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Synephrine inhibits eotaxin-1 expression via the STAT6 signaling pathway.

Abstract
Citrus contain various flavonoids and alkaloids that have multiple biological activities. It is known that the immature Citrus contains larger amounts of bioactive components, than do the mature plants. Although Citrus flavonoids are well known for their biological activities, Citrus alkaloids have not previously been assessed. In this study, we identified synephrine alkaloids as an active compound from immature Citrus unshiu, and investigated the effect of synephrine on eotaxin-1 expression. Eotaxin-1 is a potent chemoattractant for eosinophils, and a critical mediator, during the development of eosinophilic inflammation. We found that synephrine significantly inhibited IL-4-induced eotaxin-1 expression. This synephrine effect was mediated through the inhibition of STAT6 phosphorylation in JAK/STAT signaling. We also found that eosinophil recruitment induced by eotaxin-1 overexpression was inhibited by synephrine. Taken together, these findings indicate that inhibiting IL-4-induced eotaxin-1 expression by synephrine occurs primarily through the suppression of eosinophil recruitment, which is mediated by inhibiting STAT6 phosphorylation.
AuthorsKyung-Baeg Roh, Il-Hyun Kim, Young-Soo Kim, Myungjae Lee, Jung-A Lee, Eunsun Jung, Deokhoon Park
JournalMolecules (Basel, Switzerland) (Molecules) Vol. 19 Issue 8 Pg. 11883-95 (Aug 08 2014) ISSN: 1420-3049 [Electronic] Switzerland
PMID25111027 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Chemokine CCL11
  • STAT6 Transcription Factor
  • STAT6 protein, human
  • Tumor Necrosis Factor-alpha
  • Interleukin-4
  • Synephrine
Topics
  • Chemokine CCL11 (biosynthesis, drug effects)
  • Citrus (chemistry)
  • Eosinophils (drug effects)
  • Gene Expression Regulation (drug effects)
  • Humans
  • Interleukin-4 (metabolism)
  • Phosphorylation
  • STAT6 Transcription Factor (biosynthesis, genetics)
  • Signal Transduction (drug effects)
  • Synephrine (administration & dosage, chemistry, isolation & purification)
  • Tumor Necrosis Factor-alpha

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