Iron chelation effect of curcumin and baicalein on aplastic anemia mouse model with iron overload.

The current work aimed to assess whether curcumin and baicalein can chelate iron in aplastic anemia (AA) complicated with iron overload, exploring the potential mechanisms. A mouse model of AA with iron overload complication was firstly established. Low and high-dose curcumin or baicalein treatment groups were set up, as well as the deferoxamine positive control, normal and model groups (n=8). Hemogram and bone marrow mononuclear cell detection were performed, and TUNEL and immunohistochemical staining were used to evaluate hematopoiesis and apoptosis in the marrow. ELISA, Western blot, and qRT-PCR were employed to assess serum iron (SI), serum ferritin (SF), bone morphogenetic protein 6 (BMP-6), SMAD family member4 (SMAD4) and transferrin receptor 2 (TfR2) amounts. Both curcumin and baicalein improved white blood cell (increase of 0.28-0.64×109/l in high-dose groups) and hemoglobin (increase of around 10 g/l) amounts significantly, which may related to decreased apoptosis (nearly 30%-50% of that in the model group) in the bone marrow, while their effects on platelet recovery were limited and inferior to that of deferoxamine (DFO). Both test compounds up-regulated hepcidin and its regulators (BMP-6, SMAD, and TfR2) at the protein and mRNA levels; high dosage treatment may be beneficial, being better than DFO administration in lessening iron deposition in the bone marrow. Curcumin and baicalein protect hematopoiesis from immune and iron overload-induced apoptosis, exerting iron chelation effects in vivo.