水素豊富生理食塩水によるミトコンドリアATP感受性カリウムチャネル活性化を介した糖尿病性末梢神経障害への保護効果（ラット実験）
Using a streptozotocin (STZ)-induced rat model of diabetic peripheral neuropathy (DPN), this study examined the effects of hydrogen-rich saline (HS) administered intraperitoneally at doses of 2.5, 5, and 10 ml/kg daily for 4 weeks beginning at week 5 post-STZ injection. HS significantly ameliorated behavioral, biochemical, and molecular markers associated with DPN, including reductions in oxidative stress, pro-inflammatory cytokines, and apoptotic activity. Co-administration of 5-hydroxydecanoate, a selective inhibitor of mitochondrial ATP-sensitive potassium (Mito-K-ATP) channels, partially reversed these beneficial effects, implicating Mito-K-ATP channel activation as a key mechanistic component. The findings suggest that HS exerts neuroprotective effects in DPN through a pathway involving Mito-K-ATP channel activation alongside suppression of oxidative and inflammatory responses.
Hydrogen-rich saline activates mitochondrial ATP-sensitive potassium (Mito-K-ATP) channels, which in turn suppresses hyperglycemia-induced oxidative stress, pro-inflammatory cytokine release, and apoptosis, thereby reducing peripheral nerve damage in diabetic rats.
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/31746358