Effects of Astragalus and Codonopsis pilosula polysaccharides on alveolar macrophage phagocytosis and inflammation in chronic obstructive pulmonary disease mice exposed to PM2.5 |
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| Affiliation: | 1. Department of Respiratory Medicine, The Second Affiliated Hospital of Xi''an Jiaotong University, Xi''an, Shaanxi, China;2. Department of Cardiology, The Second Affiliated Hospital of Xi''an Jiaotong University, Xi''an, Shaanxi, China;3. Department of Pharmacy, The Second Affiliated Hospital of Xi''an Jiaotong University, Xi''an, Shaanxi, China;4. Department of Laboratory Examination, The Second Affiliated Hospital of Xi''an Jiaotong University, Xi''an, Shaanxi, China;5. Laboratory of Electron Microscope, Health Science Center of Xi''an Jiaotong University, Xi''an, Shaanxi, China;1. Laboratory of Environment and Health, College of Life Sciences, University of Chinese Academy of Sciences, Beijing, China;2. State Key Laboratory of Membrane Biology, Institute of Zoology, Chinese Academy of Sciences, Beijing, China |
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| Abstract: | 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 μm (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 intragastrically. COPD showed defective AM phagocytosis and increased levels of interleukin (IL)-6, IL-8, and tumor necrosis factor (TNF)-α 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. |
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| Keywords: | Pulmonary disease, Chronic obstructive PM2.5 Polysaccharides Macrophages, Alveolar Phagocytosis Inflammation |
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