Abstract
Beta-thalassemia intermedia (BTI) is characterized by ineffective erythropoiesis and iron overload due to dysregulated iron metabolism. Curcumin, a natural polyphenol, has shown potential in modulating iron homeostasis, but its effects on key iron transporter genes, SLC40A1 (ferroportin) and DMT1 (divalent metal transporter-1), remain unclear. This randomized, double-blind, placebo-controlled trial evaluated 30 transfusion-independent male BTI patients (aged 20–35 years) receiving deferasirox. Participants were assigned to either curcumin (1500 mg/day) or placebo for three months. Serum iron markers (iron, ferri-tin, transferrin saturation) and gene expression levels of SLC40A1 and DMT1 were measured before and after treatment using quantitative PCR. Statistical analyses included Mann-Whitney U tests and correlation analyses. Curcumin significantly downregulated SLC40A1 (32% reduction, p = 0.010) and DMT1 (31% reduction, p = 0.015) expression compared to placebo (p > 0.68). Negative correlations were observed between gene expression and iron markers (serum iron, ferritin, transferrin saturation; all p < 0.05), suggesting a mechanistic link between transporter modulation and improved iron homeostasis. No significant changes occurred in the placebo group. Curcumin supplementation reduces SLC40A1 and DMT1 gene expression and improves iron metabolism in BTI patients, supporting its potential as an adjunct therapy for iron overload. Further studies are needed to confirm these effects at the protein level and in broader populations.