Document Detail


Suppression of the TRIF-dependent signaling pathway of toll-like receptors by isoliquiritigenin in RAW264.7 macrophages.
MedLine Citation:
PMID:  19809799     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Toll-like receptors (TLRs) play an important role in host defense by sensing invading microbial pathogens and initiating innate immune responses. The stimulation of TLRs by microbial components triggers the activation of myeloid differential factor 88 (MyD88)- and toll-interleukin-1 receptor domain-containing adapter inducing interferon-beta (TRIF)-dependent downstream signaling pathways. Isoliquiritigen in (ILG), an active ingredient of Licorice, has been used for centuries to treat many chronic diseases. ILG inhibits the MyD88-dependent pathway by inhibiting the activity of inhibitor-kappaB kinase. However, it is not known whether ILG inhibits the TRIF-dependent pathway. To evaluate the therapeutic potential of ILG, we examined its effect on signal transduction via the TRIF-dependent pathway of TLRs induced by several agonists. ILG inhibited nuclear factor-kappaB and interferon regulatory factor 3 activation induced by lipopolysaccharide or polyinosinic-polycytidylic acid. ILG inhibited the lipopolysaccharide-induced phosphorylation of interferon regulatory factor 3 as well as interferon-inducible genes such as interferon inducible protein-10, and regulated activation of normal T-cell expressed and secreted (RANTES). These results suggest that ILG can modulate TRIF-dependent signaling pathways of TLRs, leading to decreased inflammatory gene expression.
Authors:
Se-Jeong Park; Ho-Yeon Song; Hyung-Sun Youn
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Publication Detail:
Type:  Journal Article     Date:  2009-09-30
Journal Detail:
Title:  Molecules and cells     Volume:  28     ISSN:  0219-1032     ISO Abbreviation:  Mol. Cells     Publication Date:  2009 Oct 
Date Detail:
Created Date:  2010-01-21     Completed Date:  2010-05-11     Revised Date:  2010-06-16    
Medline Journal Info:
Nlm Unique ID:  9610936     Medline TA:  Mol Cells     Country:  United States    
Other Details:
Languages:  eng     Pagination:  365-8     Citation Subset:  IM    
Affiliation:
Department of Medical Science, College of Medical Sciences, Soonchunhyang University, Asan 336-745, Korea.
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MeSH Terms
Descriptor/Qualifier:
Adaptor Proteins, Vesicular Transport / antagonists & inhibitors*
Animals
Cell Line
Chalcones / pharmacology*
Enzyme Inhibitors / pharmacology
Gene Expression
Inflammation / genetics,  prevention & control
Interferon Regulatory Factor-3
Lymphocyte Activation
Macrophages / drug effects*
Mice
NF-kappa B
Signal Transduction / drug effects*
Toll-Like Receptors / antagonists & inhibitors*
Chemical
Reg. No./Substance:
0/Adaptor Proteins, Vesicular Transport; 0/Chalcones; 0/Enzyme Inhibitors; 0/Interferon Regulatory Factor-3; 0/NF-kappa B; 0/TICAM-1 protein, mouse; 0/Toll-Like Receptors; 961-29-5/isoliquiritigenin

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