水素富化生理食塩水による非アルコール性脂肪肝疾患の改善：酸化ストレス軽減と肝臓PPARα・PPARγ活性化を介したメカニズム
Using a rat model of NAFLD induced by hyperglycemia and hyperlipidemia, this study examined the effects of hydrogen-rich saline administration. Histological evaluation via HE and TUNEL staining demonstrated marked improvement in hepatic pathology. Metabolic parameters including fasting blood glucose, insulin sensitivity, and glucose tolerance were favorably altered. Hepatic expression of pro-inflammatory cytokines TNF-α and IL-1β, along with oxidative stress markers 3-nitrotyrosine and 8-hydroxy-2'-deoxyguanosine, was significantly reduced. Notably, the expression of peroxisome proliferator-activated receptors PPARα and PPARγ in hepatocytes was substantially upregulated. These findings suggest that hydrogen-rich saline exerts beneficial effects on NAFLD through dual mechanisms: suppression of oxidative damage and activation of PPAR-mediated metabolic pathways.
Molecular hydrogen selectively scavenges peroxynitrite and hydroxyl radicals, reducing hepatic oxidative stress markers. Simultaneously, upregulation of PPARα and PPARγ in hepatocytes promotes improved lipid and glucose metabolism, collectively attenuating NAFLD progression.
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/28098910