β-Thalassemia is characterized by ineffective erythropoiesis leading to chronic anemia. Thus, increased iron absorption from the duodenum and via blood transfusions is required to maintain normal blood hemoglobin (Hb) levels and iron chelators in the removal of excessive iron. Certain agents are also needed for the improvement of stress erythropoiesis and iron dysregulation. Green tea extract (GTE), which is rich in epigallocatechin-3-gallate (EGCG), is known to possess radical scavenging and iron-chelating activities. We aimed to assess the effects of green tea extract on erythroid regulators, iron mobilization and anti–lipid peroxidation in the liver, spleen, and kidneys of iron-loaded β-globin gene knockout thalassemic (BKO) mice. Our results indicate that treatments of green tea extract and/or deferiprone (DFP) diminished levels of plasma erythropoietin (EPO) and erythroferrone (ERFE), and consistently suppressed kidney Epo and spleen Erfe mRNA expressions (p < .05) in iron- loaded BKO mice when compared with untreated mice. Coincidently, the treatments decreased plasma ferritin (Ft) levels, iron content levels in the liver (p < .05), spleen (p < .05), and kidney tissues of iron–loaded BKO mice. Furthermore, lipid-peroxidation products in the tissues and plasma were also decreased when compared with untreated mice. This is the first evidence of the orchestral role of green tea extract abundant with epigallocatechin-3-gallate in improving ineffective erythropoiesis, iron dysregulation and oxidative stress in iron-overloaded β-thalassemic mice.

Redox-active iron generates reactive oxygen species that can cause oxidative organ dysfunction. Thus, the anti-oxidative systems in the body and certain dietary antioxidants, such as anthocyanins, are needed to control oxidative stress. We aimed to investigate the effects of dielectric barrier discharge (DBD) plasma technology in the preparation of Riceberry™ rice flour (PRBF) on iron-induced oxidative stress in mice. PRBF using plasma technology was rich in anthocyanins, mainly cyanidine-3-glucoside and peonidine-3-glucoside. PRBF (5 mg AE/mg) lowered WBC numbers in iron dextran (FeDex)-loaded mice and served as evidence of the reversal of erythrocyte superoxide dismutase activity, plasma total antioxidant capacity, and plasma and liver thiobarbituric acid-reactive substances in the loading mice. Consequently, the PRBF treatment was observed to be more effective than NAC treatment. PRBF would be a powerful supplementary and therapeutic antioxidant product that is understood to be more potent than NAC in ameliorating the effects of iron-induced oxidative stress.

Hypercoagulability and increased platelet activation have been associated with iron-overloaded β−thalassemia patients resulting in thrombosis. Iron chelators, antiplatelet and antithrombosis drugs are required to alleviate these complications. Epigallocatechin−3−gallate (EGCG)−rich green tea extract (GTE) is known to exert iron-chelating and antithrombotic activities. This study aimed to assess the effects of GTE tablet consumption on coagulation, platelet function and iron overload in transfusion-dependent β-thalassemia (TDT) patients. Each day, the subjects consumed a placebo, a single GTE tablet (50 mg EGCG equivalent) or GTE tablets (2x 50 mg EGCG equivalent) over a period of two months. Blood was then collected for analyses of platelet numbers, coagulation, platelet aggregation and iron parameters. Accordingly, GTE tablets significantly reduced the aggregation of platelets that had been induced ex vivo by ADP or collagen. The tablets also increased plasma protein C and protein S activities, as well as free protein S concentration levels depending upon the time course but not the GTE dosage. Surprisingly, plasma ferritin levels were decreased in both GTE tablet groups in a time-dependent manner, for which a significant difference was observed in the second month. In conclusion, EGCG−abundant GTE improved platelet aggregation and hypercoagulability in TDT patients by increasing the antithrombotic activity of protein C and protein S. Thus, GTE can be an adjuvant to reduce the risk of thrombosis associated with iron overload.