Comparative effect of genistein and daidzein on the expression of MCP-1, eNOS, and cell adhesion molecules in TNF-alpha-stimulated HUVECs.
- Author:
Hye Yeon CHO
1
;
Chung Mu PARK
;
Mi Jeong KIM
;
Radnaabazar CHINZORIG
;
Chung Won CHO
;
Young Sun SONG
Author Information
- Publication Type:Original Article
- Keywords: Genistein; MCP-1; cell adhesion molecules; eNOS; NFkappaB
- MeSH: Cell Adhesion; Cell Adhesion Molecules; Chemokines; Down-Regulation; Endothelial Cells; Genistein; Humans; Intercellular Adhesion Molecule-1; Isoflavones; Monocytes; Nitric Oxide; Nitric Oxide Synthase Type III; RNA, Messenger; Transcriptional Activation; Tumor Necrosis Factor-alpha; Vascular Cell Adhesion Molecule-1
- From:Nutrition Research and Practice 2011;5(5):381-388
- CountryRepublic of Korea
- Language:English
- Abstract: We compared the effects of genistein and daidzein on the expression of chemokines, cell adhesion molecules (CAMs), and endothelial nitric oxide synthase (eNOS) in tumor necrosis factor (TNF)-alpha-stimulated human umbilical vascular endothelial cells (HUVECs). TNF-alpha exposure significantly increased expression of monocyte chemoattractant protein (MCP)-1, vascular adhesion molecule (VCAM)-1, and intercellular adhesion molecule-1. Genistein significantly decreased MCP-1 and VCAM-1 production in a dose-dependent manner, whereas CAM expression was not significantly lowered by genistein treatment. However, daidzein slightly decreased MCP-1 production. The effects of genistein and daidzein on MCP-1 secretion coincided with mRNA expression. Pre-treatment with either genistein or daidzein elevated eNOS expression and nitric oxide production disturbed by TNF-alpha exposure. A low concentration of isoflavones significantly inhibited nuclear factor (NF)kappaB activation, whereas a high dose slightly ameliorated these inhibitive effects. These results suggest that genistein had a stronger effect on MCP-1 and eNOS expression than that of daidzein. Additionally, NFkappaB transactivation might be partially related to the down-regulation of these mRNAs in TNF-alpha-stimulated HUVECs.
