外傷性脳損傷ラットにおける水素水の酸化ストレス軽減効果とNrf2経路の関与
Using a modified Feeney weight-drop rat model of traumatic brain injury (TBI), this study examined the neuroprotective properties of hydrogen-rich water and the underlying molecular mechanisms. Oxidative stress markers—catalase (CAT), glutathione peroxidase (GPx), and malondialdehyde (MDA)—were quantified by spectrophotometry, while Nrf2 pathway components (HO-1, NQO1) were assessed by western blotting, RT-PCR, and immunohistochemistry. TBI induced a significant decline in CAT and GPx activity alongside elevated MDA, with Nrf2 nuclear protein peaking at 24 hours post-injury without corresponding mRNA changes. Administration of hydrogen-rich water improved 7-day survival rates, reduced neurological deficit scores, and lowered intracellular oxidative stress. Additionally, nuclear translocation of Nrf2 was enhanced, leading to upregulation of downstream antioxidant genes HO-1 and NQO1. These findings indicate that hydrogen-rich water confers neuroprotection in TBI through activation of the Nrf2 antioxidant signaling pathway.
Hydrogen-rich water promotes nuclear translocation of Nrf2, upregulating downstream antioxidant enzymes HO-1 and NQO1, thereby reducing oxidative stress markers (MDA elevation, CAT and GPx suppression) following traumatic brain injury.
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/29907217