期刊名称：Journal of Nutritional Science and Vitaminology
印刷版ISSN：0301-4800
电子版ISSN：1881-7742
出版年度：2014
卷号：60
期号：4
页码：291-296
DOI：10.3177/jnsv.60.291
出版社：Center for Academic Publications Japan
摘要：S -Equol is enantioselectively produced from the isoflavone daidzein by gut microflora and is absorbed by the body. An increase of pancreatic β-cell death is directly associated with defects in insulin secretion and an increased risk of type 2 diabetes mellitus. In the present study, we demonstrate that only the S -enantiomer has suppressive effects against alloxan-induced oxidative stress in INS-1 pancreatic β-cells. S -Equol reduced alloxan-induced cell death in a dose-dependent manner, whereas R -equol had no effects. In contrast, no significant differences were observed between the enantiomers in estrogenic activity. The cytoprotective effects of S -equol were stronger than those of its precursor daidzein and were blocked by the protein synthesis inhibitor cycloheximide. The cytoprotection was diminished when cells were incubated with a protein kinase A (PKA) inhibitor (H89), but not an estrogen receptor inhibitor. S -Equol increased intracellular cAMP levels in an enantioselective manner. S -Equol, but not R -equol, induced phosphorylation of cAMP-response element-binding protein at Ser 133, and induced cAMP-response element-mediated transcription, both of which were diminished in the presence of H89. Taken together, these results show that S -equol enantioselectively increases the survival of INS-1 cells presumably through activating PKA signaling. Thus, S -equol might have applications as an anti-type 2 diabetic agent.
关键词：equol;cAMP;protein kinase A signaling;enantioselectivity;pancreatic β-cells
