外傷性脳損傷ラットの大脳皮質におけるアクアポリン1発現に対する水素富化水の影響
Using a weight-drop traumatic brain injury (TBI) model in male Sprague-Dawley rats (n=90, three groups of 30), this study examined how intraperitoneal administration of hydrogen-rich water (5 mL/kg daily for 5 days) influenced aquaporin-1 (AQP1) expression and cerebral edema. In TBI animals, AQP1 mRNA and protein levels in the cerebral cortex peaked at 24 hours post-injury (mRNA 2-ΔΔCt: 7.50±0.26; protein gray value: 1.986±0.110) and were accompanied by elevated neurological severity scores (NSS). Hydrogen-rich water administration significantly reduced AQP1 mRNA (5.40±0.21 vs. 7.50±0.26) and protein (1.246±0.137 vs. 1.986±0.110) at 24 hours, attenuated histopathological changes including irregular neuronal arrangement and hemorrhage, and lowered NSS compared with untreated TBI controls. These findings suggest that AQP1 upregulation contributes to post-TBI cerebral edema formation, and that early hydrogen-rich water administration can suppress this response.
TBI induces upregulation of AQP1 mRNA and protein in the cerebral cortex, promoting edema formation. Hydrogen-rich water suppresses this AQP1 overexpression, thereby reducing fluid accumulation and associated neurological deficits.
Intravenous hydrogen-saline infusion is a clinic-only route and is not viable for everyday self-administration. For routine hydrogen intake, inhalation is the most practical route, but inhalation carries explosion risk and concentration matters (empirical LFL of 10%; high-concentration 66% / 100% devices are not recommended).
See also:
https://h2-papers.org/en/papers/29923387