水素富化生理食塩水による全脳虚血再灌流ラットの神経保護：制御性T細胞の増加とmiR-21・miR-210・NF-κB発現の抑制
This study examined the effects of hydrogen-rich saline (HRS) in a rat model of global cerebral ischemia-reperfusion (I/R) injury. Animals receiving HRS exhibited less severe brain damage compared with untreated I/R controls. Hippocampal miR-210 expression rose significantly at 6, 24, and 96 hours post-reperfusion in the I/R group, whereas HRS administration markedly reduced this elevation. Regulatory T cell (Treg) counts declined at all measured time points in I/R animals, but recovered at 24 and 96 hours in HRS-treated rats. Strong correlations were identified among Tregs, TGF-β1, TNF-α, and NF-κB at 24 hours. These findings suggest that the neuroprotective mechanism of HRS may involve restoration of Treg populations, modulation of hypoxia-responsive microRNAs, and attenuation of NF-κB-driven neuroinflammation following global cerebral I/R.
HRS is proposed to selectively scavenge hydroxyl radicals, suppress NF-κB-mediated inflammatory cytokine signaling, restore Treg populations, and downregulate hypoxia-inducible microRNAs (miR-210, miR-21), collectively reducing cerebral I/R-induced neuronal damage.
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/27386874