4.7 Article

Chloroform Extract of Aged Black Garlic Attenuates TNF-alpha-induced ROS Generation, VCAM-1 Expression, NF-kappa B Activation and Adhesiveness for Monocytes in Human Umbilical Vein Endothelial Cells

期刊

PHYTOTHERAPY RESEARCH
卷 25, 期 1, 页码 92-100

出版社

WILEY
DOI: 10.1002/ptr.3230

关键词

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

资金

  1. Ministry for Food, Agriculture, Forestry and Fisheries, Republic of Korea [20080914000]
  2. Ministry for Health, Welfare and Family Affairs, Republic of Korea [A084711]

向作者/读者索取更多资源

Aged black garlic is a type of fermented garlic (Allium sativum) which has been used in Oriental countries for a long time because of various biological properties of garlic derivatives. The current study explored the potential of the chloroform extract of aged black garlic (CEABG) in attenuating the activities of adhesion molecules in tumor necrosis factor-alpha (TNF-alpha)-stimulated human umbilical vein endothelial cells (HUVECs). The study was performed on HUVECs that were pretreated with 30 mu g/mL of CEABG before TNF-alpha treatment. Treatment of HUVECs with CEABG significantly inhibited TNF-alpha-induced reactive oxygen species (ROS) formation. HUVECs treated with CEABG showed markedly suppressed TNF-alpha-induced mRNA expression of VCAM-1, but little alteration in ICAM-1 and E-selectin mRNA expression. CEABG treatment also significantly decreased the TNF-alpha-induced cell surface and total protein expression of VCAM-1 without affecting ICAM-1 and E-selectin expression. In addition, treatment of HUVECs with CEABG markedly reduced THP-1 monocyte adhesion to TNF-alpha-stimulated HUVECs. Furthermore, CEABG significantly inhibited NF-kappa B transcription factor activation in TNF-alpha-stimulated HUVECs. The data provide new evidence of the antiinflammatory properties of CEABG that may have a potential therapeutic use for the prevention and treatment 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) 2010 John Wiley & Sons, Ltd.

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