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目的:探讨核因子T-bet/GATA-3在支气管哮喘小鼠发病机制中的作用,观察地塞米松干预后T-bet、GATA-3mRNA的变化。方法:建立卵清蛋白(OVA)诱导的哮喘小鼠模型;24只BALB/c小鼠随机分为正常组、哮喘组及地塞米松治疗组,地塞米松腹腔注射(2mg/kg)给药。HE染色观察气道炎症变化;采用RT-PCR方法检测T-bet、GATA-3 mRNA的表达;流式细胞技术检测小鼠脾脏CD4+T细胞IFN-γ、IL-4水平。结果:与正常组相比,哮喘组小鼠GATA-3 mRNA表达显著增加(P<0.05),T-bet mRNA水平明显降低(P<0.05),IFN-γ水平明显降低(P<0.01),IL-4水平明显升高(P<0.05);经地塞米松干预后,肺组织GATA-3、T-bet mRNA均有所降低,以GATA-3m RNA降低更为明显,IL-4表达明显降低(P<0.05),而IFN-γ水平有减少倾向。结论:支气管哮喘小鼠T-bet/GATA-3表达失衡与气道炎症密切相关,地塞米松通过抑制GATA-3和T-bet的表达,调节IL-4/IFN-γ比率并纠正Th1/Th2平衡失调,可能是其治疗哮喘的机制之一。
Objective: To investigate the role of nuclear factor T-bet / GATA-3 in the pathogenesis of bronchial asthma in mice and observe the changes of T-bet and GATA-3 mRNA after dexamethasone intervention. Methods: A mouse model of asthma induced by ovalbumin (OVA) was established. Twenty-four BALB / c mice were randomly divided into normal group, asthma group and dexamethasone group. Dexamethasone was given intraperitoneally (2mg / kg) . The changes of airway inflammation were observed by HE staining. The expression of T-bet and GATA-3 mRNA were detected by RT-PCR. The levels of IFN-γ and IL-4 in CD4 + T cells were detected by flow cytometry. Results: Compared with normal group, the expression of GATA-3 mRNA in asthma group was significantly increased (P <0.05), T-bet mRNA expression was significantly decreased (P <0.05) (P <0.05). After intervention with dexamethasone, GATA-3 and T-bet mRNA in lung tissue were decreased, GATA-3 mRNA decreased more obviously and IL-4 expression was significantly higher Decreased (P <0.05), while the level of IFN-γ decreased. CONCLUSION: The imbalance of T-bet / GATA-3 expression in bronchial asthma mice is closely related to airway inflammation. Dexamethasone regulates IL-4 / IFN-γ ratio and corrects Th1 / Th2 balance disorders, may be one of the mechanisms of its treatment of asthma.