title: Astragalus polysaccharide attenuates lipopolysaccharide-induced inflammatory responses in microglial cells: regulation of protein kinase B and nuclear factor-κB signaling.
abstract: OBJECTIVE
  Microglia play an important role in immune and inflammatory responses in the central nervous system. Astragalus polysaccharide (APS) has been reported as an immune stimulant for various inflammation-associated diseases in vivo. The present study investigated the effects of APS on lipopolysaccharide-stimulated inflammatory responses in microglial cells.
  
  
  METHODS
  Cultured BV2 microglial cells were pre-treated with APS (0-200 μg/ml) prior to lipopolysaccharide (50 ng/ml) stimulation. The production of proinflammatory mediators including inducible nitric oxide synthase (iNOS)/nitric oxide (NO), cyclooxygenase-2 (COX-2)/prostaglandin E (PGE2), tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) were evaluated.
  
  
  RESULTS
  APS dose-dependently reduced lipopolysaccharide stimulated nitric oxide and PGE2 production, as well as iNOS and cyclooxygenase-2 gene expression. It also attenuated proinflammatory cytokines IL-1β and TNF-α generation. In addition, APS inhibited nuclear factor-κB translocation by blockade of IκB degradation and suppressed protein kinase B phosphorylation in lipopolysaccharide-stimulated cells.
  
  
  CONCLUSIONS
  The inhibitory effects of APS on lipopolysaccharide-stimulated inflammatory mediator production in microglia are associated with suppression of nuclear factor-κB and protein kinase B signaling pathways. APS may offer therapeutic potential for treating inflammatory and neurodegenerative diseases accompanied with microglial activation.
authors: Department of Anesthesiology, Peking University Shenzhen Hospital, Shenzhen, China, luotao_wh@yahoo.com.
authors: Tao
authors: T
authors: Luo
authors: Jian
authors: J
authors: Qin
authors: Min
authors: M
authors: Liu
authors: Jun
authors: J
authors: Luo
authors: Fang
authors: F
authors: Ding
authors: Mingling
authors: M
authors: Wang
authors: Limin
authors: L
authors: Zheng
mesh_terms: D000818:Animals; D027883:Astragalus Plant / Q000378:metabolism; D002478:Cells, Cultured; D051546:Cyclooxygenase 2 / Q000378:metabolism; D015232:Dinoprostone / Q000378:metabolism; D007249:Inflammation / Q000139:chemically induced / Q000378:metabolism / Q000517:prevention & control*; D053583:Interleukin-1beta / Q000378:metabolism; D008070:Lipopolysaccharides / Q000009:adverse effects / Q000494:pharmacology; D051379:Mice; D017628:Microglia / Q000187:drug effects / Q000378:metabolism* / Q000473:pathology; D023421:Models, Animal; D016328:NF-kappa B / Q000378:metabolism*; D009569:Nitric Oxide / Q000378:metabolism; D052247:Nitric Oxide Synthase Type II / Q000378:metabolism; D011134:Polysaccharides / Q000378:metabolism / Q000494:pharmacology* / Q000627:therapeutic use*; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism*; D015398:Signal Transduction / Q000187:drug effects*; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D053583:Interleukin-1beta; D008070:Lipopolysaccharides; D016328:NF-kappa B; D011134:Polysaccharides; D014409:Tumor Necrosis Factor-alpha; D009569:Nitric Oxide; D052247:Nitric Oxide Synthase Type II; C077623:Ptgs2 protein, mouse; D051546:Cyclooxygenase 2; D051057:Proto-Oncogene Proteins c-akt; D015232:Dinoprostone