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Inhalation Toxicology
International Forum for Respiratory Research
Volume 27, 2015 - Issue 14
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Research Article

N-acetylcysteine attenuates cigaret smoke-induced pulmonary exacerbation in a mouse model of emphysema

, , , , , , , , , & show all
Pages 802-809 | Received 02 Jun 2015, Accepted 09 Oct 2015, Published online: 16 Nov 2015
 

Abstract

Objective: The purpose of this study was to investigate the effects of cigaret 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. Method: Particulate matter (PM) in sidestream cigaret smoke aerosol was analyzed by a scanning mobility particle sizer spectrometer. A mouse model of emphysema was established by an injection of porcine pancreatic elastase (PPE) into the trachea. Mice with emphysema were then exposed to filtered air, or sidestream 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 of ≤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 d 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 of mice with emphysema to CS exacerbated the pulmonary damage, and NAC reduced the CS-mediated pulmonary damage by preventing oxidative damage and reducing inflammatory responses.

Declaration of interest

The authors declare no conflict of interest. This study was funded by grants from the National Science Foundation of China (Nos.: 91442103, 81170011 and 81200045), the Science and Technology Commission of Shanghai Municipality (12DJ1400103, 124119a9000, 12DZ1942500 and 12411950105), the Health Bureau Program of Shanghai Municipality (SHDC12014120, 2013SY047) and Tongji University (1511219020).

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