Mechanisms Of Jnk Signaling Pathway In Mouse Model Of Allergic Rhinitis

Objective: To observe the c-jun N-terminal kinase phosphorylation in allergic rhinitis (allergic rhinitis) expression in mouse models. To explore the JNK signal transduction pathway in allergic rhinitis in ratsMethods: 30 adult mice were randomly divided into three groups: normal control group (A Group), allergic rhinitis group (B), budesonide group (C), 10 in each group. To co-nasal drip intraperitoneal injection of ovalbumin (OVA) to establish mouse model of allergic rhinitis to pathological staining, immunohistochemistry and image analysis of nasal mucosa of mice was determined phosphorylation of JNK (Phospho-JNK, P -JNK) expression and morphological changes of nasal mucosa.Results: OVA sensitized and excited by the mice showed clear symptoms of allergic rhinitis, showed sneezing, clear nasal discharge, nasal scratching the face, allergic rhinitis group, nasal ciliated damage, eosinophilic granule cells than in normal group increased Immunohistochemistry showed that p-JNK nasal tissue expression of allergic rhinitis was significantly higher (P <0.05). After budesonide treatment groups of eosinophils in nasal mucosa and mucosal damage accumulation than the AR group decreasedConclusions: JNK phosphorylation in allergic rhinitis nasal mucosa of mice were increased, suggesting that JNK signal transduction pathway in the pathogenesis of allergic rhinitis-related role play. Glucocorticoid hormones Budesonide significantly inhibited the activation of JNK protein synthesis and for glucocorticoid treatment of allergic rhinitis mechanism of a new direction.