Object To establish a mouse model of chronic obstructive pulmonary disease (COPD) by cigarette smoke (CS) method, and to evaluate the model systematically. Methods Forty BALB/c mice were randomly divided into normal control group (Control group) and cigarette smoke group (CS group). The mice in CS group were subjected to passive smoking for 20 weeks and COPD model was established. Then hematoxylin-eosin staining (HE) and masson’s trichrome stain (MASSON) staining were used to observe the morphological changes of the organs and fibrosis of lung, heart, liver and kidney. The lung function, cardiac function and brain cognitive function of mice were evaluated by pulmonary function test apparatus, small animal ultrasound and Morris water maze trial. The levels of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and interleukin-1β (IL-1β) in lung and brain tissues of mice were detected by enzyme-linked immunosorbent assay (ELISA). The liver and renal function of mice were measured by biochemical method. Results The alveolar septum of CS group mice was narrowed or even broken, and the adjacent alveolar cavity was enlarged and fused, which was consistent with the pathological changes of COPD. Neuronal degeneration and necrosis were observed in the hippocampus of brain tissue. There were no significant morphological changes in other organs. MASSON staining demonstrated that there was no obvious fibrosis in lung, heart, liver and kidney of CS group mice. The results of pulmonary function test showed that compared with Control group, forced expiratory volume in 0.1s / forced vital capacity (FEV0.1/FVC) and dynamic compliance (Cydn) in CS group were significantly decreased, while airway resistance (RI) was obviously increased. Morris water maze trial confirmed the cognitive impairment of mice in CS group. The levels of TNF-α, IL-6 and IL-1β in lung and brain tissue of CS group were remarkably higher than those of Control group. The cardiac, liver and renal function of mice in CS group had no significant changes. Conclusion A mouse model of COPD can be established by cigarette smoke for 20 weeks. The lung histomorphology, lung function, brain cognitive function and the levels of inflammatory factors can be used as indicators to evaluate the success of the model.