経口水素水摂取によるグレリン分泌誘導を介した神経保護効果のマウスにおける検討
Although hydrogen-rich water (HRW) consumption is known to exert neuroprotective effects in Parkinson's disease (PD) model mice, striatal hydrogen levels remain undetectable after supplementation, implying an indirect mechanism. This study investigated that mechanism in mice and found that HRW intake elevated gastric ghrelin mRNA expression and circulating ghrelin levels. The β1-adrenoceptor antagonist atenolol blocked this ghrelin upregulation. Critically, the neuroprotective benefit of HRW was eliminated when either the ghrelin receptor antagonist D-Lys(3) GHRP-6 or atenolol was co-administered. These findings establish that ghrelin production, stimulated through adrenergic signaling in the stomach, mediates the neuroprotective action of hydrogen water in PD, identifying a previously unrecognized indirect pathway by which H2 supplementation influences neuronal survival.
Hydrogen-rich water intake stimulates gastric ghrelin mRNA expression and secretion via β1-adrenergic receptor signaling; the resulting ghrelin then activates its receptor to mediate neuroprotection, representing an indirect pathway independent of direct striatal H2 elevation.
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/24253616