Abstract: Objective To investigate the exacerbating effects of fine particulate matter (PM2.5) on lung injury in a chronic obstructive pulmonary disease (COPD) mouse model, and to provide a reliable experimental basis for further research. Methods Mice were randomly divided into four groups: control group, COPD group induced by cigarette smoke and lipopolysaccharide (LPS),KP group mice induced by intranasal instillation of Klebsiella pneumonia(KP),and PM2.5 group (COPD model) induced by intranasal instillation of PM2.5). Lung function test was used to check forced vital capacity (FVC), inspiratory capacity (IC), forced expiratory volume in 0.1 seconds (FEV0.1), FEV_0.2,FEV_0.1/FVC ratio and FEV_0.2/FVC ratio. Arterial blood gas analysis was applied to measure partial pressure of oxygen (PaO₂), partial pressure of carbon dioxide (PaCO₂), pH, and oxygen saturation (SaO₂). Lung histopathology was evaluated via hematoxylin-eosin (HE) staining microscopy. Results Compared with the control group,COPD,KP and PM2.5 groups showed significantly increased FVC,IC,FEV_0.1,FEV_0.2 and PaCO₂ (P＜0.05),along with significantly decreased FEV_0.1/FVC,FEV_0.2/FVC,PaO₂ and SaO₂ (P＜0.05). Histopathology microscopy showed typical inflammatory responses and alveolar structural damage. Compared with the COPD group,KP and PM2.5 groups exhibited further increases in FVC,FEV_0.1,and FEV_0.2(P＜0.05),reduced FEV_0.1/FVC and FEV_0.2/FVC ratios, elevated IC and PaCO₂ (PM2.5 group only,P＜0.05),and decreased SaO₂ (PM2.5 group only,P＜0.05). Histopathology microscopy confirmed aggravated inflammatory responses and alveolar destruction in these groups. Conclusions PM2.5 exacerbates pulmonary dysfunction and lung injury in COPD mice.

Key words: chronic obstructive pulmonary disease, PM2.5, pulmonary function, lung injury