国际呼吸杂志
國際呼吸雜誌
국제호흡잡지
INTERNATIONAL JOURNAL OF RESPIRATION
2012年
21期
1607-1611
,共5页
张科东%马冉%李征途%徐小明%张晨婷%巩雪芳%齐亚飞%陈豫钦%姜华%郑则广%王健%钟南山%卢文菊
張科東%馬冉%李徵途%徐小明%張晨婷%鞏雪芳%齊亞飛%陳豫欽%薑華%鄭則廣%王健%鐘南山%盧文菊
장과동%마염%리정도%서소명%장신정%공설방%제아비%진예흠%강화%정칙엄%왕건%종남산%로문국
熏烟%慢性阻塞性肺疾病模型
熏煙%慢性阻塞性肺疾病模型
훈연%만성조새성폐질병모형
Cigarette smoke%Chronic obstructive pulmonary disease mouse model
目的 建立一种熏烟诱导的小鼠慢性阻塞性肺疾病(COPD)模型.方法 将小鼠随机分为COPD模型组和正常对照组,模型组小鼠每天熏烟两次,每次2h,每周熏烟6d,香烟剂量为9支/h.模型制备期间,每星期称量一次体质量,每个月检测一次小鼠肺功能.对照组小鼠不做任何干预.熏烟满6个月后,行肺功能检测,并检测小鼠支气管肺泡灌洗液(BALF)中炎症细胞数和黏蛋白MUC5AC水平,观察气道和肺组织病理改变等.结果 与对照组相比,模型组小鼠体质量明显降低(P＜0.05),吸气阻力明显增加(P＜0.05),吸气峰流速、呼气峰流速和动态肺顺应性明显降低(P＜0.05);肺泡灌洗液中白细胞总数,中性粒细胞、巨噬细胞和淋巴细胞分类计数与对照组相比,均明显增加;模型组小鼠肺切片HE染色显示炎症浸润,PAS染色显示气道上皮中出现大量黏液分化细胞,BALF中MUC5AC表达水平较正常组增加(P＜0.01).结论 用这种熏烟的方法所建立的小鼠COPD模型符合人类COPD的病理和功能改变,是建立小鼠COPD模型的理想方法.
目的 建立一種熏煙誘導的小鼠慢性阻塞性肺疾病(COPD)模型.方法 將小鼠隨機分為COPD模型組和正常對照組,模型組小鼠每天熏煙兩次,每次2h,每週熏煙6d,香煙劑量為9支/h.模型製備期間,每星期稱量一次體質量,每箇月檢測一次小鼠肺功能.對照組小鼠不做任何榦預.熏煙滿6箇月後,行肺功能檢測,併檢測小鼠支氣管肺泡灌洗液(BALF)中炎癥細胞數和黏蛋白MUC5AC水平,觀察氣道和肺組織病理改變等.結果 與對照組相比,模型組小鼠體質量明顯降低(P＜0.05),吸氣阻力明顯增加(P＜0.05),吸氣峰流速、呼氣峰流速和動態肺順應性明顯降低(P＜0.05);肺泡灌洗液中白細胞總數,中性粒細胞、巨噬細胞和淋巴細胞分類計數與對照組相比,均明顯增加;模型組小鼠肺切片HE染色顯示炎癥浸潤,PAS染色顯示氣道上皮中齣現大量黏液分化細胞,BALF中MUC5AC錶達水平較正常組增加(P＜0.01).結論 用這種熏煙的方法所建立的小鼠COPD模型符閤人類COPD的病理和功能改變,是建立小鼠COPD模型的理想方法.
목적 건립일충훈연유도적소서만성조새성폐질병(COPD)모형.방법 장소서수궤분위COPD모형조화정상대조조,모형조소서매천훈연량차,매차2h,매주훈연6d,향연제량위9지/h.모형제비기간,매성기칭량일차체질량,매개월검측일차소서폐공능.대조조소서불주임하간예.훈연만6개월후,행폐공능검측,병검측소서지기관폐포관세액(BALF)중염증세포수화점단백MUC5AC수평,관찰기도화폐조직병리개변등.결과 여대조조상비,모형조소서체질량명현강저(P＜0.05),흡기조력명현증가(P＜0.05),흡기봉류속、호기봉류속화동태폐순응성명현강저(P＜0.05);폐포관세액중백세포총수,중성립세포、거서세포화림파세포분류계수여대조조상비,균명현증가;모형조소서폐절편HE염색현시염증침윤,PAS염색현시기도상피중출현대량점액분화세포,BALF중MUC5AC표체수평교정상조증가(P＜0.01).결론 용저충훈연적방법소건립적소서COPD모형부합인류COPD적병리화공능개변,시건립소서COPD모형적이상방법.
Objective To establish a cigarette smoke-induced chronic obstructive pulmonary disease (COPD) mouse model.Methods C57 mice were randomly divided into COPD model group and normal control group.The model group mice were exposed to cigarette smoke for twice per day,2 hours for each time with nine cigarettes per hour,6 days every week in 6 months.Control mice were exposed to room air only.During the six-month-exposure,both groups of mice were weighed every week and their pulmonary functions were measured once every month.Then the mice were dissected after the last pulmonary functions determination and the succeed of the model establishment was judged by evaluating the following parameters:the inflammatory cell numbers and mucin MUC5AC levels in bronchoalveolar lavage fluid (BALF),the phenotypes on lung pathological changes,and the parameters of pulmonary functions.Results Compared with the normal control mice,the cigarette smoked mice have lower body weights (P＜0.05),enhanced inspiratory resistance (RI),and decreases on peak inspiratory flow (PIF),peak expiratory flow (PEF) and dynamic compliance (Cdyn) (P＜0.05).The total leucocyte numbers and the numbers of neutrophils,macrophagcs and lymphocytes in BALF were increased significantly in cigarette smoked mice which developed more severe lung inflammation and more mucus cells hyperplasia assessed by HE staining and PAS staining respectively.And higher levels of MUC5AC in BALF were found in cigarette smoked mice (P ＜ 0.01 vs control mice).Conclusions The COPD mouse model established with cigarette smoke mimics the clinical situations with similar pathological changes to the COPD patients and can be taken as an effective animal model for future COPD research.
