水素分子投与によるストレプトゾトシン誘発糖尿病マウスの心機能障害軽減効果
Adult male mice received streptozotocin (50 mg/kg/day intraperitoneally for 5 days) to establish a diabetic model, followed by 8 weeks of hydrogen-rich water (1.3±0.2 mg/L) administration. Despite no significant change in blood glucose, cardiac hypertrophy markers (atrial natriuretic factor, β-myosin heavy chain) and fibrosis markers (collagen I/III, TGF-β, α-smooth muscle actin, osteopontin) were markedly reduced. Apoptotic indicators including caspase-3 activity and Bax/Bcl-2 ratio also declined. Cardiac function improved alongside reductions in oxidative stress, inflammatory signaling, and endoplasmic reticulum stress. Suppression of JNK, p38 MAPK, and NF-κB pathways was observed in cardiac tissue, suggesting these mechanisms underlie the cardioprotective effects of molecular hydrogen independent of glycemic control.
Hydrogen-rich water suppresses JNK, p38 MAPK, and NF-κB signaling pathways, thereby reducing oxidative stress, inflammation, and endoplasmic reticulum stress, which collectively attenuate cardiac hypertrophy, fibrosis, and apoptosis in diabetic hearts.
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/25979689