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Journal of Biomedicine and Biotechnology
Volume 2012 (2012), Article ID 506159, 7 pages
http://dx.doi.org/10.1155/2012/506159
Research Article

Temporal and Quantitative Analysis of Atherosclerotic Lesions in Diet-Induced Hypercholesterolemic Rabbits

1Research Institute of Atherosclerotic Disease, Xi’an Jiaotong University School of Medicine, Xi'an 710061, China
2Department of Molecular Pathology, University of Yamanashi, Chuo 409-3898, Japan
3Key Laboratory of Environment and Genes Related to Diseases of the Education Ministry, Xi’an Jiaotong University School of Medicine, Shaanxi, Xi'an 710061, China

Received 23 July 2011; Revised 24 November 2011; Accepted 12 December 2011

Academic Editor: George E. Plopper

Copyright © 2012 Qi Yu et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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.