Effects of Astragalus and Codonopsis pilosula polysaccharides on alveolar macrophage phagocytosis and inflammation in chronic obstructive pulmonary disease mice exposed to PM2.5

被引:70
|
作者
Chu, Xu [1 ]
Liu, Xiao-Ju [1 ]
Qiu, Jing-Man [1 ]
Zeng, Xiao-Li [1 ]
Bao, Hai-Rong [1 ]
Shu, Juan [1 ]
机构
[1] Lanzhou Univ, Dept Gerontal Resp Med, Hosp 1, 1 Dong Gang West Rd, Lanzhou 730000, Peoples R China
基金
中国国家自然科学基金;
关键词
Pulmonary disease; Chronic obstructive; PM2.5; Polysaccharides; Macrophages; Alveolar; Phagocytdsis; Inflammation; FINE PARTICULATE MATTER; LUNG-FUNCTION DECLINE; LONG-TERM EXPOSURE; IN-VITRO TOXICITY; CIGARETTE-SMOKE; AIRWAY INFLAMMATION; COPD; CELLS; RATS; SUSCEPTIBILITY;
D O I
10.1016/j.etap.2016.10.006
中图分类号
X [环境科学、安全科学];
学科分类号
08 ; 0830 ;
摘要
Astragalus and Codonopsis pilosula are used for their immunomodulatory and anti-inflammatory effects. Here, we investigated the effects of Astragalus polysaccharides (APS) and Codonopsis pilosula polysaccharides (CPP) on alveolar macrophage (AM) phagocytosis and inflammation in chronic obstructive pulmonary disease (COPD) associated with exposure to particulate matter with a mean aerodynamic diameter <= 2.5 mu m (PM2.5). A mouse model of COPD was established by cigarette smoke exposure. PM2.5 exposure was performed by inhalation of a PM2.5 solution aerosol. APS and CPP were administered intra-gastrically. COPD showed defective AM phagocytosis and increased levels of interleukin (IL)-6, IL-8, and tumor necrosis factor (TNF)-alpha in bronchoalveolar lavage fluid and serum. PM2.5 exposure aggravated the damage, and this effect was reversed by APS and CPP gavage. The results indicate that APS and CPP may promote defective AM phagocytosis and ameliorate the inflammatory response in COPD with or without PM2.5 exposure. (C) 2016 Elsevier B.V. All rights reserved.
引用
收藏
页码:76 / 84
页数:9
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