RESEARCH ARTICLE Open Access

Full list of author information is available at the end of the articleBackground Chronic obstructive pulmonary disease (COPD), with smoking as an important risk factor for its development [1] is an epidemic and progressive world health problem [2]. Inflammatory processes, oxidative damage, proteolysis, vascular remodeling, and lung tissue changes of COPD are well-documented changes in this disease [3]. CD68+ monocytes or macrophages in the bronchial mucosa [4], TNFα, interleukin-8, and macrophage inflammatory protein-1α (MIP-1α) which produce a positive inflam-matory chain are increased in COPD [5]. An increase in the number of neutrophils is also observed in severe COPD patients [6]. It was shown that antioxidants may have a role in the treatment of COPD patients [7]. Animal model of COPD using cigarette smoke exposure has been induced in guinea pigs which leads to emphyse-matous lung destruction and lung inflammation [8-10]. * Correspondence