Inhibitory Effects of Ginsenoside Rb₁,Rg₃, and Panax ginseng Head Butanol Fraction on Inflammatory Mediators from LPS-Stimulated RAW 264.7 Cells

Panax ginseng C.A. Mayer (Araliaceae, P. ginseng) has been used for the enhancement of vascular and immune functions in Korea and Japan for a long time. Ginsenoside <TEX>Rb₁</TEX> and <TEX>Rg₃</TEX> isolated from P. ginseng head-part butanolic extract (PGHB) were investigated for anti-inflammatory activity. Ginsenosides and PGHB did not affect the cell viability within <TEX>0\;-\;100\;μg/ml</TEX> concentration to RAW 264.7 murine macrophage cells. Ginsenosides and PGHB inhibited partly lipopolysaccharide (LPS)-induced nitrite production in a dose-dependent manner. The ginsenosides and PGHB showed partially chemical nitric oxide (NO) quenching (maximum 40%) in the cell-free system. Also, ginsenoside <TEX>Rb₁</TEX> and <TEX>Rg₃</TEX> inhibited markedly approximately 74 and 54% of inducible nitric oxide synthase (iNOS) mRNA transcription from LPS-induced RAW 264.7 cells. Taken together, the inhibitory effect of ginsenosides and PGHB on NO production did not occur as a result of cell viability, but was caused by both the chemical NO quenching and the regulation of iNOS. Additionally, the ginsenoside <TEX>Rb₁</TEX> and PGHB inhibited prostaglandin <TEX>E₂</TEX> (<TEX>PGE₂</TEX>) synthesis in a concentration-dependent manner, showed approximately 70-98% inhibition at <TEX>100\;μg/ml</TEX> concentration. And the treatment with ginsenosides and PGHB attenuated partially LPS-upregulated cyclooxygenase-2 (COX-2) gene transcription. Ginsenoside <TEX>Rg₃</TEX> suppressed LPS-stimulated interleukin-6 (IL-6) level to the basal in RAW 264.7 cells. From these results, ginsenoside <TEX>Rb₁,\;Rg₃</TEX>, and PGHB may be useful for the relief and retardation of immunological inflammatory responses and its action may occur through the reduction of inflammatory mediators, including NO, <TEX>PGE₂</TEX>, and IL-6 production.