US EPA

1456022 

Journal Article 

Inhibitory Effects of Ginsenoside Rb-1, Rg(3), and Panax ginseng Head Butanol Fraction on Inflammatory Mediators from LPS-Stimulated RAW 264.7 Cells 

Lee, JeH; Jeong, C 

2008 

16 

3 

277-285 

10.4062/biomolther.2008.16.3.277 

WOS:000260150600018 

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. 

Ginsenoside Rb-1; Ginsenoside Rg(3); Prostaglandin E-2; Nitric oxide; iNOS; COX-2; IL-6