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

• 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
• ISSN: 1340-3478; 1880-3873
• DOI: 10.5551/jat.1057

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).