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Generation of a Chronic Obstructive Pulmonary Disease Model in Mice by Repeated Ozone Exposure
Published on: August 25, 2017
The role of oxidative stress in chronic obstructive pulmonary disease
Russell P Bowler1, Peter J Barnes, James D Crapo
1Department of Medicine, National Jewish Medical and Research Center, Denver, Colorado 80206, USA. BowlerR@njc.org
Abstract:
Tobacco smoke is the number one risk factor for chronic obstructive pulmonary disease (COPD) and contains a high concentration of oxidants. The lung has a high concentration of antioxidants and antioxidant enzymes; however, COPD patients show evidence of increased oxidative stress suggesting that endogenous antioxidants may be insufficient to prevent oxidative damage from cigarette smoke. The consequences of increased oxidative stress in the lung include increased transcription of inflammatory genes, increased protease activity, and increased mucus secretion. Oxidative stress is often associated with impaired skeletal muscle function and may be one of the causes of glucocorticoid resistance. While current pharmacologic approaches to the treatment of chronic obstructive pulmonary disease do not commonly include antioxidants, preclinical studies involving animal models suggest that antioxidant superoxide dismutase mimetics offer a potential new therapeutic approach to the prevention and treatment of chronic obstructive pulmonary disease.
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