Role of TLR-NF-κB Signaling Pathway in Pathogenesis of Allergic Rhinitis in Rats and Intervention with Tripterygium wilfordii Hook

To investigate the role of TLR-NF- κB signaling pathway in pathogenesis of allergic rhinitis (AR) in rats and intervention mechanism with Tripterygium wilfordii Hook (TWH). 80 Wistar rats were randomly divided into 4 groups: normal control group (N); allergic rhinitis model group (M); allergic rhinitis+lipopolysaccharide group (LPS); TWH intervention group (TWH). Changes of nasal mucosa tissues and inflammatory cell infiltration were observed by hematoxylin and eosin (HE) staining, while neutrophil and eosinophil were counted under high power microscope. Expression of interleukin-4 (IL-4), interferon gamma (IFN-γ), and immunoglobulin E (IgE) was measured with immunohistochemical analysis. Realtime-PCR and Western-blot were used to evaluate expression of toll-like receptor (TLR4) and nuclear factor κB (NF-κB). The results indicated that both group M and LPS developed allergic rhinitis symptoms and distinct inflammatory injury of nasal mucosa. Eosinophil count was significantly higher in M group than in others (P<0.05), while neutrophil count was significantly higher in LPS group than in others (P<0.05). Expression of IL-4 in M group was significantly higher than group N, LPS, and TWH (P<0.05). IFN-γexpression significantly increased in group LPS compared with M, N and TWH (P<0.05). The IgE expression was decreased significantly in LPS and TWH group compare with the M group (P<0.05). TLR4 and NF-κB levels were significantly higher in LPS and lower in TWH group than M groups (P<0.05). In conclusion, LPS and TWH can regulate the relative balance between TH1 and TH2 in the pathogenesis of AR, and inhibits infiltration of eosinophil and expression of IgE, by regulating the levels of TLR4 and NF-κB.