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目的:研究平喘Ⅰ号在支气管哮喘小鼠气道炎症和气道重塑中的作用。方法:BALB/C雄性小鼠180只,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,每组30只,每组包括2周、4周、6周组。通过呼吸道合胞病毒(RSV)致敏和激发复制哮喘模型。除正常对照组及模型对照组用等量生理盐水外,其余各治疗组用相应药物给予干预。观察小鼠激发时的症状。通过图像分析软件测定支气管壁厚度(Wat)和平滑肌厚度(Wam),采用实时定量-聚合酶链反应(Real time PCR)测定小鼠肺组织中血小板衍生生长因子(PDGF-B mRNA)的含量,采用免疫印迹法(Western blotting)测定肺组织中细胞外信号调节激酶(extracellular regulated protein kinases,ERK1)的表达水平,直线相关分析法显示PDGF-BmRNA与ERK1的相关性。结果:与正常对照组相比较,各哮喘模型组中Wat和Wam,PDGF-BmRNA含量和ERK1水平均明显增高(P均<0.01)。与模型对照组比较,平喘I号各剂量组和地塞米松组中Wat和Wam,PDGF-BmRNA含量和ERK1水平均明显降低(P<0.01或P<0.05),其中地塞米松各组水平均高于平喘I号低剂量和中剂量组(P<0.05或P<0.01),与高剂量各组相比,地塞米松2周组水平较低(P<0.05),而4周和6周组则增高(P<0.05或P<0.01)。结论:PDGF-B与支气管哮喘气道重塑的程度相关,并与ERK信号传导途径在支气管哮喘气道重塑中起重要作用。平喘Ⅰ号可以降低PDGF-BmRNA的含量和ERK1水平,延缓哮喘小鼠的气道重塑,缓解其症状。
Objective: To study the role of Pingchuan I in airway inflammation and airway remodeling in asthmatic mice. Methods: One hundred and eighty male BALB / C male mice were randomly divided into 6 groups: normal control group, model control group, dexamethasone group and asthma Ⅰ low, medium and high dose group, 30 rats in each group, including 2 Week, 4 weeks, 6 weeks group. The asthmatic model was replicated by respiratory syncytial virus (RSV) sensitization and challenge. In addition to the normal control group and model control group with the same amount of saline, the rest of the treatment group with the appropriate drug intervention. Observe the symptoms of mice when excited. The thickness of the bronchial wall (Wat) and the thickness of the smooth muscle (Wam) were measured by image analysis software, and the content of platelet-derived growth factor (PDGF-B mRNA) in the lung tissue of the mice was measured by real time PCR. The expression of extracellular regulated protein kinases (ERK1) in lung tissue was determined by Western blotting. The correlation between PDGF-B mRNA and ERK1 was analyzed by linear correlation analysis. Results: Compared with the normal control group, the levels of Wat and Wam, PDGF-B mRNA and ERK1 in asthmatic model group were significantly increased (all P <0.01). Compared with the model control group, the levels of Wat and Wam, PDGF-B mRNA and ERK1 in each dose group and the dexamethasone group were significantly decreased (P <0.01 or P <0.05), and the dexamethasone levels (P <0.05 or P <0.01). Compared with the high-dose group, dexamethasone was lower in the 2-week group (P <0.05), and lower in the 4-week and 6-week Group was higher (P <0.05 or P <0.01). CONCLUSION: PDGF-B is associated with the degree of airway remodeling in bronchial asthma and plays an important role in the airway remodeling of bronchial asthma with the ERK signaling pathway. Pingchuan I can reduce the content of PDGF-B mRNA and ERK1 level, delay airway remodeling in asthmatic mice and relieve their symptoms.