Hydrogen Therapy Protects Lung Barriers in Severe Breathing Disorder
- Authors
- Yun Long, Yang Ang, Wei Chen, Yujie Wang, Min Shi, Fan Hu, Qingqing Zhou, Yadan Shi, Baokui Ge, Yigen Peng, Yu Wanyou, Hongguang Bao, Qian Li, Manlin Duan, Ju Gao
- Journal
- Free Radical Biology and Medicine
- Year
- 2024
- DOI
- 10.1016/j.freeradbiomed.2024.03.022
- Study Type
- Mouse
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- China
- Health Condition
- Acute Respiratory Distress Syndrome (ARDS)
- Body System
- Respiratory
TL;DR
Hydrogen gas treatment helps protect the lungs from severe damage in a condition called acute respiratory distress syndrome (ARDS) by preventing harmful changes in the cell's energy factories (mitochondria).
Key Finding
Hydrogen gas prevented harmful mitochondrial changes in lung cells of ARDS mice by activating a protective protein called Trx1, which reduced cell damage and helped restore the lung's protective barrier.
Summary
This study tested whether hydrogen gas could help repair lung damage in mice with acute respiratory distress syndrome (ARDS), a severe breathing condition. Researchers found that hydrogen reduced damage to the protective barrier lining the lungs by preventing abnormal changes in mitochondria (the energy-producing parts of cells), which was linked to reduced cell death and restored lung function.
Practical Takeaway
While this mouse study suggests hydrogen may have potential for treating severe lung injury through a specific cellular mechanism, it is a preliminary laboratory finding that has not been tested in humans. Much more research, including human clinical trials, would be needed before hydrogen could be considered a treatment for ARDS.
Abstract
Acute respiratory distress syndrome (ARDS) is an acute and severe clinical complication lacking effective therapeutic interventions. The disruption of the lung epithelial barrier plays a crucial role in ARDS pathogenesis. Recent studies have proposed the involvement of abnormal mitochondrial dynamics mediated by dynamin-related protein 1 (Drp1) in the mechanism of impaired epithelial barrier in ARDS. Hydrogen is an anti-oxidative stress molecule that regulates mitochondrial function via multiple signaling pathways. Our previous study confirmed that hydrogen modulated oxidative stress and attenuated acute pulmonary edema in ARDS by upregulating thioredoxin 1 (Trx1) expression, but the exact mechanism remains unclear. This study aimed to investigate the effects of hydrogen on mitochondrial dynamics both in vivo and in vitro. Our study revealed that hydrogen inhibited lipopolysaccharide (LPS)-induced phosphorylation of Drp1 (at Ser616), suppressed Drp1-mediated mitochondrial fission, alleviated epithelial tight junction damage and cell apoptosis, and improved the integrity of the epithelial barrier. This process was associated with the upregulation of Trx1 in lung epithelial tissues of ARDS mice by hydrogen. In addition, hydrogen treatment reduced the production of reactive oxygen species in LPS-induced airway epithelial cells (AECs) and increased the mitochondrial membrane potential, indicating that the mitochondrial dysfunction was restored. Then, the expression of tight junction proteins occludin and zonula occludens 1 was upregulated, and apoptosis in AECs was alleviated. Remarkably, the protective effects of hydrogen on the mitochondrial and epithelial barrier were eliminated after applying the Trx1 inhibitor PX-12. The results showed that hydrogen significantly inhibited the cell apoptosis and the disruption of epithelial tight junctions, maintaining the integrity of the epithelial barrier in mice of ARDS. This might be related to the inhibition of Drp1-mediated mitochondrial fission through the Trx1 pathway. The findings of this study provided a new theoretical basis for the application of hydrogen in the clinical treatment of ARDS.