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Aromadendrin Inhibits Lipopolysaccharide-Induced Nuclear Translocation of NF-κB and Phosphorylation of JNK in RAW 264.7 Macrophage Cells

  • Lee, Jae-Won (Department of Pharmacology, College of Medicine, Kangwon National University) ;
  • Kim, Nam Ho (Department of Pharmacology, College of Medicine, Kangwon National University) ;
  • Kim, Ji-Young (Department of Pharmacology, College of Medicine, Kangwon National University) ;
  • Park, Jun-Ho (Department of Pharmacology, College of Medicine, Kangwon National University) ;
  • Shin, Seung-Yeon (Department of Pharmacology, College of Medicine, Kangwon National University) ;
  • Kwon, Yong-Soo (College of Pharmacy, Kangwon National University) ;
  • Lee, Hee Jae (Department of Pharmacology, College of Medicine, Kangwon National University) ;
  • Kim, Sung-Soo (Department of Pharmacology, College of Medicine, Kangwon National University) ;
  • Chun, Wanjoo (Department of Pharmacology, College of Medicine, Kangwon National University)
  • Received : 2013.03.07
  • Accepted : 2013.04.12
  • Published : 2013.05.31

Abstract

Aromadendrin, a flavonol, has been reported to possess a variety of pharmacological activities such as anti-inflammatory, antioxidant, and anti-diabetic properties. However, the underlying mechanism by which aromadendrin exerts its biological activity has not been extensively demonstrated. The objective of this study is to elucidate the anti-inflammatory mechanism of aromadedrin in lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophage cells. Aromadendrin significantly suppressed LPS-induced excessive production of pro-inflammatory mediators such as nitric oxide (NO) and $PGE_2$. In accordance, aromadendrin attenuated LPS-induced overexpression iNOS and COX-2. In addition, aromadendrin significantly suppressed LPS-induced degradation of $I{\kappa}B$, which sequesters NF-${\kappa}B$ in cytoplasm, consequently inhibiting the nuclear translocation of pro-inflammatory transcription factor NF-${\kappa}B$. To elucidate the underlying signaling mechanism of anti-inflammatory activity of aromadendrin, MAPK signaling pathway was examined. Aromadendrin significantly attenuated LPS-induced activation of JNK, but not ERK and p38, in a concentration-dependent manner. Taken together, the present study clearly demonstrates that aromadendrin exhibits anti-inflammatory activity through the suppression of nuclear translocation of NF-${\kappa}B$ and phosphorylation of JNK in LPS-stimulated RAW 264.7 macrophage cells.

Keywords

References

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