中文摘要：

目的探讨PKC-δ/mTOR/NF-κB信号通路在喘小鼠气道重塑中的作用机制。方法 40只雄性清洁级Balb/c小鼠,随机数字表法分为4组,每组10只,分别为正常对照组;哮喘模型组;PKCδ抑制剂Rottlerin治疗组;mTOR抑制剂雷帕霉素（Rapamycin）治疗组。在末次激发24 h后小鼠肺组织行HE染色、PAS染色。用图像分析软件测定支气管壁厚度（WAt/Pbm）、支气管平滑肌厚度（WAm/Pbm）及杯状细胞百分比。用酶联免疫吸附法（ELISA）检测支气管肺泡灌洗液（BALF）中IL-4、IL-5、IL-13含量以及用Western blot检测肺组织PKC-δ、mTOR、NF-κB蛋白表达。结果哮喘模型组小鼠与正常对照组小鼠相比较BALF中IL-4、IL-5、IL-13水平增高;肺组织WAt/Pbm、WAm/Pbm、杯状细胞百分比和PKC-δ、mTOR、NF-κB蛋白表达水平显著增高（P〈0.05）。Rottlerin和Rapamycin治疗组与哮喘模型组相比较BALF中IL-4、IL-5、IL-13水平降低;肺组织WAt/Pbm、WAm/Pbm、杯状细胞百分比和PKC-δ、mTOR、NF-κB蛋白表达水平显著降低（P〈0.05）。而Rottlerin治疗组和Rapamycin治疗组之间上述各指标无显著性差异（P〉0.05）。结论 Rottlerin抑制哮喘小鼠气道重塑的发生,其机制有可能部分是通过抑制PKC-δ/mTOR/NF-κB信号通路而实现的。

英文摘要：

To explore the effect of PKC-δ/mTOR/NF-κB signaling pathway on airway remodeling, forty male Balb/c mice were recruited and randomly divided into four groups with 10 mice in each group： control group, asthma model group, Rottlerin group, and Rapamycin group. Then, cells in bronchoalveolar lavage fluid （BALF） were counted; lung tissue of mice was isolated and stained with HE and PAS for pathological examination; bronchial wall thickness （WAAm/Pbm）, bronchial smooth muscle thickness （WAAm/Pbm and goblet cell percentage were measured by Image analysis software. Furthermore, the concentrations of IL-4, IL-5, IL-13 in BALF were detected by ELISA, while PKC-δ, mTOR, NF-κB expressions in lung tissues were detected by Western blot. In asthma model group, WAAm/Pbm, WAAm/Pbm, goblet cell percentage, the concentrations of IL-4, IL-5, IL-13 in BALF and PKC-δ, roTOR, NF- κB in lung tissue were significantly higher than those in control group （P〈 0.05）. In Rottlerin group and Rapamycin group, WAAm/Pbm, WAAm/Pbm goblet cell percentage, the concentrations of IL-4, IL-5, IL-13 in BALF, and the expressions of PKC-δ, roTOR, NF-κB in lung tissue were significantly higher than those in asthma model group （P〈 0.05）. There was no significant differences in above mentioned indexes between Rottleringroup and Rapamycin group （P 〉 0.05）. All these results indicated the Rottlerin can inhibit the development of airway remodeling in asthmatic mice, and the possible mechanism may be due to inhibition of PKC-δ/mTOR/NF-κB signaling pathway.