Abstract
The objective of the current study was to determine the effect of Taraxacum officinale (TO) on the production of nitric oxide (NO). Stimulation of mouse peritoneal macrophages with TO after the treatment of recombinant interferon-γ (rIFN-γ) resulted in increased NO synthesis. TO had no effect on NO synthesis by itself. When TO was used in combination with rIFN-γ, there was a marked cooperative induction of NO synthesis in a dose-dependent manner. The optimal effect of TO on NO synthesis was shown 6 h after treatment with rIFN-γ. This increase in NO synthesis was manifested as an increased amount of inducible NO synthase (iNOS) protein. NO production was inhibited by N G-monomethyl-L-arginine. The increased production of NO from rIFN-γ plus TO-stimulated cells was decreased by treatment with a protein kinase C inhibitor such as staurosporin. In addition, synergy between rIFN-γ and TO was mainly dependent on TO-induced tumor necrosis factor-α (TNF-α) secretion. All the preparations of TO were endotoxin free. These results suggest that the capacity of TO to increase NO production from rIFN-γ-primed mouse peritoneal macrophages is the result of TO-induced TNF-α secretion.
Published Version
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