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Compound K, a ginsenoside metabolite, plays an antiinflammatory role in macrophages by targeting the AKT1-mediated signaling pathway

  • Lee, Jeong-Oog (Department of Aerospace Information Engineering, Bio-Inspired Aerospace Information Laboratory, Konkuk University) ;
  • Choi, Eunju (Department of Integrative Biotechnology, Sungkyunkwan University) ;
  • Shin, Kon Kuk (Department of Integrative Biotechnology, Sungkyunkwan University) ;
  • Hong, Yo Han (Department of Integrative Biotechnology, Sungkyunkwan University) ;
  • Kim, Han Gyung (Department of Integrative Biotechnology, Sungkyunkwan University) ;
  • Jeong, Deok (Department of Integrative Biotechnology, Sungkyunkwan University) ;
  • Hossain, Mohammad Amjad (Department of Veterinary Physiology, College of Medicine, Chonbuk National University) ;
  • Kim, Hyun Soo (Basic Research & Innovation Division, R&D Center, Amorepacific Corporation) ;
  • Yi, Young-Su (Department of Pharmaceutical Engineering, Cheongju University) ;
  • Kim, Donghyun (Basic Research & Innovation Division, R&D Center, Amorepacific Corporation) ;
  • Kim, Eunji (Department of Integrative Biotechnology, Sungkyunkwan University) ;
  • Cho, Jae Youl (Department of Integrative Biotechnology, Sungkyunkwan University)
  • 투고 : 2018.08.13
  • 심사 : 2018.10.18
  • 발행 : 2019.01.15

초록

Background: Compound K (CK) is an active metabolite of ginseng saponin, ginsenoside Rb1, that has been shown to have ameliorative properties in various diseases. However, its role in inflammation and the underlying mechanisms are poorly understood. In this report, the antiinflammatory role of CK was investigated in macrophage-like cells. Methods: The CK-mediated antiinflammatory mechanism was explored in RAW264.7 and HEK293 cells that were activated by lipopolysaccharide (LPS) or exhibited overexpression of known activation proteins. The mRNA levels of inflammatory genes and the activation levels of target proteins were identified by quantitative and semiquantitative reverse transcription polymerase chain reaction and Western blot analysis. Results: CK significantly inhibited the mRNA expression of inducible nitric oxide synthase and tumor necrosis factor-${\alpha}$ and morphological changes in LPS-activated RAW264.7 cells under noncytotoxic concentrations. CK downregulated the phosphorylation of AKT1, but not AKT2, in LPS-activated RAW264.7 cells. Similarly, CK reduced the AKT1 overexpression-induced expression of aldehyde oxidase 1, interleukin-$1{\beta}$, interferon-${\beta}$, and tumor necrosis factor-${\alpha}$ in a dose-dependent manner. Conclusion: Our results suggest that CK plays an antiinflammatory role during macrophage-mediated inflammatory actions by specifically targeting the AKT1-mediated signaling pathway.

키워드

참고문헌

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