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Anti-inflammatory activity of AP-SF, a ginsenoside-enriched fraction, from Korean ginseng

  • Baek, Kwang-Soo (Department of Genetic Engineering, Sungkyunkwan University) ;
  • Hong, Yong Deog (Skin Research Institute, AmorePacific R&D Center) ;
  • Kim, Yong (Department of Genetic Engineering, Sungkyunkwan University) ;
  • Sung, Nak Yoon (Department of Genetic Engineering, Sungkyunkwan University) ;
  • Yang, Sungjae (Department of Genetic Engineering, Sungkyunkwan University) ;
  • Lee, Kyoung Min (Department of Genetic Engineering, Sungkyunkwan University) ;
  • Park, Joo Yong (Department of Genetic Engineering, Sungkyunkwan University) ;
  • Park, Jun Seong (Skin Research Institute, AmorePacific R&D Center) ;
  • Rho, Ho Sik (Skin Research Institute, AmorePacific R&D Center) ;
  • Shin, Song Seok (Skin Research Institute, AmorePacific R&D Center) ;
  • Cho, Jae Youl (Department of Genetic Engineering, Sungkyunkwan University)
  • Received : 2014.09.23
  • Accepted : 2014.10.23
  • Published : 2015.04.15

Abstract

Background: Korean ginseng is an ethnopharmacologically valuable herbal plant with various biological properties including anticancer, antiatherosclerosis, antidiabetic, and anti-inflammatory activities. Since there is currently no drug or therapeutic remedy derived from Korean ginseng, we developed a ginsenoside-enriched fraction (AP-SF) for prevention of various inflammatory symptoms. Methods: The anti-inflammatory efficacy of AP-SF was tested under in vitro inflammatory conditions including nitric oxide (NO) production and inflammatory gene expression. The molecular events of inflammatory responses were explored by immunoblot analysis. Results: AP-SF led to a significant suppression of NO production compared with a conventional Korean ginseng saponin fraction, induced by both lipopolysaccharide and zymosan A. Interestingly, AP-SF strongly downregulated the mRNA levels of genes for inducible NO synthase, tumor necrosis factor-${\alpha}$, and cyclooxygenase) without affecting cell viability. In agreement with these observations, AP-SF blocked the nuclear translocation of c-Jun at 2 h and also reduced phosphorylation of p38, c-Jun N-terminal kinase, and TAK-1, all of which are important for c-Jun translocation. Conclusion: Our results suggest that AP-SF inhibits activation of c-Jun-dependent inflammatory events. Thus, AP-SF may be useful as a novel anti-inflammatory remedy.

Keywords

References

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