期刊
JOURNAL OF ATHEROSCLEROSIS AND THROMBOSIS
卷 16, 期 3, 页码 239-249出版社
JAPAN ATHEROSCLEROSIS SOC
DOI: 10.5551/jat.1057
关键词
Equol; Endothelial dysfunction; Oxidized low-density lipoprotein; Apoptosis
资金
- Nagano prefectural government
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).
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