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In vitro and in vivo anti-inflammatory activities of Korean Red Ginseng-derived components

  • Baek, Kwang-Soo (Department of Genetic Engineering, Sungkyunkwan University) ;
  • Yi, Young-Su (Department of Pharmaceutical Engineering, Cheongju University) ;
  • Son, Young-Jin (Department of Pharmacy, Sunchon National University) ;
  • Yoo, Sulgi (Department of Genetic Engineering, Sungkyunkwan University) ;
  • Sung, Nak Yoon (Department of Genetic Engineering, Sungkyunkwan University) ;
  • Kim, Yong (Department of Genetic Engineering, Sungkyunkwan University) ;
  • Hong, Sungyoul (Department of Genetic Engineering, Sungkyunkwan University) ;
  • Aravinthan, Adithan (Department of Physiology, College of Veterinary Medicine, Chonbuk National University) ;
  • Kim, Jong-Hoon (Department of Physiology, College of Veterinary Medicine, Chonbuk National University) ;
  • Cho, Jae Youl (Department of Genetic Engineering, Sungkyunkwan University)
  • Received : 2016.07.11
  • Accepted : 2016.08.09
  • Published : 2016.10.15

Abstract

Background: Although Korean Red Ginseng (KRG) has been traditionally used for a long time, its anti-inflammatory role and underlying molecular and cellular mechanisms have been poorly understood. In this study, the anti-inflammatory roles of KRG-derived components, namely, water extract (KRG-WE), saponin fraction (KRG-SF), and nonsaponin fraction (KRG-NSF), were investigated. Methods: To check saponin levels in the test fractions, KRG-WE, KRG-NSF, and KRG-SF were analyzed using high-performance liquid chromatography. The anti-inflammatory roles and underlying cellular and molecular mechanisms of these components were investigated using a macrophage-like cell line (RAW264.7 cells) and an acute gastritis model in mice. Results: Of the tested fractions, KGR-SF (but not KRG-NSF and KRG-WE) markedly inhibited the viability of RAW264.7 cells, and splenocytes at more than 500 mg/mL significantly suppressed NO production at $100{\mu}g/mL$, diminished mRNA expression of inflammatory genes such as inducible nitric oxide synthase, cyclooxygenase-2, tumor necrosis factor-${\alpha}$, and interferon-${\beta}$ at $200{\mu}g/mL$, and completely blocked phagocytic uptake by RAW264.7 cells. All three fractions suppressed luciferase activity triggered by interferon regulatory factor 3 (IRF3), but not that triggered by activator protein-1 and nuclear factor-kappa B. Phospho-IRF3 and phospho-TBK1 were simultaneously decreased in KRG-SF. Interestingly, all these fractions, when orally administered, clearly ameliorated the symptoms of gastric ulcer in HCl/ethanol-induced gastritis mice. Conclusion: These results suggest that KRG-WE, KRG-NSF, and KRG-SF might have anti-inflammatory properties, mostly because of the suppression of the IRF3 pathway.

Keywords

References

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