Norkurarinol inhibits toll-like receptor 3 (TLR3)-mediated pro-inflammatory signaling pathway and rotavirus replication

J Pharmacol Sci. 2012;118(2):161-70. doi: 10.1254/jphs.11077fp. Epub 2012 Jan 27.

Abstract

This study examined the effect of norkurarinol on the toll-like receptor 3 (TLR3)-mediated signaling pathways and rotavirus replication. Norkurarinol, a lavandulylated flavanone, was isolated from the roots of Sophora flavescens, which has been shown to have anti-inflammatory activity. Norkurarinol suppressed the NF-κB and AP-1 inducible secreted embryonic alkaline phosphatase (SEAP) activity induced by poly(I:C), TLR3 ligand, in THP1-Blue-CD14 cells with IC(50) values of 20.9 µM. Norkurarinol also significantly suppressed the mRNA expression of pro-inflammatory and adhesive molecules induced by poly(I:C) and rotavirus infection. Pretreatment of norkurarinol blocked the NF-κB and AP-1 signaling pathway and the phosphorylation of MAPKs induced by poly(I:C). On the other hand, norkurarinol increased the level of IRF3 phosphorylation and IFNβ expression in a dose-dependent manner. Moreover, norkurarinol inhibited the rotavirus-induced cytopathic effects. These results suggest that norkurarinol can modulate the TLR3-mediated inflammatory responses and rotavirus replication.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Anti-Inflammatory Agents / administration & dosage
  • Anti-Inflammatory Agents / isolation & purification
  • Anti-Inflammatory Agents / pharmacology*
  • Cell Line
  • Dose-Response Relationship, Drug
  • Flavanones / administration & dosage
  • Flavanones / isolation & purification
  • Flavanones / pharmacology*
  • Humans
  • Inflammation / drug therapy
  • Inflammation / physiopathology
  • Inhibitory Concentration 50
  • Macaca mulatta
  • Mitogen-Activated Protein Kinases / metabolism
  • NF-kappa B / metabolism
  • Phosphorylation / drug effects
  • Plant Roots
  • RNA, Messenger / metabolism
  • Rotavirus / drug effects
  • Signal Transduction / drug effects
  • Sophora / chemistry*
  • Toll-Like Receptor 3 / metabolism*
  • Transcription Factor AP-1 / metabolism
  • Virus Replication / drug effects

Substances

  • Anti-Inflammatory Agents
  • Flavanones
  • NF-kappa B
  • RNA, Messenger
  • Toll-Like Receptor 3
  • Transcription Factor AP-1
  • norkurarinol
  • Mitogen-Activated Protein Kinases