自然発症高血圧ラットにおけるTGF-βシグナル経路抑制を介した水素による心筋線維化の軽減
This animal study examined the effects of hydrogen-rich saline (HRS) on cardiac fibrosis using spontaneously hypertensive rats (SHRs), with pirfenidone (PFD) as a comparator. HRS administration significantly reduced left ventricular mass index and heart weight index. Myocardial collagen volume fraction, collagen I, and collagen III were all decreased compared with the model group. Serum levels of angiotensin II, PICP, and PIIINP also declined. Regarding oxidative stress markers, MDA, α-SMA, and TIMPs were downregulated while SOD activity increased. At the signaling level, HRS suppressed TGF-β1, Smad3, and Smad2/3 protein expression without altering Smad7. PFD produced comparable outcomes. These findings indicate that HRS attenuates hypertension-associated myocardial fibrosis by reducing oxidative stress and modulating collagen metabolism, with the TGF-β/Smad pathway implicated as a key mechanistic route.
HRS suppresses TGF-β1, Smad2/3, and Smad3 expression, reducing collagen I and III synthesis, while simultaneously decreasing MDA and increasing SOD activity, thereby attenuating oxidative stress-driven myocardial fibrosis.
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/34618887