Ginsenoside Rk1 suppresses pro-inflammatory responses in lipopolysaccharide-stimulated RAW264.7 cells by inhibiting the Jak2/Stat3 pathway.
10.1016/S1875-5364(17)30106-1
- Author:
Qian YU
1
;
Ke-Wu ZENG
2
;
Xiao-Li MA
2
;
Yong JIANG
2
;
Peng-Fei TU
3
;
Xue-Mei WANG
4
Author Information
1. Research Studio of Integration of Traditional and Western Medicine, First Hospital, Peking University, Beijing 100034, China.
2. State Key Laboratory of Natural and Biomimetic Drugs, School of Pharmaceutical Sciences, Peking University, Beijing 100191, China.
3. State Key Laboratory of Natural and Biomimetic Drugs, School of Pharmaceutical Sciences, Peking University, Beijing 100191, China. Electronic address: pengfeitu@vip.163.com.
4. Research Studio of Integration of Traditional and Western Medicine, First Hospital, Peking University, Beijing 100034, China. Electronic address: wangxuemeibjmu@163.com.
- Publication Type:Journal Article
- Keywords:
Ginsenoside Rk1;
Inflammation;
Jak2/Stat3;
NF-κB;
RAW264.7 cells
- MeSH:
Animals;
Anti-Inflammatory Agents;
pharmacology;
Ginsenosides;
pharmacology;
Interleukin-6;
genetics;
immunology;
Janus Kinase 2;
genetics;
immunology;
Lipopolysaccharides;
pharmacology;
Macrophages;
drug effects;
immunology;
Mice;
RAW 264.7 Cells;
STAT3 Transcription Factor;
genetics;
immunology;
Tumor Necrosis Factor-alpha;
genetics;
immunology
- From:
Chinese Journal of Natural Medicines (English Ed.)
2017;15(10):751-757
- CountryChina
- Language:English
-
Abstract:
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) in the absence or the presence of Ginsenoside Rk1 (10, 20, and 40 μmol·L). 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-1β, 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.
