【摘要】 目的观察T细胞特异转录因子T-bet/GATA-3在支气管哮喘中失衡表达,探讨地塞米松对其调节作用。方法36只雄性SPF级SD大鼠随机分为对照组(C组)、哮喘组(A组)和地塞米松组(D组)。苏木精-伊红染色观察气道病理改变;酶联免疫吸附测定(ELISA)法检测大鼠血清中IL-4、IL-5、IFN-γ含量;逆转录-聚合酶链反应(RT-PCR)和免疫印迹(Westernblot)测定法分别检测肺组织T-bet和GATA-3mRNA和蛋白表达。结果肺组织中嗜酸性粒细胞(EOS)、淋巴细胞、管壁面积/支气管管腔内周长(WA/Pi)和支气管平滑肌面积/支气管管腔内周长(ASM/Pi)A组比C组明显增多或增厚(P<0.01),D组明显低于A组(P<0.01);血清中IL-4和IL-5含量,A组高于C组(P<0.01),D组低于A组(P<0.01),IFN-γ含量A组和D组均低于C组(P<0.01);肺组织中T-betmRNA和蛋白表达A组明显低于C组(P<0.01),D组明显低于C组(P<0.01);肺组织中GATA-3mRNA和蛋白表达A组高于C组(P<0.01),D组与C组和A组比较差异均无统计学意义(P>0.05)。结论转录因子T-bet/GATA-3在哮喘中失衡表达,地塞米松明显抑制转录因子T-bet表达,但对GATA-3表达无明显影响,其抑制哮喘的气道炎症并非通过调节转录因子T-bet和GATA-3的平衡实现。更多还原

【Abstract】 Objective To investigate imbalanced expression of T cell-specific transcription factors T-bet and GATA-3 and the effects of dexamethasone on them in asthmatic rats.Methods Thirty-six male SD rats were randomly divided into control group,asthmatic group,and dexamethasone group.The changes of airway histology were observed.The concentrations of interleukin(IL)-4,IL-5,interferon γ(IFN-γ) in serum were measured by ELISA.The mRNA and protein expressions of T-bet and GATA-3 in the lungs were detected by RT-PCR and Western blot respectively.Results In asthmatic group,the numbers of eosinophils and lymphocytes,the thicknesses of WA/Pi and ASM/Pi were increased compared with those in control group and dexamethasone group(P<0.01).So did the concentrations of IL-4 and IL-5 in serum(P<0.01).In asthmatic group,the concentration of IFN-γ in serum was decreased compared with that in control group(P<0.01).So did the expressions of T-bet mRNA and protein(P<0.01).In asthmatic group,the levels of GATA-3 mRNA and protein expression were significantly increased compared with those in control group(P<0.01).Conclusion The expressions of T cell-specific transcription factors T-bet and GATA-3 are imbalanced,and dexamethasone inhibits T-bet,but has no effect on GATA-3 in asthmatic rats.Dexamethasone inhibits the asthmatic airway inflammation without regulating the balance of transcription factors T-bet and GATA-3.更多还原