Subject(s)
Bioprosthesis , Cor Triatriatum/diagnostic imaging , Heart Valve Prosthesis , Mitral Valve/diagnostic imaging , Prosthesis Failure , Adult , Cor Triatriatum/surgery , Diagnosis, Differential , Echocardiography, Three-Dimensional/methods , Echocardiography, Transesophageal/methods , Female , Humans , Mitral Valve/surgeryABSTRACT
The preventive and therapeutic effects of eicosapentaenoic acid (EPA) on diet-induced hyperlipidemia in rabbits have been investigated. Eighteen New Zealand rabbits were randomly divided into three groups of 6 subjects each; experimental group-I (EG-I) was administered a cholesterol rich diet, experimental group-II (EG-II) was treated with EPA (300 mg/kg/d) following a cholesterol-rich diet and the control group (CG) had a standard diet. Blood samples were collected at day 0 and at the 4th and 12th weeks of EG-II to obtain serum levels of total cholesterol (TC), high density lipid-cholesterol (HDL-C), low density lipid-cholesterol (LDL-C) and triglyceride (TG). From each group tissue samples were collected from the carotid artery for immunohistochemistry and electron microscopy. Our results showed that EPA could significantly lower (p<0.001) serum TC, LDL-C, HDL-C and TG levels with a reduction of 35%; 55%; 44% and 51%, respectively. Scanning and transmission electron microscopy results revealed that endothelial damage was more prominent in EG-I when compared to EG-II. The ruptured endothelial lining and damaged cellular surface was increased in EG-I when compared to EG-II. Ultrastructural observations showed that after EPA treatment, the degeneration and cellular surface damage on the endothelium were also decreased. These biochemical and ultrastructural results suggest that EPA is a potential drug which significantly lowers the serum lipid profile and partially repairs endothelial dysfunction due to hyperlipidemia.
Subject(s)
Carotid Arteries/drug effects , Carotid Artery Diseases/prevention & control , Cholesterol, Dietary/administration & dosage , Eicosapentaenoic Acid/pharmacology , Endothelium, Vascular/drug effects , Hypercholesterolemia/drug therapy , Hypolipidemic Agents/pharmacology , Animals , Biomarkers/blood , Carotid Arteries/metabolism , Carotid Arteries/ultrastructure , Carotid Artery Diseases/etiology , Carotid Artery Diseases/metabolism , Carotid Artery Diseases/pathology , Disease Models, Animal , Endothelium, Vascular/metabolism , Endothelium, Vascular/ultrastructure , Hypercholesterolemia/etiology , Hypercholesterolemia/metabolism , Hypercholesterolemia/pathology , Immunohistochemistry , Lipids/blood , Microscopy, Electron, Scanning , Microscopy, Electron, Transmission , Rabbits , Time FactorsABSTRACT
The aim of this study was to investigate the pleotropic effects of an extract of a traditional herb, Tribulus terrestris (TT), on the lipid profile and vascular endothelium of the abdominal aorta in New Zealand rabbits fed a cholesterol-rich diet. Eighteen rabbits were randomly divided into three groups (n=6 for each). One experimental group (EG-I) was given a cholesterol-rich diet, a second experimental group (EG-II) was treated with TT following a cholesterol-rich diet, and a control group (CG) was fed a standard diet. Blood samples were collected on day 0 and then at weeks 4 and 12 to determine total serum cholesterol (TC), high density lipid-cholesterol (HDL-C), low density lipid-cholesterol (LDL-C) and triglyceride (TG) levels. Tissues were collected from the abdominal aorta for immunohistochemistry and transmission and scanning electron microscopy. In EG-II, the serum lipid profile was significantly lower than that of EG-I at week 12 with a reduction of TC: 65%; LDL-C: 66%; HDL-C: 64%; TG: 55%. Ultrastructural analysis revealed that endothelial damage was more prominent in EG-I compared to EG-II. The ruptured endothelial linings and damaged cellular surfaces increased in EG-I compared to EG-II. Our data indicate that dietary intake of TT can significantly lower serum lipid profiles, decrease endothelial cellular surface damage and rupture and may partially repair the endothelial dysfunction resulting from hyperlipidemia.