水素水による炎症・酸化ストレスの相互促進の遮断が反復性軽度外傷性脳損傷マウスのミエリン再生と神経細胞生存を介して認知機能低下およびうつ様行動を改善する
Using a mouse model of repetitive mild traumatic brain injury (rmTBI), this study examined the effects of early hydrogen-rich water (HRW) administration on neuroinflammatory and oxidative pathways. NLRP3 inflammasome activation peaked at 7–14 days post-injury (DPI), while oxidative stress persisted throughout the 30-day observation period. HRW significantly reduced Nrf2 expression in the prefrontal cortex at 14 DPI and in hippocampal CA2 at 30 DPI. Magnetic resonance spectroscopy revealed an elevated tCho/tCr ratio and a reduced tNAA/tCr ratio in rmTBI animals, indicating metabolic disruption. Behavioral assessments showed anhedonia in the sucrose preference test and prolonged platform-finding latency in the Morris water maze in rmTBI mice, both of which were attenuated in the HRW group. The findings suggest that HRW suppresses inflammasome assembly and sustained oxidative stress, thereby facilitating oligodendrocyte recovery, myelin repair, and prevention of axonal and neuronal apoptotic damage, ultimately improving depression-like behavior and spatial cognitive function.
HRW suppresses NLRP3 inflammasome assembly and reduces sustained oxidative stress, which restores oligodendrocyte function, promotes myelin repair, and prevents neuronal apoptosis following repetitive mild traumatic brain injury.
Hydrogen-rich water is a low-risk delivery route, but the achievable systemic hydrogen dose is bounded. For clinical applications, inhalation is the most efficient route; inhalation, however, carries explosion risk, and concentration matters (empirical LFL of 10% applies to inhalation environments; high-concentration devices are documented in the Consumer Affairs Agency accident database and are not recommended).
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https://h2-papers.org/en/papers/38479178