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Green tea extract modulates oxidative tissue injury in beta-thalassemic mice by chelation of redox iron and inhibition of lipid peroxidation
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Metadata
Document Title
Green tea extract modulates oxidative tissue injury in beta-thalassemic mice by chelation of redox iron and inhibition of lipid peroxidation
Author
Koonyosying P., Kongkarnka S., Uthaipibull C., Svasti S., Fucharoen S., Srichairatanakool S.
Name from Authors Collection
Affiliations
Department of Biochemistry, Faculty of Medicine, Chiang Mai University, Chiang Mai, Thailand; Department of Pathology, Faculty of Medicine, Chiang Mai University, Chiang Mai, Thailand; Protein-Ligand Engineering and Molecular Biology Laboratory, National Center for Genetic Engineering and Biotechnology (BIOTEC), National Science and Technology Development Agency, Thailand Science ParkPathum Thani, Thailand; Thalassemia Research Center, Institute of Molecular Bioscience, Mahidol University Salaya CampusNakornpathom, Thailand
Type
Article
Source Title
Biomedicine and Pharmacotherapy
ISSN
07533322
Year
2018
Volume
108
Page
1694-1702
Open Access
Hybrid Gold
Publisher
Elsevier Masson SAS
DOI
10.1016/j.biopha.2018.10.017
Abstract
Iron overload in patients with β-thalassemia can cause oxidative organ dysfunction. Iron chelation along with antioxidant supplementation can ameliorate such complications and prolong lives. Green tea extract (GTE) rich in epigallocatechin-3-gallate (EGCG) exhibits anti-oxidation and iron chelation properties in β-knockout thalassemic (BKO) mice diagnosed with iron overload. We investigated the effects of GTE and deferiprone (DFP) alone in combination with one another, and upon the levels of redox-active iron, lipid-peroxidation product, insulin and hepcidin in BKO mice. A state of iron overload was induced in the mice via a trimethylhexanoyl-ferrocene supplemented (Fe) diet for 3 months, and the mice were treated daily with either: DFP (50 mg/kg), DFP (50 mg/kg) plus GTE (50 mg EGCG equivalent/kg), or GTE alone for 2 months. Plasma non-transferrin bound iron (NTBI), malondialdehyde (MDA), alanine aminotransferase (ALT), aspartate aminotransferase (AST), hepcidin and insulin; tissue iron and MDA were measured. DFP, GTE and GTE + DFP effectively decreased plasma MDA (p < 0.05), NTBI and ALT, and increased plasma hepcidin and insulin. All the treatments also reduced iron accumulation and MDA production in both the pancreas and liver in the mice. However, the combination therapy demonstrated no advantages over monotherapy. The findings suggest GTE improved liver and pancreatic β-cell functions in iron-overloaded β-thalassemia mice by diminishing redox iron and free radicals, while inhibiting lipid peroxidation. Consequently, there are indications that GTE holds significant potential for clinical use. © 2018 Elsevier Masson SAS
Keyword
EGCG | Green tea | Iron overload | Oxidative stress | Thalassemia
Industrial Classification
Knowledge Taxonomy Level 1
Knowledge Taxonomy Level 2
Knowledge Taxonomy Level 3
Funding Sponsor
Thailand Research Fund
License
CC BY-NC-ND
Rights
Elsevier B.V.
Publication Source
Scopus