Hydrogen Repairs LPS-Induced Endothelial Progenitor Cells Injury via PI3K/AKT/eNOS Pathway.

ABSTRACT: Endotoxins and other harmful substances may cause an increase in permeability in endothelial cells (ECs) monolayers, as well as ECs shrinkage and death to induce lung damage. Lipopolysaccharide (LPS) can impair endothelial progenitor cells (EPCs) functions, including proliferation, migration, and tube formation. EPCs can migrate to the damaged area, differentiate into ECs, and participate in vascular repair, which improves pulmonary capillary endothelial dysfunction and maintains the integrity of the endothelial barrier. Hydrogen (H₂) contributes to the repairment of lung injury and the damage of ECs. We therefore speculate that H₂ protects the EPCs against LPS-induced damage, and it's mechanism will be explored. The bone marrow-derived EPCs from ICR Mice were treated

SUBMITTER: Mu Q 

PROVIDER: S-EPMC9133378 | biostudies-literature | 2022

REPOSITORIES: biostudies-literature