Hydrogen sulfide attenuates hydrogen peroxide-induced injury in human lung epithelial A549 cells

Abstract

Lung tissues are frequently exposed to a hyperoxia environment, which leads to oxidative stress injuries. Hydrogen sulfide (H2 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 (H2 O2) as an oxidative damage model to investigate the protective mechanism of H2 S in lung injury. Cell death induced by H2 O2 treatment could be significantly attenuated by the pre-treatment of H2 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 H2 S decreased reactive oxygen species (ROS), as well as neutralized the damaging effects of H2 O2 in mitochondria energy-producing and cell metabolism. Pre-treatment of H2 S also decreased H2 O2-induced suppression of endogenous H2 S production enzymes, cystathionine-beta-synthase (CBS), cystathionine-gamma-lyase (CSE), and 3-mercapto-pyruvate sulfurtransferase (MPST). Furthermore, the administration of H2 S attenuated [Ca2+] overload and endoplasmic reticulum (ER) stress through the mitogen-activated protein kinase (MAPK) signaling pathway. Therefore, H2 S might be a potential therapeutic agent for reducing ROS and ER stress-associated apoptosis against H2 O2-induced lung injury.