title: Temporal and quantitative analysis of atherosclerotic lesions in diet-induced hypercholesterolemic rabbits.
abstract: The diet-induced atherosclerotic rabbit is an ideal model for atherosclerosis study, but temporal changes in atherosclerotic development in hypercholesterolemic rabbits are poorly understood. Japanese white rabbits were fed a high-cholesterol diet to induce sustained hypercholesterolemia, and each group of 10-12 animals was then sacrificed at 6, 12, 16, or 28 weeks. The rabbit aortas were harvested, and the sizes of the gross and intima atherosclerotic lesions were quantified. The cellular component of macrophages (Mφs) and smooth muscle cells (SMCs) in aortic intimal lesions was also quantified by immunohistochemical staining, and the correlation between plasma cholesterol levels and the progress of atherosclerotic lesions was studied. The ultrastructure of the atherosclerotic lesions was observed by transmission electron microscopy (TEM). Widely variable atherosclerotic plaques were found from 6 weeks to 28 weeks, and the lesional progress was closely correlated with cholesterol exposure. Interestingly, a relatively reduced accumulation of Mφ, an increased numbers of SMCs, and a damaged endothelial layer were presented in advanced lesions. Moreover, SMCs were closely correlated with cholesterol exposure and lesional progress for the whole period. Cholesterol exposure directly determines atherosclerotic progress in a rabbit model, and the changes in the cellular component of advanced lesions may affect plaque stability in an atherosclerotic rabbit model.
authors.affiliation: Research Institute of Atherosclerotic Disease, Xi'an Jiaotong University School of Medicine, Xi'an 710061, China.
authors.forename: Qi
authors.initials: Q
authors.lastname: Yu
authors.forename: Yafeng
authors.initials: Y
authors.lastname: Li
authors.forename: Ahmed Bilal
authors.initials: AB
authors.lastname: Waqar
authors.forename: Yanli
authors.initials: Y
authors.lastname: Wang
authors.forename: Bingqiao
authors.initials: B
authors.lastname: Huang
authors.forename: Yulong
authors.initials: Y
authors.lastname: Chen
authors.forename: Sihai
authors.initials: S
authors.lastname: Zhao
authors.forename: Peigang
authors.initials: P
authors.lastname: Yang
authors.forename: Jianglin
authors.initials: J
authors.lastname: Fan
authors.forename: Enqi
authors.initials: E
authors.lastname: Liu
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D001011:Aorta / Q000166:cytology / Q000473:pathology; D019540:Area Under Curve; D050197:Atherosclerosis / Q000097:blood / Q000209:etiology / Q000473:pathology*; D002097:C-Reactive Protein / Q000378:metabolism; D002791:Cholesterol, Dietary / Q000008:administration & dosage / Q000009:adverse effects*; D059305:Diet, High-Fat; D006937:Hypercholesterolemia / Q000097:blood / Q000209:etiology / Q000473:pathology*; D008055:Lipids / Q000097:blood; D008264:Macrophages / Q000378:metabolism / Q000473:pathology; D008297:Male; D032389:Myocytes, Smooth Muscle / Q000378:metabolism / Q000473:pathology; D058226:Plaque, Atherosclerotic / Q000097:blood / Q000209:etiology / Q000473:pathology*; D011817:Rabbits
chemical_list: D002791:Cholesterol, Dietary; D008055:Lipids; D002097:C-Reactive Protein