目的观察祛风宣肺方对豚鼠咳嗽敏感性增高模型的肺组织病理及磷酸化p38丝裂原活化蛋白激酶(p-p38MAPK)的影响。方法将40只雄性SPF级健康豚鼠随机分为空白对照组、模型组、祛风宣肺方组、西药对照组4组,每组10只。采用卵蛋白和氢氧化铝腹腔注射及卵蛋白溶液雾化的方法建立豚鼠咳嗽敏感性增高模型,造模成功后连续灌胃给药10 d,取材留取肺组织,应用电镜和光镜观察各组肺组织病理变化,应用免疫组化方法观察肺组织p-p38MAPK的表达情况。结果光镜下,空白对照组结构基本正常,模型组可见支气管管腔狭窄、上皮细胞脱落、黏膜皱襞增厚,且可见支气管黏膜层及黏膜下层、肺泡腔内及周围等炎症细胞浸润,其中以单核细胞、嗜酸性粒细胞为主。病理变化程度由重到轻依次为模型组、西药对照组、祛风宣肺方组。电镜下,空白对照组结构基本正常,模型组可见肺毛细血管增厚、基底膜增厚、肺泡炎症细胞浸润及Ⅱ型肺泡上皮细胞结构改变。病理变化程度由重到轻依次为模型组、西药对照组、祛风宣肺方组。肺组织pp38MAPK的分布情况,光镜下4组均有p-p38MAPK的阳性表达,主要表达于支气管、肺泡、肺毛细血管周围,阳性表达程度由强到弱依次为模型组、西药对照组、祛风宣肺方组、空白对照组。各组肺组织p-p38MAPK平均积分光密度数值比较,模型组、祛风宣肺方组、西药对照组较空白对照组均升高,差异均有统计学意义(P<0.05),提示咳嗽敏感性增高动物模型造模成功;祛风宣肺方组、西药对照组较模型组均降低,差异均有统计学意义(P<0.05);祛风宣肺方组较西药对照组降低,差异有统计学意义(P<0.05)。结论祛风宣肺方对豚鼠咳嗽敏感性增高模型有较好的治疗作用,其作用机制可能与修复气道损伤、抑制气道炎症细胞分泌及影响p-p38MAPK的表达水平等有关,从而减轻气道神经源性炎症,进而降低了咳嗽敏感性。 Objective To observe the effect of Qufeng Xuanfei Recipe on lung histopathology and phospho-p38 mitogen-activated protein kinase (p-p38MAPK) in a guinea pig model with increased sensitivity to cough. Methods Forty male SPF healthy guinea pigs were randomly divided into blank control group, model group, Qufeng Xuanfei Fang group and western medicine control group, with 10 rats in each group. Cigarette cough hypersensitivity model was established by intraperitoneal injection of ovalbumin and aluminum hydroxide and atomization of egg protein solution. After successful establishment of model, the rats were given gavage for 10 days continuously. The lung tissues were drawn and taken out by electron microscope and light microscope Lung tissue pathological changes, immunohistochemistry method to observe the expression of p-p38MAPK in lung tissue. Results Under the light microscope, the structure of the blank control group was basically normal. In the model group, bronchial stenosis, epithelial cell shedding and thickening of mucosal folds were observed. Inflammatory cells infiltration in the bronchial mucosa and submucosa, alveolar cavity and surrounding were visible Monocytes, eosinophils dominated. The severity of pathological changes from heavy to light were model group, western medicine control group and Qufeng Xuanfei Fang group. Under the electron microscope, the structure of the blank control group was basically normal. In the model group, pulmonary capillary thickening, basement membrane thickening, alveolar inflammatory cell infiltration and structure change of type II alveolar epithelial cells were observed. The severity of pathological changes from heavy to light were model group, western medicine control group and Qufeng Xuanfei Fang group. The distribution of pp38MAPK in the lung tissue was positive in all the four groups, which were mainly expressed in the bronchi, alveoli and pulmonary capillaries. The expression of pp38MAPK in the lung tissue from strong to weak was the model group, the western medicine control group, Wind Xuanfei Fang group, blank control group. Compared with the blank control group, the average integral optical density of p-p38MAPK in model group, model group, Qufeng Xuanfei Fang group and western medicine control group were significantly increased (P <0.05), suggesting cough sensitivity Qufengxuanfeifang group and western medicine control group were lower than the model group, the differences were statistically significant (P <0.05); Qufeng Xuanfei group was lower than the western medicine control group, the difference was Statistical significance (P <0.05). Conclusion Qufeng Xuanfei Fang has a better therapeutic effect on the model of increased cough sensitivity in guinea pigs, and its mechanism may be related to the repair of airway injury, inhibition of airway inflammatory cell secretion and the expression of p-p38MAPK, Road neurogenic inflammation, thereby reducing the cough sensitivity.