Hydrogen Gas Protects Heart Function During Life-Threatening Infections
- Authors
- Shuqi Meng, Jianfeng Liu, Yanhua Luo, Yan Fan, Zhiwei Wang, Yu Song, Shuaijie Pei, Xiaofan Huang, Lina Zhao, Keliang Xie
- Journal
- British Journal of Pharmacology
- Year
- 2025
- DOI
- 10.1111/bph.70132
- Study Type
- Mouse
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- China
- Health Condition
- Sepsis-Induced Cardiomyopathy
- Body System
- Cardiovascular
TL;DR
Breathing 2% hydrogen gas helped protect the heart in septic mice by reducing stress in heart cells and lowering inflammation, cell death, and overactive cleanup processes.
Key Finding
Inhaling 2% hydrogen gas improved survival rates and cardiac function in mice with sepsis-induced heart damage, with the protective effect specifically linked to reducing Golgi stress and its downstream effects on inflammation and cell death.
Summary
Researchers studied whether inhaling hydrogen gas could protect the heart during sepsis (a life-threatening infection response). Using mice with induced sepsis, they found that 2% hydrogen gas improved survival rates, restored heart function, and reduced heart damage. The protective effect appeared to work by reducing stress in a cellular structure called the Golgi apparatus, which then decreased harmful processes like inflammation and cell death in heart tissue.
Practical Takeaway
This early research in mice suggests hydrogen gas may have heart-protective potential during severe infections, but it is a preliminary finding that has not been tested in humans. Much more research, including human clinical trials, would be needed before hydrogen therapy could be considered a treatment for sepsis-related heart problems.
Abstract
Background and purpose: Sepsis-induced cardiomyopathy (SIC) is the primary cause of mortality among people with sepsis. Hydrogen (H2) has a cardioprotective effect in SIC; however, its specific mechanism remains unclear. We thus explored whether 2% H2 treatment mitigates SIC through inhibiting Golgi stress and investigated the specific molecular pathways underlying this protective effect. Experimental approach: Male C57BL/6J mice were subjected to caecal ligation and puncture (CLP) to establish the sepsis model. We measured the 7-day survival rates, cardiac function, myocardial damage enzymes, and myocardial haematoxylin and eosin (H&E) staining to evaluate the 2% H2 on SIC. Immunofluorescence and electron microscopy were used to observe the morphological changes in the Golgi apparatus (GA). Additionally, a Golgi stress-specific agonist (Brefeldin A) was administered to observe whether the therapeutic effect of inhalation of 2% H2 could be reversed. Finally, we examined the indicators of autophagy, inflammation and apoptosis to explore how 2% H2 affects the downstream mechanisms of Golgi stress. Key results: The 7-day survival rate of mice decreased, cardiac function deteriorated and myocardial damage enzymes increased after CLP. Golgi stress was associated with elevated levels of autophagy, inflammation and apoptosis levels. These levels decreased following the treatment with 2% H₂ inhalation. However, administration of the Golgi stress-specific agonist Brefeldin A reversed the therapeutic effects of 2% H₂. Conclusions and implications: We found that 2% H2 exerted a protective effect on SIC, and we determined that its mechanism is related to improving Golgi stress-mediated autophagy, inflammation and apoptosis. Keywords: Golgi stress; apoptosis; autophagy; hydrogen; inflammation; sepsis‐induced cardiomyopathy.