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Pristimerin Inhibits Inducible Nitric Oxide Synthase Expression Induced by TLR Agonists

  • Kim, Su-Yeon (Department of Biomedical Laboratory Science, College of Medical Sciences, SoonChunHyang University) ;
  • Heo, Sung-Hye (Department of Biomedical Laboratory Science, College of Medical Sciences, SoonChunHyang University) ;
  • Park, Sin-Aye (Department of Biomedical Laboratory Science, College of Medical Sciences, SoonChunHyang University) ;
  • Youn, Hyung-Sun (Department of Biomedical Laboratory Science, College of Medical Sciences, SoonChunHyang University)
  • Received : 2019.01.14
  • Accepted : 2019.03.14
  • Published : 2019.03.31

Abstract

Toll-like receptors (TLRs) are one of the families of pattern recognition receptors (PRR) operating in the innate immunity. TLRs have the ability to recognize relatively conserved microbial components, which are generally referred to as pathogen-associated molecular patterns (PAMPs). The activation of TLRs signaling leads to the activation of $NF-{\kappa}B$ and the expression of pro-inflammatory gene products such as cytokines and inducible nitric oxide synthase (iNOS). To evaluate the therapeutic potential of pristimerin, which is a naturally occurring triterpenoid compound from Celastraceae plants, iNOS expression induced by MALP-2 (TLR2 and TLR6 agonist), Poly[I:C] (TLR3 agonist), or LPS (TLR4 agonist) were examined. Pristimerin suppressed the iNOS expression induced by MALP-2, Poly[I:C], or LPS. These results suggest that pristimerin can modulate TLRs signaling pathways leading to decreased inflammatory gene expression.

Keywords

References

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