The Establishment and Characteristics of Rat Model of Atherosclerosis Induced by Hyperuricemia.

The Establishment and Characteristics of Rat Model of Atherosclerosis Induced by Hyperuricemia.
复制标题

高尿酸血症大鼠动脉粥样硬化模型的建立及特点

DOI:
10.1155/2016/1365257
复制
发表时间:
2016
影响因子:
4.3
通讯作者:
Li C
Li C
中科院分区:
医学3区
文献类型:
--
作者:
Liu Z;Chen T;Niu H;Ren W;Li X;Cui L;Li C

文献摘要

被引文献

相似文献

流行病学研究已经确定高尿酸血症是心血管疾病的一个独立危险因素。然而,高尿酸血症导致动脉粥样硬化的机制尚不清楚。本研究旨在建立高尿酸血症致动脉粥样硬化大鼠模型。Wistar-Kyoto大鼠被随机分配到正常饮食(ND)、高脂肪饮食(HFD)或高腺嘌呤饮食(HAD),然后在4、8或12周后牺牲。分析血清尿酸、血脂水平,苏木精、伊红染色观察主动脉病理变化,实时定量聚合酶链反应检测mRNA表达。与ND组相比,HAD组在4周时血清尿酸和TC显著升高,但ND组和HFD组之间血清尿酸无显著差异。与HFD组相比,HAD组主动脉钙化发生更早、更严重。与ND组相比,HFD组和HAD组增殖细胞核抗原、单核细胞趋化因子-1、细胞间粘附分子-1和血管细胞粘附分子-1 mRNA水平升高。这种新的动物模型将为研究高尿酸血症诱导动脉粥样硬化的机制提供有用的工具。
Epidemiological studies have identified hyperuricemia as an independent risk factor for cardiovascular disease. However, the mechanism whereby hyperuricemia causes atherosclerosis remains unclear. The objective of the study was to establish a new rat model of hyperuricemia-induced atherosclerosis. Wistar-Kyoto rats were randomly allocated to either a normal diet (ND), high-fat diet (HFD), or high-adenine diet (HAD), followed by sacrifice 4, 8, or 12 weeks later. Serum uric acid and lipid levels were analyzed, pathologic changes in the aorta were observed by hematoxylin and eosin staining, and mRNA expression was evaluated by quantitative real-time polymerase chain reaction. Serum uric acid and TC were significantly increased in the HAD group at 4 weeks compared with the ND group, but there was no significant difference in serum uric acid between the ND and HFD groups. Aorta calcification occurred earlier and was more severe in the HAD group, compared with the HFD group. Proliferating cell nuclear antigen, monocyte chemotactic factor-1, intercellular adhesion molecule-1, and vascular cell adhesion molecule-1 mRNA levels were increased in the HFD and HAD groups compared with the ND group. This new animal model will be a useful tool for investigating the mechanisms responsible for hyperuricemia-induced atherosclerosis.