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논문 기본 정보

자료유형
학술저널
저자정보
Lee, Je-Hyuk (Plant Resources Research Institute, Duksung Women's University) Zhou, Hong-Yu (National Products Research Institute, College of Pharmacy, Seoul National University) Cho, So-Yean (National Products Research Institute, College of Pharmacy, Seoul National University) Kim, Yeong-Shik (National Products Research Institute, College of Pharmacy, Seoul National University) Lee, Yong-Soo (College of Pharmacy, Duksung Women's University) Jeong, Choon-Sik (College of Pharmacy, Duksung Women's 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 제30권 제10호
발행연도
2007.1
수록면
1,318 - 1,327 (10page)

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The aim of this study was to clarify the anti-inflammatory mechanism of apigenin. Apigenin inhibited the collagenase activity involved in rheumatoid arthritis (RA) and suppressed lipopolysaccharide (LPS)-induced nitric oxide (NO) production in a dose dependent manner in RAW 264.7 macrophage cells. Pretreatment with apigenin also attenuated LPS-induced cyclooxygenase-2 (COX-2) expression. In addition, apigenin profoundly reduced the tumor necrosis factor-${\alpha}$ (TNF-${\alpha}$)-induced adhesion of monocytes to HUVEC monolayer. Apigenin significantly suppressed the TNF-${\alpha}$-stimulated upregulation of vascular cellular adhesion molecule-1 (VCAM-1 )-, intracellular adhesion molecule-1 (ICAM-1)-, and E-selectin-mRNA to the basal levels. Taken together, these results suggest that apigenin has significant anti-inflammatory activity that involves blocking NO-mediated COX-2 expression and monocyte adherence. These results further suggest that apigenin may be useful for therapeutic management of inflammatory diseases.

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