水素水がラット心筋虚血再灌流傷害におけるPI3K/AKTシグナル経路に及ぼす影響
Using a Langendorff isolated heart preparation, 60 rats were allocated to hydrogen-rich water or control groups, each subdivided into pre-ischemic, ischemic, and reperfusion subgroups (n=10 per subgroup). Control hearts received Krebs-Ringer solution alone, while the hydrogen-rich water group received Krebs-Ringer solution supplemented with hydrogen-rich water. Gene and protein expression of PI3K, AKT, phosphorylated AKT, FoxO1, Bim, and Caspase-3 were quantified by RT-qPCR, immunohistochemistry, and Western blotting, with Caspase-3 enzymatic activity assessed spectrophotometrically. In the hydrogen-rich water reperfusion subgroup, PI3K, AKT, and p-AKT expression were elevated, whereas FoxO1, Bim, and Caspase-3 levels were significantly reduced relative to the corresponding control subgroup (P<0.05). These findings indicate that hydrogen-rich water activates the PI3K/AKT signaling cascade, thereby suppressing cardiomyocyte apoptosis and reducing myocardial ischemia-reperfusion injury in isolated rat hearts.
Hydrogen-rich water activates the PI3K/AKT signaling pathway, leading to downregulation of FoxO1, Bim, and Caspase-3 expression, which collectively reduces cardiomyocyte apoptosis during ischemia-reperfusion.
Hydrogen-rich water is a low-risk delivery route, but the achievable systemic hydrogen dose is bounded. For clinical applications, inhalation is the most efficient route; inhalation, however, carries explosion risk, and concentration matters (empirical LFL of 10% applies to inhalation environments; high-concentration devices are documented in the Consumer Affairs Agency accident database and are not recommended).
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https://h2-papers.org/en/papers/31702499