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).
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).
Authors: Xiao Zhang; Cole V Veliky; Rahel L Birru; Emma Barinas-Mitchell; Jared W Magnani; Akira Sekikawa Journal: Nutrients Date: 2021-10-23 Impact factor: 5.717
Authors: Daniele Del Rio; Ana Rodriguez-Mateos; Jeremy P E Spencer; Massimiliano Tognolini; Gina Borges; Alan Crozier Journal: Antioxid Redox Signal Date: 2012-08-27 Impact factor: 8.401