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.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
