中文摘要：

目的利用雷帕霉素探讨哺乳动物雷帕霉素靶蛋白（mTOR）在支气管哮喘小鼠气道重塑中的作用机制。方法30只6清洁级BABL／c小鼠，随机数字表法分为3组，每组10只，分别为生理盐水对照组、卵蛋白（OVA）哮喘组、雷帕霉素治疗组。在末次激发24h后所有小鼠取左肺组织行苏木精-伊红（HE）染色，PAS染色及mTOR免疫组织化学染色。分别用酶联免疫吸附法（ELISA）和Westei＇nblot检测支气管肺泡灌洗液（BALF）中IL4、IL-5、IL-13含量以及右肺组织mTOR蛋白表达。应用小鼠肺功能仪检测气道阻力的变化。结果哮喘模型组小鼠与对照组相比较BALF中IL-4、IL-5、IL-13水平增高；肺组织mTOR蛋白表达水平明显高于对照组（P〈0．01）。雷帕霉素治疗组与哮喘模型组相比较BALF中IL-4、IL-5、IL-13含量及肺组织mTOR表达水平均降低，差异具有显著性（P〈0．05）。结论雷帕霉素可抑制哮喘小鼠气道重塑的发生，其机制有可能是通过阻断mTOR信号通路而实现的。

英文摘要：

Aim To explore the effect of rapamycin on airway remodeling and the expression of mTOR in asth- matic mice. Methods Thirty male BABL/c mice were randomly divided into three groups with 10 mice in each group： control group, OVA group, and rapam- yein group. The left lung was isolated for pathological examination. Lung sections were stained with HE and PAS,immunohistochemistry. The concentrations of IL- 4,IL-5,IL-3 in BALF were examined by ELISA, and the mTOR from the right lung tissues was detected by Western blot. The changes of the airway resistance and lung function were analyzed by means of animal lungs function analysis system. Results In OVA group, the number of inflammatory cells and the concentrations of IL-4, IL-5, IL-3 in BALF and bronchial airway thickness, bronchial smooth muscle thickness, and mTOR in lung tissue were significantly higher than those in control group （P 〈 0.05）. In rapamycin group, the number of inflammatory cells, the concentrations of IL- 4,IL-5 ,IL-3 in BALF and bronchial airway thickness, bronchial smooth muscle thickness, and mTOR in lung tissue were significantly lower than those in OVA group （P 〈 0. 05）. The above indices of Rapamycin group were significantly lower than those of OVA group （ P 〈 0. 05 ）. Conclusion Rapamycin can inhibit the de- velopment of airway remodeling in asthmatic mice, and the possible mechanism may be due to its inhibition of roTOR signaling.