Expression of inducible nitric oxide synthase by Corydalis turtschaninovii on interferon-gamma stimulated macrophages.

OBJECTIVE

Corydalis turtschaninovii (CT) has been used for tumor therapy. However, it is still unclear how this herb prevents the diseases in experimental models. Nitric oxide (NO) as a potent macrophage-derived effector molecule against a variety of tumors has received increasing attention.

METHODS

In this study, using mouse peritoneal macrophages, we have examined the mechanism by which CT regulates NO production.

RESULTS

When CT was used in combination with recombinant interferon-gamma (rIFN-gamma), there was a marked cooperative induction of NO production. However, CT had no effect on NO production by itself. The increase in NO synthesis was reflected as an increased amount of inducible NO synthase (iNOS) protein. The increased production of NO from rIFN-gamma plus CT-stimulated peritoneal macrophages was decreased by the treatment with N(G)-monomethyl-L-arginine or N(alpha)-Tosyl-Phe Chloromethyl Ketone, iNOS inhibitor. The increased production of NO from rIFN-gamma plus CT-stimulated cells was almost completely inhibited by pre-treatment with pyrrolidine dithiocarbamate, an inhibitor of nuclear factor kappa B (NF-kappaB). However, treatment of peritoneal macrophages with rIFN-gamma plus CT had no effect on the increase in tumor necrosis factor-alpha (TNF-alpha) production.

CONCLUSIONS

Our findings demonstrate that CT increases the production of NO and TNF-alpha by rIFN-gamma-primed macrophages and suggest that NF-kappaB plays a critical role in mediating these effects of CT.