Obstructive Lung Diseases: COPD: Etiology |

N-Acetylcysteine Attenuates Cigarette Smoke-Induced Pulmonary Exacerbation in a Mouse Model of Emphysema FREE TO VIEW

Liusheng Wang, MD; Yang Hu, PhD; Yan Li, PhD; Yaru Wei, PhD; Zhaofang Yin, MD; Yukui Du, MD; Dong Weng, PhD; Huiping Li, PhD
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Hang Zhou First People's Hospital, Hangzhou Hospital Affiliated to Nanjing Medical University, Hangzhou, China

Copyright 2016, American College of Chest Physicians. All Rights Reserved.

Chest. 2016;149(4_S):A350. doi:10.1016/j.chest.2016.02.365
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SESSION TYPE: Original Investigation Poster

PRESENTED ON: Saturday, April 16, 2016 at 11:45 AM - 12:45 PM

PURPOSE: The purpose of this study was to investigate the effects of cigarette smoke (CS) on a mouse model of emphysema and examine the protective role of N-acetylcysteine (NAC) in the CS-induced exacerbation of pulmonary damage in the mice.

METHODS: Particulate matter (PM) in cigarette smoke aerosol was analyzed by a scanning mobility particle sizer spectrometer. A mouse model of emphysema was established by injection of porcine pancreas elastase (PPE) into the trachea. Mice with emphysema were then exposed to filtered air, or cigarette smoke (CS) with intragastric administration of NAC or normal saline. Mouse body weight, survival, pulmonary tissue histology, total antioxidant capacity (T-AOC) and malonaldehyde (MDA) contents in lung tissue, and inflammatory responses were examined.

RESULTS: Particles with a size ≤346 nm constituted 99.06% of CS PM. Mice exhibited ruptured alveolar septal, alveolar fusion, significantly increased mean lining interval, and reduced mean alveolar number (all P<0.05) 21 days after PPE injection. Exposure of mice with emphysema to CS exacerbated the pulmonary tissue damage, caused weight loss, significantly increased mortality, decreased T-AOC, elevated MDA contents in lung tissue, and increased interleukin (IL)-1β levels in bronchoalveolar lavage (BAL) fluids (all P<0.05). Administration of NAC attenuated those CS-induced adverse effects in the mice and increased anti-inflammatory factor IL-10 levels in BAL fluids significantly (all P<0.05).

CONCLUSIONS: Exposure to CS can trigger pulmonary exacerbation in a mouse model of emphysema by reducing antioxidant capacity and increasing inflammatory responses. NAC blocks the CS-induced pulmonary injury by maintaining antioxidant capacity and reducing inflammatory responses in the mice with emphysema.

CLINICAL IMPLICATIONS: These findings suggest that NAC might be a promising therapy to attenuate the exacerbation of emphysema that caused by cigarette smoke. (All the work is done at Shanghai Pulmonary Hospital)

DISCLOSURE: The following authors have nothing to disclose: Liusheng Wang, Yang Hu, Yan Li, Yaru Wei, Zhaofang Yin, Yukui Du, Dong Weng, Huiping Li

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