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Molecular mechanism of protopanaxadiol saponin fraction-mediated anti-inflammatory actions

  • Yang, Yanyan (Department of Genetic Engineering, Sungkyunkwan University) ;
  • Lee, Jongsung (Department of Dermatological Health Management, Eulji University) ;
  • Rhee, Man Hee (College of Veterinary Medicine, Kyungpook National University) ;
  • Yu, Tao (Department of Genetic Engineering, Sungkyunkwan University) ;
  • Baek, Kwang-Soo (Department of Genetic Engineering, Sungkyunkwan University) ;
  • Sung, Nak Yoon (Department of Genetic Engineering, Sungkyunkwan University) ;
  • Kim, Yong (Department of Genetic Engineering, Sungkyunkwan University) ;
  • Yoon, Keejung (Department of Genetic Engineering, Sungkyunkwan University) ;
  • Kim, Ji Hye (Department of Genetic Engineering, Sungkyunkwan University) ;
  • Kwak, Yi-Seong (Ginseng Corporation Central Research Institute) ;
  • Hong, Sungyoul (Department of Genetic Engineering, Sungkyunkwan University) ;
  • Kim, Jong-Hoon (Department of Veterinary Physiology, College of Veterinary Medicine, Biosafety Research Institute, Chonbuk National University) ;
  • Cho, Jae Youl (Department of Genetic Engineering, Sungkyunkwan University)
  • Received : 2014.05.07
  • Accepted : 2014.06.07
  • Published : 2015.01.15

Abstract

Background: Korean Red Ginseng (KRG) is a representative traditional herbal medicine with many different pharmacological properties including anticancer, anti-atherosclerosis, anti-diabetes, and anti-inflammatory activities. Only a few studies have explored the molecular mechanism of KRG-mediated anti-inflammatory activity. Methods: We investigated the anti-inflammatory mechanisms of the protopanaxadiol saponin fraction (PPD-SF) of KRG using in vitro and in vivo inflammatory models. Results: PPD-SF dose-dependently diminished the release of inflammatory mediators [nitric oxide (NO), tumor necrosis factor-${\alpha}$, and prostaglandin $E_2$], and downregulated the mRNA expression of their corresponding genes (inducible NO synthase, tumor necrosis factor-${\alpha}$, and cyclooxygenase-2), without altering cell viability. The PPD-SF-mediated suppression of these events appeared to be regulated by a blockade of p38, c-Jun N-terminal kinase (JNK), and TANK (TRAF family member-associated NF-kappa-B activator)-binding kinase 1 (TBK1), which are linked to the activation of activating transcription factor 2 (ATF2) and interferon regulatory transcription factor 3 (IRF3). Moreover, this fraction also ameliorated HCl/ethanol/-induced gastritis via suppression of phospho-JNK2 levels. Conclusion: These results strongly suggest that the anti-inflammatory action of PPD-SF could be mediated by a reduction in the activation of p38-, JNK2-, and TANK-binding-kinase-1-linked pathways and their corresponding transcription factors (ATF2 and IRF3).

Keywords

Acknowledgement

Supported by : Korean Society of Ginseng

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