水素含有培地はROCKを介してLPS誘発性の単球-内皮細胞接着および血管内皮透過性を抑制する
To investigate the mechanisms underlying vascular endothelial dysfunction in sepsis, this in vitro study examined the effects of hydrogen-rich medium on lipopolysaccharide (LPS)-stimulated vascular endothelial cells. Hydrogen-rich medium reduced the adhesion of both monocytes and polymorphonuclear neutrophils to endothelial cells and lowered the expression of adhesion molecules. Concurrently, transepithelial/endothelial electrical resistance values and VE-cadherin expression were elevated, indicating improved endothelial barrier integrity. Notably, the expression of Rho-associated coiled-coil protein kinase (ROCK) was diminished by hydrogen-rich medium, an outcome comparable to that produced by the ROCK inhibitor Y-27632. These findings suggest that hydrogen-rich medium modulates endothelial permeability and leukocyte adhesion at least partly through suppression of ROCK protein expression.
Hydrogen-rich medium downregulates ROCK protein expression, thereby reducing LPS-induced adhesion molecule upregulation and endothelial hyperpermeability while preserving VE-cadherin-mediated barrier function.
This is basic research at the cellular or molecular level. 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 not recommended).
See also:
https://h2-papers.org/en/papers/25895142