变应性鼻炎嗅觉障碍大鼠嗅感受神经元的实验研究

目的 通过锰增强磁共振成像技术(manganese-enhanced magnetic resonance imaging,MEMRI)观察变应性鼻炎(AR)嗅觉障碍大鼠嗅觉传导通路的改变,并用病理学方法 观察嗅黏膜形态结构的改变和相关免疫组织化学变化,来探讨AR对嗅黏膜感受神经元的影响.方法40只SD大鼠,随机分为实验组(30只)和对照组(10只).实验组应用卵清蛋白致敏并激发SD大鼠,应用埋藏食物小球实验评估AR大鼠嗅觉功能,建立AR嗅觉障碍的大鼠模型.ELISA法测定并比较血清IgE水平.MEMRI观察大鼠嗅球中锰增强的对比显影.HE染色及免疫组化法观察嗅黏膜的组织形态学变化及嗅标记蛋白表达的变化.结果 对成功建模的AR大鼠进行嗅觉功能评估,40%(12/30)的AR大鼠在AR的基础上伴有嗅觉障碍.MEMRI示对照组大鼠嗅球锰增强显影显著,AR伴嗅觉障碍组大鼠嗅球几乎无锰增强显影,AR不伴嗅觉障碍组大鼠嗅球有部分锰增强显影.AR伴嗅觉障碍组大鼠嗅黏膜的上皮层明显变薄,阳性的嗅感受神经元的层数减少,与不伴嗅觉障碍组和对照组相比差异存在统计学意义(P均<0.05).结论 通过卵清蛋白致敏激发可以成功建立AR嗅觉障碍的大鼠模型.AR可导致嗅黏膜感受神经元的变化,并由此导致嗅觉传导通路的改变,有可能是AR引起嗅觉障碍的发病机制之一.

Experimental research of the olfactory receptor neurons of olfactory dysfunction by allergic rhinitis

OBJECTIVE To set up an intranasal ovalbumin-induced animal model of allergic rhinitis(AR) accompanied with olfactory dysfunction in mice. By observing the olfactory pathway in mice using manganese-enhanced magnetic resonance imaging (MEMRI) and the relatively morphologic structural and immunological changes in olfactory epithelium, the influence of AR on olfactory receptor neurons(ORNs) was studied.METHODS Forty SD mice were randomly divided into two groups, the research group(n=30) and the control group(n=10). The research group was intraperitoneally injected and intranasal application of ovalbumin to establish an AR mice model. The olfactory function of the mice was evaluated by buried food test(BFT). ELISA was performed to measure the level of IgE in serum. MEMRI images were acquired with a 7.0 T micro-MR scanner. HE staining and immunohistochemistry were used to observe the tissues morphology change of olfactory mucosa and OMP expression.RESULTS The olfactory function evaluation of the AR mice model indicated that the incidence of olfactory dysfunction in AR mice was 40.0%. The AR mice with olfactory dysfunction had no signal enhancement in MEMRI. The olfactory epithelium became thinner, layer numbers of ORNs were decreased with disorder arrangement and the OMP expression was decreased in AR mice with olfactory dysfunction compared with that in AR mice without olfactory dysfunction(P=0.018) and the control group(P=0.0141).CONCLUSION An animal model of AR accompanied with olfactory dysfunction in mice was successfully established. The influence of AR on ORNs and thus cause the change of the olfactory pathway is one of the major pathogenesis of olfactory dysfunction in AR.