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Stylopine from Chelidonium mrajus Inhibits LPS-Induced Inflammatory Mediators un RAW 264.7 Cells  

Seon Il, Jang (Department of Skin & beauty, Seojeong College)
Byung Hee, Kim (Department of Bionanochemistry and Basic Sciences Research Institute, Wonkwang University)
Woo-Yiel, Lee (Department of Bionanochemistry and Basic Sciences Research Institute, Wonkwang University)
Sang Jin, An (Department of Bionanochemistry and Basic Sciences Research Institute, Wonkwang University)
Han Gil, Choi (Division of Biological Science, College of Natural Sciences, Wonkwang University)
Byung Hun, Jeon (Department of Pathology, College of Oriental Medicine, Wonkwang University)
Hun-Taeg, Chung (Department of Immunology, Institute of Immtec Korea, Medicinal Resources Research Center of Wonkwang University)
Jung-Rae, Rho (Department of Oceanography, Kunsan National University)
Publication Information
Archives of Pharmacal Research / v.27, no.9, 2004 , pp. 923-929 More about this Journal
Abstract
Stylopine is a major component of the leaf of Chelidonium majus L. (Papaveraceae), which has been used for the removal of warts, papillomas and condylomas, as well as the treatment of liver disease, in oriental countries. Stylopine per se had no cytotoxic effect in unstimulated RAW 264.7 cells, but concentration-dependently reduced nitric oxide (NO), prostaglandin E$_2$ (PGE$_2$), tumor necrosis factor-a (TNF-$\alpha$) and interleukin-1$\beta$(IL-1$\beta$), and the IL-6 production and cyclooxygenase-2 (COX-2) activity caused by the LPS stimulation. The levels of inducible nitric oxide synthase (iNOS) and COX-2 protein expressions were markedly suppressed by stylopine in a concentration dependent manner. These results suggest that stylopine suppress the NO and PGE$_2$ production in macrophages by inhibiting the iNOS and COX-2 expressions. These biological activities of stylopine may contribute to the anti-inflammatory activity of Cheli-donium majus.
Keywords
Chelidonium majus; Stylopine; Nitric oxide; Tumor necrosis factor-$\alpha$; Interleukin-1$\beta$; Interleukin-6;
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