Kim Kang-Hyun, Park Tai Sun, Kim You-Sun, Lee Jae Seung, Oh Yeon-Mok, Lee Sang-Do, Lee Sei Won
Asan Institute for Life Sciences, University of Ulsan College of Medicine, Seoul, Republic of Korea.
Department of Pulmonology and Critical Care Medicine, Clinical Research Center for Chronic Obstructive Airway Diseases, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Republic of Korea; Department of Pulmonology and Critical Care Medicine, University of Ulsan College of Medicine, Seoul, Republic of Korea.
Int J Chron Obstruct Pulmon Dis. 2016 May 27;11:1119-28. doi: 10.2147/COPD.S100198. eCollection 2016.
Emphysema is an irreversible disease that is characterized by destruction of lung tissue as a result of inflammation caused by smoking. Resolvin D1 (RvD1), derived from docosahexaenoic acid, is a novel lipid that resolves inflammation. The present study tested whether RvD1 prevents smoking-induced emphysema and promotes lung tissue regeneration.
C57BL/6 mice, 8 weeks of age, were randomly divided into four groups: control, RvD1 only, smoking only, and smoking with RvD1 administration. Four different protocols were used to induce emphysema and administer RvD1: mice were exposed to smoking for 4 weeks with poly(I:C) or to smoking only for 24 weeks, and RvD1 was injected within the smoking exposure period to prevent regeneration or after completion of smoking exposure to assess regeneration. The mean linear intercept and inflammation scores were measured in the lung tissue, and inflammatory cells and cytokines were measured in the bronchoalveolar lavage fluid.
Measurements of mean linear intercept showed that RvD1 significantly attenuated smoking-induced lung destruction in all emphysema models. RvD1 also reduced smoking-induced inflammatory cell infiltration, which causes the structural derangements observed in emphysema. In the 4-week prevention model, RvD1 reduced the smoking-induced increase in eosinophils and interleukin-6 in the bronchoalveolar lavage fluid. In the 24-week prevention model, RvD1 also reduced the increased neutrophils and total cell counts induced by smoking.
RvD1 attenuated smoking-induced emphysema in vivo by reducing inflammation and promoting tissue regeneration. This result suggests that RvD1 may be useful in the prevention and treatment of emphysema.
肺气肿是一种不可逆的疾病，其特征是由于吸烟引起的炎症导致肺组织破坏。源自二十二碳六烯酸的消退素D1（RvD1）是一种可消退炎症的新型脂质。本研究测试了RvD1是否能预防吸烟引起的肺气肿并促进肺组织再生。
将8周龄的C57BL/6小鼠随机分为四组：对照组、仅给予RvD1组、仅吸烟组和吸烟并给予RvD1组。采用四种不同方案诱导肺气肿并给予RvD1：小鼠暴露于吸烟环境4周并同时给予聚肌胞苷酸（poly(I:C)），或仅暴露于吸烟环境24周，在吸烟暴露期内注射RvD1以预防组织再生，或在吸烟暴露结束后注射RvD1以评估组织再生情况。测量肺组织中的平均线性截距和炎症评分，并检测支气管肺泡灌洗液中的炎症细胞和细胞因子。
平均线性截距测量结果显示，在所有肺气肿模型中，RvD1均显著减轻了吸烟引起的肺组织破坏。RvD1还减少了吸烟引起的炎症细胞浸润，而这种浸润会导致肺气肿中观察到的结构紊乱。在4周预防模型中，RvD1降低了吸烟引起的支气管肺泡灌洗液中嗜酸性粒细胞和白细胞介素-6的增加。在24周预防模型中，RvD1还降低了吸烟引起的中性粒细胞增加和总细胞计数增加。
RvD1通过减轻炎症和促进组织再生，在体内减轻了吸烟引起的肺气肿。该结果表明，RvD1可能对肺气肿的预防和治疗有用。
