Ginsenoside Rc from Panax ginseng exerts anti-inflammatory activity by targeting TANK-binding kinase 1/interferon regulatory factor-3 and p38/ATF-2
- J Ginseng Res. 2017 Apr;41(2):127-133. doi: 10.1016/j.jgr.2016.02.001.
- 1. Department of Genetic Engineering, Sungkyunkwan University, Suwon, Korea.
- 2. Institute of Translational Medicine, Qingdao University, Qingdao, China.
- 3. Korean Ginseng Corporation, Central Research Institute, Daejeon, Korea.
- 4. Division of Rheumatology, Department of Internal Medicine, Korea University Guro Hospital, Seoul, Korea.
- 5. Department of Bioinformatics and Life Science, Soongsil University, Seoul, Korea.
- 6. College of Veterinary Medicine, Kyungpook National University, Daegu, Korea.
Background: Ginsenoside Rc (G-Rc) is one of the major protopanaxadiol-type saponins isolated from Panax ginseng, a well-known medicinal herb with many beneficial properties including Anticancer, anti-inflammatory, antiobesity, and antidiabetic effects. In this study, we investigated the effects of G-Rc on inflammatory responses in vitro and examined the mechanisms of these effects.
Methods: The in vitro inflammation system used lipopolysaccharide-treated macrophages, tumor necrosis factor-α/interferon-γ-treated synovial cells, and HEK293 cells transfected with various inducers of inflammation.
Results: G-Rc significantly inhibited the expression of macrophage-derived cytokines, such as tumor necrosis factor-α and interleukin-1β. G-Rc also markedly suppressed the activation of TANK-binding kinase 1/IκB kinase ε/interferon regulatory factor-3 and p38/ATF-2 signaling in activated RAW264.7 macrophages, human synovial cells, and HEK293 cells.
Conclusion: G-Rc exerts its anti-inflammatory actions by suppressing TANK-binding kinase 1/IκB kinase ε/interferon regulatory factor-3 and p38/ATF-2 signaling.
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