中文摘要：

目的探讨A20重组蛋白对支气管哮喘小鼠气道重构及NF-κB信号通路的影响。方法 40只雄性清洁级Balb/c小鼠,随机数字表法分为4组,每组10只,分别为：生理盐水对照组;卵蛋白（OVA）哮喘组;A20重组蛋白治疗3 d组;A20重组蛋白治疗7 d组。在末次激发24 h后所有小鼠取左肺组织行苏木精-伊红（HE）染色及PAS染色。取右肺组织分别用酶联免疫吸附法（ELISA）,RT-PCR和Western blote检测支气管肺泡灌洗液（BALF）中IL-4、IL-5、TNF-α及IFN-γ含量以及肺组织中结缔组织生长因子（Connective tissue growth factor,CTGF）、转化生长因子-β1（trailsforming growth factor-β1,TGF-β1）的mRNA表达和核转录因子（nuclear factor kappa B,NF-κB）的表达。结果哮喘模型组小鼠与对照组相比较BALF中炎症细胞计数、IL-4、IL-5、TNF-α水平增高,而IFN-γ水平降低;肺组织CTGF、TGF-β1的转录和表达水平以及NF-κB表达水平均显著高于对照组（P〈0.01）。A20重组蛋白3 d和7 d干预组小鼠与哮喘模型组相比较BALF中炎症细胞计数、IL-4、IL-5、TNF-α水平,CTGF、TGF-β1的转录和表达水平,NF-κB表达水平均显著降低,而BALF中IFN-γ水平明显上升,具有显著差异（P〈0.05）,但2个不同治疗组之间上述各指标间差异无统计学意义（P〉0.05）。结论 A20重组蛋白可抑制哮喘小鼠气道重构的发生,其机制有可能是通过抑制NF-κB/TGF-β1/CTGF信号通路而实现的。

英文摘要：

To explore the effects of A20 domain protein on airway remodeling and the expression of NF-κB in asthmatic mice,40 male Balb/c mice were randomly divided into four groups with 10 mice in each group： control group,OVA group,A20 domain protein 3 d group,A20 domain protein 7 d group.The left lung of all groups was isolated and stained with HE and PAS for pathological examination.The concentrations of IL-4,IL-5,TNF-α,and IFN-γ in BALF were measured by ELISA;the RT-PCR and Western blotting were performed to detect the mRNA expression of CTGF/TGF-β1 mRNA and NF-κB in the right lung tissues.In OVA group,all these detected index were higher,including the number of inflammatory cells,the concentrations of IL-4,IL-5,and TNF-α in BALF,the Bronchial airway thickness,the bronchial smooth muscle thickness,the collagen deposition area,as well as the expression of CTGF/TGF-β1 mRNA and NF-κB in lung tissue,but IFN-γ were lower than those in group B（P 0.01）.On the contrary,A20 domain protein 3 d group and A20 domain protein 7 d group demonstrated lower level of all these index（P0.05）,except IFN-γ which was higher than that in group B（P 0.01）.For index mentioned above,there were no significant differences between A20 domain protein 3 d group and A20 domain protein 7 d group（P0.05）.All these results indicated that the A20 domain protein can inhibit the development of airway remodeling in asthmatic mice,and the possible mechanism may be due to inhibition of NF-κB/ TGF-β1/CTGF signaling.