of hydrogen sulfide

Research on the phototoxicity of blue light (BL) to the skin is increasing. Although blue light can induce oxidative stress, inflammation, and inhibition of proliferation in skin cells, the mechanism by which blue light damages the skin is not yet clear. Endoplasmic reticulum (ER) stress and autophagy are two mechanisms by which cells resist external interference factors and maintain cell homeostasis and normal function, and both can affect cell apoptosis. Interestingly, we have found that blue light (435 nm ~ 445 nm, 8000 lx, 6–24 h)-induced oxidative stress triggers the ER stress-CHOP (C/EBP homologous protein) signal and affects the protein levels of B-cell lymphoma-2 (Bcl-2) and Bcl2-associated X (Bax), thereby promoting apoptosis. In addition, blue light activates autophagy in skin cells, which intensifies cell death. When ER stress is inhibited, autophagy is subsequently inhibited, suggesting that blue light-induced autophagy is influenced by ER stress. These evidences suggest that blue light induces activation of reactive oxygen species (ROS)-ER stress-autophagy-apoptosis axis signaling, which further induces skin injury and apoptosis. This is the first report on the relationships among oxidative stress, ER stress, autophagy, and apoptosis in blue light-induced skin injury. Furthermore, we have studied the effect of hydrogen sulfide (H2S) on blue light-induced skin damage, and found that exogenous H2S can protect skin from blue light-induced damage by regulating the ROS-ER stress-autophagy-apoptosis axis. Our data shows that when we are exposed to blue light, such as sunbathing and jaundice treatment, H2S may be developed as a protective agent.