High-Dose Hydrogen Gas Protects Lungs from Sepsis Damage in Mice
- Authors
- Ruiqiang Sun, Nan Zhao, Yuzun Wang, Yanchao Su, Jiayan Zhang, Yaoqi Wang, Yonghao Yu, Guolin Wang, Zhen Wang, Keliang Xie
- Journal
- International Immunopharmacology
- Year
- 2021
- DOI
- 10.1016/j.intimp.2021.108198
- Study Type
- Mouse
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- China
- Health Condition
- Sepsis
- Body System
- Respiratory
TL;DR
Breathing in high concentrations of hydrogen gas can significantly reduce lung damage caused by a bacterial toxin, likely by activating a protective cellular pathway and reducing inflammation and cell death.
Key Finding
High-concentration hydrogen gas (67%) significantly reduced lung injury, inflammation, and cell death in mice exposed to bacterial toxin, but only when the Nrf2 cellular defense pathway was functional.
Summary
Researchers exposed mice to a bacterial toxin (lipopolysaccharide) to create lung injury similar to what happens in severe infections. They then treated some mice by having them breathe high-concentration hydrogen gas (67%) and found it reduced lung damage, inflammation, and cell death. The protective effect appeared to work through a cellular defense mechanism called the Nrf2 pathway, since mice genetically unable to use this pathway did not benefit from the hydrogen treatment.
Practical Takeaway
This mouse study suggests hydrogen gas may help protect lungs during severe infections by activating natural cellular defense mechanisms. However, this is early-stage animal research—human studies would be needed to determine if these results apply to people, and the very high hydrogen concentration used (67%) differs from typical hydrogen water products.
Abstract
Background and aims: The lung is the first organ to fail in sepsis. Our previous studies have proven that 2% molecular hydrogen (H2) inhalation remain a protective effect on a septic animal model via its anti-inflammatory and anti-apoptosis properties. This current research aims to observe the therapeutic effect of high concentration hydrogen (67%, HCH) on lipopolysaccharide (LPS) induced acute lung injury (ALI), and further investgate the role of Nrf2 signaling pathway. Methods: ALI model was induced by LPS areosol inhalation. HCH were treated for 1 h at 1 and 6 h after modelling. Lung tissues and bronchoalveolar lavage fluid (BALF) were collected 4 and 24 h after the exposure of LPS. The histological scores, wet/dry weight ratios, myeloperoxidase (MPO) activity, protein content and cytokine levels in BALF, apoptosis condition of lung cells, expression of Nrf2 and NF-κB were assessed in both wild type and Nrf2-knockout mice. Results: HCH Inhalation significantly alleviated LPS-induced pathological alterations of lung, and reduced the protein concentration, the wet/dry weight ratio, and the MPO activity of lung tissue. HCH Inhalation improved LPS-induced increasement in caspase-3 activity and the number of TUNEL-positive cells. HCH inhalation attenuated the LPS induced increased total cell content and polymorphonuclear granulocyte content, and pro-inflammatory cytokines, Nrf2 and NF-κB expression. HCH could not produce protective effct in Nrf2-knockout mice. Conclusion: HCH can effectively alleviate LPS-induced ALI, which may be related to activation of Nrf2 signaling pathway and inhibition of inflammatory response and cell apoptosis mediated by NF-κB.