Hydrogen Sulfide Attenuates Hydrogen Peroxide-Induced Injury in Human Lung Epithelial A549 Cells

Lung tissues are frequently exposed to a hyperoxia environment, which leads to oxidative stress injuries. Hydrogen sulfide (H(2)S) is widely implicated in physiological and pathological processes and its antioxidant effect has attracted much attention. Therefore, in this study, we used hydrogen peroxide (H(2)O(2)) as an oxidative damage model to investigate the protective mechanism of H(2)S in lung injury. Cell death induced by H(2)O(2) treatment could be significantly attenuated by the pre-treatment of H(2)S, resulting in a decrease in the Bax/Bcl-2 ratio and the inhibition of caspase-3 activity in human lung epithelial cell line A549 cells. Additionally, the results showed that H(2)S decreased reactive oxygen species (ROS), as well as neutralized the damaging effects of H(2)O(2) in mitochondria energy-producing and cell metabolism. Pre-treatment of H(2)S also decreased H(2)O(2)-induced suppression of endogenous H(2)S production enzymes, cystathionine-beta-synthase (CBS), cystathionine-gamma-lyase (CSE), and 3-mercapto-pyruvate sulfurtransferase (MPST). Furthermore, the administration of H(2)S attenuated [Ca(2+)] overload and endoplasmic reticulum (ER) stress through the mitogen-activated protein kinase (MAPK) signaling pathway. Therefore, H(2)S might be a potential therapeutic agent for reducing ROS and ER stress-associated apoptosis against H(2)O(2)-induced lung injury.