Antioxidant Properties of Hydrogen Gas Attenuates Oxidative Stress in Airway Epithelial Cells

Abstract

Oxidative stress plays a crucial role in the development of airway diseases. Recently, hydrogen (H2) gas has been explored for its antioxidant properties. This study investigated the role of H2 gas in oxidative stress-induced alveolar and bronchial airway injury, where A549 and NCI-H292 cells were stimulated with hydrogen peroxide (H2O2) and lipopolysaccharide (LPS) in vitro. Results show that time-dependent administration of 2% H2 gas recovered the cells from oxidative stress. Various indicators including reactive oxygen species (ROS), nitric oxide (NO), antioxidant enzymes (catalase, glutathione peroxidase), intracellular calcium, and mitogen-activated protein kinase (MAPK) signaling pathway were examined to analyze the redox profile. The viability of A549 and NCI-H292 cells and the activity of antioxidant enzymes were reduced following induction by H2O2 and LPS but were later recovered using H2 gas. Additionally, the levels of oxidative stress markers, including ROS and NO, were elevated upon induction but were attenuated after treatment with H2 gas. Furthermore, H2 gas suppressed oxidative stress-induced MAPK activation and maintained calcium homeostasis. This study suggests that H2 gas can rescue airway epithelial cells from H2O2 and LPS-induced oxidative stress and may be a potential intervention for airway diseases.

Study details

Article type

Original Research

Disease / injury model

Oxidative stress-induced airway injury (in vitro, using H2O2 and LPS)

Dose comparison

The study compared the effects of 30 min and 60 min exposures to 2% H2 gas, showing a time-dependent effect with 60 min being more effective.

Dose-dependent effect

Yes

Outcome

Positive

Findings

Hydrogen gas (2%) significantly attenuated oxidative stress in airway epithelial cells (A549 and NCI-H292) induced by H2O2 and LPS, restoring cell viability, reducing ROS and NO, enhancing antioxidant enzyme activity, maintaining calcium homeostasis, and suppressing MAPK pathway activation in a time-dependent manner.