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Ginsenoside‐Rh1 and Rh2 inhibit the induction of nitric oxide synthesis in murine peritoneal macrophages
Author(s) -
Park Young Chul,
Lee Chang Hoon,
Kang Ho Sung,
Kim KyuWon,
Chung Hun Taeg,
Kim Han Do
Publication year - 1996
Publication title -
iubmb life
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.132
H-Index - 113
eISSN - 1521-6551
pISSN - 1521-6543
DOI - 10.1080/15216549600201353
Subject(s) - nitric oxide , stimulation , ginsenoside , lipopolysaccharide , pharmacology , chemistry , inhibitory postsynaptic potential , ginsenoside rg1 , interferon gamma , priming (agriculture) , ginseng , in vitro , endocrinology , biology , medicine , biochemistry , pathology , alternative medicine , botany , germination
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.