HIF-1 alpha plays a key role in iron uptake and transport in the liver, whose activity is tightly linked to the repression of hepcidin (Hamp). Hump prevents intestinal iron uptake and cellular efflux by negatively modulating ferroportin. Hump is also expressed in the kidneys, where transcriptional control by HIF-1 alpha remains poorly understood. We show that the administration of epigallocatechin gallate (EGCG) results in a considerable Hump expression in rat kidneys. We also provide evidence to show that EGCG inhibited prolyl hydroxylase (PHD) activity, essential for HIF-1 alpha degradation in vivo and in vitro. Rats that were dosed with EGCG (60 mg/kg, intraperitoneal) over a 7 day time course stabilized HIF-1 alpha protein in kidney tissues. Interestingly. Hump gene expression was induced, even after subjecting rats to a 4 h hypoxia treatment (8% oxygen). Using Hep3B cells, we determined that EGCG conferred its inhibitory action by complexing with PHD, altering its catalytic iron center and thus preventing HIF-1 alpha hydroxylation. These data demonstrate EGCG's therapeutic potential in modulating hepcidin expression in diseases associated with altered iron metabolism. Published by Elsevier Inc.