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

In-Soo You,Ailyn Fadriquela,So-Yeon Lee,Kyu-Jae Lee,Jaeyong Sung,Johny Bajgai,Md Habibur Rahman,Subham Sharma,Cheol-Su Kim,Hwang-Un Kwon,Thuy Trinh Thi

doi:10.3390/molecules26216375

In-Soo You, Ailyn Fadriquela + Show 9 more

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https://doi.org/10.3390/molecules26216375

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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.

Highlights

Oxidative stress indicates an imbalance of reactive oxygen species (ROS) and antioxidants, leading to disturbance of redox homeostasis and cellular damage
Our results showed that H2 O2 induction reduced the cell viability in the A549 cell line compared with the control (p < 0.001), but this effect was significantly increased after treatment with H2 gas
In A549 cells, the results showed that upon H2 O2 induction, levels of the mitogen-activated protein kinase (MAPK) pathway proteins increased significantly compared with controls (p-Jun N-terminal kinase (JNK) (p < 0.001), p-extracellular signal-regulated kinase (ERK) (p < 0.01), and p-p38 (p < 0.001))

Summary

Introduction

Oxidative stress indicates an imbalance of reactive oxygen species (ROS) and antioxidants, leading to disturbance of redox homeostasis and cellular damage. Pulmonary epithelial cells are always exposed to varieties of stress inducers, and are the main target of ROS. Studies have shown that hydrogen peroxide (H2 O2 ) and lipopolysaccharide (LPS) can be used as a strong oxidizing agent to induce oxidative stress and inflammation. With exposure to these compounds, alveolar and bronchial epithelial cell line such as A549 and NCI-H292 respond sensitively in lung injury due to oxidative stress [8,9,10]. Another study revealed that LPS activates endoplasmic reticulum stress and induces apoptosis in human airway NCI-H292 cells, resulting in acute lung injury [10]

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