水素水によるTGF-β1誘導性Sirt1調節を介した腎障害および腎線維化の抑制
This study examined the effects of hydrogen-rich water (HW) on renal fibrosis and epithelial-mesenchymal transition (EMT) using a unilateral ureteral obstruction (UUO) mouse model and TGF-β1-stimulated human proximal tubular epithelial cells (HK-2). UUO induced marked interstitial fibrosis, glomerular shrinkage, and basement membrane disruption, accompanied by elevated serum creatinine and blood urea nitrogen. HW administration reduced these pathological changes and improved renal function markers. In HK-2 cells, HW pretreatment blocked TGF-β1-induced EMT, as reflected by altered expression of α-SMA, fibronectin, E-cadherin, and Smad2. TGF-β1-mediated downregulation of Sirt1 was restored by HW, and the Sirt1 inhibitor sirtinol abolished HW's protective effects, confirming that Sirt1 acts as a key downstream mediator of HW's anti-fibrotic action.
HW restores TGF-β1-suppressed Sirt1 expression, thereby inhibiting downstream EMT markers (α-SMA, fibronectin upregulation; E-cadherin loss) and reducing renal interstitial fibrosis via a Sirt1-dependent pathway.
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).
See also:
https://h2-papers.org/en/papers/28458345