4.7 Article

5-Hydroxymethylfurfural from Black Garlic Extract Prevents TNFα-induced Monocytic Cell Adhesion to HUVECs by Suppression of Vascular Cell Adhesion Molecule-1 Expression, Reactive Oxygen Species Generation and NF-κB Activation

期刊

PHYTOTHERAPY RESEARCH
卷 25, 期 7, 页码 965-974

出版社

WILEY
DOI: 10.1002/ptr.3351

关键词

5-hydroxymethylfurfural; aged black garlic; human umbilical vein endothelial cells; cell adhesion molecules; reactive oxygen species; NF-kappa B transcription factor

资金

  1. Medical Research Institute, Pusan National University Hospital [2007-14]

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5-Hydroxymethylfurfural (5-HMF) is a common Maillard reaction product; the reaction occurs during heat-processing and the preparation of many types of foods and beverages. Although 5-HMF has been proposed to have harmful effects, recently, its beneficial effects, including antioxidant, cytoprotective and antitumor effects have become increasingly apparent. It was found recently that a chloroform extract of aged black garlic shows antiinflammatory properties when administered to human umbilical vein endothelial cells (HUVECs). This study investigated the antiinflammatory potential of 5-HMF purified from the chloroform extract of aged black garlic in tumor necrosis factor-alpha (TNF-alpha)-stimulated HUVECs. Treatment of HUVECs with 5-HMF strongly suppressed TNF-alpha-induced cell surface and total protein expression of vascular cell adhesion molecule-1 (VCAM-1) and intercellular cell adhesion molecule-1 (ICAM-1) as well as their mRNA expression. In addition, 5-HMF significantly inhibited TNF-alpha-induced reactive oxygen species formation, and markedly reduced THP-1 monocyte adhesion to TNF-alpha-stimulated HUVECs. Furthermore, 5-HMF significantly inhibited NF-kappa B transcription factor activation in TNF-alpha-stimulated HUVECs. The data provide new evidence of the antiinflammatory properties of 5-HMF in support of its potential therapeutic use for the prevention and management of vascular diseases such as atherosclerosis through mechanisms involving the inhibition of VCAM-1 expression and NF-kappa B activation in vascular endothelial cells. Copyright (C) 2011 John Wiley & Sons, Ltd.

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