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目的 用新西兰白兔 (NZW )作为Cpn感染和AS的模型 ,来进一步探索Cpn和AS之间的关系。 方法 35只健康NZW兔分为 4组 ,分别为Cpn感染组 (I)、Cpn感染组同时予以高脂饮食组 (HI)、高脂饮食组 (H)和对照组 (C)。I和HI组于实验 1、3周经鼻腔每次感染 1mlCpn(1× 1 0 6IFU/ml)。H和HI组同时喂予高脂饲料。初次感染后 1 2周全部处死 ,取心、肺、肝和血管组织进行病理学、直接微量免疫荧光 (IF)和PCR检测。结果 HI组血管组织最大内膜厚 (MIT)和斑块面积指数 (PAI)均大于H组 (P <0 .0 5 )。I组血管未发现AS病变。Cpn抗原和DNA在 1 0只HI组家兔中检测到。 结论 Cpn感染和高脂饮食可促进并加重AS病变
Objective To further explore the relationship between Cpn and AS using New Zealand white rabbits (NZW) as a model of Cpn infection and AS. Methods 35 healthy NZW rabbits were divided into 4 groups: Cpn infection group (I), high fat diet group (HI), high fat diet group (H) and control group (C). The I and HI groups were infected with 1 ml of Cpn (1 × 10 6 IFU / ml) through the nasal cavity one and three weeks after the experiment. H and HI group also fed high fat diet. All the patients were sacrificed at 12 weeks after primary infection, and pathology, direct microinjection of immunofluorescence (IF) and PCR were performed on the heart, lung, liver and blood vessels. Results The maximal intimal thickening (MIT) and plaque area index (PAI) in HI group were significantly higher than those in H group (P <0.05). I group of vascular disease was not found in AS. Cpn antigen and DNA were detected in 10 HI group rabbits. Conclusion Cpn infection and high-fat diet can promote and aggravate AS lesions