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目的研究信号转导与转录活化因子3(STAT3)在支气管哮喘(哮喘)小鼠呼吸道中的表达及STAT3与呼吸道重塑的关系,探讨STAT3信号传导途径在哮喘发病机制中的作用。方法Balb/c小鼠30只随机分为正常对照组、哮喘未干预组和AG490干预组,每组各10只。建立鸡卵白蛋白(OVA)致敏的小鼠哮喘模型,HE染色光镜下观察其肺组织结构改变,病理图像分析系统测量其支气管壁厚度(Wat)和平滑肌厚度(Wam),并采用Masson染色观察其肺组织胶原纤维的变化,免疫组织化学染色检测各组小鼠肺组织STAT3表达,免疫印迹法检测磷酸化STAT3(p-STAT3)水平。应用SPSS13.0软件进行统计学分析。结果1.OVA致敏的哮喘模型组小鼠可见支气管壁增厚和管腔狭窄、呼吸道壁周围有大量胶原纤维沉积等呼吸道重塑表现;2.哮喘未干预组小鼠呼吸道上皮细胞STAT3蛋白表达水平、肺组织p-STAT3水平明显高于正常对照组(Pa<0.01,0.05),AG490干预组小鼠肺组织p-STAT3水平、Wat和Wam明显低于哮喘未干预组(Pa<0.05);3.哮喘未干预组小鼠呼吸道上皮细胞STAT3蛋白阳性信号积分吸光度及肺组织p-STAT3水平分别与Wat(r=0.58,P<0.05;r=0.61,P<0.05)、Wam(r=0.46,P<0.05;r=0.53,P<0.05)呈正相关。结论呼吸道重塑是哮喘的基本病理学特征,哮喘小鼠呼吸道上皮细胞STAT3蛋白表达水平及活化程度增加,其增加水平与呼吸道重塑程度相关,阻断STAT3的磷酸化可减轻呼吸道重塑程度,上皮细胞STAT3信号通路可能参与呼吸道重塑过程。
Objective To investigate the expression of STAT3 in the respiratory tract of asthmatic mice and the relationship between STAT3 and airway remodeling and to explore the role of STAT3 signaling pathway in the pathogenesis of asthma. Methods Thirty Balb / c mice were randomly divided into normal control group, untreated asthma group and AG490 intervention group, 10 rats in each group. A mouse model of asthma induced by chicken ovalbumin (OVA) was established. The lung tissue structure was observed under HE staining, and the bronchial wall thickness (Wat) and smooth muscle thickness (Wam) were measured by pathological image analysis system. Masson staining The changes of collagen fibers in the lung tissue were observed. The expression of STAT3 in the lung tissue of each group was detected by immunohistochemical staining. The level of phospho-STAT3 (p-STAT3) was detected by immunoblotting. Application SPSS13.0 software for statistical analysis. Results 1.Among them, asthma model group showed bronchial wall thickening and lumen stenosis, and a large number of respiratory remodeling around the airway wall, such as airway remodeling.2. STAT3 protein expression in the airway epithelial cells of mice without asthma The level of p-STAT3 in lung tissue was significantly higher than that in normal control group (P <0.01, 0.05). The level of p-STAT3 in lung tissue of AG490 intervention group was significantly lower than that in asthma group (P <0.05) The positive signal integral absorbance of STAT3 protein and the level of p-STAT3 in lung tissue of asthmatic untreated group were significantly lower than those of Wat (r = 0.58, P <0.05; r = 0.61, , P <0.05; r = 0.53, P <0.05). Conclusions Respiratory remodeling is the basic pathological feature of asthma. STAT3 protein expression and activation are increased in the airway epithelial cells of asthmatic mice. The increased level is associated with the degree of airway remodeling. Blocking the phosphorylation of STAT3 can reduce the degree of airway remodeling, Epithelial cells STAT3 signaling pathway may be involved in respiratory remodeling process.