| Summary: | Lung tissues are frequently exposed to a hyperoxia environment, which leads to oxidative stress injuries. Hydrogen sulfide (H<sub>2</sub>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<sub>2</sub>O<sub>2</sub>) as an oxidative damage model to investigate the protective mechanism of H<sub>2</sub>S in lung injury. Cell death induced by H<sub>2</sub>O<sub>2</sub> treatment could be significantly attenuated by the pre-treatment of H<sub>2</sub>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<sub>2</sub>S decreased reactive oxygen species (ROS), as well as neutralized the damaging effects of H<sub>2</sub>O<sub>2</sub> in mitochondria energy-producing and cell metabolism. Pre-treatment of H<sub>2</sub>S also decreased H<sub>2</sub>O<sub>2</sub>-induced suppression of endogenous H<sub>2</sub>S production enzymes, cystathionine-beta-synthase (CBS), cystathionine-gamma-lyase (CSE), and 3-mercapto-pyruvate sulfurtransferase (MPST). Furthermore, the administration of H<sub>2</sub>S attenuated [Ca<sup>2+</sup>] overload and endoplasmic reticulum (ER) stress through the mitogen-activated protein kinase (MAPK) signaling pathway. Therefore, H<sub>2</sub>S might be a potential therapeutic agent for reducing ROS and ER stress-associated apoptosis against H<sub>2</sub>O<sub>2</sub>-induced lung injury.
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