Abstract
Human vascular endothelial cells (HUVECs) were exposed to CoCl2 as an in vitro model of hypoxia. Expression of VCAM-1 (vascular cell adhesion molecule), reduction of PECAM-1 (platelet endothelial cell adhesion molecule) and cytoskeletal changes without alterations in cell viability were observed. HUVECs were also exposed to Escherichia coli lipopolysaccaride (LPS) as an in vitro model of inflammation: significant IL-6 release was measured. Pre-treatment of HUVECs with aescin prevented, in a concentration-dependent fashion (0.1-1 microM), the action of CoCl2 on VCAM-1 and PECAM-1, also preserving endothelial cell morphology. Furthermore, aescin pre-treatment reduced IL-6 release from LPS-activated vascular endothelium.
MeSH terms
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Aesculus*
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Cell Survival / drug effects
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Cobalt
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Dose-Response Relationship, Drug
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Endothelium, Vascular / drug effects*
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Endothelium, Vascular / metabolism
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Escherichia coli
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Escin / administration & dosage
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Escin / pharmacology*
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Escin / therapeutic use
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Fruit
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Humans
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Hypoxia / chemically induced
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Hypoxia / prevention & control*
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Inflammation / chemically induced
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Inflammation / prevention & control*
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Interleukin-6 / metabolism
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Lipopolysaccharides
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Phytotherapy*
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Plant Extracts / administration & dosage
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Plant Extracts / pharmacology
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Plant Extracts / therapeutic use
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Platelet Endothelial Cell Adhesion Molecule-1 / metabolism
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Vascular Cell Adhesion Molecule-1 / metabolism
Substances
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Interleukin-6
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Lipopolysaccharides
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Plant Extracts
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Platelet Endothelial Cell Adhesion Molecule-1
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Vascular Cell Adhesion Molecule-1
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Cobalt
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Escin
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cobaltous chloride