变应性鼻炎大鼠TNFAIP3基因在鼻腔上皮细胞的表达

TNFAIP3 Gene Expression in Nasal Epithelial Cells of Allergic Rhinitis Rats

目的研究致敏-治疗过程中肿瘤坏死因子α诱导蛋白3(tumor necrosis factor alpha-induced protein 3,TNFAIP3)基因在大鼠鼻腔黏膜上皮的表达,探讨TNFAIP3基因在变应性鼻炎免疫进程中的作用。方法本实验于在2019年1月—2020年1月开展,将24只Wistar大鼠,随机分为对照组、模型组、治疗组各8只。卵清蛋白构建变应性鼻炎(allergic rhinitis,AR)大鼠模型并评价造模效果;免疫组化法检测大鼠鼻腔黏膜组织中促炎因子核因子κB(nuclear factor kappa B,NF-κB)、TNFAIP3的表达情况;采用qRT-PCR检测鼻黏膜中NF-κB和TNFAIP3基因表达的情况。结果AR大鼠模型构建成功,模型组鼻腔黏膜组织中可见大量嗜酸性粒细胞浸润,NF-κB阳性显色密集,TNFAIP3阳性显色罕见。鼻黏膜中NF-κB基因表达在模型组中高于治疗组与对照组(P<0.05)。TNFAIP3基因表达在模型组中低于治疗组与对照组(P<0.05)。结论锌指蛋白TNFAIP3作为炎症触发因子NF-κB的负调控因素,可阻止机体变应性炎症反应的发展。

Objective To investigate the expression of tumor necrosis factor alpha-induced protein 3(TNFAIP3)gene in the nasal mucosa of rats in the process of sensitization-therapy and to explore the role of TNFAIP3 in the immune progression of allergic rhinitis.Methods From January 2019 to January 2020,a total of 24 Wistar rats were randomly divided into control group,model group and treatment group,there were 8 rats in each.Rats were sensitized by ovalbumin for establishment of allergic rhinitis(AR)model and the modeling effect was evaluated.The expression of nuclear factor kappa B(NF-κB)and TNFAIP3 in nasal mucosa of rats were detected by immunohistochemical techniques.And the expression of NF-κB and TNFAIP3 genes in nasal mucosa were determined by reverse transcription-quantitative polymerase chain reaction.Results The AR rat model was successfully constructed.A large number of eosinophil cells infiltration were observed in nasal mucosa of rats with allergic rhinitis and NF-κB positive coloration was dense in model group,while TNFAIP3 positive coloration was rare.Expression levels of NF-κB gene in nasal mucosa was significantly upregulated in model group than in control and treatment group(P<0.05).Relatively TNFAIP3 gene expression in model group was lower than that in control group and treatment group(P<0.05).Conclusion Zinc finger protein TNFAIP3,acts as a negative regulator of NF-κB,can prevents the development of allergic inflammatory response.