Hydrogen Gas Protects Brain Function During Sepsis in Mice Study
- Authors
- Yan Cui, Shuqi Meng, Nannan Zhang, Jingya Liu, Lina Zheng, Wanjie Ma, Yu Song, Zhiwei Wang, Yuehao Shen, Jianfeng Liu, Keliang Xie
- Journal
- CNS Neuroscience & Therapeutics
- Year
- 2024
- DOI
- 10.1111/cns.70021
- Study Type
- Mouse
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- China
- Health Condition
- Sepsis
- Body System
- Nervous System
TL;DR
Breathing in a high concentration of hydrogen gas helps mice with sepsis-related brain damage survive longer and remember better by improving the health of their brain cell powerhouses.
Key Finding
Mice with sepsis that inhaled 67% hydrogen gas showed improved survival rates and better cognitive function, with evidence of restored mitochondrial health and reduced brain inflammation.
Summary
This study tested whether inhaling high-concentration hydrogen gas (67%) could protect the brains of mice with sepsis (a severe infection). Researchers found that mice given hydrogen inhalation had better survival rates, improved memory function, and showed signs of healthier brain cells. The protective effect appeared to work by improving how mitochondria (the energy-producing parts of cells) function and reducing harmful inflammation and oxidative stress in the brain.
Practical Takeaway
This is an early-stage animal study suggesting hydrogen gas inhalation may protect brain function during severe infections by improving cellular energy production. However, this research was conducted only in mice, and much more work—including human studies—would be needed before any conclusions could be drawn about hydrogen's usefulness for sepsis patients.
Abstract
Background: Sepsis-associated encephalopathy (SAE) is a neuronal injury with poor prognosis. Mitochondrial dysfunction is critical in SAE development, and hydrogen gas (H2) has a protective effect on septic mice. This study aimed to investigate the effect of high concentration (67%) of H2 on SAE and whether it is related to mitochondrial biogenesis and mitochondrial dynamics. Methods: A mouse sepsis model was induced by cecal ligation and puncture. The mice inhalated 67% H2 for 1 h at 1 and 6 h post-surgery, respectively. The 7-day survival rate was recorded. Cognitive function was assessed using the Y-maze test and Morris water maze test. Serum inflammatory factors, antioxidant enzymes, as well as mitochondrial function indexes including mitochondrial membrane potential (MMP) and ATP in the hippocampal tissue were evaluated 24 h after surgery. Mitochondrial dynamic proteins (DRP1 and MFN2) and biosynthetic proteins (PGC-1α, NRF2, and TFAM) in the hippocampal tissue were detected. Moreover, the morphology of mitochondria was observed by transmission electron microscopy. Results: Inhalation of 67% H2 improved the 7-day survival rates and recognition memory function of septic mice, alleviated brain antioxidant enzyme activity (SOD and CAT), and reduced serum proinflammatory cytokine levels. H2 inhalation also enhanced the expression of MFN2 and mitochondrial biogenesis-related factors (PGC-1α, NRF2, and TFAM) and decreased the expression of fission protein (DRP1), leading to improvement in mitochondrial function, as evidenced by MMP and ATP levels. Conclusions: Inhalation of high concentration (67%) of H2 in septic mice improved the survival rate and reduced neuronal injury. Its mechanism might be mediated by enhancing mitochondrial biogenesis and mitochondrial dynamics.