Tenuigenin inhibits LPS-induced inflammatory responses in microglia via activating the Nrf2-mediated HO-1 signaling pathway

Eur J Pharmacol. 2017 Aug 15:809:196-202. doi: 10.1016/j.ejphar.2017.05.004. Epub 2017 May 3.

Abstract

Tenuigenin (TGN), a major active component of polygala tenuifolia root, has been reported to have anti-inflammatory effect. In this study, we investigated the anti-neuroinflammatory effects of TGN on LPS-induced inflammation both in vitro and in vivo. The levels of tumor necrosis factor -α (TNF-α), Interleukin-1β (IL-1β), Interleukin-6 (IL-6), and prostaglandin E2 (PGE2) were measured by ELISA. The expression of Nuclear factor E2-related factor 2 (Nrf2) and heme oxygenase 1 (HO-1) were detected by western blot analysis. The results showed that TGN strongly inhibited LPS-induced TNF-α, IL-1β, IL-6, and PGE2 production. The expression of Nrf2 and HO-1 were up-regulated by TGN in a dose-dependent manner. Furthermore, the anti-inflammatory effects of TGN were significantly inhibited by transfection with Nrf2 siRNA or protoporphyrin (SnPP), an HO-1 activity inhibitor. In vivo, TGN attenuated LPS-induced memory deficit in the Morris water maze and passive avoidance tasks. Also, TGN inhibited LPS-induced TNF-α and IL-1β expression in brain tissues. In conclusion, the results of this study indicated that TGN inhibited LPS-induced inflammatory responses in microglia via activating the Nrf2-mediated HO-1 signaling pathway.

Keywords: Inflammatory response; LPS; Nrf2; Tenuigenin.

MeSH terms

  • Animals
  • Anti-Inflammatory Agents / pharmacology*
  • Anti-Inflammatory Agents / therapeutic use
  • Brain / drug effects
  • Brain / metabolism
  • Brain / pathology
  • Brain / physiopathology
  • Cell Line
  • Cell Survival / drug effects
  • Dinoprostone / biosynthesis
  • Drugs, Chinese Herbal / pharmacology*
  • Drugs, Chinese Herbal / therapeutic use
  • Gene Expression Regulation, Enzymologic / drug effects
  • Heme Oxygenase-1 / metabolism*
  • Inflammation / drug therapy
  • Inflammation / pathology
  • Interleukin-1beta / biosynthesis
  • Interleukin-6 / biosynthesis
  • Lipopolysaccharides / pharmacology*
  • Memory / drug effects
  • Mice
  • Mice, Inbred ICR
  • Microglia / drug effects*
  • Microglia / pathology
  • NF-E2-Related Factor 2 / metabolism*
  • Signal Transduction / drug effects*
  • Tumor Necrosis Factor-alpha / biosynthesis

Substances

  • Anti-Inflammatory Agents
  • Drugs, Chinese Herbal
  • Interleukin-1beta
  • Interleukin-6
  • Lipopolysaccharides
  • NF-E2-Related Factor 2
  • Tumor Necrosis Factor-alpha
  • tenuigenin
  • Heme Oxygenase-1
  • Dinoprostone