title: Hydrogen-Rich Medium Attenuated Lipopolysaccharide-Induced Monocyte-Endothelial Cell Adhesion and Vascular Endothelial Permeability via Rho-Associated Coiled-Coil Protein Kinase.
abstract: Sepsis is the leading cause of death in critically ill patients. In recent years, molecular hydrogen, as an effective free radical scavenger, has been shown a selective antioxidant and anti-inflammatory effect, and it is beneficial in the treatment of sepsis. Rho-associated coiled-coil protein kinase (ROCK) participates in junction between normal cells, and regulates vascular endothelial permeability. In this study, we used lipopolysaccharide to stimulate vascular endothelial cells and explored the effects of hydrogen-rich medium on the regulation of adhesion of monocytes to endothelial cells and vascular endothelial permeability. We found that hydrogen-rich medium could inhibit adhesion of monocytes to endothelial cells and decrease levels of adhesion molecules, whereas the levels of transepithelial/endothelial electrical resistance values and the expression of vascular endothelial cadherin were increased after hydrogen-rich medium treatment. Moreover, hydrogen-rich medium could lessen the expression of ROCK, as a similar effect of its inhibitor Y-27632. In addition, hydrogen-rich medium could also inhibit adhesion of polymorphonuclear neutrophils to endothelial cells. In conclusion, hydrogen-rich medium could regulate adhesion of monocytes/polymorphonuclear neutrophils to endothelial cells and vascular endothelial permeability, and this effect might be related to the decreased expression of ROCK protein.
authors.affiliation: *Department of Anesthesiology, Tianjin Institute of Anesthesiology, General Hospital of Tianjin Medical University, Tianjin, China; †Department of Anesthesiology, Tianjin Hospital, Tianjin, China; and ‡Institute of Acute Abdominal Disease, Tianjin Nan Kai Hospital, Tianjin, China.
authors.forename: Keliang
authors.initials: K
authors.lastname: Xie
authors.forename: Weina
authors.initials: W
authors.lastname: Wang
authors.forename: Hongguang
authors.initials: H
authors.lastname: Chen
authors.forename: Huanzhi
authors.initials: H
authors.lastname: Han
authors.forename: Daquan
authors.initials: D
authors.lastname: Liu
authors.forename: Guolin
authors.initials: G
authors.lastname: Wang
authors.forename: Yonghao
authors.initials: Y
authors.lastname: Yu
mesh_terms: D000577:Amides / Q000494:pharmacology; D002199:Capillary Permeability / Q000187:drug effects*; D002448:Cell Adhesion / Q000187:drug effects; D003470:Culture Media / Q000494:pharmacology*; D004730:Endothelium, Vascular / Q000378:metabolism* / Q000473:pathology; D005260:Female; D015971:Gene Expression Regulation, Enzymologic / Q000187:drug effects; D061307:Human Umbilical Vein Endothelial Cells / Q000378:metabolism* / Q000473:pathology; D006801:Humans; D006859:Hydrogen / Q000494:pharmacology*; D008070:Lipopolysaccharides / Q000633:toxicity*; D008297:Male; D009000:Monocytes / Q000378:metabolism* / Q000473:pathology; D009504:Neutrophils / Q000378:metabolism / Q000473:pathology; D011725:Pyridines / Q000494:pharmacology; D020298:U937 Cells; D054460:rho-Associated Kinases / Q000096:biosynthesis*
chemical_list: D000577:Amides; D003470:Culture Media; D008070:Lipopolysaccharides; D011725:Pyridines; C108830:Y 27632; D006859:Hydrogen; D054460:rho-Associated Kinases