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Effects of Simvastatin on Cigarette Smoking-Induced Structural and Functional Changes in Rat Lungs

Sang Do Lee, MD; Ji-Hyun Lee, MD; Eun Kyung Kim, MD; Kang-Hyun Choi, MD; Yeon Mok Oh, MD; Tae Sun Shim, MD
Author and Funding Information

*From the Division of Pulmonary and Critical Care Medicine (Drs. S.D. Lee, Oh, and Shim), Asan Medical Center, University of Ulsan, Seoul, Korea; Department of Internal Medicine (Drs. J.H. Lee and Kim), Bundang CHA Hospital, Seoul, Korea; and the Department of Internal Medicine (Dr. Choi), College of Medicine, Chungbuk National University, Cheongju, Korea.

Correspondence to: Sang Do Lee, MD, Asan Medical Center, Internal Medicine, University of Ulsan, 388–1 Poongnab-dong SongpaGu, Seoul 138–736, South Korea; e-mail: sdlee@amc.seoul.kr



Chest. 2005;128(6_suppl):574S. doi:10.1378/chest.128.6_suppl.574S
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Cigarette smoking-induced chronic inflammation is known to be the main cause of COPD, which is progressive and not fully reversible. Statins, particularly 3-hydroxy-3-methyl-glutaryl coenzyme A reductase inhibitors, have been employed as lipid-lowering agents, but they can critically affect various cellular processes. Well-known functions of statins are antiinflammation, antioxidation, restoration of endothelial dysfunction, and antithrombogenesis, which act in opposition to the effects of cigarette smoking. Therefore, we hypothesized that simvastatin, a 3-hydroxy-3-methyl-glutaryl coenzyme A reductase inhibitor, may attenuate structural and functional changes of rat lungs induced by cigarette smoking.

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