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目的:探讨地塞米松对哮喘小鼠模型肺组织中肿瘤坏死因子样弱凋亡诱导因子(TWEAK)及受体成纤维细胞生长因子诱导的早期反应蛋白14(Fn14)表达的调节作用。方法:采用卵清蛋白致敏方法建立经典哮喘模型。将36只雌性BALB/c小鼠,随机分为对照组、哮喘组、地塞米松组,每组12只。HE染色评估各组小鼠气道炎症程度;采用逆转录聚合酶链反应(RT-PCR)方法检测各组肺组织TWEAK、Fn14mRNA表达水平;采用免疫组化方法检测各组肺组织TWEAK、Fn14蛋白表达水平。结果:哮喘组小鼠肺组织TWEAK、Fn14 mRNA水平高于对照组(P<0.01),地塞米松组TWEAK、Fn14 mRNA水平低于哮喘组(P<0.01)。TWEAK、Fn14蛋白的表达水平哮喘组较对照组明显升高(P<0.01),地塞米松组表达量较哮喘组明显降低(P<0.01)。结论:地塞米松可抑制哮喘小鼠肺组织中TWEAK及Fn14表达,从而减少气道炎症反应。
Objective: To investigate the regulatory effect of dexamethasone on tumor necrosis factor-like weak-inducing factor (TWEAK) and receptor fibroblast growth factor-induced early reactive protein 14 (Fn14) expression in the lung tissue of asthmatic mice. Methods: A classic asthma model was established by ovalbumin sensitization. 36 female BALB / c mice were randomly divided into control group, asthma group and dexamethasone group, with 12 mice in each group. HE staining was used to evaluate the degree of airway inflammation in each group. The expression of TWEAK and Fnl4 mRNA in lung tissues of each group was detected by reverse transcription-polymerase chain reaction (RT-PCR). The expressions of TWEAK and Fn14 The expression level. Results: The TWEAK and Fn14 mRNA levels in asthmatic mice were significantly higher than those in control group (P <0.01). The TWEAK and Fn14 mRNA levels in dexamethasone group were lower than those in asthma group (P <0.01). The expression of TWEAK and Fn14 protein in asthma group was significantly higher than that in control group (P <0.01). The expression of TWEAK and Fn14 in asthma group was significantly lower than that in asthma group (P <0.01). Conclusion: Dexamethasone can inhibit the expression of TWEAK and Fn14 in the lung tissue of asthmatic mice and thus reduce airway inflammation.