Hydrogen Gas Protects Against Heart Inflammation in Mice Study
- Authors
- Shuang Pan, Mengshu Yu, Bowei Fan, Bin Wang, Xinrui Yang, Jiawen Zhang, Xiaoqi Liu, Xiaojian Hong, Wei Yang
- Journal
- Clinical Immunology
- Year
- 2025
- DOI
- 10.1016/j.clim.2025.110577
- Study Type
- Mouse
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- China
- Health Condition
- Autoimmune Myocarditis
- Body System
- Cardiovascular
TL;DR
Inhaling hydrogen gas helped reduce heart inflammation and improve function in a mouse model of autoimmune myocarditis.
Key Finding
Hydrogen gas inhalation reduced heart inflammation and improved cardiac function in mice with autoimmune myocarditis by blocking a specific cell death pathway (necroptosis) linked to tumor necrosis factor signaling.
Summary
This study tested whether hydrogen gas could help treat autoimmune myocarditis (inflammation of the heart muscle caused by the immune system attacking itself) in mice. Mice with artificially induced heart inflammation were given hydrogen gas to breathe twice daily for 21 days. Hydrogen treatment reduced immune cell activity, lowered inflammatory chemicals in the blood, improved heart function, and decreased markers of a type of cell death called necroptosis that was occurring in damaged heart tissue.
Practical Takeaway
While this early-stage mouse study suggests hydrogen may have anti-inflammatory effects on heart disease, it is not yet evidence that hydrogen would work in humans with myocarditis. Much more research, including human clinical trials, would be needed before hydrogen could be considered a treatment option. This remains a laboratory finding with no established safety or efficacy in people.
Abstract
Autoimmune myocarditis refers to the inflammation of myocardial tissue caused by innate and adaptive immune responses, characterized by elevated levels of tumour necrosis factor-α (TNF-α), a classic pro-inflammatory factor. Although hydrogen exhibits anti-inflammatory and antioxidant properties, its therapeutic effects in autoimmune myocarditis have not been evaluated. Therefore, the present study aimed to explore whether hydrogen can alleviate autoimmune myocarditis via TNF-α. An experimental autoimmune myocarditis (EAM) model was established in BALB/c mice via subcutaneous injection of pig-derived myocardial myoglobin emulsified with complete Freund's adjuvant. The treatment group received 2 % hydrogen inhalation twice a day (3 h each time) for 21 days. CD4+ T cell expression was higher in the EAM group than in the Control group, and this increase was attenuated following treatment with hydrogen. Additionally, the levels of TNF-α and related inflammatory factors were substantially higher in the EAM group than in the Control group, and these changes were reversed following hydrogen treatment. Echocardiography assessments demonstrated a significant improvement in heart function following treatment with hydrogen compared to that in the EAM group. Pathological results revealed significant inflammatory cell infiltration and fibrosis in the hearts of the untreated EAM group. Tissue immunofluorescence and protein immunoblotting indicated elevated necroptosis markers in the EAM group, which were downregulated after treatment with hydrogen. This study demonstrates that hydrogen effectively ameliorated autoimmune myocarditis by modulating necroptosis via the TNF/TNFR1 signalling pathway, making it a promising novel therapeutic strategy for myocarditis.