Hydrogen Gas Protects Brain Function During Sepsis in Mice
- Authors
- Lingling Liu, Keliang Xie, Hongguang Chen, Xiaoqing Dong, Yuan Li, Yong-Hao Yu
- Journal
- Chinese Medical Journal
- Year
- 2014
- DOI
- 10.3760/cma.j.issn.0376-2491.2014.40.015
- Study Type
- Mouse
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- China
- Health Condition
- Sepsis-Associated Encephalopathy
- Body System
- Nervous System
TL;DR
Breathing in hydrogen gas helps improve brain function and reduce brain damage in mice with a condition similar to brain inflammation caused by severe infection.
Key Finding
Inhaled hydrogen gas significantly improved cognitive function and reduced brain cell damage in mice with sepsis-associated encephalopathy, with improvements linked to increased antioxidant enzyme activity and reduced oxidative stress markers.
Summary
Researchers tested whether inhaled hydrogen gas could protect the brains of mice with sepsis-associated encephalopathy (a type of brain dysfunction that occurs during severe infection). Mice with sepsis that received hydrogen gas inhalation showed improved memory and learning abilities, less brain cell damage, and better antioxidant enzyme activity (protective proteins that fight cellular damage) compared to mice with sepsis that didn't receive hydrogen gas.
Practical Takeaway
This early evidence from mouse studies suggests hydrogen gas inhalation may help protect brain function during severe infection, but these results cannot yet be applied to humans. Further research in larger animal models and eventually clinical trials would be needed to determine if this approach could benefit sepsis patients.
Abstract
To evaluate protective effects of inhaled hydrogen gas (H2) on cognitive function in a murine model of sepsis-associated encephalopathy (SAE). A total of 84 male ICR mice, weighing 20-25 g, aged 6-8 weeks, were randomly divided into 4 groups of sham, sham+H2, sepsis and sepsis+H2. Sepsis was established by cecal ligation and puncture (CLP). Mice in sham+H2 and sepsis+H2 groups received 2% H2 inhalation for 1 h at 1 h and 6 h after sham operation or CLP operation respectively. The changes of neurological function and neuronal damage in hippocampal CA1 region were observed at 24 h post-operation. The activities of superoxide dismutase (SOD) and catalase (CAT) and the levels of malondialdehyde (MDA) and 8-iso-prostaglandin F2α (8-iso-PGF2α) in sera and hippocampus were detected at 24 h post-operation. The changes of cognitive function were observed by Y-maze test and fear conditional test at days 3 to 14 post-operation. Compared with sham group, the neurological function significantly declined and neurons in hippocampal CA1 region were significantly damaged; the activities of SOD and CAT markedly decreased while the levels of MDA and 8-iso-PGF2α markedly increased in sera and hippocampus; the time in new zone and the percentage of freezing time dramatically decreased at days 3 to 14 post-operation in sepsis group (P < 0.05) . Compared with sepsis group, neurological function significantly improved and damaged neurons in hippocampal CA1 region significantly reduced; the activities of SOD and CAT markedly increased and the levels of MDA and 8-iso-PGF2α markedly decreased in sera and hippocampus; the time in new zone and the percentage of freezing time dramatically increased at days 3 to 14 post-operations in sepsis+H2 group (P < 0.05). H2 inhalation can significantly alleviate neuronal damage and improve cognitive dysfunction in CLP-induced SAE mice. And it is probably associated with the increased activities of antioxidant enzymes and the reduced levels of oxidative products.