| ObjectiveThe most important risk factor for chronic obstructive pulmonary disease(COPD)is cigarette smoke,which is in direct contact with lung tissue at the core of COPD,causing persistent decline in lung function and a series of respiratory Symptoms seriously affect the patient’s quality of life and activity participation.The pathogenesis of COPD is complex,and inflammatory response is one of the basic pathways involved in the pathogenesis of COPD.Cigarette smoke,as the original stimulus of the disease,will induce the body’s inflammatory response to aggravate,activate a variety of inflammatory cells,release a large number of inflammatory cytokines,and then damage the normal structure of lung tissue.The longer the smoking time and the greater the amount of smoking,the higher the prevalence of COPD,the worse the body functions,and the more likely to have other complications.There are many ways to build COPD animal models.Past studies have confirmed that simple cigarette smoke exposure can successfully build COPD animal models,but few studies have adopted long-term incremental cigarette smoke exposure regimens.Based on this,this study adopted a 25-week incremental cigarette smoke exposure regimen to observe the effects of this regimen on lung function,lung structure and lung tissue inflammation in mice,and further improve the preparation of COPD animal models.Methods16 male SPF grade 8-week-old C57BL/6J mice were randomly divided into a smoking group and a blank group.The conditions of the two groups of mice were observed at any time during the experimental period.After smoking,the two groups of mice were tested for lung function first,and then sacrificed for sampling,sample collection and analysis.HE staining and Masson staining were used to observe and compare the morphological similarities and differences of the lung tissue of the two groups of mice,and ELISA was used to detect the inflammatory factors IL-6,IL-8,IL-6,IL-8 and IL-6 in the bronchial lavage alveolar fluid and lung tissue of the two groups of mice,respectively.17 and TNF-α expression levels.Results1.The results of pulmonary function test showed that compared with the mice in the blank group,the pulmonary function parameters(FEV20,FEV50,PEF,MMEF,FRC)of the mice after 25 weeks of smoking were significantly different(P<0.05).There was a downward trend in FVC,but it did not reach statistical significance.2.The Masson staining results of lung histopathology showed that compared with the blank group mice,the tracheal wall thickness of the smoked mice was increased,the airway lumen was narrowed,the airway epithelial cells were arranged disorderly,and the airway wall had obvious collagen fibers accumulation The results of HE staining showed that inflammatory cell infiltration was seen in the lung tissue of the mice in the smoking group,the bronchial terminals were significantly enlarged,the alveolar septum was obviously thinned,and even some of them were broken to form pulmonary bullae.Calculated by the software,the cross-sectional area of alveoli in the smoking group was significantly higher than that in the blank group(P=0.005).3.The ELISA test results of lung inflammation showed that compared with the mice in the blank group,the expression levels of IL-6,IL-8 and IL-17 in the BALF of the smoked mice were significantly different,and the expression levels of TNF-α were significantly different.There was an upward trend,but it did not reach statistical significance;IL-6,IL-8,IL-17 and TNF-α in the lung tissue of the smoked mice were significantly increased.Conclusion1.After 25 weeks of incremental cigarette smoke exposure,the lung volume of mice was destroyed,and the ventilation function and small airway function decreased;there were obvious pathological changes of small airway lesions and emphysema;the lung tissue and small airway of mice were formed.The inflammatory response was significantly increased;2.The 25-week incremental cigarette smoke exposure regimen can successfully build a COPD mouse model. |
PDF Full Text Request