2015 · Yu et al. — Protective effects of hydrogen-rich medium on lipopolysaccharide-induced monocytic adhesion and vascular endothelial permeability through regulation of vascular endothelial cadherin.
Super-Abstract
In endothelial cell culture, hydrogen-rich medium reduced the inflammation-triggered adhesion of monocytes to vessel walls and preserved the integrity of the endothelial barrier — effects mediated through the adhesion protein VE-cadherin. This is an in-vitro study; these cell culture findings have not been validated in animals or humans. (Genetics and Molecular Research, 2015.)
Commentary
Yu and colleagues used LPS-stimulated human umbilical vein endothelial cells (HUVECs) to model inflammatory vascular injury. H₂-rich medium reduced the expression of adhesion molecules VCAM-1, ICAM-1, and E-selectin, and reduced monocyte-endothelial cell adhesion. Importantly, it also preserved or restored VE-cadherin — the key protein that keeps endothelial junctions tight and the vascular barrier intact. The transendothelial electrical resistance (TEER) measurement confirmed reduced permeability. This is a mechanistically coherent in-vitro study, adding VE-cadherin regulation as a candidate mechanism for H₂'s vascular protective effects. No animal or human data is included.
Key quotes
- „Liquid rich in hydrogen could reduce LPS-induced production of adhesion molecules and endothelium-hyaline leukocyte conglutination, and influence the expression and distribution of VE-cadherin to regulate the permeability of the endothelium.“ — the summary finding: H₂ protects the vascular barrier via VE-cadherin
- „Compared with LPS cells, the VE-cadherin in LPS+H2 cells was even and complete at the cell joints.“ — fluorescence imaging confirmed restored VE-cadherin distribution at cell junctions
- „There was an increase in endothelium-hyaline leukocyte conglutination, a reduction in VCAM-1, ICAM-1, and E-selectin, and the TEER value increased obviously.“ — quantitative evidence of reduced inflammation and improved barrier function in H₂-treated cells
Our assessment
A focused in-vitro study identifying VE-cadherin regulation as a mechanism by which H₂ may protect vascular endothelium from inflammatory damage. The methodology — combining flow cytometry, ELISA, TEER, Western blot, and immunofluorescence — is multi-faceted and internally consistent. All findings are from cell culture and cannot be directly applied to cardiovascular or inflammatory disease management in humans. The VE-cadherin finding adds a specific, testable molecular target for future in-vivo H₂ research.
Study design
- Type: in-vitro study · Model: LPS-stimulated HUVECs (human umbilical vein endothelial cells), 4 treatment groups · H₂ delivery: saturated hydrogen-rich medium applied to cell culture
- Result: H₂-rich medium reduced VCAM-1, ICAM-1, E-selectin; decreased monocyte-endothelial adhesion; increased TEER (lower permeability); restored VE-cadherin expression and distribution at cell junctions
Abstract
We observed the effect of hydrogen-rich medium on lipopolysaccharide (LPS)-induced human umbilical vein endothelial cells (HUVECs), hyaline leukocyte conglutination, and permeability of the endothelium. Endotheliocytes were inoculated on 6-well plates and randomly divided into 4 groups: control, H2, LPS, LPS+H2, H2, and LPS+H2 in saturated hydrogen-rich medium. We applied Wright's stain-ing to observe conglutination of hyaline leukocytes and HUVECs, flow cytometry to determine the content of vascular cell adhesion protein 1 (VCAM-1) and intercellular adhesion molecule 1 (ICAM-1), enzyme-linked immunosorbent assay to measure the E-selectin concentration in the cell liquor, the transendothelial electrical resistance (TEER) to test the permeability of endothelial cells, and Western blot and immunofluorescence to test the expression and distribution of vascular endothelial (VE)-cadherin. Compared with control cells, there was an increase in endothelium-hyaline leukocyte conglutination, a reduction in VCAM-1, ICAM-1, and E-selectin, and the TEER value increased obviously. Compared with LPS, there was an obvious reduction in the conglutination of LPS+H2 cells, a reduction in VCAM-1, ICAM-1, and E-selectin levels, and a reduction in the TEER-resistance value, while the expression of VE-cadherin increased. Fluorescence results showed that, compared with control cells, the VE-cadherin in LPS cells was in-complete at the cell joints. Compared with LPS cells, the VE-cadherin in LPS+H2 cells was even and complete at the cell joints. Liquid rich in hydrogen could reduce LPS-induced production of adhesion molecules and endothelium-hyaline leukocyte conglutination, and influence the expression and distribution of VE-cadherin to regulate the permeability of the endothelium.
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