动脉粥样硬化_____动脉粥样硬化；Ⅰ型胶原；

Ⅰ型胶原及NFκB与动脉粥样硬化关系的实验研究

http://www.100md.com 《西安交通大学学报》 2005年第5期

动脉粥样硬化,,动脉粥样硬化；Ⅰ型胶原；,NFκB；,1材料与方法,2结果,3讨论,参考文献

     摘要：目的探讨动脉粥样硬化(AS)时血脂成分的改变以及Ⅰ型胶原mRNA与其蛋白、NFκBmRNA与其蛋白在兔AS发生中的作用及其机制，为临床预防及治疗AS斑块提供新的理论依据。方法采用HE、免疫组化及原位杂交法染色，光镜观察AS病变，并应用CMIAS真彩色医学图像分析系统分析；检测40只食饵性AS新西兰兔血脂成分的改变及血管壁的病理变化、Ⅰ型胶原mRNA与其蛋白、NFκBmRNA与其蛋白的表达情况。结果实验兔15周时血胆固醇(TC)升高约43倍，血低密度脂蛋白(LDL)升高约37倍。主动脉内壁可见脂质条纹形成。主动脉AS病变Ⅰ型胶原、NFκB蛋白及Ⅰ型胶原mRNA、NFκBmRNA表达定量(A值)分别为0.27±0.02、0.19±0.01及0.30±0.03、0.35±0.03，显著高于对照组(0.08±0.01、0.09±0.01及0.11±0.01、0.10±0.09，P<0.05)。结论 AS时Ⅰ型胶原增多刺激NFκB的活性，可能参与了血管AS的形成。

    关键词：动脉粥样硬化；Ⅰ型胶原； NFκB；

    Study on relationship between typeⅠcollagen, NFκB and atherosclerosis in rabbits

    Zheng Jianjie, Ma Aiqun, Wang Hongyan, Bai Xiaojun, Bai Ling

    (1. Department of Cardiosurgery; 2. Department of Cardiology; 3. Department of Pathology, First Hospital of Xian Jiaotong University, Xian 710061, China)

    ABSTRACT: Objective To study the serum lipid (TC, TG, LDLC) and the role of typeⅠcollagen, NFκB, typeⅠcollagen mRNA and NFκB mRNA levels and their mechanisms in the occurrence and progress of atherosclerosis in order to provide theoretical gist for its prevention. Methods Blood vessel wall pathological and the serum lipid changes,the expressions of typeⅠcollagen, NFκB, typeⅠcollagen mRNA and NFκB mRNA levels were observed in dietary induced atherosclerosis rabbit model by morphology study, immunohistochemistry, in situ hybridization technique and color image analyzer(CMAIS). Results The model of AS was established successfully after rabbits were fed with cholesterol, who developed the fatty streak lesion in the aortic intrawall. In the rabbit model, TC and LDL were respectively increased 43 times and 37 times and there were no difference in TG and body weight. Type I collagen, NFκB, type I collagen mRNA and NFκB mRNA were 0.27±0.02, 0.19±0.01 and 0.30±0.03, 0.35±0.03, respectively, which were higher than those of control group(0.08±0.01, 0.09±0.01 and 0.11±0.01, 0.10±0.09, respectively) (P<0.05). Conclusion We understand further that hyperlipidemia is one of the uppermost causes of AS and provide theoretical gist for preventing AS. In other words, elevation of type I collagen in atherosclerotic lesions can stimulate NFκB activity , which is one of the mechanisms causing AS. ......

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