Hydrogen Therapy Improves Memory Loss from Sleep Deprivation in Mice
- Authors
- QiFan Xiao, ShiRui Zhou, Bin Tang, YuQing Zhu
- Journal
- CNS Neuroscience & Therapeutics
- Year
- 2026
- DOI
- 10.1002/cns.70770
- Study Type
- Mouse
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- China
- Health Condition
- Sleep Deprivation
- Body System
- Nervous System
TL;DR
Hydrogen improved cognitive performance in sleep-deprived mice by reducing oxidative stress and inflammation via activation of the Nrf2/HO-1 pathway.
Key Finding
Hydrogen gas treatment improved cognitive performance in sleep-deprived mice by activating a cellular protective pathway (Nrf2/HO-1) that reduced brain inflammation and oxidative stress.
Summary
Researchers gave sleep-deprived mice hydrogen gas and tested whether it could improve their memory and thinking abilities. Mice that received hydrogen performed better on memory tests and showed reduced inflammation and oxidative stress (cellular damage from unstable molecules) in their brains compared to untreated sleep-deprived mice. The improvement appeared to work through activation of a specific cellular protective pathway called Nrf2/HO-1.
Practical Takeaway
This is an early-stage animal study suggesting hydrogen may have protective effects on cognition during sleep deprivation, but it was conducted only in mice and does not establish whether these effects would occur in humans. Much more research, including human trials, would be needed before any health recommendations could be made.
Abstract
Aims: This study investigated the effects of hydrogen (H2) on cognitive impairment in sleep-deprived mice mediated by the nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) signaling pathway. Methods: A chronic sleep deprivation (SD) model was established using the modified multiple platform method, with 18 h of deprivation daily for 28 consecutive days. Cognitive function was evaluated using the Morris water maze and novel object recognition (NOR) test. Histopathological and biochemical analyses, including hematoxylin and eosin staining, Nissl staining, immunohistochemistry, and enzyme-linked immunosorbent assay, were performed to assess oxidative stress and inflammation-related markers. Results: The results demonstrated that H2-treated mice showed significantly shorter escape latency, longer target quadrant duration, and higher NOR index compared to controls. Concurrently, Nrf2/HO-1 expression was significantly upregulated, while interleukin-1β and tumor necrosis factor-alpha levels were reduced. Additionally, glutathione peroxidase and superoxide dismutase activities were restored. Conclusion: These results indicate that H2 alleviates oxidative stress and neuroinflammation through Nrf2/HO-1 pathway activation, mitigating SD-induced cognitive impairment. This research provides a theoretical foundation for potential clinical applications.