Abstract：
:Cigarette smoking is the principal cause of chronic obstructive pulmonary disease (COPD), especially emphysema, which is characterized by alveolar wall destruction and airspace enlargement. Apoptosis of lung structural cells is involved in the pathogenesis of COPD. Xanthine derivatives (aminophylline or theophylline) have been used for the treatment of COPD as a bronchodilator. But the effects of xanthine derivatives on apoptosis of the lung structural cells remain poorly understood, even though it is known that theophylline protects against ultraviolet irradiation-induced cell death in corneal epithelial cells. This study was designed to determine whether aminophylline would protect against cigarette smoke extract (CSE)-induced apoptosis in lung fibroblasts. We demonstrated that aminophylline protected against apoptosis of MRC-5 cells at a relatively lower therapeutic range (10 μg/ml), resulting in a significant increase in cell viability occurring at 20% concentration after 8-hr exposure. Annexin staining decreased from 68 ± 4% of the control to 12 ± 2% of aminophylline (10 μg/ml) pre-treatment after 20% CSE exposure for 12 hr (p < 0.05). Aminophylline decreased caspase 3 and 8 activities and nuclear condensation or fragmentation in MRC-5 cells after exposure to 20% CSE for 12 hr compared with control and high levels of aminophylline (>50 μg/ml) pre-treatment. These findings suggest that aminophylline protected apoptosis of MRC-5 cells through the inactivation of caspases 3 and 8 and could be an effective agent to reduce cigarette smoking-induced lung structural cell apoptosis.
journal_name
Basic Clin Pharmacol Toxicoljournal_title
Basic & clinical pharmacology & toxicologyauthors
Kim YJ,Kim JY,Yoon JY,Kyung SY,Lee SP,Jeong SH,Moon C,Park JWdoi
10.1111/j.1742-7843.2011.00673.xsubject
Has Abstractpub_date
2011-07-01 00:00:00pages
17-22issue
1eissn
1742-7835issn
1742-7843journal_volume
109pub_type
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