beta-escin and cobaltous-chloride

beta-escin has been researched along with cobaltous-chloride* in 1 studies

Other Studies

1 other study(ies) available for beta-escin and cobaltous-chloride

Article	Year
Aescin protection of human vascular endothelial cells exposed to cobalt chloride mimicked hypoxia and inflammatory stimuli. Planta medica, 2007, Volume: 73, Issue:3 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. Topics: Aesculus; Cell Survival; Cobalt; Dose-Response Relationship, Drug; Endothelium, Vascular; Escherichia coli; Escin; Fruit; Humans; Hypoxia; Inflammation; Interleukin-6; Lipopolysaccharides; Phytotherapy; Plant Extracts; Platelet Endothelial Cell Adhesion Molecule-1; Vascular Cell Adhesion Molecule-1	2007

Article

Year

Aescin protection of human vascular endothelial cells exposed to cobalt chloride mimicked hypoxia and inflammatory stimuli.

Planta medica, 2007, Volume: 73, Issue:3

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.

Topics: Aesculus; Cell Survival; Cobalt; Dose-Response Relationship, Drug; Endothelium, Vascular; Escherichia coli; Escin; Fruit; Humans; Hypoxia; Inflammation; Interleukin-6; Lipopolysaccharides; Phytotherapy; Plant Extracts; Platelet Endothelial Cell Adhesion Molecule-1; Vascular Cell Adhesion Molecule-1

2007