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豚鼠动脉粥样硬化模型形成机制:LDL-C代谢异常
引用本文:杨润梅,陈慧敏,高南南,宋鑫,李金莲,蔡大勇. 豚鼠动脉粥样硬化模型形成机制:LDL-C代谢异常[J]. 中国实验动物学报, 2011, 19(3): 237-241,280,281. DOI: 10.3969/j.issn.1005-4847.2011.03.013
作者姓名:杨润梅  陈慧敏  高南南  宋鑫  李金莲  蔡大勇
作者单位:中国医学科学院北京协和医学院药用植物研究所药理毒理研究中心,北京,100193
基金项目:科技部"重大新药创制"科技重大专项-综合性新药研究开发技术大平台-创新药物研究开发技术平台建设
摘    要:目的建立豚鼠动脉粥样硬化模型并探讨其形成机制,同时与大鼠进行比较,阐明模型特点及优势。方法应用高脂饲料诱导方法,观察豚鼠和大鼠动脉粥样硬化病变的形成情况。HE染色法分析主动脉内膜-中膜厚度、内膜炎性细胞浸润和内膜表层斑块的形成情况;酶法检测血脂,酶联免疫吸附法测定血清Ox-LDL浓度,实时定量PCR检测肝脏LDL-R mRNA表达的变化,免疫组化检测血管内膜CD36蛋白表达的变化。结果与对照组比较,豚鼠模型组动脉内膜明显增厚,单核细胞、巨噬细胞浸润与聚集增加,大量的泡沫细胞聚集形成斑块,而大鼠模型组未出现类似动脉粥样硬化病理改变。机制研究表明豚鼠较大鼠易于诱发形成动脉粥样硬化原因主要在于豚鼠血清Ox-LDL水平明显升高,肝脏LDL-R mRNA表达下调,动脉内膜CD36蛋白表达明显增强等。结论与大鼠不同,经高脂饲料诱导10周后,豚鼠可形成典型动脉粥样硬化病变,其机制主要在于LDL-C代谢异常。

关 键 词:豚鼠  动脉粥样硬化  Ox-LDL  LDL-R  CD36

Mechanism of early atherosclerosis in guinea pigs: abnormal metabolism of LDL-C
YANG Run-mei,CHEN Hui-min,GAO Nan-nan,SONG Xin,LI Jin-lian,CAI Da-yong. Mechanism of early atherosclerosis in guinea pigs: abnormal metabolism of LDL-C[J]. Acta Laboratorium Animalis Scientia Sinica, 2011, 19(3): 237-241,280,281. DOI: 10.3969/j.issn.1005-4847.2011.03.013
Authors:YANG Run-mei  CHEN Hui-min  GAO Nan-nan  SONG Xin  LI Jin-lian  CAI Da-yong
Affiliation:YANG Run-mei,CHEN Hui-min,GAO Nan-nan,SONG Xin,LI Jin-lian,CAI Da-yong(Research Center for Pharmacology and Toxicology,Institute of Medicinal Plant Development,Chinese Academy of Medical Sciences and Peking Union Medical College,Beijing 100193,China)
Abstract:Objective To establish a model of early atherosclerosis in guinea pig and explore its pathogenetic mechanisms,compared with the modeling in rats,and to clarify the characteristics and advantages of this guinea pig model of atherosclerosis.Methods The differences of early atherosclerosis induced by high lipid diets in guinea pig and rat were investigated.Aortic intima-media thickness,intimal inflammatory cells infiltration and plaque development were observed by pathology with HE staining.Serum lipid levels ...
Keywords:Ox-LDL  LDL-R  CD36
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