Hydrogen Gas Protects Lungs from Infection-Induced Injury in Mice
- Authors
- Hongling Yin, Yajing Feng, Yi Duan, Shaolin Ma, Zhongliang Guo, Youzhen Wei
- Journal
- Journal of Inflammation
- Year
- 2022
- DOI
- 10.1186/s12950-022-00314-x
- Study Type
- Mouse
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- China
- Health Condition
- Acute Lung Injury
- Body System
- Respiratory
TL;DR
Breathing in hydrogen gas can help mice recover from a type of acute lung injury caused by bacterial toxins, likely by reducing inflammation and oxidative stress.
Key Finding
Hydrogen gas inhalation increased survival rates to 80% in mice with acute lung injury and reduced inflammatory markers and oxidative stress in the lungs.
Summary
Researchers tested whether hydrogen gas could protect mice from acute lung injury (severe lung damage caused by a bacterial toxin called lipopolysaccharide). Mice that received hydrogen gas had better survival rates (80%), less lung damage, and lower levels of inflammatory chemicals and harmful molecules in their lungs compared to mice that didn't receive hydrogen. The study suggests hydrogen may work by blocking a specific pathway in immune cells that normally triggers inflammation.
Practical Takeaway
This early evidence from mice suggests hydrogen gas may have protective effects against severe lung injury, but this is animal research only and does not yet demonstrate safety or effectiveness in humans. Much more research, including human studies, would be needed before hydrogen could be considered a treatment for lung conditions.
Abstract
Background: Chronic inflammation and oxidant/antioxidant imbalance are two main pathological features associated with lipopolysaccharide (LPS)-induced acute lung injury (ALI). The following study investigated the protective role of hydrogen (H2), a gaseous molecule without known toxicity, in LPS-induced lung injury in mice and explored its potential molecular mechanisms. Methods: Mice were randomly divided into three groups: H2 control group, LPS group, and LPS + H2 group. The mice were euthanized at the indicated time points, and the specimens were collected. The 72 h survival rates, cytokines contents, pathological changes, expression of Toll-like receptor 4 (TLR4), and oxidative stress indicators were analyzed. Moreover, under different culture conditions, RAW 264.7 mouse macrophages were used to investigate the potential molecular mechanisms of H2 in vitro. Cells were divided into the following groups: PBS group, LPS group, and LPS + H2 group. The cell viability, intracellular ROS, cytokines, and expression of TLR4 and nuclear factor kappa-B (NF-κB) were observed. Results: Hydrogen inhalation increased the survival rate to 80%, reduced LPS-induced lung damage, and decreased inflammatory cytokine release in LPS mice. Besides, H2 showed remarked anti-oxidative activity to reduce the MDA and NO contents in the lung. In vitro data further indicated that H2 down-regulates the levels of ROS, NO, TNF-α, IL-6, and IL-1β in LPS-stimulated macrophages and inhibits the expression of TLR4 and the activation of nuclear factor kappa-B (NF-κB). Conclusion: Hydrogen gas alleviates lipopolysaccharide-induced acute lung injury and inflammatory response most probably through the TLR4-NF-κB pathway.