| 王 贞,辛丽红,张 雯.过表达XB130抑制哮喘小鼠气道高反应性和气道炎症[J].,2017,17(13):2440-2443 |
| 过表达XB130抑制哮喘小鼠气道高反应性和气道炎症 |
| Overexpression of XB130 Inhibited the Airway Inflammation and Hyperresponsiveness in a Murine Asthmatic Model |
| 投稿时间：2016-05-30 修订日期：2016-06-25 |
| DOI：10.13241/j.cnki.pmb.2017.13.010 |
| 中文关键词: XB130 哮喘 气道高反应 气道炎症 |
| 英文关键词: XB130 Asthma Airway hyperresponsiveness Airway inflammation |
| 基金项目: |
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| 中文摘要: |
| 摘要 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IgE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-?酌的分泌。结果：哮喘小鼠肺组织中XB130表达减少，过表达XB130其mRNA和蛋白表达水平显著升高。过表达XB130降低醋甲胆碱（metha- choline，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）IgE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。 |
| 英文摘要: |
| ABSTRACT Objective: To investigate the effect of XB130 on the airway inflammation and hyperresponsiveness in a murine asth- matic model. Methods: C57 mice were randomly divided into 4 groups with 9 mice each: control group (CON), Asthma group (AS), Adenovirus contral group (Ad-vector+AS) and XB130 overexpression group (Ad-XB130+AS). A murine asthmatic model was induced by ovalbumin (OVA) administration. Ad-vector and Ad-XB130 were injected intravenously. After the last antigen challenge for 24 h, the bronchi alveolar lavage fluids (BALF)have been collected. Airway hyperresponsiveness to methacholine (Mch) was measured. The ex- pression of XB130 in lung tissues was evaluated using RT-PCR and Western blotting respectively. The content of OVA-specific IgE in serum was detected using ELISA. The cell counts of eosinophile granulocyte (EOS) were calculated. The secretion of IL-4, IL-5, IL-13 and IFN-γ were determined using ELISA. Results: XB130 was reduced in the lung tissue of asthma mice. The mRNA and protein expression of XB130 were increased in Ad-XB130 asthmatic mice. Overexpression XB130 reduced the airway hyperresponsiveness induced by methacholine (Mch). The number of EOS in Ad-XB130+AS group (17±4) was decreased compared with Ad-vector+AS group (48±3). Moreover, forcing expression of XB130 (0.051±0.002) reduced the content of OVA-specific IgE compared with vector control group (0.128±0.007). In addition, XB130 inhibited the secretion of IL-4, IL-5 and IL-13, promoted the production of IFN-γ in BALF and lung tissues. Conclusion: Overexpression of XB130 inhibited the airway inflammation and hyperresponsiveness in asthmatic mice. |
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