Abstract ▼ AI-Helper

Nitric oxide(NO) is an anti-tumor molecule produced in activated macrophages. Aralia continentalis Kitagawa(ACK) is an oriental medicine, which has been used to treat rheumatic conditions. In this study, we have examined the mechanism by which ACK regulates NO production, using mouse peritoneal macr...

Nitric oxide(NO) is an anti-tumor molecule produced in activated macrophages. Aralia continentalis Kitagawa(ACK) is an oriental medicine, which has been used to treat rheumatic conditions. In this study, we have examined the mechanism by which ACK regulates NO production, using mouse peritoneal macrophages. Water extract(WE) and ethanol extract(EE) of ACK were investigated. When ACK WE and EE was used in combination with 10 U/㎖ of recombinant interferon-γ(rIFN-γ), there was a marked cooperative induction of NO production. The increase in NO synthesis was reflected as an increased expression of inducible NO synthase(iNOS) protein. The production of NO from rIFN-γ plus ACK-stimulated peritoneal macrophages was decreased by treatment with N^(G)-monomethyl-L-arginine, iNOS inhibitor. Additionally, the increased production of NO from rIFN-γ plus ACK-stimulated cells was almost completely inhibited by pre-treatment with 100 μM of pyrrolidine dithiocarbamate, an inhibitor of nuclear factor kappa B(NF-κB). Furthermore, ACK increased activation of NF-κB. These findings suggest that ACK increases the production of NO by rIFN-γ-primed macrophages and NF-κB plays a critical role in mediating these effects of ACK.