protective effect of EGCG on mouse islets
Takata, Atsushi Tokushima University
Wada, Yuma Tokushima University
Ikemoto, Tetsuya Tokushima University Tokushima University Educator and Researcher Directory KAKEN Search Researchers
Morine, Yuji Tokushima University Tokushima University Educator and Researcher Directory KAKEN Search Researchers
Imura, Satoru Tokushima University Tokushima University Educator and Researcher Directory KAKEN Search Researchers
Saito, Yu Tokushima University Tokushima University Educator and Researcher Directory KAKEN Search Researchers
Epigallocatechin 3-gallate (EGCG)
Reactive oxygen species (ROS)
Nuclear factor erythroid 2-related factor 2 (Nrf2)
Reactive oxygen species (ROS) production
Thesis or Dissertation
Purpose: Epigallocatechin 3-gallate (EGCG), a green tea polyphenol, has been shown to have anti-oxidant and anti-inflammatory effects in vitro and in vivo. The aim of this study was to investigate the effects and mechanism of EGCG on isolated pancreatic islets as pre-conditioning for pancreatic islet transplantation.
Methods: The pancreatic islets were divided into two groups: an islet culture medium group (control) and an islet culture medium with EGCG (100 μM) group. We investigated the islet viability, Nrf2 expression, reactive oxygen species (ROS) production, and heme oxygenase-1 (HO-1) mRNA. Five hundred islet equivalents after 12 h of culture for the EGCG 100 μM and control group were transplanted under the kidney capsule of streptozotocin (STZ)-induced diabetic ICR mice.
Results: The cell viability and insulin secretion ability in the EGCG group were preserved, and the nuclear translocation of Nrf2 was increased in the EGCG group (p<0.01). While the HO-1 mRNA levels were also higher in the EGCG group than in the control group (p<0.05), the ROS production was lower (p<0.01). An in vivo functional assessment showed that the blood glucose level had decreased in the EGCG group after transplantation (p<0.01).
Conclusion: EGCG protects the viability and function of islets by suppressing ROS production via the Nrf2 pathway.
Springer|Japan Surgical Society
This is a post-peer-review, pre-copyedit version of an article published in Surgery Today. The final authenticated version is available online at: https://doi.org/10.1007/s00595-019-1761-0
|DOI (Published Version)|
|URL ( Publisher's Version )|
k3342_abstract_review.pdf 265 KB
k3342_fulltext.pdf 292 KB
|MEXT report number||
Doctor of Medical Science