Esculentoside A inhibits LPS-induced BV2 microglia activation through activating PPAR-γ

Eur J Pharmacol. 2017 Oct 15:813:61-65. doi: 10.1016/j.ejphar.2017.07.029. Epub 2017 Jul 19.

Abstract

Neuroinflammation has been recognized as a factor in the pathogenesis of neurodegenerative diseases. Esculentoside A (EsA), a saponin isolated from Phytolacca esculenta, has been reported to have anti-inflammatory activity. However, little research has been reported on the anti-neuroinflammatory effects of EsA. EsA concentration-dependently suppressed LPS-induced TNF-α, IL-1β, and PGE2 production. LPS-induced NF-κB activation was inhibited by treatment of EsA. Furthermore, EsA concentration-dependently up-regulated the expression of PPAR-γ. In addition, GW9662, a specific PPAR-γ inhibitor, reversed the anti-inflammatory effects of EsA. In conclusion, these results indicate that EsA exerts anti-inflammatory effects by activating PPAR-γ.

Keywords: Esculentoside A; Inflammatory response; LPS; PPAR-γ.

MeSH terms

  • Animals
  • Anti-Inflammatory Agents / pharmacology*
  • Cell Line
  • Cell Survival / drug effects
  • Lipopolysaccharides / pharmacology*
  • Mice
  • Microglia / cytology
  • Microglia / drug effects*
  • Microglia / metabolism*
  • NF-kappa B / metabolism
  • Oleanolic Acid / analogs & derivatives*
  • Oleanolic Acid / pharmacology
  • PPAR gamma / metabolism*
  • Saponins / pharmacology*

Substances

  • Anti-Inflammatory Agents
  • Lipopolysaccharides
  • NF-kappa B
  • PPAR gamma
  • Saponins
  • esculentoside A
  • Oleanolic Acid