MRNA expression of complement C3 and C4 in rat nasal mucosa with allergic rhinitis / 中华耳鼻咽喉头颈外科杂志

<p><b>OBJECTIVE</b>To investigate the level of mRNA expression of complement C3 and C4 in rat nasal mucosa and to reveal the relationship with the pathogenesis of allergic rhinitis (AR) .</p><p><b>METHODS</b>Twenty healthy SD rats were randomly divided into AR group and control group, 10 rats for each group. Ten rats was sensitized and intranasally challenged by ovalbumin and Al (OH)3 (as supplement) as allergic rhinitis models, and the control group was treated by saline. RT-PCR was performed to investigate the level of mRNA expression of complement C3 and C4 in nasal mucosa of both groups.</p><p><b>RESULTS</b>C3 and C4 mRNA were detected in both groups. The relative intensity of gene expression was measured. The relative intensity of C3 mRNA expression was 6183+/-1376 in AR group, 4444+/-989 in control group, C4 mRNA was 4398 +/-948 in AR group, and 2771+/-407 in control group. Expression of C3 and C4 in AR group was higher than that of the controls ( P < 0. 05) .</p><p><b>CONCLUSION</b>The high level of C3 and C4 mRNA expression in nasal mucosa of rats with allergic rhinitis suggests that C3 and C4 are involved in the immunopathology of allergic rhinitis. The result implies that complement system involved in the rat's allergic rhinitis is possibly activated through the classical pathway.</p>

Expression of complement regulatory protein C1-INH and CD46 in nasal mucosa of allergic rhinitis rats / 第二军医大学学报

Objective: To determine the expression of complement regulatory proteins (CRPs) C1-INH, MCP (CD46) in the nasal mucosa of allergic rhinitis rats and to study the role of CRPs in the pathogenesis of allergic rhinitis. Methods: Nine healthy SD rats were sensitized and intranasally challenged with ovalbumin and Al(OH)3 (as supplement) to establish allergic rhinitis models and another 9 SD rats treated with saline were taken as control. The nasal mucosa in respiratory area of both groups was obtained. Then Western blotting was performed to investigate the expression levels of C1-INH and CD46. Results: Western blotting showed that both C1-INH and CD46 had been detected in rat nasal mucosa. Expression level of CD46 in the nasal mucosa of allergic rhinitis was significantly higher than that in control rats(P<0.01); whereas the level of C1-INH was lower than that in control rats(P<0.05). Conclusion: It is suggested that both C1-INH and CD46 maybe involved in the pathogenesis of rat allergic rhinitis. The regulatory role of CRPs may be related to the classical pathway of complement activation.