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      Ginsenoside Rk1 suppresses pro-inflammatory responses in lipopolysaccharide-stimulated RAW264.7 cells by inhibiting the Jak2/Stat3 pathway

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          The saponin ginsenoside Rk1 is a major compound isolated from ginseng. Ginsenoside Rk1 has been reported to have anti-inflammatory and anti-tumor properties and to be involved in the regulation of metabolism. However, the effect and mechanism of anti-inflammatory action of ginsenoside Rk1 has not been fully clarified. We investigated whether ginsenoside Rk1 could suppress the inflammatory response in lipopolysaccharide-stimulated RAW264.7 macrophages and to explore its mechanism of the action. RAW264.7 cells were treated with LPS (1 μg·mL −1) in the absence or the presence of Ginsenoside Rk1 (10, 20, and 40 μmol·L −1). Then the inflammatory factors were tested with Griess reagents, ELISA, and RT-PCR. The proteins were analyzed by Western blotting. Ginsenoside Rk1 inhibited lipopolysaccharide-induced expression of nitric oxide (NO), interleukin (IL)-6, IL-1 β, tumor necrosis factor (TNF)- α, and monocyte chemotactic protein (MCP)-1. Ginsenoside Rk1 inhibited the lipopolysaccharide-stimulated phosphorylation of NF-κB and janus kinase (Jak)2 and signal transducer and activator of transcription (Stat)3 at Ser727 and Tyr705. These data suggested that ginsenoside Rk1 could inhibit expression of inflammatory mediators and suppress inflammation further by blocking activation of NF-κB and the Jak2/Stat3 pathway in LPS-stimulated RAW264.7 cells.

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          Author and article information

          Chinese Journal of Natural Medicines
          20 October 2017
          : 15
          : 10
          : 751-757
          1Research Studio of Integration of Traditional and Western Medicine, First Hospital, Peking University, Beijing 100034, China
          2State Key Laboratory of Natural and Biomimetic Drugs, School of Pharmaceutical Sciences, Peking University, Beijing 100191, China
          Author notes
          *Corresponding author: Tu Peng-Fei, E-mail: pengfeitu@ ; WANG Xue-Mei, E-mail: wangxuemeibjmu@

          These authors have no conflict of interest to declare.

          Copyright © 2017 China Pharmaceutical University. Published by Elsevier B.V. All rights reserved.
          Funded by: National Natural Science Foundation of China
          Award ID: 81173369
          Award ID: 81303253
          Award ID: 81530097
          Award ID: 81222051
          Funded by: National Key Technology R&D Program “New Drug Innovation” of China
          Award ID: 2012ZX09301002-002-002
          Award ID: 2012ZX09304-005
          Funded by: Natural Science Foundation of Beijing, China
          Award ID: 132210
          Funded by: Doctoral Scientific Fund Project of the Ministry of Education of China
          Award ID: 20120001110105
          This work was supported by the National Natural Science Foundation of China (Nos. 81173369, 81303253, 81530097, and 81222051), the National Key Technology R&D Program “New Drug Innovation” of China (Nos. 2012ZX09301002-002-002 and 2012ZX09304-005), the Natural Science Foundation of Beijing, China (No. 132210), and the Doctoral Scientific Fund Project of the Ministry of Education of China (No. 20120001110105)].


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