Shu Jiaze, Lu Wenju, Li Defu, Liang Zhihao, Xu Xiaoming, Zhang Bo, Wang Jian
Guangzhou Institute of Respiratory Disease, State Key Laboratory of Respiratory Diseases, the 1st Affiliated Hospital of Guangzhou Medical University, Guangzhou 510120, China.
Guangzhou Institute of Respiratory Disease, State Key Laboratory of Respiratory Diseases, the 1st Affiliated Hospital of Guangzhou Medical University, Guangzhou 510120, China; Email:
Zhonghua Jie He He Hu Xi Za Zhi. 2015 Dec;38(12):907-11.
To establish a mouse model of chronic obstructive pulmonary disease (COPD) and associated pulmonary hypertension (COPD-PH) induced by nose-only cigarette smoking exposure plus airway lipopolysaccharide (LPS) inhalation.
There were 24 male C57B6 mice divided into a control group and a model group at random. The model group was given LPS by intranasal inhalation on day 1 and day 14 and exposed to the cigarette smoke in a nose-only exposure system, while the control group was given physiological saline and exposed to normal air. The model establishment was evaluated according the following parameters: the lung function and the right heart pressure, the total and differential cell numbers in bronchial alveolar lavage fluid (BALF), and the pathological changes of lung tissues.
The functional residual capacity data of the model group and the control group were (0.402 ± 0.057) and (0.243 ± 0.064) ml respectively (P<0.05). The inspiratory resistance data of the model group and the control group were (1.056 ± 0.121) and (0.789 ± 0.063) cmH(2)O · ml(-1) · s(-1) (1 cmH(2)O=0.098 kPa) respectively (P<0.05). The static lung compliance data of the model group and the control group were (0.084 ± 0 .007) and (0.056 ± 0.004) cmH(2)O/ml respectively (P<0.05). The right ventricular mean pressure of the model group and the control group were (11.3 ± 1.3) and (7.9 ± 1.1) mmHg (1 mmHg=0.133 kPa) respectively (P<0.05), while the right ventricular hypertrophy index of the model group and the control group were (0.267 ± 0.019) and (0.195 ± 0.023) respectively (P<0.05). Moreover, the histological staining showed that goblet cell hyperplasia, lung inflammation and thickening of smooth muscle layers of bronchial and pulmonary small vessels occurred in the model group, which indicated ongoing airway and blood vessel remodeling.
A COPD-PH mouse model was established by nose-only cigarette smoking exposure plus airway LPS inhalation in a short period of time, and this method was more similar to the smoking behavior of human.
通过仅经鼻暴露于香烟烟雾加气道内吸入脂多糖（LPS）建立慢性阻塞性肺疾病（COPD）及相关肺动脉高压（COPD-PH）的小鼠模型。
将24只雄性C57B6小鼠随机分为对照组和模型组。模型组在第1天和第14天经鼻吸入LPS，并在仅经鼻暴露系统中暴露于香烟烟雾，而对照组给予生理盐水并暴露于正常空气中。根据以下参数评估模型建立情况：肺功能和右心压力、支气管肺泡灌洗液（BALF）中的细胞总数和分类细胞数，以及肺组织的病理变化。
模型组和对照组的功能残气量数据分别为（0.402±0.057）和（0.243±0.064）ml（P<0.05）。模型组和对照组的吸气阻力数据分别为（1.056±0.121）和（0.789±0.063）cmH₂O·ml⁻¹·s⁻¹（1 cmH₂O = 0.098 kPa）（P<0.05）。模型组和对照组的静态肺顺应性数据分别为（0.084±0.007）和（0.056±0.004）cmH₂O/ml（P<0.05）。模型组和对照组的右心室平均压力分别为（11.3±1.3）和（7.9±1.1）mmHg（1 mmHg = 0.133 kPa）（P<0.05），而模型组和对照组的右心室肥厚指数分别为（0.267±0.019）和（0.195±0.023）（P<0.05）。此外，组织学染色显示模型组出现杯状细胞增生、肺部炎症以及支气管和肺小血管平滑肌层增厚，这表明存在气道和血管重塑。
通过仅经鼻暴露于香烟烟雾加气道内吸入LPS在短时间内建立了COPD-PH小鼠模型，且该方法更类似于人类的吸烟行为。
