论文部分内容阅读
目的:探讨重组激活基因1(RAG1)在变应性鼻炎(AR)发病机制中的作用及其与IL4、IL10和IgE之间的关系及意义。方法:用卵清蛋白(OV)建立大鼠AR模型并用地塞米松(DEX)进行干预,用被动皮肤过敏原试验(PCA)测试皮肤反应并与正常对照组进行比较;用RTPCR技术检测各组鼻黏膜中RAG1基因mRNA的表达水平,并对RAG1基因的DNA进行测序;用ELISA法检测各组大鼠外周血清IL4、IL10和IgE的水平变化。结果:RAG1基因的mRNA在正常对照组鼻黏膜中未见表达,在AR组和DEX干预组均有明显表达;DNA测序未发现RAG1基因有突变发生;AR组血清IL4[(106.31±12.90)ng/L]和IgE[(38.67±4.13)ng/L]水平均显著高于正常对照组[(93.65±7.78)ng/L,(23.27±1.36)ng/L](均P<0.05),IL10[(38.15±4.89)ng/L]水平显著低于正常对照组[(48.74±3.49)ng/L](P<0.05);经DEX干预后,血清IL4[(92.67±16.40)ng/L]和IgE[(24.23±4.38)ng/L]水平均较AR组显著下降(均P<0.05),而IL10[(46.18±5.01)ng/L]水平较AR组显著升高(P<0.05);PCA试验在AR组90%呈阳性反应,在正常对照组和DEX干预组均呈阴性反应。结论:RAG1的高表达与AR的发病密切相关,并介导了IL4和IgE的分泌及抑制IL10的分泌。其DNA序列在AR鼻黏膜中具有保守性,糖皮质激素不影响RAG1基因的表达,推测在AR发病机制中,RAG1基因通过一个较高层面的免疫调节环节发生作用。
Objective: To investigate the role of RAG1 in the pathogenesis of allergic rhinitis (AR) and its relationship with IL4, IL10 and IgE. Methods: Rat AR model was established with ovalbumin (OV) and treated with dexamethasone (DEX). The skin reaction was tested by Passive Skin Allergen Test (PCA) and compared with the normal control group. The RTPCR The expression of RAG1 mRNA in nasal mucosa was detected, and the DNA of RAG1 gene was sequenced. The levels of IL4, IL10 and IgE in peripheral blood were detected by ELISA. Results: The mRNA of RAG1 gene was not expressed in the nasal mucosa of normal control group and was significantly expressed in AR and DEX intervention groups. No mutation of RAG1 gene was found in DNA sequencing. The level of IL4 [(106.31 ± 12.90) ng / L] and IgE [(38.67 ± 4.13) ng / L] were significantly higher than those in the normal control group [(93.65 ± 7.78) ng / L, The level of IL-4 [(92.67 ± 16.40) ng / L] was significantly lower than that of the normal control group [(48.15 ± 4.49) ng / L] (24.23 ± 4.38) ng / L] were significantly lower than those in AR group (all P <0.05), while those of IL10 [(46.18 ± 5.01) ng / L] ; PCA test in 90% of AR group was positive, in the normal control group and DEX intervention group were negative reactions. Conclusion: The high expression of RAG1 is closely related to the pathogenesis of AR and mediates the secretion of IL4 and IgE and the secretion of IL10. Its DNA sequence is conserved in the nasal mucosa of AR. Glucocorticoid does not affect the expression of RAG1 gene. It is speculated that RAG1 gene acts through a higher level of immunoregulation in AR pathogenesis.