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Korean Society for Biochemistry and Molecular Biology (생화학분자생물학회)
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Salicortin suppresses lipopolysaccharide-stimulated inflammatory responses via blockade of NF-κB and JNK activation in RAW 264.7 macrophages

  • Kwon, Dong-Joo (Department of Biomedical Science and Research Institute for Bioscience & Biotechnology, Hallym University) ;
  • Bae, Young-Soo (Department of Forest Biomaterials Engineering, Kangwon National University) ;
  • Ju, Sung Mi (Department of Biomedical Science and Research Institute for Bioscience & Biotechnology, Hallym University) ;
  • Youn, Gi Soo (Department of Biomedical Science and Research Institute for Bioscience & Biotechnology, Hallym University) ;
  • Choi, Soo Young (Department of Biomedical Science and Research Institute for Bioscience & Biotechnology, Hallym University) ;
  • Park, Jinseu (Department of Biomedical Science and Research Institute for Bioscience & Biotechnology, Hallym University)
  • Received : 2013.09.03
  • Accepted : 2013.09.09
  • Published : 2014.06.30
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Abstract

We isolated the phenolic glucoside salicortin from a Populus euramericana bark extract, and examined its ability to suppress inflammatory responses as well as the molecular mechanisms underlying these abilities, using lipopolysaccharide (LPS)-stimulated RAW264.7 cells. Salicortin inhibited iNOS expression and the subsequent production of NO in a dose-dependent manner in the LPS-stimulated RAW 264.7 cells. Salicortin significantly suppressed LPS-induced signal cascades of NF-${\kappa}B$ activation, such as IKK activation, $I{\kappa}B{\alpha}$ phosphorylation and p65 phosphorylation in RAW 264.7 cells. In addition, salicortin inhibited the LPS-induced activation of JNK, but not ERK or p38 MAPK. Furthermore, salicortin significantly inhibited production of pro-inflammatory cytokines, such as TNF-${\alpha}$, IL-$1{\beta}$ and IL-6 in the LPS-stimulated RAW 264.7 cells. These findings suggest that salicortin may show its anti-inflammatory activity by suppressing the LPS-induced expression of pro-inflammatory mediators through inhibition of NF-${\kappa}B$ and JNK MAPK signaling cascades in macrophages.

Keywords

References

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