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논문 기본 정보

자료유형
학술저널
저자정보
Han, Shin-Ha (Department of Pharmacy, Sahmyook University) Kim, Kwang-Hee (Department of Pharmacy, Sahmyook University) Kim, Hyun-Yul (Department of Pharmacy, Sahmyook University) Kwon, Jeung-Hak (Department of Pharmacy, Sahmyook University) Lee, Young-Hee (College of Pharmacy, Chungbuk National University) Lee, Chong-Kil (College of Pharmacy, Chungbuk National University) Song, Young-Cheon (Department of Pharmacy, Sahmyook University) Lee, Sang-Jin (College of Pharmacy, Chungbuk National University) Ha, Nam-Joo (Department of Pharmacy, Sahmyook University) Kim, Kyung-Jae (Department of Pharmacy, Sahmyook 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 제31권 제1호
발행연도
2008.1
수록면
67 - 74 (8page)

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Auranofin (AF), a gold compound, is an orally active therapeutic agent used to treat rheumatoid arthritis (RA), a self-perpetuating inflammatory disease. RA is characterized by autoimmune-mediated proliferation of synovial cells that leads to inflammation, pain, and swelling in most major joints. However, the mechanism as to how AF relieves RA symptoms has not been fully elucidated. The object of this study was to examine the ability of AF to immunomodulate macrophages as antigen presenting cells (APCs). Macrophages are recognized as playing an important role in the pathogenesis of RA, in that there is a relative abundance of macrophagederived cytokines, such as tumor necrosis $factor-{\alpha}$ ($TNF-{\alpha}$), $interleukin-1{\beta}$ ($IL-1{\beta}$) and interleukin-6 (IL-6) in rheumatoid synovium. In this work, we tested whether AF (2.5-20 mM) could inhibit inflammatory activity in the macrophage cell line RAW 264.7. AF decreased production of nitric oxide (NO) and the pro-inflammatory cytokines, $TNF-{\alpha}$, $IL-1{\beta}$ and IL-6 in macrophages. Furthermore, AF inhibited cyclooxygenase-2 (COX-2)-dependent prostaglandin E2 (PGE2) production in a concentration-dependent manner. In conclusion, these findings may provide an explanation for the clinical effects of AF in patients with RA.

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