分子状水素は胆管閉塞性胆管炎誘発性肝機能障害においてギャップ結合およびタイト結合を回復させることで肝機能の改善を促進する
Acute obstructive cholangitis (AOC) disrupts hepatocyte gap junctions (GJs) and tight junctions (TJs) through elevated biliary pressure and lipopolysaccharide (LPS) exposure, resulting in liver dysfunction. A rat AOC model was constructed by infusing LPS via a bile duct catheter with the distal duct occluded; biliary drainage was then established 12 hours later. Molecular hydrogen (H2) was administered following drainage. AOC caused marked disruption of both GJ and TJ proteins, whereas H2 administration reversed these junction abnormalities. The underlying mechanism appears to involve attenuation of inflammatory responses, reduction of oxidative damage, and decreased matrix metalloproteinase activity. These findings indicate that H2 can accelerate the restoration of liver function in AOC, with the effect dependent on the recovery of GJ and TJ integrity.
H2 attenuates inflammatory signaling and oxidative damage while suppressing matrix metalloproteinase activity, thereby preventing disruption of gap junction and tight junction proteins and facilitating restoration of hepatocyte function.
This study is at the animal-experiment stage. For human application, inhalation is the most promising delivery route, but inhalation carries explosion risk and concentration matters (empirical LFL of 10%; high-concentration devices are documented in the Consumer Affairs Agency accident database and are not recommended).
See also:
https://h2-papers.org/en/papers/31059036