PDF(Pubmed)
Abstract：
Acute thrombosis secondary to atherosclerotic plaque rupture is the main cause of acute cardiac and cerebral ischemia. An animal model of unstable atherosclerotic plaques is highly important for investigating the mechanism of plaque rupture and thrombosis. However, current animal models involve complex operations, are costly, and have plaque morphologies that are different from those of humans. We aimed to establish a simple animal model of vulnerable plaques similar to those of humans. Rabbits were randomly divided into three groups. Group A was given a normal formula diet for 13 weeks. Group C underwent surgery on the intima of the right carotid artery with - 80 °C cryofluid-induced injury after 1 week of a high-fat diet and further feeding a 12-week high-fat diet. Group B underwent the same procedure as Group C but without the - 80 °C cryofluid. Serum lipid levels were detected via ELISA. The plaque morphology, stability and degree of stenosis were evaluated through hematoxylin-eosin (HE) staining, Masson trichrome staining, Elastica van Gieson staining (EVG), and oil red O staining. Macrophages and inflammatory factors in the plaques were assessed via immunohistochemical analysis. The serum low-density lipoprotein cholesterol (LDL-C), triglyceride (TG), and total cholesterol (TC) levels in groups B and C were significantly greater than those in group A. No plaque formation was observed in group A. The plaques in group B were very small. In group C, obvious plaques were observed in the blood vessels, and the plaques exhibited a thin fibrous cap, a large lipid core, and partially visible neovascularization, which is consistent with the characteristics of vulnerable plaques. In the plaques of group C, a large number of macrophages were present, and matrix metalloproteinase 9 (MMP-9) and lectin-like oxidized LDL receptor 1 (LOX-1) were abundantly expressed. We successfully established a rabbit model of vulnerable carotid plaque similar to that of humans through the combination of cryofluid-induced endothelial injury and a high-fat diet, which is feasible and cost effective.
摘要：
继发于动脉粥样硬化斑块破裂的急性血栓形成是急性心、脑缺血的主要原因。不稳定动脉粥样硬化斑块的动物模型对于研究斑块破裂和血栓形成的机制非常重要。然而,目前的动物模型涉及复杂的操作，是昂贵的,斑块形态与人类不同。我们的目的是建立一个简单的类似于人类的易损斑块的动物模型。将兔随机分为三组。A组给予正常配方饮食13周。C组在高脂饮食1周并进一步喂养12周高脂饮食后，在-80°C的低温下对右颈动脉内膜进行手术。B组经历与C组相同的程序,但没有-80°C的冷冻流体。通过ELISA检测血清脂质水平。斑块形态,稳定性和狭窄程度通过苏木精-伊红（HE）染色，Masson三色染色,ElasticavanGieson染色(EVG),油红O染色。通过免疫组织化学分析评估斑块中的巨噬细胞和炎症因子。血清低密度脂蛋白胆固醇（LDL-C），甘油三酯（TG），B组和C组的总胆固醇（TC）水平明显高于A组。A组未观察到斑块形成。B组斑块很小。C组,在血管中观察到明显的斑块，斑块显示出薄的纤维帽，一个大的脂质核心，和部分可见的新生血管形成，这与易损斑块的特征是一致的。在C组的斑块中,大量的巨噬细胞存在，基质金属蛋白酶9（MMP-9）和凝集素样氧化LDL受体1（LOX-1）大量表达。我们通过结合冷冻液致内皮损伤和高脂饮食，成功建立了与人类相似的兔颈动脉易损斑块模型。这是可行的和成本有效的。
