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Isobavachalcone suppresses expression of inducible nitric oxide synthase induced by Toll-like receptor agonists.

Abstract
Toll-like receptors (TLRs) play an important role by recognizing many pathogen-associated molecular patterns and inducing innate immunity. Dysregulated activation of TLR signaling pathways induces the activation of various transcription factors such as nuclear factor-κB, leading to the induction of pro-inflammatory gene products such as inducible nitric oxide synthase (iNOS). The present study investigated the effect of isobavachalcone (IBC), a natural chalcone component of Angelica keiskei, on inflammation by modulating iNOS expression induced by TLR agonists in murine macrophages. IBC suppressed iNOS expression induced by macrophage-activating lipopeptide 2-kDa, polyriboinosinic polyribocytidylic acid, or lipopolysaccharide. These results indicate the potential of IBC as a potent anti-inflammatory drug.
AuthorsHwa-Jeong Shin, Dong-Hwa Shon, Hyung-Sun Youn
JournalInternational immunopharmacology (Int Immunopharmacol) Vol. 15 Issue 1 Pg. 38-41 (Jan 2013) ISSN: 1878-1705 [Electronic] Netherlands
PMID23164691 (Publication Type: Journal Article)
CopyrightCrown Copyright © 2012. Published by Elsevier B.V. All rights reserved.
Chemical References
  • Adaptor Proteins, Vesicular Transport
  • Anti-Inflammatory Agents
  • Chalcones
  • Enzyme Inhibitors
  • Lipopeptides
  • Lipopolysaccharides
  • Myd88 protein, mouse
  • Myeloid Differentiation Factor 88
  • TICAM-1 protein, mouse
  • Toll-Like Receptors
  • isobavachalcone
  • macrophage stimulatory lipopeptide 2
  • Nitric Oxide Synthase Type II
  • Nos2 protein, mouse
  • Poly I-C
Topics
  • Adaptor Proteins, Vesicular Transport (metabolism)
  • Animals
  • Anti-Inflammatory Agents (pharmacology)
  • Cell Line
  • Chalcones (pharmacology)
  • Enzyme Inhibitors (pharmacology)
  • Lipopeptides (pharmacology)
  • Lipopolysaccharides (pharmacology)
  • Mice
  • Myeloid Differentiation Factor 88 (metabolism)
  • Nitric Oxide Synthase Type II (antagonists & inhibitors)
  • Poly I-C (pharmacology)
  • Toll-Like Receptors (agonists)

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