水素富化生理食塩水による圧負荷誘発性心肥大の抑制：JAK-STATシグナル経路の関与
This study examined whether hydrogen-rich saline (HRS) exerts cardioprotective effects in a rat model of pressure overload induced by abdominal aortic constriction (AAC). Sixty Sprague-Dawley rats underwent AAC surgery and were allocated to four groups: sham, AAC-model, low-dose HRS (3 mL/kg/day intraperitoneally), and high-dose HRS (6 mL/kg/day intraperitoneally), each administered for 6 weeks. Heart weight-to-body weight and left ventricular weight-to-body weight ratios were elevated in the model group and reduced in both HRS groups in a dose-dependent manner. Elevated expression of atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP), along with cardiac fibrosis, were similarly suppressed by HRS. Janus kinase–signal transducer and activator of transcription (JAK-STAT) signaling molecule expression was downregulated following HRS administration, suggesting this pathway may mediate the observed cardioprotective effects.
HRS administration downregulated JAK-STAT signaling molecules, which was associated with reduced ANP and BNP expression and decreased cardiac fibrosis, suggesting that JAK-STAT pathway inhibition underlies the cardioprotective effect against pressure overload-induced hypertrophy.
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/29433438