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Inflamm Res. 2015 Apr;64(3-4):205-12. doi: 10.1007/s00011-015-0798-9. Epub 2015 Feb 11.

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

Author information

1
Department of Anesthesiology, Peking University Shenzhen Hospital, Shenzhen, China, luotao_wh@yahoo.com.

Abstract

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 (0-200 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.

PMID:
25669325
DOI:
10.1007/s00011-015-0798-9
[Indexed for MEDLINE]

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