title: Astragalus polysaccharides mediated preventive effects on bronchopulmonary dysplasia in rats.
abstract: BACKGROUND
  Bronchopulmonary dysplasia (BPD) is a multifactor chronic lung disease that mainly affects premature infants. In this study, we investigate the preventive effects of Astragalus polysaccharides (APS) on BPD, and explore its potential molecular mechanisms.
  
  
  METHODS
  Lung tissues of newborn Sprague-Dawley rats from the control group, the room air plus low-dose APS group, the room air plus high-dose APS group, the BPD model group, the low-dose APS group (20 mg/kg d), and the high-dose APS group (40 mg/kg d) were examined at the 4th, 10th, and 14th d of life. The pathomorphological change was evaluated by hematoxylin-eosin staining. The content levels of superoxide dismutase (SOD) and malondialdehyde (MDA) were measured by the assay kit. Moreover, the protein and/or mRNA expression levels of NF-κBp65, CD31, ICAM-1, and TNF-α were also detected by corresponding methods.
  
  
  RESULTS
  APS decreased the inflammatory cells infiltrating compared with the BPD group. For the APS group, the activity of SOD was increased and the content of MDA was reduced compared with the BPD group at any time point. The protein and mRNA expression levels of NF-κBp65, ICAM-1, and TNF-α were all decreased, while the protein expression level of CD31 was increased in the APS-treated group, with the most significant difference of the high-dose group (P < 0.01) compared with the BPD group after birth on the 4th, 10th, and 14th d.
  
  
  CONCLUSIONS
  APS can reduce airway remodeling and alveolar damage by its modulation of inflammatory mediators and antioxidation, suggesting some protective effects on BPD of neonatal rats.
authors.affiliation: Department of Neonatology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, China.
authors.forename: Xiao-Hong
authors.initials: XH
authors.lastname: Wang
authors.affiliation: Key Laboratory of Functional Protein Research of Guangdong Higher Education Institutes, Institute of Life and Health Engineering, College of Life Science and Technology, Jinan University, Guangzhou, Guangdong, China.
authors.forename: Hong-Ling
authors.initials: HL
authors.lastname: Jia
authors.affiliation: Department of Pneumology, Guangzhou Women and Children's Medical Center, Guangzhou, Guangdong, China.
authors.forename: Li
authors.initials: L
authors.lastname: Deng
authors.affiliation: Department of Neonatology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, China.
authors.forename: Wei-Min
authors.initials: WM
authors.lastname: Huang
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D027883:Astragalus Plant / Q000737:chemistry*; D015153:Blotting, Western; D001992:Bronchoalveolar Lavage Fluid; D001997:Bronchopulmonary Dysplasia / Q000517:prevention & control*; D018799:Intercellular Adhesion Molecule-1 / Q000235:genetics; D008168:Lung / Q000187:drug effects / Q000201:enzymology / Q000378:metabolism; D008315:Malondialdehyde / Q000378:metabolism; D011134:Polysaccharides / Q000494:pharmacology*; D012333:RNA, Messenger / Q000235:genetics; D051381:Rats; D017207:Rats, Sprague-Dawley; D060888:Real-Time Polymerase Chain Reaction; D013482:Superoxide Dismutase / Q000378:metabolism; D051996:Transcription Factor RelA / Q000235:genetics; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics
chemical_list: D011134:Polysaccharides; D012333:RNA, Messenger; C498145:Rela protein, rat; D051996:Transcription Factor RelA; D014409:Tumor Necrosis Factor-alpha; D018799:Intercellular Adhesion Molecule-1; D008315:Malondialdehyde; D013482:Superoxide Dismutase