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

• Published in: Journal of ethnopharmacology Vol. 122; no. 3; pp. 573 - 578
• Main Authors: An, Hyo-Jin, Rim, Hong-Kun, Chung, Hwan-Suck, Choi, In-Young, Kim, Na-Hyung, Kim, Su-Jin, Moon, Phil-Dong, Myung, Noh-Yil, Jeong, Hyun-Ja, Jeong, Chang-Hyun, Chung, Seok-Hee, Um, Jae-Young, Hong, Seung-Heon, Kim, Hyung-Min
• Format: Journal Article
• Language: English
• Published: Shannon Elsevier Ireland Ltd 21.04.2009; Amsterdam; New York: Elsevier; Elsevier
• Subjects: Animals; anticarcinogenic activity; Antioxidants - pharmacology; Biological and medical sciences; Corydalis; Corydalis turtschaninovii; Drug Synergism; General pharmacology; Interferon-gamma - pharmacology; interferons; macrophages; Macrophages, Peritoneal - drug effects; Macrophages, Peritoneal - metabolism; Male; Medical sciences; medicinal plants; medicinal properties; Mice; Mice, Inbred C57BL; Mouse peritoneal macrophages; NF-kappa B; NF-kappa B - antagonists & inhibitors; Nitric oxide; Nitric Oxide - biosynthesis; nitric oxide synthase; Nitric Oxide Synthase Type II - antagonists & inhibitors; Nitric Oxide Synthase Type II - metabolism; Pharmacognosy. Homeopathy. Health food; Pharmacology. Drug treatments; Plant Extracts - pharmacology; pyrrolidine dithiocarbamate; Pyrrolidines - pharmacology; Recombinant Proteins; Thiocarbamates - pharmacology; traditional medicine; tumor necrosis factor-alpha; South Korea; Corydalis turtschaninovii; Mouse peritoneal macrophages; Nitric oxide; Enzyme; Pharmacognosy; Rodentia; Fumariaceae; Nitric-oxide synthase; Medicinal plant; Vertebrata; Mammalia; Mouse; Dicotyledones; Animal; Angiospermae; Plant origin; Spermatophyta; Oxidoreductases; Gamma interferon; Macrophage; Peritoneum
• ISSN: 0378-8741; 1872-7573
• DOI: 10.1016/j.jep.2008.12.030

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