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目的:研究XB130在哮喘小鼠气道高反应(airway hyperresponsiveness,AHR)和气道炎症中的作用。方法:36只C57小鼠分为4组:正常对照组(Control,CON)、哮喘组(Asthma,AS)、腺病毒载体组(Ad-vector+AS)和腺病毒过表达XB130组(Ad-XB130+AS)。采用卵白蛋白(ovalbumin,OVA)建立小鼠过敏性哮喘模型,后两组小鼠分别尾静脉注射Ad-vector和Ad-XB130。最后一次雾化吸入后24小时进行气道高反应试验,收集支气管灌洗液(bronchi alveolar lavage fluids,BALF)。采用RT-PCR和Western blotting方法检测XB130表达。ELISA法检测血清中OVA特异性Ig E的含量。直接计数法计算BALF中嗜酸性粒细胞(eosinophile granulocyte,EOS)数量。ELISA方法用于检测BALF和肺组织中IL-4、IL-5、IL-13和IFN-γ的分泌。结果:哮喘小鼠肺组织中XB130表达减少,过表达XB130其m RNA和蛋白表达水平显著升高。过表达XB130降低醋甲胆碱(methacholine,Mch)诱导的气道高反应。与载体对照组(48±3)相比,XB130过表达(17±4)EOS数量显著减少。同时,过表达XB130(0.051±0.002)较载体对照组(0.128±0.007)Ig E含量减少。此外,XB130抑制哮喘小鼠中IL-4、IL-5和IL-13并促进IFN-γ分泌。结论:过表达XB130可抑制哮喘模型小鼠气道高反应性和炎症反应。
AIM: To investigate the role of XB130 in airway hyperresponsiveness (AHR) and airway inflammation in asthmatic mice. Methods: Thirty-six C57 mice were divided into four groups: Control, CON, Asthma, AS, Ad-vector + AS and Ad- XB130 + AS). The mice model of allergic asthma was established by ovalbumin (OVA), and the mice in the two groups were injected with Ad-vector and Ad-XB130 respectively via tail vein. Airway hyperresponsiveness tests were performed 24 hours after the last nebulization and bronchoalveolar lavage fluids (BALF) were collected. The expression of XB130 was detected by RT-PCR and Western blotting. Serum levels of OVA-specific IgE were measured by ELISA. The number of eosinophile granulocytes (EOS) in BALF was calculated by direct counting method. The ELISA method was used to detect the secretion of IL-4, IL-5, IL-13 and IFN-γ in BALF and lung tissue. Results: The expression of XB130 decreased in the lung tissue of asthmatic mice. The expression of mBNA and protein in XB130 cells was significantly increased. Overexpression of XB130 reduced methacholine (Mch) -induced airway hyperresponsiveness. Compared with the vehicle control group (48 ± 3), XB130 overexpression (17 ± 4) significantly reduced the number of EOS. At the same time, the IgE level of over-expressed XB130 (0.051 ± 0.002) was lower than that of the vehicle control group (0.128 ± 0.007). In addition, XB130 inhibits IL-4, IL-5 and IL-13 in asthmatic mice and promotes IFN-γ secretion. Conclusion: Overexpression of XB130 can inhibit airway hyperresponsiveness and inflammatory response in asthmatic mice.