分子状水素はROSを介したPTEN-AKT-mTORシグナル経路の調節により腹膜透析関連腹膜線維化を軽減する
Peritoneal dialysis is used by approximately 11% of end-stage renal disease patients globally, yet prolonged use leads to peritoneal fibrosis. This study established a high-glucose-induced peritoneal fibrosis mouse model via intraperitoneal injection of high-glucose dialysate, followed by intervention with hydrogen-rich dialysate. Parallel in vitro experiments were conducted using MeT-5A mesothelial cells. Both in vivo and in vitro findings demonstrated that molecular hydrogen effectively suppressed the progression of high-glucose-induced peritoneal fibrosis. Mechanistically, hydrogen eliminated intracellular reactive oxygen species and blocked activation of the PTEN/AKT/mTOR signaling pathway. These results indicate that the ROS/PTEN/AKT/mTOR axis mediates the anti-fibrotic action of molecular hydrogen in the peritoneal environment.
Molecular hydrogen selectively scavenges intracellular ROS, thereby preventing activation of the PTEN/AKT/mTOR signaling cascade and inhibiting high-glucose-driven peritoneal fibrosis progression.
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/31930571