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. 2018 Jul;16(1):113-120.
doi: 10.3892/etm.2018.6143. Epub 2018 May 10.

A cynomolgus monkey model of carotid atherosclerosis induced by puncturing and scratching of the carotid artery combined with a high-fat diet

Lei Zhang  1 , Yan Zeng  1 , Ji Qi  2 , Yanxiao Xu  2 , Shaoqun Zhang  2 , Xin Zhou  2 , Ruiyue Ping  3 , Shijie Fu  1
Affiliations

A cynomolgus monkey model of carotid atherosclerosis induced by puncturing and scratching of the carotid artery combined with a high-fat diet

Lei Zhang et al. Exp Ther Med. 2018 Jul.

Abstract

Cardio-cerebrovascular disease is one of the three major causes of mortality in humans and constitutes a major socioeconomic burden. Carotid atherosclerosis (CAS) is a very common lesion of the arterial walls, which leads to narrowing of the arteries, in some cases occluding them entirely, increasing the risk of cardiovascular events. The aim of the present study was to evaluate a cynomolgus monkey model of carotid atherosclerosis (CAS) induced by puncturing and scratching combined with a high-fat diet. A total of 12 cynomolgus monkeys were randomly divided into four groups: A, puncturing and scratching carotid artery intimas + high-fat diet (n=3); B, puncturing and scratching carotid artery intimas + regular diet (n=3); C, high-fat diet only (n=3); and D, regular diet only (n=3). Blood was harvested at weeks 4, 6 and 8 and plasma lipid levels were assessed. At week 8, monkeys were sacrificed and carotid arteries were harvested for hematoxylin and eosin (H&E) staining to observe pathological changes. The results revealed that a high-fat diet led to increased plasma lipid levels and accelerated plaque formation. Carotid color Doppler ultrasonography was performed and, along with H&E staining, revealed plaque formation in group A. In summary, the results of the present study suggest that a cynomolgus monkey model of CAS model may be successfully constructed by puncturing and scratching of the carotid artery intimas in combination with a high-fat diet.

Keywords: animal models; carotid atherosclerosis; high-fat diet.

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Figures

Figure 1.
Figure 1.
The cynomolgus monkey model of carotid atherosclerosis was constructed by puncturing the carotid artery and scratching the intima. The white arrow indicates the point at which the carotid artery was pierced with a needle.
Figure 2.
Figure 2.
Plasma lipid levels in each group prior to intervention. No statistically significant differences were observed. TG, triglycerides; TC, total cholesterol; HDL-C, high-density lipoprotein cholesterol; LDL-C, low-density lipoprotein cholesterol.
Figure 3.
Figure 3.
Plasma (A) TG, (B) TC, (C) HDL-C and (D) LDL-C levels in each group at different time points. #P<0.05 vs. 6 weeks in the same group; $P<0.05 vs. 8 weeks in the same group; %P<0.05 vs. group B at the same time; &P<0.05 vs. group C at the same time; *P<0.05 vs. group D at the same time. TG, triglycerides; TC, total cholesterol; HDL-C, high-density lipoprotein cholesterol; LDL-C, low-density lipoprotein cholesterol.
Figure 4.
Figure 4.
Color Doppler ultrasound of the carotid artery. Images of (A) an artery transect and (B) a longitudinal section were obtained. White arrows indicate plaque formation.
Figure 5.
Figure 5.
Hematoxylin and eosin staining revealed the morphological characteristics of carotid atherosclerosis. (A) Transect and (B) longitudinal section of the carotid artery in group A. (C) Transect and (D) longitudinal section of the carotid artery in group B. (E) Transect and (F) longitudinal section of the carotid artery in group C. (G) Transect and (H) longitudinal section of the carotid artery in group D. Black arrows indicate scratch injuries on the carotid intima. White arrows indicate the location of atherosclerotic plaques. In groups C and D, the arterial wall was complete, the endothelial cell layer maintained its integrity and the diameter of the lumen was uniform.
See this image and copyright information in PMC

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