Hydrogen Gas Inhalation Protects Against Lung Disease in Rats
- Authors
- Chenting Zhang, Yue Xing, Xuefen Wu, Qian Jiang, Xiaoyun Luo, Wei He, Shiyun Liu, Wenju Lu, Jian Wang
- Journal
- Respiratory Research
- Year
- 2024
- DOI
- 10.1186/s12931-024-02906-y
- Study Type
- Rat
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- China
- Health Condition
- Pulmonary Veno-Occlusive Disease
- Body System
- Respiratory
TL;DR
Breathing in hydrogen gas can help prevent and treat a severe lung disease called pulmonary veno-occlusive disease (PVOD) in rats.
Key Finding
Inhaled hydrogen gas prevented and reversed pulmonary veno-occlusive disease in rats, improving heart function and reducing lung damage through antioxidant and anti-inflammatory mechanisms.
Summary
Researchers tested whether inhaled hydrogen gas could prevent or treat a serious lung disease called pulmonary veno-occlusive disease (PVOD) in rats. They induced PVOD using a drug called mitomycin C, then gave some rats hydrogen gas to breathe either at the same time as the drug or two weeks after. Hydrogen gas treatment improved heart function, reduced lung damage, and lowered markers of oxidative stress (cellular damage from harmful molecules) and inflammation in the rats' lungs and blood.
Practical Takeaway
This rat study suggests hydrogen gas inhalation may have potential as a treatment for a severe form of pulmonary hypertension, but this is very early-stage research. The findings cannot yet be applied to humans, and much more research would be needed before hydrogen inhalation could be considered a viable therapy for this condition in people.
Abstract
Background: As a subtype of pulmonary hypertension (PH), pulmonary veno-occlusive disease (PVOD) is devastating and life-threatening disease without effective therapy. Hydrogen has been reported to exhibits antioxidant and anti-inflammatory effects in a rat model induced by monocrotaline of PH. In this study, we investigated the effects of inhaled hydrogen gas on the prevention and treatment of PVOD induced by mitomycin C (MMC) in rats. Methods: PVOD was induced in female Sprague-Dawley rats through intraperitoneal injection of MMC at a concentration of 3 mg·kg- 1·wk- 1 for 2 weeks. Inhalation of hydrogen gas (H2) was administered through a designed rat cage concurrently or two weeks after MMC administration. The severity of PVOD was assessed by using hemodynamic measurements and histological analysis. The expression levels of general control nonderepressible 2 (GCN2), nuclear factor erythroid 2-related factor-2 (Nrf2), heme oxygenase-1 (HO-1) and endothelial-to-mesenchymal transition (EndoMT) related proteins in lung tissue were measured. Levels of lipid peroxidation pro-inflammatory cytokines in serum were determined. Results: Inhaled H2 improved hemodynamics and right heart function, reversed right ventricular hypertrophy, and prevented pulmonary vessel reconstitution in both prevention and treatment approaches. It decreased malondialdehyde (MDA) levels in the serum and the expression of NADPH oxidase 1 (NOX-1) in lung tissue. It regulated Nrf2/HO-1 signaling pathway and anti-inflammatory factor GCN2 in lung tissue, accompanied by a decrease in macrophages and pro-inflammatory cytokines. Our data suggested that H2 inhalation effectively countered EndoMT induced by MMC, as evidenced by the detection of endothelial markers (e.g., VE-cadherin and CD31) and mesenchymal markers (e.g., vimentin and fibronectin). Further research revealed that H2 preserved p-Smad3 and induced p-Smad1/5/9. Conclusion: Inhalation of H2 effectively inhibits the pathogenesis of PVOD induced by MMC in rats. This inhibitory effect may be attributed to the antioxidant and anti-inflammatory properties of H2.