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

Abstract

Aim of the study 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. Materials and 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-γ (rIFN-γ), 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-γ plus CT-stimulated peritoneal macrophages was decreased by the treatment with N G-monomethyl- l-arginine or N α-Tosyl-Phe Chloromethyl Ketone, iNOS inhibitor. The increased production of NO from rIFN-γ plus CT-stimulated cells was almost completely inhibited by pre-treatment with pyrrolidine dithiocarbamate, an inhibitor of nuclear factor kappa B (NF-κB). However, treatment of peritoneal macrophages with rIFN-γ plus CT had no effect on the increase in tumor necrosis factor-α (TNF-α) production. Conclusions Our findings demonstrate that CT 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 CT.