动物造模 z-bo 2022-02-03 418

　　Chronic obstructive pulmonary disease (COPD) is a chronic respiratory system disease. Its airflow limitation is characterized by inflammation and the concentrated effect of the lungs on harmful gases (such as cigarette smoke and harmful particles (especially smoking)). . .. Including the association of chronic bronchitis and/or emphysema characterized by airway obstruction.

　　[Modeling mechanism] Smoking is the most important cause of human COPD. Harmful components of tobacco attack the epithelium of the respiratory tract, directly impairing the cleansing and defense functions of the airway, increasing the burden of inhaled particles and the total amount of lung smoke that causes it. Airway inflammation and secondary emphysema can also exacerbate respiratory symptoms and promote COPD. Therefore, the changes formed by the COPD animal model established by passive smoking are the closest to all current models of human COPD.

　　[Modeling method] Prepare a plexiglass smoke box (20 cm x 25 cm x 30 cm), leave a 0.5 cm diameter vent at the lower end of one side of the smoke box, and connect the other side to the stainless steel smoke box (straight through ), the air inlet of the smoke chamber is connected to a small fan, and the cigarette smoke enters the cigarette case through the power of the fan, so the smoke is evenly distributed in the cigarette case, and there is enough oxygen in the cigarette case. The rats in the smoking group passively smoke once every morning and afternoon. Put three rats from the smoking group in each smoking box, each box contains 3 fresh commercially available unfiltered Sungai cigarettes (about 25 mg tar, 1.4 mg nicotine in the smoke) . Inhale the smoke for 1 hour. [Characteristics of the model] The rats in the smoking group have characteristic pathological changes in the trachea, bronchi and lung tissues of chronic bronchitis and obstructive emphysema, and the overall symptoms are ciliated epithelium. Dissociation, proliferation and thickening of bronchial epithelium and fibroblasts. , Mucous glands and goblet cells proliferate, mucus accumulates in the lumen, and macrophages and lymphocytes infiltrate the airway wall and the alveolar area around small blood vessels. After 10 weeks of smoking, ciliated epithelium becomes abnormal and mucus secretion increases. After 12 weeks of smoking, the airway ciliary epithelium was partially detached. 12 to 24 weeks after smoking, some alveoli fuse to form blisters, which are visible 24 to 36 weeks after smoking. The above-mentioned pathological changes were more obvious, especially after 36 weeks of smoking, the alveolar cavity was significantly enlarged, the airway wall was significantly thickened, fibrosis, and many inflammatory cell infiltrations were observed. [Model Evaluation and Application] Establish a rat COPD model by smoking for 36 weeks, and establish a rat COPD model that meets the characteristics of human COPD. Various inflammatory cells participate in the development of COPD. The inflammatory cells in the airway are mainly neutrophils, macrophages and lymphocytes. The lung parenchyma is mainly composed of macrophages (CD68 +) and T lymphocytes, especially CD3 + and CD8 +. Mainly cell infiltration. IL-2, IL-4, IL-6, IL-10, IL-13, IL-18, IFN-γ, monocyte chemotactic protein (McP-1), endothelin (ET)-1 in inflammation makes an important impact. Excessive secretion of airway mucus, increased inflammatory cells, thickening of the airway wall, and excessive deposition of collagen-based extracellular matrix are important pathological changes in COPD airway remodeling and are the main causes of obstructive ventilation dysfunction. This is the reason. Airway resistance and lung compliance-RC system (BUXCO) is used to detect airway resistance and lung compliance in rats. This model is mainly used to study the pathology, pathophysiological changes and drug treatment of COPD.