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Korean Red Ginseng Saponin Fraction Downregulates Proinflammatory Mediators in LPS Stimulated RAW264.7 Cells and Protects Mice against Endotoxic Shock

  • Yayeh, Taddessee (College of Veterinary Medicine and Stem Cell Research Therapeutic Institute, Kyungpook National University) ;
  • Jung, Kun-Ho (College of Veterinary Medicine, Chungnam National University) ;
  • Jeong, Hye-Yoon (Department of Genetic Engineering, Sungkyunkwan University) ;
  • Park, Ji-Hoon (College of Veterinary Medicine and Stem Cell Research Therapeutic Institute, Kyungpook National University) ;
  • Song, Yong-Bum (Ginseng Corporation Central Research Institute) ;
  • Kwak, Yi-Seong (Ginseng Corporation Central Research Institute) ;
  • Kang, Heun-Soo (Metabolab Inc.) ;
  • Cho, Jae-Youl (Department of Genetic Engineering, Sungkyunkwan University) ;
  • Oh, Jae-Wook (College of Animal Bioscience & Technology, Konkuk University) ;
  • Kim, Sang-Keun (College of Veterinary Medicine, Chungnam National University) ;
  • Rhee, Man-Hee (College of Veterinary Medicine and Stem Cell Research Therapeutic Institute, Kyungpook National University)
  • Received : 2012.03.02
  • Accepted : 2012.03.24
  • Published : 2012.07.15

Abstract

Korean red ginseng has shown therapeutic effects for a number of disease conditions. However, little is known about the anti-inflammatory effect of Korean red ginseng saponin fraction (RGSF) in vitro and in vivo. Therefore, in this study, we showed that RGSF containing 20(S)-protopanaxadiol type saponins inhibited nitric oxide production and attenuated the release of tumor necrotic factor (TNF)-${\alpha}$, interleukin (IL)-6, granulocyte monocyte colony stimulating factor (GMCSF), and macrophage chemo-attractant protein-1 in lipopolysaccharide (LPS) stimulated murine macrophage RAW264.7 cells. Moreover, RGSF down-regulated the mRNA expressions of inducible nitric oxide synthase, cyclooxyginase-2, IL-$1{\beta}$, TNF-${\alpha}$, GMCSF, and IL-6. Furthermore, RGSF reduced the level of TNF-${\alpha}$ in the serum and protected mice against LPS mediated endotoxic shock. In conclusion, these results indicated that ginsenosides from RGSF and their metabolites could be potential sources of therapeutic agents against inflammation.

Keywords

References

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