外傷性脳損傷ラットの脳組織におけるミトコンドリア障害とサイトカインに対する水素水の影響
Using a rat model of traumatic brain injury (TBI) established by a modified free-fall impact method, this study examined the effects of intraperitoneally administered hydrogen-rich water (5 mL/kg daily) on mitochondrial integrity and inflammatory cytokine profiles. Fifty-four male SD rats were allocated to sham, TBI, and TBI plus hydrogen-rich water groups, with assessments at 1, 3, and 7 days post-injury. Neurological severity scores (NSS) were significantly reduced in the hydrogen-rich water group at days 3 and 7 compared with the TBI-only group. Elevated levels of TNF-α, IL-1β, mitochondrial reactive oxygen species, and Bax protein observed after TBI were all attenuated by hydrogen-rich water administration. Conversely, mitochondrial membrane potential, membrane permeability transition pore activity, and Bcl-2 protein expression—each diminished by TBI—were partially restored. These findings indicate that hydrogen-rich water suppresses neuroinflammation, mitigates mitochondrial dysfunction, and reduces neuronal apoptosis in the early phase following TBI.
Hydrogen-rich water reduces mitochondrial ROS accumulation after TBI, preserves membrane potential and permeability transition pore function, shifts the Bax/Bcl-2 ratio toward survival, and lowers TNF-α and IL-1β levels, collectively attenuating neuroinflammation and apoptosis.
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/29663991