Please use this identifier to cite or link to this item: http://cmuir.cmu.ac.th/jspui/handle/6653943832/67624
Title: Decrement in Cellular Iron and Reactive Oxygen Species, and Improvement of Insulin Secretion in a Pancreatic Cell Line Using Green Tea Extract
Authors: Pimpisid Koonyosying
Chairat Uthaipibull
Suthat Fucharoen
Evangelia Vlachodimitropoulou Koumoutsea
John B. Porter
Somdet Srichairatanakool
Authors: Pimpisid Koonyosying
Chairat Uthaipibull
Suthat Fucharoen
Evangelia Vlachodimitropoulou Koumoutsea
John B. Porter
Somdet Srichairatanakool
Keywords: Biochemistry, Genetics and Molecular Biology;Medicine
Issue Date: 1-May-2019
Abstract: © Wolters Kluwer Health, Inc. All rights reserved. Objectives We have investigated the efficacy of mono- and combined therapy with green tea extract (GTE) in mobilizing redox iron, scavenging reactive oxygen species (ROS), and improving insulin production in iron-loaded pancreatic cells. Methods Rat insulinoma pancreatic β-cells were iron-loaded using culture medium supplemented with either fetal bovine serum or ferric ammonium citrate and treated with various doses of GTE for epigallocatechin-3-gallate (EGCG) equivalence and in combination with iron chelators. Cellular iron, ROS, and secretory insulin were measured. Results The rat insulinoma pancreatic cells took up iron from fetal bovine serum more rapidly than ferric ammonium citrate. After treatment with GTE (0.23-2.29 μg EGCG equivalent), cellular levels of iron and ROS were dose dependently decreased. Importantly, secretory insulin levels were increased nearly 2.5-fold with 2.29 μg of EGCG equivalent GTE, indicating a recovery in insulin production. Conclusions Green tea EGCG ameliorated oxidative damage of iron-loaded β-cells by removing redox iron and free radicals and attenuating insulin production. The impact can result in the restoration of pancreatic functions and an increase in insulin production. Green tea extract exerts iron-chelating, free-radical scavenging, and pancreato-protective effects in the restoration of β-cell functions, all of which we believe can increase insulin production in diabetic β-thalassemia patients.
URI: https://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=85066822022&origin=inward
http://cmuir.cmu.ac.th/jspui/handle/6653943832/67624
ISSN: 15364828
08853177
Appears in Collections:CMUL: Journal Articles

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