Abstract
Using mouse peritoneal macrophages, we have examined the mechanism by which, Smilacis rhizoma (SR) regulates nitric oxide (NO) production. When SR was used in combination with recombinant interferon-γ (rIFN-γ), there was a marked cooperative induction of NO production. However, SR had no effect on NO production by itself. The increased production of NO from rIFN-γ plus SR-stimulated cells was almost completely inhibited by pre-treatment with pyrrolidine dithiocarbamate (PDTC), an inhibitor of nuclear factor kappa B (NF-κB). Furthermore, treatment of peritoneal macrophages with rIFN-γ plus SR caused a significant increase in tumor necrosis factor-α (TNF-α) production. PDTC also decreased the effect of SR on TNF-α production significantly. These findings demonstrate that SR increases the production of NO and TNF-α by rIFN-γ-primed macrophages and suggest that NF-κB plays a critical role in mediating these effects of SR.
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