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Resveratrol blunts tumor necrosis factor-${alpha}$-induced monocyte adhesion and transmigration
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  • Resveratrol blunts tumor necrosis factor-${alpha}$-induced monocyte adhesion and transmigration
  • Resveratrol blunts tumor necrosis factor-${alpha}$-induced monocyte adhesion and transmigration
저자명
Kim. Dong-Shoo,Kwon. Hyang-Mi,Choi. Jung-Suk,Kang. Sang-Wook,Ji. Geun-Eog,Kang. Young-Hee
간행물명
Nutrition research and practice
권/호정보
2007년|1권 4호|pp.285-290 (6 pages)
발행정보
한국영양학회
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정기간행물|ENG|
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이 논문은 한국과학기술정보연구원과 논문 연계를 통해 무료로 제공되는 원문입니다.
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기타언어초록

The leukocyte recruitment and transmigration across the endothelial barrier into the vessel wall are crucial steps in atherosclerosis. Leukocyte trafficking on the endothelium is elicited by induction of endothelial adhesion molecules, and its transmigration is mediated by degradation of basement membrane proteins through enzymatic activity of matrix metalloproteinases (MMP). The current study investigated whether resveratrol, a polyphenol present in grapes and red wine, was capable of inhibiting leukocyte adhesion to tumor necrosis factor (TNF)-${alpha}$-activated endothelium. It was found that resveratrol inhibited the TNF-${alpha}$-activated endothelial expression of vascular cell adhesion molecule-1 in a dose-dependent manner. In addition, resveratrol hampered THP-1 monocyte adhesion to activated endothelial cells. This study further examined whether resveratrol interfered with transendothelial migration of leukocytes. The MMP-2 gelatinolytic activity of endothelial cells was enhanced by TNF-${alpha}$, which was attenuated by an addition of ${geq}25{mu}M$ resveratrol. In addition, 25 ${mu}M$ resveratrol mitigated the MMP-9 activity of THP-1 cells, followed by a marked inhibition of transendothelial migration. These results demonstrated that resveratrol suppressed monocyte adhesion and migration induced by TNF-${alpha}$ through modulating expression of adhesion molecules and gelatinolytic activity of MMP. These findings suggest that dietary resveratrol may be therapeutic agent for inhibiting leukocyte recruitment into the subendothelium during inflammatory atherosclerosis.