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Curcumol exhibits anti-inflammatory properties by interfering with the JNK-mediated AP-1 pathway in lipopolysaccharide-activated RAW264.7 cells.

Abstract
Curcumol is one of the major components of the essential oil of Rhizoma Curcumae, a common traditional Chinese medicine with anti-inflammatory properties. However, the anti-inflammatory activity and the underlying molecular mechanisms of this compound remain unclear. In the present study, the anti-inflammation effect of curcumol on lipopolysaccharide (LPS)-induced RAW264.7 cells is demonstrated along with its underlying mechanisms. We show that curcumol inhibits LPS-induced NO production by suppressing iNOS mRNA expression and protein level but not iNOS activity. Moreover, curcumol inhibits LPS-induced production of TNF-α, IL-1β and IL-6 at both the transcriptional and translational levels. Further investigations reveal that these effects mainly act via suppressing JNK-mediated AP-1 rather than the NF-κB pathway; these effects include a decrease in the phosphorylation level of JNK and a direct inhibition of the activity of p-JNK. These data provide scientific molecular evidence that curcumol may be a potential lead compound for a novel anti-inflammatory drug because of its inhibitory activity on the production of various inflammatory mediators.
AuthorsXi Chen, Chuanjie Zong, Yuan Gao, Runlan Cai, Lei Fang, Juan Lu, Fen Liu, Yun Qi
JournalEuropean journal of pharmacology (Eur J Pharmacol) Vol. 723 Pg. 339-45 (Jan 15 2014) ISSN: 1879-0712 [Electronic] Netherlands
PMID24269960 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Copyright© 2013 Published by Elsevier B.V.
Chemical References
  • Anti-Inflammatory Agents
  • Cytokines
  • Lipopolysaccharides
  • RNA, Messenger
  • Sesquiterpenes
  • Transcription Factor AP-1
  • Nitric Oxide
  • curcumol
  • Nitric Oxide Synthase Type II
  • Nos2 protein, mouse
  • JNK Mitogen-Activated Protein Kinases
Topics
  • Animals
  • Anti-Inflammatory Agents (pharmacology)
  • Cell Line
  • Cytokines (metabolism)
  • JNK Mitogen-Activated Protein Kinases (metabolism)
  • Lipopolysaccharides
  • Mice
  • Nitric Oxide (metabolism)
  • Nitric Oxide Synthase Type II (genetics, metabolism)
  • RNA, Messenger (metabolism)
  • Sesquiterpenes (pharmacology)
  • Signal Transduction (drug effects)
  • Transcription Factor AP-1 (metabolism)

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