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

Author:

Yu Qi1,Li Yafeng1,Waqar Ahmed Bilal2,Wang Yanli1,Huang Bingqiao1,Chen Yulong1,Zhao Sihai13,Yang Peigang1,Fan Jianglin2,Liu Enqi13

Affiliation:

1. Research Institute of Atherosclerotic Disease, Xi’an Jiaotong University School of Medicine, Xi’an 710061, China

2. Department of Molecular Pathology, University of Yamanashi, Chuo 409-3898, Japan

3. Key Laboratory of Environment and Genes Related to Diseases of the Education Ministry, Xi’an Jiaotong University School of Medicine, Shaanxi, Xi’an 710061, China

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.

Funder

National Natural Science Foundation of China

Publisher

Hindawi Limited

Subject

Health, Toxicology and Mutagenesis,Genetics,Molecular Biology,Molecular Medicine,General Medicine,Biotechnology

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