机构地区:[1]吉林大学中日联谊医院耳鼻咽喉头颈外科,长春130033 [2]吉林大学中日联谊医院中心研究室,长春130033 [3]吉林大学基础医学院病理生物学教育部重点实验室
出 处:《中华耳鼻咽喉头颈外科杂志》2008年第6期443-446,共4页Chinese Journal of Otorhinolaryngology Head and Neck Surgery
摘 要:目的建立豚鼠实验性变应性鼻炎最轻持续炎性反应(minimal persistent inflammation,MPI)模型,并初步探讨其病理机制及意义。方法60只健康雄性Hartley系豚鼠,随机分为A~D共4组,每组15只。A组为阳性对照组,B组为实验组即MPI组,C组为阴性对照组,D组为空白对照组。首先以含卵清蛋白和氢氧化铝凝胶的生理盐水混合液对A、B、C3组行基础致敏和强化致敏,再分别用1%和0.01%的卵清蛋白溶液或生理盐水长期鼻腔激发。D组始终以生理盐水进行致敏和激发。观察豚鼠鼻腔激发后症状(喷嚏)变化并检测鼻黏膜中嗜酸粒细胞(eosinophils,EOS)浸润程度及上皮细胞内细胞间黏附分子1(intercellular adhesion molecule1,ICAM-1)的表达情况。结果MPI模型组在以1%卵清蛋白溶液激发时,喷嚏平均次数明显多于D组(P〈0.05),而与A、C组相比差异无统计学意义(P值均〉0.05);改用0.01%卵清蛋白溶液鼻腔激发后,变应性鼻炎症状基本消失,与D组相比差异无统计学意义(P〉0.05),但鼻黏膜内仍有少量EOS浸润,EOS计数明显多于D组(P〈0.05),并可见上皮细胞轻度表达ICAM-1,而D组无ICAM-1表达。结论通过长期低浓度卵清蛋白鼻腔激发,可成功建立豚鼠实验性变应性鼻炎MPI模型,将为深入探讨变应性鼻炎病理机制和制定干预策略提供实验参考。Objective To develop an animal model of minimal persistent inflammation (MPI) in allergic rhinitis guinea pigs and to investigate its significance. Methods Sixty male Hartley guinea pigs were divided into four groups : group A ( positive control group ) , B ( MPI model group ), C ( negative group ) and D(bland group) respectively, with fifteen animals in each group. Guinea pigs from group A, B and C were sensitized intraperitoneally by injection of suspension of ovalbumin(OVA) and aluminum hydroxide in 0. 9% physiological saline. Then, repeated local booster sensitization with different concentration of OVA suspension( 1% and 0.01% ) or physiological saline into the nasal cavity of those guinea pigs were performed. For group D, physiological saline was used only. Symptoms (sneezing) of guinea pigs after antigen challenge were observed and the infiltration of eosinophils (EOS) together with the expression of intercellular adhesion molecule 1 ( ICAM-1 ) in the nasal epithelial cells were also examined. Results When challenged with 1% OVA, the sneezing number of guinea pigs in group B was increased markedly than that in group D( P 〈 0. 05 ). However, there was no difference between group B, A and C( P 〉 0. 05 ). When challenged with 0. 01% OVA, the symptom of sneezing almost disappeared in group B just like that in group D and there was no difference between the two groups ( P 〉 0. 05 ). Besides, there was still more EOS infiltrated in the nasal mucosa of guinea pigs in group B than that in group D ( P 〈 0. 05 ). There was no expression of ICAM-1 in nasal epithelium of guinea pigs in group D, nevertheless, ICAM-1 was found mildly expressed in group B. Conclusions MPI models have been established successfully through long term challenge with lower density of OVA in the sensitized guinea pigs, which will provide us with a new method for further research in the mechanism and treatment of allergic rhinitis.
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