N-acetylcysteine attenuates cigaret smoke-induced pulmonary exacerbation in a mouse model of emphysema
N-acetylcysteine attenuates cigaret smoke-induced pulmonary exacerbation in a mouse model of emphysema
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DOI：
10.3109/08958378.2015.1110217
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发表时间：
2015-11
影响因子：
2.1
通讯作者：
Liusheng Wang;Yang Hu;Chun-Lin Li;Yan Li;Ya-Ru Wei;Zhao-Fang Yin;Yu-Kui Du;Z. Min;D. Weng;Jian-min Chen;Huiping Li
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文献类型：
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作者：
Liusheng Wang;Yang Hu;Chun-Lin Li;Yan Li;Ya-Ru Wei;Zhao-Fang Yin;Yu-Kui Du;Z. Min;D. Weng;Jian-min Chen;Huiping Li
摘要目的：研究香烟烟雾(CS)对小鼠肺气肿模型的影响及N-乙酰半胱氨酸(NAC)对CS所致小鼠肺损伤加重的保护作用。方法：采用扫描流动粒度仪对侧流卷烟烟雾气溶胶中的颗粒物进行分析。采用气管内注射猪胰腺弹性酶(PPE)的方法建立小鼠肺气肿模型。然后，将患有肺气肿的小鼠暴露于过滤空气中，或侧流CS中，灌胃NAC或生理盐水。观察小鼠体重、存活时间、肺组织学、肺组织总抗氧化能力(T-AOC)、肺组织丙二醛(MDA)含量及炎症反应。结果：≤为346 nm的颗粒占CS PM的99.06%注射PPE后21d，小鼠出现肺泡间隔破裂，肺泡融合，平均内衬间隔显著增加，平均肺泡数减少(均P<；0.05)。肺气肿小鼠暴露于CS后，肺组织损伤加重，体重减轻，死亡率显著增加，总抗氧化能力下降，肺组织丙二醛含量升高，支气管肺泡灌洗液中IL-1β水平升高(P均<0.05)。给予NAC可显著减轻CS所致小鼠的上述不良反应，显著提高BAL液中抗炎因子IL-10的水平(均P<0.05)。结论：肺气肿小鼠暴露于CS可加重肺损伤，而NAC可通过防止氧化损伤和减轻炎症反应来减轻CS介导的肺损伤。
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.