水素富化生理食塩水による心筋細胞アポトーシス抑制：miR-124-3pを介したcalpain1発現低下の関与
This study investigated the cardioprotective mechanisms of hydrogen-rich saline (HRS) in myocardial ischemia-reperfusion (I/R) injury using adult C57BL/6 mice and neonatal rat cardiomyocytes subjected to I/R and hypoxia/reoxygenation (H/R) conditions. miR-124-3p expression was markedly reduced in both injury models, and HRS pretreatment partially restored its levels. HRS suppressed apoptotic cell death and improved cell viability under I/R conditions; however, silencing miR-124-3p abolished these benefits. Calpain1 was identified as a direct downstream target of miR-124-3p. When calpain1 was overexpressed, caspase-3 activity increased, cleaved-caspase-3 and Bax protein levels rose, and Bcl-2 expression declined, collectively diminishing the cytoprotective effect of HRS in the H/R model. These findings indicate that the miR-124-3p–calpain1 signaling axis is a key mediator of HRS-induced cardioprotection against I/R injury.
HRS elevates miR-124-3p, which directly suppresses calpain1 expression and activity. Reduced calpain1 limits caspase-3 activation and maintains a favorable Bcl-2/Bax ratio, thereby attenuating cardiomyocyte apoptosis during ischemia-reperfusion.
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/37602925