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

Authors

  • Baodong Ye Department of Hematology, First Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, Zhejiang, China
  • Dijiong Wu Department of Hematology, First Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, Zhejiang, China
  • Huijin Hu Department of Hematology, First Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, Zhejiang, China
  • Linglong Xu Department of Hematology, Taizhou Central Hospital, Taizhou, Zhejiang, China
  • Wenbin Liu Department of Hematology, First Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, Zhejiang, China
  • Xiaowen Wen Department of Internal Medicine, Central Hospital of Jinhua Affiliated to Zhejiang University, Jinhua, Zhejiang, China
  • Yuhong Zhou Department of Hematology, First Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, Zhejiang, China
Abstract:

Objective(s): 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.Materials and Methods: 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. Results: 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.Conclusion: Curcumin and baicalein protect hematopoiesis from immune and iron overload-induced apoptosis, exerting iron chelation effects in vivo.

Download for Free

Sign up for free to access the full text

Already have an account?login

similar resources

A composite mouse model of aplastic anemia complicated with iron overload

Iron overload is commonly encountered during the course of aplastic anemia (AA), but no composite animal model has been developed yet, which hinders drug research. In the present study, the optimal dosage and duration of intraperitoneal iron dextran injection for the development of an iron overload model in mice were explored. A composite model of AA was successfully established on the principl...

full text

IRON METABOLISM Iron overload and chelation

Iron is one of the most common elements in nature. As a transition metal it is very efficient in electron transport and redox reactions. The proteins and enzymes in which iron is an essential component play a key role in respiration, energy production, detoxification of harmful oxygen species and cell replication. Despite the abundance of iron in nature, the solubility of its stable ferric form...

full text

Overview of guidelines on iron chelation therapy in patients with myelodysplastic syndromes and transfusional iron overload

Between 2002 and 2008, a number of consensus statements and guidelines were developed by various groups around the world to educate healthcare professionals on the treatment of myelodysplastic syndromes (MDS), including the management of transfusional iron overload with iron chelation therapy. Guidelines have been developed by The Italian Society of Hematology, The UK MDS Guidelines Group, The ...

full text

Effect of Systemic Iron Overload and a Chelation Therapy in a Mouse Model of the Neurodegenerative Disease Hereditary Ferritinopathy

Mutations in the ferritin light chain (FTL) gene cause the neurodegenerative disease neuroferritinopathy or hereditary ferritinopathy (HF). HF is characterized by a severe movement disorder and by the presence of nuclear and cytoplasmic iron-containing ferritin inclusion bodies (IBs) in glia and neurons throughout the central nervous system (CNS) and in tissues of multiple organ systems. Herein...

full text

Iron kinetics with emphasis on iron overload.

BODY IRON IN MAN is estimated at 35 to 45 mg/kg or a total of about 3 g.1 The major portion of body iron, some 30 mg/kg, is held in the circulating red cell mass and erythroid marrow as hemoglobin. The only other fraction of quantitative significance is storage iron, amounting to another 15 mg/kg in the adult male and varying from 0 to 10 mg/kg in the female. The manner in which body iron is ma...

full text

Iron Chelation Therapy with Deferasirox in the Management of Iron Overload in Primary Myelofibrosis

Deferasirox (DSX) is the principal option currently available for iron-chelation-therapy (ICT), principally in the management of myelodysplastic syndromes (MDS), while in primary myelofibrosis (PMF) the expertise is limited. We analyzed our experience in 10 PMF with transfusion-dependent anemia, treated with DSX from September 2010 to December 2013. The median dose tolerated of DSX was 750 mg/d...

full text

My Resources

Save resource for easier access later

Save to my library Already added to my library

{@ msg_add @}


Journal title

volume 22  issue 6

pages  660- 668

publication date 2019-06-01

By following a journal you will be notified via email when a new issue of this journal is published.

Hosted on Doprax cloud platform doprax.com

copyright © 2015-2023