title: Emodin-6-O-β-D--glucoside inhibits high-glucose-induced vascular inflammation.
abstract: Emodin-6-O-β-D-glucoside (EG), a new active compound from Reynoutria japonica, has recently been shown to exert potent anti-inflammatory and barrier protective effects in human umbilical vein endothelial cells (HUVECs) and in mice. Vascular inflammatory process has been suggested to play a key role in initiation and progression of atherosclerosis, a major complication of diabetes mellitus. Thus, we attempted to determine whether EG can suppress the vascular inflammatory process induced by high glucose (HG) in HUVECs and mice. Data showed that HG induced markedly increased vascular permeability, monocyte adhesion, expressions of CAMs, formation of ROS, and activation of NF-κB. Remarkably, all of the above-mentioned vascular inflammatory effects of HG were attenuated by pretreatment with EG. Vascular inflammatory responses induced by HG are critical events underlying development of various diabetic complications; therefore, our results suggest that EG may have significant therapeutic benefits against diabetic complications and atherosclerosis.
authors.affiliation: College of Pharmacy, CMRI, Research Institute of Pharmaceutical Sciences, Kyungpook National University, 80 Dahak-ro, Buk-gu, Daegu, 702-701, Republic of Korea.
authors.forename: Wonhwa
authors.initials: W
authors.lastname: Lee
authors.forename: Sae-Kwang
authors.initials: SK
authors.lastname: Ku
authors.forename: Doohyun
authors.initials: D
authors.lastname: Lee
authors.forename: Taeho
authors.initials: T
authors.lastname: Lee
authors.forename: Jong-Sup
authors.initials: JS
authors.lastname: Bae
mesh_terms: D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology*; D002199:Capillary Permeability / Q000187:drug effects; D002448:Cell Adhesion / Q000187:drug effects; D015815:Cell Adhesion Molecules / Q000378:metabolism; D002478:Cells, Cultured; D018920:Coculture Techniques; D003925:Diabetic Angiopathies / Q000139:chemically induced / Q000276:immunology / Q000378:metabolism / Q000517:prevention & control*; D004195:Disease Models, Animal; D004305:Dose-Response Relationship, Drug; D004642:Emodin / Q000031:analogs & derivatives* / Q000494:pharmacology; D042783:Endothelial Cells / Q000187:drug effects* / Q000276:immunology / Q000378:metabolism; D005947:Glucose; D005960:Glucosides / Q000494:pharmacology*; D061307:Human Umbilical Vein Endothelial Cells / Q000187:drug effects / Q000378:metabolism; D006801:Humans; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D009000:Monocytes / Q000187:drug effects / Q000378:metabolism; D016328:NF-kappa B / Q000378:metabolism; D018384:Oxidative Stress / Q000187:drug effects; D017382:Reactive Oxygen Species / Q000378:metabolism; D014657:Vasculitis / Q000139:chemically induced / Q000276:immunology / Q000378:metabolism / Q000517:prevention & control*
chemical_list: D000893:Anti-Inflammatory Agents; D015815:Cell Adhesion Molecules; D005960:Glucosides; D016328:NF-kappa B; D017382:Reactive Oxygen Species; C583240:emodin-6-O-glucoside; D005947:Glucose; D004642:Emodin