摘要
目的 通过重新评价卵蛋白致小鼠哮喘模型,寻找一种简便易行的气道高反应动物模型和相应的检测指标,为研发治疗本类疾病药物和研究气道高反应发病机制提供新的实验手段.方法 小鼠采用卵白蛋白（OVA）致敏;致敏后（15～21）d给予10% OVA雾化吸入激发哮喘,在末次激发24 h内测量小鼠辣椒素引咳的半数有效浓度,处死小鼠取肺组织测定匀浆中NO、IL-13、ET-1的含量.结果 卵蛋白致敏模型小鼠随辣椒素浓度的升高其咳嗽反应阳性率、咳嗽次数明显增加（与对照组相比较P〈0.01）.模型组辣椒素引咳的半数有效浓度为89.39 μmol/L,对照组、地塞米松组分别为204.84、220.02 μmol/L;小鼠肺匀浆NO、ET-1、IL-13含量均明显增加,地塞米松可明显抑制NO的升高（与对照组相比较P〈0.01）.结论小鼠经卵蛋白致敏并连续激发7 d与临床气道高反应性（AHR）的多种特征相似,操作简便易行,稳定性高,故可作为气道高反应性的模型.辣椒素引咳阈值的测定、动物肺组织中NO、IL-13、ET-1含量的变化,可作为评价模型严重程度的指标.
Objective To reappraise the mouse model of ovalbumin （OVA） -induced asthma and to develop a new model of airway hyperresponsiveness （AHR） and its evaluation indicators. Methods Mice were sensitized with ovalbumin （OVA） and induced asthma by inhalation of 10% OVA at 15 -21 days after the sensitization. The threshold value of capsaicin cough sensitivity test, and content of NO, ET-1, IL-13 in the lung homogenate were measured at 24 h after the last inhalation. Results The positive rate of cough reflex aroused by capsaicin was significantly increased with the raise of concentration of capsaicin （ compared with the control group, P 〈 0. O1 ）. The EDs0 of capsaicin cough of the model group was 89.39 p.mol/L, significantly lower than that of the control group （204.84 μmol/L） and dexamethasone group （220. 02 μmol/L）. The contents of NO, ET-1, IL-13 in the lung homogenate of the model group were significantly increased, and dexamethasone significantly inhibited the increase of NO （ compared with the control group, P 〈 0.01 ）. Conclusions The characteristics of the OVA-sensitized mouse model are resemble to that of clinical airway hyperresponsiveness. This model is simple to generate and stable, therefore, can be used as a model of AHR. The threshold value of capsaicin cough sensitivity test and the content of NO, ET-1, IL-13 in the long homogenate can be used to evaluate the disease severity of the mouse models.
出处
《中国比较医学杂志》
CAS
2014年第2期20-23,共4页
Chinese Journal of Comparative Medicine
基金
北京中医药大学科研创新团队资助项目(编号:2011-CXTD-12)
