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

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-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.

The saponin ginsenoside Rkl is a major compound isolated from ginseng. Ginsenoside Rkl has been reported to have anti-inflammat ）ry and anti-tumor properties and to be involved in the regulation of metabolism. However, the effect and mechanism of anti-inflammat ）ry action of ginsenoside Rkl has not been fully clarified. We investigated whether ginsenoside Rkl could suppress the inflammatory esponse in lipopolysaccharide-stimulated RAW264.7 macrophages and to explore its mechanism of the action. RAW264.7 cels were treated with LPS （1 μg.mL-l） in the absence or the presence of Ginsenoside Rkl （10, 20, and 40 μmol.L-1）. Then the inflammat（ ry factors were tested with Griess reagents, ELISA, and RT-PCR. The proteins were analyzed by Western blotting. Ginsenoside Pd ：1 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 Rkl inhibited the lipopolysaccharide-stimulated phosphorylation of NF-κB and anus kinase （Jak）2 and signal transducer and activator of transcription （Stat）3 at Ser727 and Tyr705. These data sug- gested that gin： enoside Rkl could inhibit expression of inflammatory mediators and suppress inflammation further by blocking activa- tion ofNF-B and the Jak2/Stat3 pathway in LPS-stimulated RAW264.7 ceils.