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目的通过早期营养过剩建立肥胖小鼠模型,探讨肥胖对哮喘小鼠肺部炎症及气道反应性的影响。方法采用小窝喂养的方法建立早期营养过剩肥胖小鼠模型,实验组采用鸡卵白蛋白(OVA)腹腔注射致敏及雾化吸入激发的方法建立哮喘模型,对照组采用等量生理盐水腹腔注射及雾化吸入,分组为肥胖哮喘组、单纯哮喘组、单纯肥胖组和正常对照组。最后一次激发后行肺功能测定检测肥胖对哮喘气道反应性的影响,行肺泡灌洗术分析灌洗液中炎症细胞总数和分类、肺组织HE染色检测肥胖对哮喘炎症的影响。结果 1)哮喘小鼠气道反应性明显高于对照组,肥胖哮喘小鼠较单纯肥胖组和哮喘组小鼠气道反应性明显升高(P均<0.05)。2)与哮喘组和肥胖组相比,肥胖哮喘组灌洗液炎症细胞总数和分类炎症细胞明显升高(P均<0.05),与对照组相比,单纯肥胖组炎症细胞总数和巨噬细胞增多(P均<0.05),其他炎症细胞无差异(P均>0.05)。3)与肥胖组相比,肥胖哮喘组支气管周围和肺泡间隙炎症细胞明显增多(P均<0.05),与哮喘组相比,仅表现为支气管周围炎症细胞增多(P<0.05)。结论早期营养过剩诱导的肥胖小鼠可明显增加哮喘小鼠气道反应性及肺组织炎症。
OBJECTIVE: To establish an obese mouse model through early over-nutrition to investigate the effect of obesity on lung inflammation and airway responsiveness in asthmatic mice. Methods The model of early overweight obesity mice was established by the method of feeding the small intestine. The experimental group was sensitized by intraperitoneal injection of chicken ovalbumin (OVA) and challenged by inhalation of atomization. The rats in the control group were injected intraperitoneally with normal saline Inhaled inhalation, divided into obese asthma group, simple asthma group, simple obesity group and normal control group. Pulmonary function tests were performed to determine the effect of obesity on the airway responsiveness of asthma. The total number and classification of inflammatory cells in lavage fluid were analyzed by alveolar lavage, and the effect of obesity on asthmatic inflammation was examined by HE staining. Results 1) The airway responsiveness in asthmatic mice was significantly higher than that in the control group. The airway responsiveness in the obese asthmatic mice was significantly higher than that in the obesity group and asthmatic mice (all P <0.05). 2) Compared with the asthma group and the obesity group, the number of inflammatory cells and inflammatory cells in the lavage fluid in obese asthma group were significantly increased (P <0.05). Compared with the control group, the number of inflammatory cells and macrophages (P <0.05), but no difference in other inflammatory cells (all P> 0.05). Compared with the obese group, the number of inflammatory cells around the bronchi and alveolar spaces in the obese asthmatic group increased significantly (P <0.05). Compared with the asthma group, the number of inflammatory cells in the bronchial periphery increased (P <0.05). Conclusion Overexpression induced obese mice can significantly increase airway responsiveness and lung inflammation in asthmatic mice.