Anti-inflammatory potential of saponins derived from cultured wild ginseng roots in lipopolysaccharide-stimulated RAW 264.7 macrophages.

Ginseng, namely the root of Panax ginseng Meyer, is a well-known traditional medicine that has been used in Asian countries for thousands of years. Ginseng saponins have been shown to exert a variety of prominent pharmacological effects in a number of diseases. The aim of the present study was to identify the anti-inflammatory effects of total saponins extracted from cultured wild ginseng roots (TSWG) on lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophages. An elevated production of nitric oxide (NO) was detected in the RAW 264.7 cells in response to stimulation with LPS, as shown by NO detection assay using Griess reagent. However, pre-treatment with TSWG inhibited the production of NO through the suppression of inducible NO synthase gene expression. Furthermore, the LPS-induced gene expression and production of tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) were significantly reduced by treatment with TSWG, as shown by ELISA, and western blot analysis and RT-PCR, respectively. In the LPS-stimulated RAW 264.7 cells, nuclear factor-κB (NF-κB) was translocated from the cytosol to the nucleus, while pre-treatment with TSWG induced the sequestration of NF-κB in the cytosol through the inhibition of the inhibitor of κB degradation, as shown by immunofluorescence staining. TSWG also contributed to the downregulation of mitogen-activated protein kinases and Akt in the LPS-stimulated RAW 264.7 cells. Additionally, in the TSWG-treated RAW 264.7 cells, we observed the activation of nuclear factor (erythroid-derived 2)-like 2 and an increase in heme oxygenase-1 expression; these effects were associated with the inhibition of the generation of reactive oxygen species. The results from the present study indicate that TSWG exerts anti-inflammatory and antioxidant effects, suggesting that TSWG may be an effective therapeutic agent for inflammatory diseases and prevent cellular damage induced by oxidative stress.