Hydrogen Inhalation Slows COPD-Like Lung Disease in Smoke-Exposed Rats
- Authors
- Xiaoyu Liu, Cuiqing Ma, Xiaoyu Wang, Wenjing Wang, Zhu Li, Xiansheng Wang, Pengyu Wang, Wuzhuang Sun, Baojian Xue
- Journal
- International Journal of Chronic Obstructive Pulmonary Disease
- Year
- 2017
- DOI
- 10.2147/COPD.S124547
- Study Type
- Rat
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- China
- Health Condition
- Chronic Obstructive Pulmonary Disease (COPD)
- Body System
- Respiratory
TL;DR
Breathing in hydrogen gas can help reduce lung damage and improve lung and heart functions in rats with a disease similar to human COPD.
Key Finding
Hydrogen gas inhalation reduced inflammatory markers and slowed lung disease progression in rats with cigarette smoke-induced COPD-like disease, with higher hydrogen concentrations showing greater benefit.
Summary
Researchers exposed rats to cigarette smoke to create a model of COPD (a lung disease that makes breathing difficult), then gave some rats different concentrations of hydrogen gas to breathe. Rats that inhaled hydrogen showed less lung damage, better lung function, and reduced markers of inflammation (the body's harmful response to injury) compared to rats that didn't receive hydrogen. Higher concentrations of hydrogen (22% and 41.6%) worked better than lower concentrations (2%).
Practical Takeaway
This rat study suggests hydrogen gas may help slow COPD development, but it's important to note this is animal research only—human studies are needed before any conclusions can be drawn about hydrogen's effects on people with COPD. The study also tested inhaled hydrogen gas rather than hydrogen water, so the findings may not directly apply to hydrogen water consumption.
Abstract
Background: Chronic obstructive pulmonary disease (COPD) is a progressive pulmonary disease caused by harmful gases or particles. Recent studies have shown that 2% hydrogen or hydrogen water is effective in the treatment and prevention of a variety of diseases. This study investigated the beneficial effects and the possible mechanisms of different hydrogen concentrations on COPD. Methods: A rat COPD model was established through smoke exposure methods, and inhalation of different concentrations of hydrogen was used as the intervention. The daily condition of rats and the weight changes were observed; lung function and right ventricular hypertrophy index were assessed. Also, white blood cells were assessed in bronchoalveolar lavage fluid. Pathologic changes in the lung tissue were analyzed using light microscopy and electron microscopy; cardiovascular structure and pulmonary arterial pressure changes in rats were observed using ultrasonography. Tumor necrosis factor alpha, interleukin (IL)-6, IL-17, IL-23, matrix metalloproteinase-12, tissue inhibitor of metalloproteinase-1, caspase-3, caspase-8 protein, and mRNA levels in the lung tissue were determined using immunohistochemistry, Western blot, and real-time polymerase chain reaction. Results: The results showed that hydrogen inhalation significantly reduced the number of inflammatory cells in the bronchoalveolar lavage fluid, and the mRNA and protein expression levels of tumor necrosis factor alpha, IL-6, IL-17, IL-23, matrix metalloproteinase-12, caspase-3, and caspase-8, but increased the tissue inhibitor of metalloproteinase-1 expression. Furthermore, hydrogen inhalation ameliorated lung pathology, lung function, and cardiovascular function and reduced the right ventricular hypertrophy index. Inhalation of 22% and 41.6% hydrogen showed better outcome than inhalation of 2% hydrogen. Conclusion: These results suggest that hydrogen inhalation slows the development of COPD-like lung disease in a cigarette smoke-induced rat model. Higher concentrations of hydrogen may represent a more effective way for the rat model.