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, R ginseng) has been used for the enhancement of vascular and immune functions in Korea and Japan for a long time. Ginsenoside Rb-1 and Rg(3) 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 0 - 100 mu g/ml 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 Rb, and Rg(3) 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 Rb, and PGHB inhibited prostaglandin E-2 (PGE(2)) synthesis in a concentration-dependent manner, showed approximately 70-98% inhibition at 100 mu g/ml concentration. And the treatment with ginsenosides and PGHB attenuated partially LPS-upregulated cyclooxygenase-2 (COX-2) gene transcription. Ginsenoside Rg(3) suppressed LIPS-stimulated intedeukin-6 (IL-6) level to the basal in RAW 264.7 cells. From these results, ginsenoside Rb-1, Rg(3), 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, PGE2, and IL-6 production.