支气管肺发育不良小鼠模型的建立

目的建立支气管肺发育不良小鼠模型。方法将30只4日龄雌性昆明小鼠随机分为2组,每组15只,氧气组置于氧箱（FiO20.6）,空气组置于空气中（FiO20.21）,分别于暴露7 d、14 d、21 d时每组随机选取5只,称重后处死,观察肺组织形态学、放射状肺泡计数（radical alveolar counts,RAC）及肺胶原含量变化。结果氧气组各时间点体重较空气组均明显降低（P〈0.001）;实验21 d时氧气组肺组织HE染色下见正常肺泡结构破坏,肺泡隔增厚,肺泡融合;氧气组RAC较空气组显著降低（P〈0.001）;肺胶原天狼猩红特殊染色见Ⅰ型、Ⅲ型胶原增生,较空气组显著增加（P〈0.001）。结论中等浓度氧（FiO20.6）暴露21 d可致小鼠肺发生类似人类支气管肺发育不良改变。

Establishment of a Mouse Model of Bronchopulmonary Dysplasia

Objective To establish a mouse model of bronchopulmonary dysplasia. Method Thirty female mouse pups were randomly devided into two groups： the normoxia group（FiO2 0,21, n = 15） and hyperoxia group（FiO2 0.6, n = 15）. Morphological changes of lung tissue, radical alveolar counts （RAC） and collagen were detected on the 7th, 14th and 21th days after exposure. Results Hyperoxia-treated mice had lower body weight than those of normoxia group （P 〈 0.001 ）. The lung tissues stained with HE of the hyperoxia group showed loss of normal alveoli, alveolar fusion and increased septal wall thickness. The RAC value was significantly decreased in the hyperoxia group （P 〈 0.001 ）. Mice of hyperoxia group dipicted prominent proliferation of collagen （P 〈 0.001 ）. Conclusion Exposure to oxygen （FiO2 0.6）can induce BPD-1ike changes in the lung structure of mice.