General Research
Model: mouse
Hydrogen gas alleviates lipopolysaccharide-induced acute lung injury and inflammatory response in mice
Simplified Version Available
How Hydrogen Gas May Help Reduce Lung Inflammation
A recent study found that hydrogen gas reduced lung inflammation in mice with acute lung injury. This breakthrough could lead to new treatments for conditions like acute respiratory distress syndrome. Hydrogen gas therapy may also have benefits for other inflammatory conditions, such as liver damage and chronic fatigue syndrome.
Read Simplified ArticleAbstract
Publish Year 2022 Country China Rank Positive Journal Journal of Inflammation Primary Topic Lung Secondary TopicSepsis Model Mouse Tertiary TopicLung Injury Vehicle Gas pH N/A Application Inhalation Comparison Complement Oxygen
Background
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.
Methods
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).
Results
Conclusion: Hydrogen gas alleviates lipopolysaccharide-induced acute lung injury and inflammatory response most probably through the TLR4-NF-κB pathway.