S-Equol Enantioselectively Activates cAMP-Protein Kinase A Signaling and Reduces Alloxan-Induced Cell Death in INS-1 Pancreatic β-Cells

DOI Web Site PubMed 被引用文献11件 参考文献29件
  • HORIUCHI Hiroko
    Division of Applied Life Sciences, Graduate School of Life and Environmental Sciences, Osaka Prefecture University
  • HARADA Naoki
    Division of Applied Life Sciences, Graduate School of Life and Environmental Sciences, Osaka Prefecture University
  • ADACHI Tetsuya
    Laboratory of Food and Health Sciences, Minatogawa College
  • NAKANO Yoshihisa
    Osaka Women’s Junior College
  • INUI Hiroshi
    Division of Applied Life Sciences, Graduate School of Life and Environmental Sciences, Osaka Prefecture University
  • YAMAJI Ryoichi
    Division of Applied Life Sciences, Graduate School of Life and Environmental Sciences, Osaka Prefecture University

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タイトル別名
  • <i>S</i>-Equol Enantioselectively Activates cAMP-Protein Kinase A Signaling and Reduces Alloxan-Induced Cell Death in INS-1 Pancreatic β-Cells
  • S-Equol Enantioselectively Activates cAMP-Protein Kinase A Signaling and Reduces Alloxan-Induced Cell Death in INS-1 Pancreatic ^|^beta;-Cells

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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.

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