| Background: Allergic rhinitis (AR)is clinically defined as a symptomaticdisorder of the nose induced by an IgE-mediated inflammation after allergen exposure. Rhinitis includes rhinorrhea, nasal obstruction, nasal itching and sneezing which are reversible spontaneously or under treating. In recent decades, its incidence has been increasing and has impaired severely on people's life. Further more, it could also induce asthma, sinusitis and polyps. Now it has been becoming a global health problem to be solved rapidly.Many studies had shown that both IgE-mediated I type allergic reaction and nerve or its transmitters were involved in the AR's mechanisms. Immune cell and cytokines played the key role. Yssel ( 2000 ) and others found that the expressive level of interleukin-4 mRNA, interleukin-5 mRNA and GM-CSF mRNA rosed in nose tracheal mucous membrane by ISH technique and significient difference (SD) was obvious. Primary studies had shown that IL-4 had extensive bio-function such as stimulating B Cell differentiation, activation and producing of immunoglobulin E, being responsible for the isotype switching of immunoglobulin, up-regulating VCAM-1 expression, enhancing the adhesion of inflammation cell, attracting eosinophilia into inflammation site. It was more important that IL-4 could promote the ThO cell differentiating into T help-2 cell which secret T helper-2 cytokines (IL-4,IL-5,GM-CSF etc) inducing to enhance immune reaction and improve AR' spathophysiological action severe. IL-5 play a significant role in increasing the number of eosinophils and sustaining the chronic inflammation variety in AR as an special regulating factor. It could enhance the producting and releasing of eosinophils progenitors, activate eosinophil, support the recruitment, maturation and survival of eosinophils. In addition, it could up-regulat adhesion molecule (AM) expression and enhance the adhesion of inflammation cell to membrane. Obviously, IL-4 and IL-5 dominated pathohysiological development and variety in AR. GM-CSF was also a key factor as for EOS' differentiating, activating, prolonging it's life. In consequence, it could promote the late phase action. But its eternal effects in AR were yet unclear completely. As a consequence the inhibition or modulation of allergen-specific Th2 cells and their cytokines had become an attractive target for novel therapeutic intervention strategies in allergy.(Cohn and Ray 2000).It's well known that expression of cytokines and other inflammation factors were dependented on such nuclear transcripts factor as NFkB, NFAT, AP-1 etc. Hart found that there were a lot of activated NF K B in trachea! mucous membrane of patient suffering bronchitis. Freter' s study indicated NF K B was a crucial nuclear transcript factor in regulating inflammation actions. All those suggested that NF K B took part in the proceeds of allergic pathohysiological action.Many kinds of drug were applied to therapy for AR in clinic. Glucocorticosteroids were selected firstly due to its good effect; but its side effect limited its broadening usage. Triptolide(TP), one of the extracts of Tripterygium wilfordii Hook f, had the same .extensive effects of suppressing immunology as glucocorticosteroids without its side effects and had been successfully applied to treating asthma which had more common in atrophy, tissue, pathophsiology and therapy with AR, but no report had been appearing in AR.Aim: This experiment explored how TP took effect on gene transcripts in AR animal model so that provided the evidence of applying TP to clinics. Materials and Methods:Adult guinea pigs,300-400g, were employed and divided into four groupsrandomly(n=20). They were:OV(ovalbumin,OV) group, TP group was conducted by TP, Dexamethasone(DM) group by DM and 0.9% Sodium Chloride(SC) group.Model was estab!ished:Basic sensitive: OV. 0.3mg; A1(OH)3 30mg was added with 0.9% SC to lml,and was injected into abdominal cavty(ia). qid. The times was sumed to 7. then they were sensitized with 0.25% OV/0.9%NS aerosol thought in...
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