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Background : Ginseng (Panax ginseng) has been reported to exert an anti-inflammatory activity in a variety of inflammatory. However, inflammation-regulatory activity of wood-cultivated ginseng has not been thoroughly evaluated. In this study, we evaluated the anti-inflammatory effect of wood-cultivated ginseng and elucidated the potential mechanisms in LPS-stimulated RAW264.7 cells.
Methods and Results : Inhibitory effects of the old wood-cultivated ginseng (WCG-O), young wood-cultivated ginseng (WCG-Y) and ginseng (G) on NO and PGE2 production were examined using the Griess assay and ELISA kit. Suppressive effects of WCG-O on inflammatory gene expression, transcriptional activation, and inflammation signaling events were investigated using Western blot analysis, RT-PCR analysis and luciferase activity reporter gene assay. WCG-O dose-dependently suppressed nitric oxide (NO) and Prostaglandin E2 (PGE2) production in LPS-stimulated RAW264.7 cells. In addition, WCG-O attenuated LPS-mediated overexpression of iNOS and COX-2. In addition, WCG-O blocked the expression of TNF-α and IL-1β in LPS-stimulated RAW264.7 cells. In elucidation of the potential mechanisms for anti-inflammatory effect, WCG-O inhibited the activation of IκK-α/β, the phosphorylation of IκB-α, and degradation of IκB-α, which results in the inhibition of p65 nuclear accumulation and NF-κB activation. In addition, WCG-O suppressed the activation of ERK1/2, p38 and JNK, which results in the inhibition of ATF2 nuclear accumulation.
Conclusion : These results indicate that WCG-O may exert anti-inflammatory activity through the inhibiting NF-κB and MAPK signaling. From these findings, WCG-O has potential to be a candidate for the development of chemoprevention or therapeutic agents for the inflammatory diseases.
