title: Vasoprotective effect of vitamin E: rescue of ethanol-induced atherosclerosis and inflammatory stress in rat vascular wall.
abstract: Chronic ethanol consumption increases the incidence of cardiovascular disease. The mechanisms underlying ethanol-induced susceptibility to cardiovascular disease continue to be defined. This study examines the hypothesis that chronic ethanol consumption plausibly induces vascular wall abnormalities via inflammatory reactions. In addition, it intends to find out whether vitamin E inhibits the abnormalities induced by ethanol in rats' vascular wall. Twenty four male Wistar rats were divided into three groups (n=8): Control ©, ethanol (E), and vitamin E treated ethanol (VETE) group. After 6weeks, the aortic and coronary wall changes, vascular endothelial growth factor (VEGF), alpha-1 glycoprotein and haptoglobin amounts in plasma, C-reactive protein levels(CRP), as well as the amount of aortic IL-6 were evaluated. The results revealed the elevation of polymorphonuclear (PMN) leukocyte in the vascular wall, disorganization of endothelium with ballooning of cells, proliferation of vasa-vasorum with an increase in the IL-6, CRP, as well as a decrease in VEGF and an increase in alpha-1 glycoprotein and haptoglobin in the ethanol group compared to the control group. Significant amelioration of aortic and coronary wall changes, along with the restoration of elevated level of IL6, CRP, and the decreased level of VEGF compared to that of the controls were found in vitamin E-treated animals. These findings strongly support the idea that heavy and chronic ethanol consumption initiates atherosclerosis by inflammatory stress, and that these effects can be alleviated by vitamin E as an anti-inflammatory agent.
authors.affiliation: Department of Physiology, Faculty of Medicine, Urmia University of Medical Sciences, Urmia, Iran. ashirpoor@yahoo.com
authors.forename: Alireza
authors.initials: A
authors.lastname: Shirpoor
authors.forename: Leila
authors.initials: L
authors.lastname: Norouzi
authors.forename: Mohammad-Hasan
authors.initials: MH
authors.lastname: Khadem Ansari
authors.forename: Behrouz
authors.initials: B
authors.lastname: Ilkhanizadeh
authors.forename: Rasool
authors.initials: R
authors.lastname: Gharaaghaji
mesh_terms: D000818:Animals; D000893:Anti-Inflammatory Agents / Q000008:administration & dosage / Q000627:therapeutic use*; D001011:Aorta / Q000187:drug effects* / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D050197:Atherosclerosis / Q000139:chemically induced / Q000276:immunology / Q000473:pathology / Q000517:prevention & control*; D001798:Blood Proteins / Q000378:metabolism; D049109:Cell Proliferation / Q000187:drug effects; D003331:Coronary Vessels / Q000187:drug effects* / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D004730:Endothelium, Vascular / Q000187:drug effects / Q000276:immunology / Q000473:pathology; D000431:Ethanol / Q000633:toxicity*; D008297:Male; D009131:Muscle, Smooth, Vascular / Q000187:drug effects / Q000276:immunology / Q000473:pathology; D051381:Rats; D017208:Rats, Wistar; D013312:Stress, Physiological / Q000187:drug effects / Q000276:immunology; D014651:Vasa Vasorum / Q000187:drug effects / Q000276:immunology / Q000473:pathology; D042461:Vascular Endothelial Growth Factor A / Q000378:metabolism; D014810:Vitamin E / Q000008:administration & dosage / Q000627:therapeutic use*
chemical_list: D000893:Anti-Inflammatory Agents; D001798:Blood Proteins; D042461:Vascular Endothelial Growth Factor A; C467498:vascular endothelial growth factor A, rat; D014810:Vitamin E; D000431:Ethanol