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자료유형
학술저널
저자정보
Jang Seon Il (Department of Skin & Beauty, Seojeong College) Kim Young-Jun (Department of Bionanochemistry and Basic Sciences Research Institute, Wonkwang University) Lee Woo-Yiel (Department of Bionanochemistry and Basic Sciences Research Institute, Wonkwang University) Kwak Kyung Chell (Department of Bionanochemistry and Basic Sciences Research Institute, Wonkwang University) Baek Seung Hwa (Department of Bionanochemistry and Basic Sciences Research Institute, Wonkwang University) Kwak Gyu Beum (Department of New Material Science, Chunbuk National University) Yun Young-Gab (Department of Prescription, School of Oriental Medicine, Wonkwang University) Kwon Tae-Oh (College of Life Science and Natural Resources, Wonkwang University) Chung Hun Taeg (Medicinal Resources Research Center of Wonkwang University) Chai Kyu-Yun (Department of Bionanochemistry and Basic Sciences Research Institute, Wonkwang University)
저널정보
대한약학회 Archives of pharmacal research : a publication of the Pharmaceutical Society of Korea Archives of pharmacal research : a publication of the Pharmaceutical Society of Korea 제28권 제2호
발행연도
2005.1
수록면
203 - 208 (6page)

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Scoparone is a major component of the shoot of Artemisia capillaris (Compositae), which has been used for the treatment of hepatitis and biliary tract infection in oriental countries. In the present study we observed that, scorparone exhibited no cytotoxic effect in unstimulated macrophages, but reduced the release of nitric oxide (NO) and prostaglandin $E_2\;(PGE_2)$ upon stimulation by IFN-${\gamma}$/LPS or LPS. The inhibitory effects were found to be in conjuction with the suppression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) in IFN-${\gamma}$/LPS stimulated RAW 264.7 cells. Moreover, scoparone also attenuated the production of tumor necrosis factor (TNF)-${\alpha}$, interleukin (IL)-$1{\beta}$ and IL-6 in LPS-stimulated RAW264.7 cells. These results suggest that scoparone decreases the production of the inflammatory mediators such as NO and $PGE_2$ in macrophages by inhibiting iNOS and COX-2 expression.

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