Total saponin of heat-processed ginseng (TSHG) stimulated the production of nitric oxide (NO) in interferon-γ (IFN-γ)-primed macrophages through the increased expression of inducible nitric oxide synthase (iNOS). However, TSHG by itself had a very weak effect on the NO synthesis without IFN-γ priming. The saponins of white ginseng inhibited the NO production in lipopolysaccharide (LPS)/IFN-γ activated macrophages rather than the stimulation of NO production found in IFN-γ primed macrophages. The NO production by TSHG-stimulated macrophages was inhibited by the NOS inhibitor (NG-monomethyl-L-arginine (L-NMMA)) and nuclear factor-kappaB inhibitor (pyrrolidine dithiocarbamate (PDTC)). TSHG showed different serum-dependence from LPS on the activation of IFN-γ primed macrophages. This property of TSHG may explain the intensified anti-tumor properties of heat-processed ginseng through its immunostimulating activity.
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