IL-4/STAT6在变应性鼻炎豚鼠鼻黏膜的表达及鼻用糖皮质激素对其表达的影响

目的:研究IL-4/STAT-6在变应性鼻炎豚鼠鼻黏膜的表达和丙酸氟替卡松鼻喷雾剂对其表达的影响,进一步探讨变应性鼻炎的发病机制。方法:45只豚鼠随机分为对照组(NC组)、变应性鼻炎无干预组(AR组)和变应性鼻炎糖皮质激素干预组(Glu组),每组15只。其中AR、Glu组采用卵清白蛋白致敏法制备变应性鼻炎豚鼠模型;NC组用生理盐水替代卵清白蛋白进行同步处理。动物建模后用丙酸氟替卡松鼻喷雾剂(每次50μl/侧)治疗,每天2次,连续5d。观察各组大鼠行为学改变及鼻黏膜病理学改变,免疫组织化学法检测各组豚鼠鼻黏膜中IL-4、STAT6蛋白的表达并观察其变化情况及相关性。结果:与NC组比较,AR组豚鼠喷嚏及搔鼻次数明显增加,IL-4、STAT6表达增强;与AR组比较,Glu组激素干预后豚鼠喷嚏及搔鼻次数明显减少,IL-4、STAT6表达减弱,NC组与Glu组相比结果无明显差异。结论:IL-4/STAT6在Th2分化中起关键作用,丙酸氟替卡松鼻喷雾剂干预后可以通过影响IL-4/STAT6的表达发挥治疗作用。

Histologic expressions of IL-4/STAT6 in nasal mucosa of guinea pig allergic rhinitis models and effect of glucocorticoid on them

Objective:To investigate the relation between IL-4/STAT6 and allergic rhinitis by comparing expressions of IL-4 and STAT6 in normal nasal mucosa and allergic rhinitis models,to explore the influence of glucocorticoid on IL-4,and STAT6 expression,and then to elucidate further the pathogenesis of AR and the mechanism of glucocorticoid.Method:Forty-five guinea pigs were divided into three groups: normal control(NC) group,allergic rhinitis group(AR) and glucocorticoid(Glu) group(15 each).Animals in AR and Glu groups were sensitized with egg albumin,and in NC group were treated with normal saline as control.After sensitization and reproduction of AR model,rats in AR group received no treatment,while those in Glu group were treated with glucocorticoid(50 μl/one side/time,once a day) for 5 days.The changes in behavior was examined,and pathology of nasal mucosa were observed with HE staining,and the protein expressions of IL-4 and STAT6 in the nasal mucosa were detected by immunohistochemical technique.Result:Compared with NC group,the frequency of sneezing and nose-scratching,and the expressions of IL-4 and STAT6 were increased obviously,but the opposite findings were observed in Glu group.Conclusion:IL-4 and STAT6 are related to the pathogenesis of allergic rhinitis and may be the main factors for eosinophil infiltration in allergic rhinitis.Glucocorticoid may produce a therapeutic effect by intervening the expression of IL-4 and STAT6.