水素水がカルシウム緩衝タンパク質の調節を介してラット脳虚血傷害を軽減する
This study examined whether hydrogen-rich water (HRW) could influence the expression of two calcium-buffering proteins, parvalbumin and hippocalcin, in the context of cerebral ischemia and glutamate-induced neuronal death. Male Sprague-Dawley rats underwent middle cerebral artery occlusion (MCAO), and HRW (6 ml/kg) was administered before and after the procedure. Cortical tissue was collected at 1, 7, and 14 days post-MCAO. HRW-treated animals showed reduced infarct volume and improved neurological scores. Ischemia-induced decreases in parvalbumin and hippocalcin levels were prevented by HRW in vivo. In vitro experiments demonstrated that HRW dose-dependently reduced glutamate toxicity-associated neuronal death and suppressed the accompanying rise in intracellular Ca²⁺ concentration. These findings indicate that preservation of calcium-buffering protein levels may contribute to the neuroprotective mechanism of HRW during ischemic brain injury.
HRW preserves the expression of calcium-buffering proteins parvalbumin and hippocalcin, thereby attenuating intracellular Ca²⁺ overload triggered by glutamate toxicity and ischemia-reperfusion, which reduces neuronal apoptosis.
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/25920370