Intraperitoneal injection of cigarette smoke extract induced emphysema, and injury of cardiac and skeletal muscles in BALB/C mice.

BACKGROUND: Chronic obstructive pulmonary disease (COPD) is a chronic, progressive, airway disease. In order to recognize mechanisms of COPD, various types of COPD animal models have been established, and the pathogenesis are different. The present study was designed to establish a COPD animal model by intraperitoneal injection of cigarette smoke extract (CSE) in BALB/C mice.
METHODS: Mice were injected intraperitoneally with PBS/CSE and sacrificed at day 28. Pulmonary function, pathology of lung tissue, morphology of hearts and skeletal muscle, leukocytes count and antioxidant activity of bronchoalveolar lavage fluid (BALF), pulmonary parenchymal apoptosis index (AI), expression of cleaved caspase-3, expression of MMP-2 and MMP-9 mRNA, and activity of MMP-2 and MMP-9 in lung tissue were measured.
RESULTS: Intraperitoneal injection of CSE induced pulmonary parenchymal destruction, pulmonary function reduction, leukocytes count, injury of cardiac and peripheral muscles, and increased pulmonary parenchymal AI, cleaved caspase-3 protein, expression of MMP-2 and MMP-9 mRNA, activity of MMP-2 and MMP-9 protein in lung tissue, and suppressed antioxidant activity in BALF (P < 0.05).
CONCLUSIONS: Intraperitoneal injection of CSE produced emphysema, pulmonary parenchymal apoptosis, and injury of cardiac and skeletal muscles in mice. All pathobiologically relevant mechanisms in this model are shared with the COPD patients.