飲料水中の分子状水素が外傷性脳損傷による神経変性変化を抑制する
Traumatic brain injury (TBI) is recognized as a risk factor for neurodegenerative conditions such as Alzheimer's and Parkinson's diseases, partly through oxidative stress and neuroinflammation. Using a controlled cortical impact (CCI) mouse model, this study evaluated the effects of hydrogen-rich drinking water (mHW) on acute post-injury changes. mHW reduced CCI-induced cerebral edema by approximately 50%, completely suppressed pathological tau expression, and normalized protein levels of aquaporin-4, HIF-1, MMP-2, and MMP-9. Cytokine responses were modulated: an early elevation was accentuated, but by day 7 the increase was attenuated. Gene expression changes related to oxidative metabolism, cytokine release, and leukocyte migration observed 4 hours post-CCI were reversed by mHW. ATP levels were preserved or elevated, and the authors propose that the Jagendorf reaction may underlie this effect. Amyloid beta peptides 1-40 and 1-42 were not significantly altered. These findings indicate that hydrogen-rich water can mitigate multiple molecular and cellular consequences of experimental TBI.
Hydrogen-rich water is proposed to exert neuroprotection by reducing oxidative stress, normalizing aquaporin-4, HIF-1, and MMP-2/9 protein levels, suppressing pathological tau, modulating cytokine dynamics, and enhancing ATP production via the Jagendorf reaction.
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).
See also:
https://h2-papers.org/en/papers/25251220