The Research Of The Anti-inflammation And Analgesic Mechanisms Of Tongfengning Granule Based On "TLR/NF-κB" Signal Pathway

ObjectiveThe study will further explore the Tongfengning’s microscopic mechanism and provide the data for the drug’s clinical application based on "TLR/NF-κB " signal pathway, by observing the generally information, inflammatory cells and PGE2, IL-8content in the synovial fluid and the expression of IκB-α, KK-ain joint synovial organization of rat’s acute gouty arthritis model.Methods45(male, SPF, SD) rats randomly divided into normal control group, model control group, Tongfengning group, Tongfengding group and Celecoxib group, using monosodium urate crystal (MSU) to set up the acute gouty arthritis model. Three days after treatment, use the pathology testing, enzyme linked immunosorbent assay, immunohistochemical technology to observe, compare and analyze the pathological form of joint synovial organization, cytokines PGE2, IL-8content in the synovial fluid, and the expression of IκB-α, IKK-ain joint synovial organization.Results1. Tongfengning granule plays a significant role in rat’s acute gouty arthritis models of inflammation and swelling;also can significantly inhibit joint swelling and local inflammatory cells infiltrating and synovial cells’proliferation. The inhibition, Tongfengning granule, is inferior to Celecoxib capsule, but better than the Tongfengding capsule, and high safety;rats with no adverse reaction.2. Enzyme league immune analysis shows that Tongfengning granule can reduce the content of PGE2, IL-8in synovial fluid. The results between Tongfengning group and model control group have significant difference (P<0.05).3. Immunohistochemical analysis shows that the Tongfengning granule can lower the expression of I KK-a and promote the expression of IκB-α.ConclusionTongfengning granule has an obvious effect of anti-inflammation and detumescence to acute gouty arthritis, its mechanism may realse to Tongfengning granule influence key signaling molecules IκB-α and IKK-a’s expression in "TLR/NF-κB" signal pathway, thus inhibit the expression of PGE2, IL-8, and then reduce infiltration of local tissue inflammatory cells and proliferation of synovial membrane cells;relieve the inflammatory response.