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Title: Inhibition of tumor necrosis factor-{alpha}-induced expression of adhesion molecules in human endothelial cells by the saponins derived from roots of Platycodon grandiflorum

Journal Article · · Toxicology and Applied Pharmacology
 [1];  [2];  [1];  [3];  [4];  [5];  [1]
  1. Department of Pharmacy, College of Pharmacy, Research Center for Proteineous Materials, Chosun University, Kwangju (Korea, Republic of)
  2. Department of Pathology, College of Oriental Medicine, Daejeon University, Daejeon (Korea, Republic of)
  3. Department of Pharmacy, College of Pharmacy, Chungnam National University, Taejon (Korea, Republic of)
  4. Division of Food Science, Chinju International University, Chinju (Korea, Republic of)
  5. Jangsaeng Doraji Research Institute of Biotechnology, Jangsaeng Doraji Co., Ltd., Chinju (Korea, Republic of)

Adhesion molecules play an important role in the development of atherogenesis and are produced by endothelial cells after being stimulated with various inflammatory cytokines. This study examined the effect of saponins that were isolated from the roots of Platycodon grandiflorum A. DC (Campanulaceae), Changkil saponins (CKS), on the cytokine-induced monocyte/human endothelial cell interaction, which is a crucial early event in atherogenesis. CKS significantly inhibited the TNF{alpha}-induced increase in monocyte adhesion to endothelial cells as well as decreased the protein and mRNA expression levels of vascular adhesion molecule-1 and intercellular cell adhesion molecule-1 on endothelial cells. Furthermore, CKS significantly inhibited the TNF{alpha}-induced production of intracellular reactive oxygen species (ROS) and activation of NF-{kappa}B by preventing I{kappa}B degradation and inhibiting I{kappa}B kinase activity. Overall, CKS has anti-atherosclerotic and anti-inflammatory activity, which is least in part the result of it reducing the cytokine-induced endothelial adhesion to monocytes by inhibiting intracellular ROS production, NF-{kappa}B activation, and cell adhesion molecule expression in endothelial cells.

OSTI ID:
20783413
Journal Information:
Toxicology and Applied Pharmacology, Vol. 210, Issue 1-2; Other Information: DOI: 10.1016/j.taap.2005.09.015; PII: S0041-008X(05)00582-X; Copyright (c) 2005 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved; Country of input: International Atomic Energy Agency (IAEA); ISSN 0041-008X
Country of Publication:
United States
Language:
English