Effects of Equol on Oxidized Low-Density Lipoprotein-Induced Apoptosis in Endothelial Cells

Aim: Equol is the main active product of daidzein metabolism, produced via specific microflora in the gut. This study aimed to clarify the effects of equol on oxidized low-density lipoprotein (OX-LDL)-stimulated apoptosis in human umbilical vein endothelial cells (HUVECs). Methods: HUVECs were cultu...

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Bibliographic Details
Published in:Journal of Atherosclerosis and Thrombosis 2009, Vol.16(3), pp.239-249
Main Authors: Kamiyama, Masumi, Kishimoto, Yoshimi, Tani, Mariko, Utsunomiya, Kazunori, Kondo, Kazuo
Format: Article
Language:English
Subjects:
Apoptosis
Apoptosis - drug effects
Cells, Cultured
Endothelial Cells
Endothelial dysfunction
Endothelium, Vascular - cytology
Equol
Humans
Isoflavones - pharmacology
Lipoproteins, LDL - physiology
Nitric Oxide - biosynthesis
Oxidized low-density lipoprotein
Phytoestrogens
Reactive Oxygen Species - analysis
Superoxides - analysis
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Summary:Aim: Equol is the main active product of daidzein metabolism, produced via specific microflora in the gut. This study aimed to clarify the effects of equol on oxidized low-density lipoprotein (OX-LDL)-stimulated apoptosis in human umbilical vein endothelial cells (HUVECs). Methods: HUVECs were cultured in the presence of OX-LDL, and cell apoptosis was monitored by evaluating of DNA fragmentation and the production of cytoplasmic histone-associated DNA fragments. We simultaneously evaluated the level of cellular superoxide and nitric oxide (NO) and the effects of the anti-oxidant activity of equol on apoptosis. Results: We found that equol inhibited the induction of apoptosis in response to exposure of HUVECs to OX-LDL. Treatment of cells with equol led to a significant reduction in superoxide production by NAD(P)H oxidase and also to a significant increase in NO production. We further observed an effect of equol on the suppression of OX-LDL uptake. Conclusions: These results suggested that equol might contribute to a reduced level of OX-LDL-stimulated apoptosis linked to the reduced generation of intracellular reactive oxygen species (ROS).
ISSN:1340-3478
1880-3873
DOI:10.5551/jat.1057