NF-κB在变应性鼻炎发病中的调节作用  

Role of NF-κB in pathogenesis of allergic rhinitis

作　　者：张敏[1] 吴聃 刘黎星[1] 侯赛榕[1] 蔡丽希[1] ZHANG Min;WU Dan;LIU Li-xing;HOU Sai-rong;CAI Li-xi(Department of Anatomy and Physiology,Basic Medical College of Putian University,Putian 351100,FujianProvince,China)

机构地区：[1]莆田学院基础医学院解剖生理学教研室

出　　处：《中国临床解剖学杂志》2019年第4期421-424,430,共5页Chinese Journal of Clinical Anatomy

基　　金：莆田学院育苗基金资助课题(2014058;2016111);国家自然青年基金(81502360)

摘　　要：目的探讨变应性鼻炎(allergic rhinitis,AR)病理过程中TLR-NF-κB信号传导通路的调节机制及核因子-κB(NF-κB)对嗜酸性粒细胞聚集的调节作用。方法 50只大鼠随机分成A组(对照组)、B组(AR组)、C组(AR+PGN)、D组(AR+PGN+Pam3CSK4)、E组(AR+PGN+BEL),应用卵清蛋白建造AR模型,HE染色观察鼻黏膜形态改变并计数炎症细胞浸润数,ELISA法检测鼻腔清洗液IFN-γ、IL-4、嗜酸性粒细胞主要碱性蛋白(MBP)及IgE的含量,Real-Time PCR及Western blot法检测Toll样受体2(TLR2)、NF-κB的表达情况。结果 B组变应性损伤明显,鼻黏膜嗜酸性粒细胞浸润数多于其他组,IL-4、MBP及IgE的表达较A组增高(P<0.05);C组鼻黏膜以中性粒细胞浸润为主,IFN-γ、TLR2及NF-κB的表达较B组增高(P<0.05);D、E组炎症细胞浸润数、IL-4、MBP及IgE的表达较B组降低(P<0.05)。结论调控TLR-NF-κB传导通路的表达即抑制NF-κB的过度表达,有利于调节变应性鼻炎病理过程中嗜酸性粒细胞的增值聚集。Objective To experimentally investigate a potential mechanism of the TLR-NF-κB signaling pathway in the pathogenesis of allergic rhinitis(AR), and the role of NF-κB in eosinophil aggregation. Methods A total of 50 rats were randomly divided into five groups with A(control group), B(AR group), C(group of AR+PGN), D(group of AR+PGN+Pam3 CSK4), and E(group of AR +PGN+BEL).AR model was established with ovalbumin. Hematoxylin and eosin(H&E) staining was used to detect the morphologic change of nasal mucosa and count the number of infiltrated inflammatory cell. The contents of IFN-γ, IL-4, MBP and IgE in nasal cleanser were detected by ELISA. Expression of NF-κB and TLR2 was measured by Real-Time polymerase chain reaction(PCR) and Western blot. Results Obvious allergic injury was observed in AR rats(B group). The number of infiltrated eosinophils in nasal mucosa in group B was higher than in other groups. The expressions of IL-4, MBP and IgE in group B were higher than in group A(P<0.05). Neutrophil infiltration was predominant in nasal mucosa of group C, and the expression of IFN-γ, TLR2 and NF-κB was higher in group B(P<0.05). Inflammatory cell infiltration, IL-4, MBP and IgE expression in group D and E were lower than in group B(P<0.05). Conclusions Regulating the expression of TLR-NF-κB pathway and inhibiting the over-expression of NF-κB is beneficial to regulating the aggregation of eosinophils in the pathogenesis of allergic rhinitis.

关 键 词：核因子-ΚB TOLL样受体 肽聚糖 嗜酸性粒细胞 变应性鼻炎 

分 类 号：R765[医药卫生—耳鼻咽喉科] R392.3[医药卫生—临床医学]