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Ginsenoside‐Rh1 and Rh2 inhibit the induction of nitric oxide synthesis in murine peritoneal macrophages

The effects of ginsenoside‐Rh1 and Rh2 in the induction of nitric oxide (NO) synthesis by IFN‐γ plus LPS were investigated using murine peritoneal macrophages. The NO production from rIFNγ plus LPS‐treated macrophages was markedly reduced by ginsenoside‐Rh1 or Rh2 in a dose dependent manner, but had no inhibitory effects by ginsenoside‐Rb1, Rc or Re. In addition, treatment of the cells with ginsenoside‐Rh2 6 hr before the stimulation with IFN‐γ plus LPS showed more inhibitory effect than the treatment with ginsenoside‐Rh2 6 hr after or simultaneously with the stimulation with IFN‐γ plus LPS in the NO production. Ginsenoside‐Rh2 also effectively inhibited IFN‐γ‐induced NO production when the cells were treated with IFN‐γ 6 hr after the treatment with ginsenoside‐Rh2. Our findings suggest that this phenomenon might be caused by inhibition of priming signal such as IFN‐γ for the synergistic induction of NO synthesis.