パーキンソン病モデルマウスにおける分子状水素が誘導する胃脳相関の複雑性
This study examined the role of ghrelin in the neuroprotective effects of hydrogen-rich water (HW) in a mouse model of Parkinson's disease (PD) induced by MPTP. Ghrelin knockout (KO) mice retained the neuroprotective response to HW, indicating that ghrelin is not indispensable. Subdiaphragmatic vagotomy did not abolish the protective effect observed in the substantia nigra, ruling out vagal afferent nerve involvement. Furthermore, the ghrelin receptor antagonist D-Lys-GHRP-6 failed to cancel HW-mediated neuroprotection in ghrelin-KO mice, unlike in wild-type animals. These findings collectively suggest that additional H2-responsive factors can compensate for the absence of ghrelin, pointing to a more complex stomach-brain interaction than previously recognized.
Neuroprotection by hydrogen-rich water does not depend solely on ghrelin or vagal afferent signaling; when ghrelin is absent, alternative H2-responsive factors appear to compensate, maintaining substantia nigra protection in MPTP-treated mice.
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/28462451