雷公藤多苷干预TLR-NF-κB通路发挥免疫抑制作用  

Immunosuppression of tripterygium glycosides via TLR-NF-κB signaling pathway

作　　者：张敏[1] 王守安[1] 刘黎星[1] 

机构地区：[1]莆田学院基础医学院生理学教研室,福建莆田351100

出　　处：《中草药》2014年第9期1288-1292,共5页Chinese Traditional and Herbal Drugs

基　　金：莆田市科技局课题(2010S06);福建省教育厅课题(JK2013045)

摘　　要：目的探讨雷公藤多苷在变应性鼻炎(allergic rhinitis,AR)发病中干预TLR-NF-κB通路的机制。方法 100只大鼠随机分成4组:对照组、模型组、雷公藤多苷组、倍氯米松组,每组25只。应用卵清白蛋白制备AR模型,施加雷公藤多苷干预。HE染色观察鼻黏膜形态改变并计数炎性细胞浸润数,免疫组化法检测肿瘤坏死因子-α(TNF-α)、白细胞介素-5(IL-5)及免疫球蛋白(IgE)的量,实时定量PCR及Western blotting检测Toll样受体(TLR4)和核因子-κB(NF-κB)的表达情况。结果模型组变应性损伤明显,鼻黏膜以嗜酸性粒细胞浸润为主,TNF-α、IL-5及IgE的表达较对照组明显增高,TLR4和NF-κB的表达较对照组也明显增高(P<0.05);雷公藤多苷及倍氯米松组鼻黏膜以少量中性粒细胞浸润为主,IL-5、IgE、TLR4和NF-κB的表达较模型组明显降低(P<0.05)。结论雷公藤多苷可通过影响TLR-NF-κB信号传导通路,降低TLR4及NF-κB的表达发挥免疫调节作用。Objective To investigate the intervention of tripterygium glycosides （TG） on TLR-NF-k3 signaling pathway in pathogenesis of allergic rhinitis （AR）. Methods Ovalbumin was provided to build AR model, TG was used to interfere the rats, and 100 rats were randomly divided into four groups such as control （group A）, model （group B）, TG （group C）, BDP （group D） groups （n = 25）. Changes of nasal mucosa tissues and inflammatory cell infiltration were observed by HE staining, while neutrophil and eosinophil count was performed under high power microscope. Expression of IL-5, TNF-α, and IgE in nasal mucosa tissues was measured with immunohistochemical method. Realtime-PCR and Westem-blotting were used to evaluate the expression levels of TLR4 and NF-kB. Results Developed AR injury of nasal mucosa was observed in group B. Eosinophil count and the expression of IL-5, TNF-α, and IgE were significantly higher in group B than those in group A; The expression levels of TLR4 and NF-kB were significantly higher than those in group A （P 〈 0.05）, and IL-5, IgE, TLR4, and NF-kB were significantly decreased in groups C and D than those in group B （P 〈 0.05）. Conclusion TG could decrease the expression of TLR and NF-kB to suppress immunity via TLR-NF-kB signaling pathway in pathogenesis of AR.

关 键 词：雷公藤多苷 TOLL样受体 核因子-KB TLR-NF-kB通路 变应性鼻炎 

分 类 号：R765.21[医药卫生—耳鼻咽喉科]