STAT6在哮喘小鼠肺组织的表达及激素的影响作用

目的探讨信号转导和转录激活因子(STAT)-6在支气管哮喘发病机制中的作用及激素的影响作用。方法经腹腔注射与鼻腔滴注卵白蛋白(OVA)制作小鼠哮喘模型,并设对照组和地塞米松干预组,激发后观察各组肺组织病理学改变,采用反转录-聚合酶链反应(RT-PCR)和免疫组织化学检测肺组织STAT6mRNA和蛋白表达。结果OVA末次激发24h后,病理组织学显示哮喘组小鼠肺组织可见大量炎细胞浸润,STAT6mRNA(2.46±0.24与1.41±0.26,P<0.01)及蛋白表达水平较对照组明显增加,地塞米松治疗后,小鼠肺组织炎细胞浸润减轻,STAT6mRNA(1.80±0.36与2.46±0.24,P<0.01)及蛋白表达水平下降。结论哮喘气道中STAT6过度表达,地塞米松可通过调控STAT6表达发挥抗炎作用。

The expression of STAT6 in murine asthma model and the effect of dexamethasone

Objective To investigate the role of STAT6 in development of asthma and its response to treatment with dexamethasone. Methods Murine asthma models was created by intranasal and intraperitoneal dosing of OVA, and then randomized to control group and dexamethasone-treated group. After challenge, the lung tissues were subjected to histological study and the expression of STAT6 mRNA in the lungs was detected using semi-quantitative RTPCR and immmunohistochemistry. Results 24 hours after the last challenge, massive infiltration of inflammatory cells in lung tissues and significant elevated expression of STAT6 mRNA from baseline （2.46±0.24 vs 1.41±0.26, P〈0.01） was found in the untreated OVA-sensitized mice. In contrast, dexamethasone-treated mice showed less inflammatory infiltration and lower level of STAT6 mRNA expression （1.80±0.36 vs 2.46±0.24,P〈0.01）. Conclusion Over-xpression of STAT6 was demonstrated in the airways with asthma, and dexmathesone may be effective as an anti-inflammatory agent by inhibiting STAT6 expression.