Effect Of Deer Goose Rhinitis On Th1 / Th2 Cells And Related Cytokines In Allergic Rhinitis Model Rats

ObjectiveAllergic rhinitis is mediated by IgE allergic disease, is the most common form of the upper respiratory tract disease, prevalence rate increased significantly in recent years.Although allergic rhinitis will not threat to life, but the number of patients is large, except lead to local organs such as the nose and eye symptoms, it can also be induced bronchial asthma and other complications, will serious impact on individuals and society.Chinese medicine has certain advantages in treating allergic rhinitis,and Lu E Bi Yan formula(LEBYF) is uesd to treat allergic rhinitis in our clinical,which mechanism of treatment is not clear at present. We establish allergic rhinitis rats model by ovalbumin sensitization,to study the treatment of LEBYF to allergic rhinitis rats model and the effect of regulating Thl\Th2 cells.Methods60 SD rats were randomly divided into 6 groups:normal group,model group,cetirizine group,high LEBYF group,middle LEBYF group and low LEBYF group.Rats were made into AR models by ovalbumin sensitization,after the completion of the modeling were given appropriate drug intervention,all rats were killed after 14 days and Obtain serum and nasal mucosa tissue.Using ELISA method to detect serum OVA-sIgE, IL-4 and IFN-gamma level, HE、PAS and A& S staining observation of nasal mucosa pathological morphological changes and detecting the change of the number of mast cells and goblet cells, immunohistochemical to detect nasal mucosa tissues expression of IL-4 and IFN-gamma, western blot and RT-PCR method to detect the expression of T-bet and GATA-3 in nasal mucosa tissue which is specific transcription factor of Th1、Th2 cells.Results1) After model, the behavioral scores were greater than five points in model group and treatment group,and high than normal group.2) The nasal pathomorphology performance of normal group rats included pseudostratified ciliated columnar epithelial was complete and smooth,no inflammatory response performance;the nasal epithelial of model group rats was shedding necrosis and discontinous,inflammatory cell infiltration,tissue clearance bleeding,gland hyperplasis and swelling,goblet cells inceased,secretions on mucosal surface increased; the nasal of cetirizine group rats basicly returned to normal,and there was no significant inflammation; the nasal of treatment group rats have a significantly improved,only exsist a small amout inflammatory cell infiltration and part of epithelial cell sheded. Compared with normol group and treatment group,the numberofmast cells and goblet cells in nasal mucosal increased obviously in model group rats.3.Serum ELISA test, compared with normal group,IgE、IL-4 level is increase and IFN-y level is decrease in model group;after treatment, compared with model group, IgE、IL-4 level is decrease and IFN-y level is increase in treatment groupAimmunohistochemical test, compared with normal group,the expression of IL-4 is increase and IFN-y is decrease in model group; after treatment, compared with model group, the expression of IL-4 decrease and IFN-y is increase in treatment group.5. Western blot and RT-PCR test, compared with normal group,the expression of GATA-3is increase and T-bet is decrease in model group; after treatment, compared with model group, the expression of GATA-3 is decrease and T-bet is increase in treatment group.Conclusions1) LEBYF can effectively relieve nasal symptoms of allergic rhinitis rats,such as runny nose, sneezing,and reduce the level of serum OVA-sIgE and nasal inflammation,have treatment of allergic rhinitis.2) LEBYF can reduce allergic rhinitis rats Th2 cytokines IL-4 levels, elevated Thl cytokines IFN-gamma content, correcting imbalances of Th1Th2 cells, relieve their immune allergy. The mechanism may be down-regulated by expression of Th2-specific transcription factor GATA-3, and promote the expression of Th1-specific transcription factor T-bet,through regulatory Thl/Th2 cells to reversing the cellular immune response to Th2 dominated immune imbalance.