Astragalus polysaccharide attenuates lipopolysaccharide-induced inflammatory responses in microglial cells: regulation of protein kinase B and nuclear factor-κB signaling

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• 作者：Tao Luo ; Jian Qin ; Min Liu ; Jun Luo ; Fang Ding ; Mingling Wang…
• 关键词：Microglia ; Neuroinflammation ; Astragalus polysaccharide ; Lipopolysaccharide
• 刊名：Inflammation Research
• 出版年：2015
• 出版时间：April 2015
• 年：2015
• 卷：64
• 期：3-4
• 页码：205-212
• 全文大小：861 KB
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• 刊物类别：Biomedical and Life Sciences
• 刊物主题：Biomedicine
  Immunology
  Pharmacology and Toxicology
  Allergology
  Dermatology
  Neurology
  Rheumatology
  
• 出版者：Birkh盲user Basel
• ISSN：1420-908X

文摘

Objectives and design 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. Materials and methods Cultured BV2 microglial cells were pre-treated with APS (0-00?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.