平喘Ⅰ号对哮喘鼠气道重塑ERK信号转导的干预

Intervention effect of Pingchuan Ⅰ Formula on the ERK signaling pathway in mice with asthma airway remodeling

目的:观察支气管哮喘模小型鼠在平喘Ⅰ号干预下不同时期细胞外信号调节激酶(ERK)及c-fos的表达变化,探讨其防治支气管哮喘气道重塑的作用及其作用机制。方法:复制小鼠哮喘模型,随机分为正常对照组、模型对照组、地塞米松组、平喘Ⅰ号低、中、高剂量组6组,各组包括2、4、6周组。采用呼吸道合胞病毒(RSV)致敏和激发复制哮喘模型。实时定量-聚合酶链反应(Real-time PCR)测定肺组织中c-fos mRNA含量,免疫印迹法(Western blot)测定肺组织中ERK1蛋白表达水平。结果:模型对照组ERK1蛋白含量和c-fos mRNA水平较正常对照组明显增高(P<0.01);与模型组对照组比较,各干预组显著降低(P<0.05),平喘Ⅰ号高剂量4周及6周组优于地塞米松组(P<0.05)。结论:ERK信号转导途径在支气管哮喘气道重塑中起重要作用。平喘Ⅰ号可能通过调控ERK信号通路相关因子,缓解气道重塑,改善呼吸道症状。

Objective： By observation of the changes of extracellular regulated protein kinases （ERK） and c-fos in mice with asthma airway remodeling to explore its preventive and therapeutic mechanism. Methods： Mice were randomly divided into normal control group, model control group, dexamethasone group, Pingchuan I Formula low, middle and high-dose groups. According to the experimental period, each treatment group was divided into 2 weeks group, 4 weeks group and 6 weeks group. Asthma model was established and induced with respiratory syncytial virus. Real time PCR and Western blot were used to measure the levels of c-los mRNA and ERK1 protein in the lung tissue, respectively. Results： The values of Wat and Wam and the levels of c-fos mRNA and ERK1 protein in model control group were all significantly higher than those in normal control group （P〈0.01）. While, the values of Wat and Warn and the levels of c-fos mRNA and ERK1 protein in all treatment group were all significantly lower than those in model control group （P〈0.05）. And, those in Pingchuan I Formula high-dose group were superior to those in dexamethasone group during the 4th week and the 6th week （P〈0.05）. Conclusion： ERK signal transduction pathway plays an important role in asthma airway remodeling. Pingchuan I may regulate the related factor of ERK signal transduction pathway, which could relieve the airway remodelin~ of asthma and imorove the resoiratorv svmotoms.