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The Pharmaceutical Society of Korea (대한약학회)
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Manassantin A and B Isolated from Saururus chinensis Inhibit $TNF-{\alpha}-Induced$ Cell Adhesion Molecule Expression of Human Umbilical Vein Endothelial Cells

  • Kwon Oh Eok (Laboratory of Lipid Metabolism, Korea Research Institute of Bioscience and Biotechnology) ;
  • Lee Hyun Sun (Laboratory of Lipid Metabolism, Korea Research Institute of Bioscience and Biotechnology) ;
  • Lee Seung Woong (Laboratory of Lipid Metabolism, Korea Research Institute of Bioscience and Biotechnology) ;
  • Chung Mi Yeon (Laboratory of Lipid Metabolism, Korea Research Institute of Bioscience and Biotechnology) ;
  • Bae Ki Hwan (College of Pharmacy, Chungnam National University) ;
  • Rho Mun-Chual (Laboratory of Lipid Metabolism, Korea Research Institute of Bioscience and Biotechnology) ;
  • Kim Young-kook (Laboratory of Lipid Metabolism, Korea Research Institute of Bioscience and Biotechnology)
  • Published : 2005.01.01
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Abstract

Leukocyte adhesion to the vascular endothelium is a critical initiating step in inflammation and atherosclerosis. We have herein studied the effect of manassantin A (1) and S (2), dineolignans, on interaction of THP-1 monocytic cells and human umbilical vein endothelial cells (HUVEC) and expression of intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), and E-selectin in HUVEC. When HUVEC were pretreated with 1 and 2 followed by stimulation with $TNF-{\alpha}$, adhesion of THP-1 cells to HUVEC decreased in dose-dependent manner with $IC_{50}$ values of 5 ng/mL and 7 ng/mL, respectively, without cytotoxicity. Also, 1 and 2 inhibited $TNF-{\alpha}-induceda$ up-regulation of ICAM-1, VCAM-1 and E-selectin. The present findings suggest that 1 and 2 prevent monocyte adhesion to HUVEC through the inhibition of ICAM-1, VCAM-1 and E-selectin expression stimulated by $TNF-\alpha$, and may imply their usefulness for the prevention of atherosclerosis relevant to endothelial activation.

Keywords

References

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