AI Article Synopsis
- TLRs are essential for the innate immune response against infections, activating signaling pathways through MyD88 and TRIF.
- Cardamonin, a compound from Alpinia species, shows anti-inflammatory effects by inhibiting TLR-induced NF-κB and COX-2 activation, as well as interferon-related proteins.
- This study suggests that cardamonin could be a promising new anti-inflammatory agent by modulating TLR signaling pathways.
Article Abstract
Toll-like receptors (TLRs) play a crucial role in the induction of innate immune response against bacterial and viral infections. TLRs induce downstream signaling via MyD88- and TRIF-dependent pathways. Cardamonin is a naturally occurring chalcone from Alpinia species exhibiting anti-inflammatory effects. However, the principal molecular mechanisms remain unclear. The objective of this study was to investigate the role of cardamonin in TLR signaling pathways. Cardamonin inhibited NF-κB activation as well as COX-2 expression induced by TLR agonists. Cardamonin inhibited the activation of IRF3 and the expression of interferon-inducible protein-10 (IP-10) induced by TLR3 or TLR4 agonists. Cardamonin also inhibited ligand-independent NF-κB activation overexpressed by MyD88, IKKβ, or p65 and IRF3 activation overexpressed by TRIF, TBK1, or IRF3. However, cardamonin had no effect on TBK1 kinase activity in vitro. These results suggest that cardamonin modulates both the MyD88- and TRIF-dependent pathways of TLRs and represents a potentially new anti-inflammatory candidate.
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| http://dx.doi.org/10.1016/j.intimp.2018.08.018 | DOI Listing |
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