Hydrogen Gas Reduces Asthma Inflammation in Mice Study
- Authors
- Wenjing He, Md Habibur Rahman, Johny Bajgal, Sofian Abdul-Nasir, Chaodeng Mo, Hui Ma, Seong Hoon Goh, Kim Bomi, Hyeran Jung, Cheol-Su Kim, Lee Hyungdon, Kyu-Jae Lee
- Journal
- Antioxidants
- Year
- 2024
- DOI
- 10.3390/antiox13111328
- Study Type
- Mouse
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- South Korea
- Health Condition
- Allergic Asthma
- Body System
- Respiratory
TL;DR
Breathing in hydrogen gas reduced signs of asthma-like lung inflammation in mice.
Key Finding
In asthmatic mice, inhaled hydrogen gas significantly reduced inflammatory cell buildup, decreased pro-inflammatory immune chemicals, and boosted the activity of antioxidant enzymes compared to untreated asthmatic mice.
Summary
Researchers tested whether inhaled hydrogen gas could reduce airway inflammation in mice with asthma-like symptoms caused by a protein called ovalbumin. They found that mice breathing 3% hydrogen gas showed reduced inflammation, lower levels of immune chemicals that trigger allergic responses, and increased activity of the body's natural antioxidant defenses (molecules that protect cells from damage).
Practical Takeaway
This early evidence from mouse studies suggests hydrogen gas inhalation may help reduce airway inflammation and oxidative stress in asthma. However, this is a single animal study with unknown duration and sample size details; human clinical trials would be needed to determine whether these effects translate to people with asthma.
Abstract
Airway inflammatory diseases, such as asthma, are a global public health concern owing to their chronic inflammatory effects on the respiratory mucosa. Molecular hydrogen (H2) has recently been recognized for its antioxidant and anti-inflammatory properties. In this study, we examined the therapeutic potential of H2 in airway inflammation using an ovalbumin (OVA)-induced BALB/c mouse model of allergic asthma. Female BALB/c mice were sensitized and challenged with OVA to induce airway inflammation, and 30 mice were randomly divided into five groups: NT (non-treatment), HTC (3% H2 treatment only), NC (negative control, OVA only), PC (positive control, OVA + intranasal 1 mg/mL salbutamol 50 μL), and HT (H2 treatment, OVA + inhaled 3% H2). Various inflammatory and oxidative stress (OS)-induced markers such as white blood cells (WBCs) and their differential counts, lung histology, cytokine levels such as interleukin (IL)-4, (IL)-5, (IL)-13, interferon-gamma (IFN-γ), tumor necrosis factor-alpha (TNF-α), granulocyte-macrophage colony-stimulating factor (GM-CSF), (IL)-10, reactive oxygen species (ROS), nitric oxide (NO), glutathione peroxidase (GPx), and catalase (CAT), and total immunoglobulin E (IgE) levels were investigated. Our results showed that inhaled H2 significantly reduced inflammatory cell infiltration, OS markers, and pro-inflammatory cytokine expression while upregulating antioxidant enzyme activity. Furthermore, H2 also significantly decreased serum IgE levels, a marker of allergic inflammation. Collectively, our findings suggest that H2 inhalation is a promising treatment option for airway inflammation, offering a novel approach with potential clinical applications.