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目的研究咳喘宁对RSV诱发哮喘大鼠气道重塑形态学及ICAM-1表达的影响,阐明其防治哮喘的作用机制。方法将60只幼年SD雄性大鼠随机分为6组,即正常组,模型组,泼尼松与沙丁胺醇治疗组(简称泼+沙治疗组),咳喘宁大、中、小剂量组,每组10只。用卵清蛋白复制大鼠哮喘模型,并予呼吸道合胞病毒(RSV)激发哮喘。大鼠处死后肺组织行HE染色观察炎症反应;图像分析软件测定支气管壁厚度及气道壁面积;免疫组化pv-9000二步法检测ICAM-1表达水平。结果与模型组相比,各治疗组炎症反应较轻。各治疗组支气管壁厚度及气道壁面积改变较小,与模型组相比差异有统计学意义(P<0.01);咳喘宁中剂量组较泼+沙治疗组作用略差,但差异无统计学意义(P>0.05);咳喘宁大、小剂量组与泼+沙治疗组相比,其作用明显较差,有统计学意义(P<0.05)。各治疗组与模型组比较,其肺组织中ICAM-1表达均降低,有显著性差异(P<0.01);泼+沙治疗组ICAM-1表达稍低于咳喘宁中剂量组,但差异无统计学意义(P>0.05﹚。结论咳喘宁可有效抑制气道重塑,其机制可能与降低肺组织中ICAM-1表达有关。
Objective To study the effect of Kechuanning on airway remodeling morphology and ICAM-1 expression in RSV-induced asthmatic rats, and to clarify its mechanism of action in preventing and treating asthma. Methods Sixty male Sprague-Dawley rats were randomly divided into 6 groups: normal group, model group, prednisone and salbutamol treatment group, Kechuanning large, medium and low dose groups Group of 10. Ovalbumin was used to replicate the rat asthma model and challenged with respiratory syncytial virus (RSV) to stimulate asthma. Inflammatory reaction was observed by HE staining. The thickness of bronchial wall and the area of airway wall were measured by image analysis software. The expression of ICAM-1 was detected by immunohistochemistry pv-9000 two-step method. Results Compared with the model group, the inflammatory response in each treatment group was lighter. The bronchial wall thickness and airway wall area of each treatment group changed little, compared with the model group, the difference was statistically significant (P <0.01); Kechuanning middle dose group than the injection of + Sha treatment group slightly worse, but no difference Statistically significant (P> 0.05); Kechuanning large and small dose group and the injection of + sand treatment group, the effect was significantly poorer, with statistical significance (P <0.05). The expression of ICAM-1 in the lung tissue of each treatment group was significantly lower than that of the model group (P <0.01). The ICAM-1 expression of the treatment group was slightly lower than that of the Kechuanning middle dose group No statistical significance (P> 0.05). Conclusion Kechuanning can effectively inhibit airway remodeling, the mechanism may be related to reducing the expression of ICAM-1 in lung tissue.