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目的:观察支气管哮喘模型小鼠肺部相关病理改变及大承气汤的干预作用,为开展支气管哮喘“从肠论治”效应机制研究,探讨“肺合大肠”脏腑相关联络机制奠定基础。方法:40只C57BL/6小鼠随机分为正常组、模型组、模型给药组及正常给药组,采用卵清蛋白(OVA)致敏激发法建立支气管哮喘小鼠模型。造模第15～21天,正常组、模型组蒸馏水灌胃,模型给药组、正常给药组以大承气汤灌胃,连续7天。观察各组小鼠整体情况和肺组织病理学改变,收集肺支气管肺泡灌洗液(BALF)进行细胞分类计数。结果:OVA致敏哮喘模型小鼠可见剧烈咳嗽、呼吸急促、喘息、打喷嚏、哮鸣音、腹肌抽搐、大小便失禁等症,BALF中淋巴细胞、嗜酸性粒细胞和中性粒细胞比例均明显升高(P<0.01);肺组织病理学存在支气管上皮损坏、肺泡周围充血,伴淋巴细胞浸润等明显改变。经大承气汤从肠干预后,上述症状、体征及病理改变有所减轻。结论:采用OVA致敏法制备的支气管哮喘小鼠模型,存在明显的气道高反应性及炎症性病理改变。通腑法即采用大承气汤通利大肠,能够在一定程度上改善小鼠模型肺部的症状及病理变化,其作用调节机制,有待进一步研究。
OBJECTIVE: To observe the lung-related pathological changes in bronchial asthma model mice and the intervention effect of Dachengqi Decoction in order to explore the mechanism of “treating the bowel from bronchial asthma” and to explore the related mechanism of “lung and intestine” Lay the foundation. Methods: Forty C57BL / 6 mice were randomly divided into normal group, model group, model group and normal group. A mouse model of bronchial asthma was established by ovalbumin (OVA) sensitization. On the 15th to 21th day of modeling, normal group and model group were given gavage with distilled water, model group and normal group with Dachengqi Decoction for 7 consecutive days. Observe the overall situation of mice in each group and lung histopathological changes, lung bronchoalveolar lavage fluid (BALF) were collected for cell counting. Results: The mice with OVA-sensitized asthma showed severe cough, shortness of breath, wheezing, sneezing, wheeze, abdominal convulsion, incontinence embolism, the proportion of lymphocytes, eosinophils and neutrophils in BALF (P <0.01). The histopathology of lung showed bronchial epithelial damage, hyperemic alveolar congestion and lymphocyte infiltration. The Dachengqi decoction from the intestine after the above symptoms, signs and pathological changes have been alleviated. Conclusion: The bronchial asthma mouse model induced by OVA sensitization has obvious airway hyperresponsiveness and inflammatory pathological changes. Tongfu method that the use of Dachengqi Tonglida intestine, to a certain extent, improve the mouse model of lung symptoms and pathological changes, the role of regulatory mechanisms, pending further study.