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

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.

MicroRNA-486-5p functions as a diagnostic marker for carotid artery stenosis and prevents endothelial dysfunction through inhibiting inflammation and oxidative stress

“…Endothelial cell damage is the initiating pathological basis of arteriosclerosis, and runs through the whole process of arteriosclerosis development. The dysfunction of vascular endothelial cells and activation of the inflammatory response ultimately cause the occurrence of CAS [ 3 ]. In the current study, HAECs were recruited for cell function experiments and treated with oxLDL.…”

“…The main cause of CAS is the dysfunction of endothelial cells caused by atherosclerotic plaque, and the apoptosis of vascular endothelial cells induced by oxidized low-density lipoprotein (ox-LDL) is a vital link leading to the lesion [ 2 ]. It is demonstrated that age, hypertension, diabetes, and hyperlipidemia are all risk inducements for CAS [ 3 ]. Clinical intervention for asymptomatic CAS patients can effectively reduce the risk of stroke, which has an important clinical significance.…”

LncRNA THRIL Functions as a Marker for Carotid Artery Stenosis and Affects the Biological Function of Human Aortic Endothelial Cell

“…4 The main pathological changes include vascular endothelial cell damage, inflammatory cell infiltration, abnormal lipid deposition, foam cell formation, and atherosclerotic plaque formation. 5 The risk factors of CAS factors include obesity, hypertension, hyperlipidemia, smoking, chronic infection, and genetic factors. Many patients with CAS often have no obvious clinical symptoms, while acute ischemic symptoms, such as sudden stroke and hemiplegia, are often caused by carotid plaques or thrombus on the surface of plaque, leading to intracranial arteriovenous ischemia.…”