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dc.contributor.authorPimpisid Koonyosyingen_US
dc.contributor.authorSarawut Kongkarnkaen_US
dc.contributor.authorChairat Uthaipibullen_US
dc.contributor.authorSaovaros Svastien_US
dc.contributor.authorSuthat Fucharoenen_US
dc.contributor.authorSomdet Srichairatanakoolen_US
dc.description.abstract© 2018 Elsevier Masson SAS 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.en_US
dc.subjectPharmacology, Toxicology and Pharmaceuticsen_US
dc.titleGreen tea extract modulates oxidative tissue injury in beta-thalassemic mice by chelation of redox iron and inhibition of lipid peroxidationen_US
article.title.sourcetitleBiomedicine and Pharmacotherapyen_US
article.volume108en_US Mai Universityen_US National Science and Technology Development Agencyen_US Universityen_US
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