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Beta-thalassemia major(β-TM)is an inherited disease caused by a defect in the synthesis of globin. The disease requires long-term blood transfusion and iron chelator treatment, which can cause various secondary changes in the body and eye tissues. Compared with normal peers, β-TM patients will show changes in the eye such as steeper corneal curvature, shallower anterior chamber, increased lens thickness, shorter axial length, and reduced tear secretion. At the same time, nutritional deficiencies and the use of iron chelator drugs will increase the risk of complicated cataract and retinal degeneration, thus affecting the quality of life of β-TM patients.This article combines relevant domestic and foreign literatures to explore and review the changes in the eye of β-TM patients, with a view to providing valuable insights for clinical practice.
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BACKGROUND:With the aging of the global population,the incidence rate of osteoporosis is also increasing.It is very important to further understand its pathogenesis and propose new therapeutic targets.Recent studies have shown that ferroptosis is closely related to the pathogenesis of some bone diseases,such as inflammatory arthritis,osteoporosis and osteoarthritis. OBJECTIVE:To summarize the previous studies on the mechanism of ferroptosis in osteoporosis,so as to provide new therapeutic ideas and potential therapeutic targets for osteoporosis. METHODS:The first author used the computer to search the documents published from 2000 to 2022 in CNKI,WanFang,VIP,PubMed and Web of Science with the key words of"ferroptosis,osteoporosis,osteoblasts,osteoclasts,iron chelators,reactive oxygen species,nuclear factor erythroid 2-related factor 2,heme oxygenase-1,glutathione peroxidase 4,review"in Chinese and English.A total of 70 articles were finally included according to the inclusion criteria. RESULTS AND CONCLUSION:Ferroptosis is significantly different from necrosis,apoptosis and autophagy.In terms of cell morphology and function,it does not have the morphological characteristics of typical necrosis,nor does it have the characteristics of traditional apoptosis,such as cell contraction,chromatin condensation,the formation of apoptotic bodies and the disintegration of cytoskeleton.Contrary to autophagy,ferroptosis does not form a classical closed bilayer membrane structure(autophagic vacuole).Morphologically,ferroptosis is mainly manifested by obvious contraction of mitochondria,increased membrane density,and reduction or disappearance of mitochondrial cristae,which are different from other cell death modes.Iron overload can destroy bone homeostasis by significantly inhibiting osteogenic differentiation and stimulating osteoclast formation,leading to osteoporosis.Iron overload interferes with the differentiation of stem cells to osteoblasts,leading to a weakened osteoblast function and further imbalance of bone metabolism in the body,which eventually leads to osteoporosis.Stimulated by iron overload,osteoclast bone resorption is enhanced and bone loss exceeds new bone formation.Iron chelators have been proved to have osteoprotective effects by inhibiting osteoclast activity and stimulating osteogenic differentiation of osteoblasts.Its potential mechanism is related to inhibiting osteoclast differentiation and promoting osteoblast differentiation.Antioxidants can prevent reactive oxygen species production and inhibit bone absorption,thus improving bone metabolism and effectively preventing osteoporosis.
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BACKGROUND:Aside from iron chelating,deferoxamine is also considered as an effective hypoxia mimetic agent and hypoxia inducible factor-1α stabilizer.Deferoxamine has played a favorable effect on bone regeneration in both basic and clinical research recently.Deferoxamine solutions or deferoxamine loaded bio-scaffolds have been locally applied in bone tissue engineering,and their promotion of bone repair involves various functional properties and molecular mechanisms which have not been entirely clarified.Moreover,their advances in research of bone regeneration lack comprehensive summary as well. OBJECTIVE:To review the functional properties,relative merits and advances in basic research and clinical practice of deferoxamine applied in bone regeneration,attempting to provide references and strategies for further studies. METHODS:Relevant articles were searched with the key words of"deferoxamine OR desferrioxamine OR desferal OR DFO,""bone tissue engineering OR bone regeneration OR bone remodeling OR bone repair OR bone healing OR osteogenesis,""angiogenesis OR vascularized bone regeneration OR angiogenic-osteogenic coupling"in English and Chinese by using PubMed,WanFang and CNKI databases.Eventually,88 articles were selected for review. RESULTS AND CONCLUSION:Deferoxamine can recruit stem cells and regulate their function,activate relevant signaling pathways to advance hypoxia adaptation of the cells,exert anti-inflammatory and antioxidant properties to improve local inflammatory environment,and promote bone regeneration by coupling osteogenesis and angiogenesis as well as inhibiting bone resorption.Compared with growth factors or peptides loaded in conventional bone tissue engineering,deferoxamine has its unique advantages as a small molecule drug,while it also has toxic reactions and application limitations.Therefore,it is necessary to optimize its loading form and dosagey.The unique angiogenic-osteogenic coupling ability of deferoxamine can be used in different types of bone injuries including fractures,osteonecrosis,distraction osteogenesis,bone grafting,oral related osteogenesis,and bone defects.Due to the enhancement of angiogenesis,this ability enables deferoxamine to better adapt and solve the difficulties in bone repair caused by the complex and variable clinical situations and individual differences.However,it is also necessary to compare and optimize the application methods and safe dosage of deferoxamine to expand its application scope and enhance its clinical value.
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Objective:To observe the effect of α-lipoic acid(ALA) on the intracerebroventricular injection(icv) of streptozotocin(STZ)-induced spatial learning memory impairments in rats and the underlying molecular mechanisms.Methods:Forty-five male SD rats were assigned into 3 groups, control group, icv-STZ group and icv-STZ+ ALA group, 15 rats each. STZ was dissolved in artificial cerebrospinal fluid then injected into the lateral ventricles of the rat by using stereotaxic device. ALA was administrated by gavage after STZ injection. The spatial learning memory was examined by using Morris water maze test after 4 weeks of treatment. Immunohistochemistry was performed to detect the number of microglia and astrocytes, electron microscopy was applied to detect mitochondrial integrity, Western blotting was used to detect the protein expression levels, and the changes of lipid peroxidation and redox system were examined by kit.Results:Spatial learning memory was impaired in rats after 4 weeks of STZ injection, and ALA treatment ameliorated STZ-induced cognitive dysfunction in rats. Iron concentration, lipid peroxidation, neuroinflammation, Tau hyperphosphorylated were enhanced markedly after STZ injection, along with and the activation of MAPK and GSK-3β, which were ameliorated by ALA. Further examination revealed that STZ activated the JAK2/STAT3 pathway and transcriptionally inhibited the expression of peroxidase GPX. Inhibition of STAT3 activity can block STZ-induced downregulation of GPX4 and Tau hyperphosphorylation.Conclusion:ALA ameliorated STZ-induced spatial learning memory impairments in rats via deactivation of JAK2/STAT3 pathway, restored GPX4 protein level, resulting in chelating iron, improving mitochondrial function, balancing the redox system, ameliorating Tau hyperphosphorylation and neuroinflammation.
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Background: Ocular involvement in β-thalassemia major is very common. Iron chelators like Desferrioxamine and Deferiprone avoid systemic complications but chelate metals in retina. Objectives: 1.To study the relation of oral iron chelator (Deferiprone) on various ocular manifestations in β-thalassemia major patients. 2. To study the relation of serum ferritin with various ocular manifestations. Methods: 100β-thalassemia major patients out of those attending our thalassemia clinic were selected for the study as per our inclusion and exclusion criteria. They were divided into two major groups based on whether they were taking oral iron chelator (Deferiprone) or not. Detailed history, examination and investigations were done and recorded. Results: The study revealed that 52% of the patients had ocular involvement with 86.5% of them taking Deferiprone (p<0.0001), 13% had retinal pigment epithelium (RPE) degeneration with 92.3% of them on Deferiprone (p=0.003) and 18% had RPE mottling with 88.8% of them taking Deferiprone (p=0.001). Other ocular changes like lens opacity, disc hyperemia, best corrected visual acuity (BCVA) and venous tortuosity showed some difference between the two groups but that was insignificant. Further the study also showed that higher serum ferritin levels were significantly associated with ocular changes like decreased BCVA (p<0.001), RPE degeneration (p<0.001), RPE mottling (p<0.001) and venous tortuosity (p<0.025). Conclusion: Ocular changes in β-thalassemia major increases with greater duration of the disease and increased number of blood transfusions due to increased serum ferritin levels. Using iron chelators may reduce iron overload but they causechelator induced ocular involvement.
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Iron is an essential nutrient that not only participates in cell oxidative phosphorylation, DNA synthesis and replication, but also regulates cancer associated genes through hypoxia-inducible factor (HIF).In the process of cancerization, cells change the way of iron metabolism resulting in a high consumption of iron.In this case, pathways of iron acquisition, efflux, storage and regulation are perturbed.Therefore, iron can significantly contribute to tumor growth, cell survival and metastasis.In this paper, we summarize the iron changes in cancer cells and the relationship between the changes and tumorigenesis.We also briefly state the potential problems of current clinical using iron chelating agents in oncotherapy.Targeting iron metabolic pathways may provide new tools for cancer prognosis and therapy.
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Objective To explore the clinical effectiveness of deferasirox, deferiprone and desferrioxamine in the treatment of iron overload in patients with thalassemia major.Methods Among the severe thalassemia patients with iron overload being diagnosis,treated and followed up in Guigang City People′s Hospital,fifty cases were tested by MRI T2 and were detected with cardiac and liver iron overload,the patients were selected and randomly divided into the deferoxamine treatment(DFO)group(18 case),deferiprone treatment(DFP)group(22 cases)and deferasirox treatment(DFX)group(10 case),The baseline data of the three groups were statistically analyzed.the serum ferritin(SF)value,the cardiac MRI T2 value and the liver MRI T2 value before and after treatment were measured.Results The patients completed the treatment,after 1 years of treatment,the serum SF value,cardiac and liver MRI T2 values of the patients were improved than those before the treatment(P<0.05); the differences in serum SF among the three groups were not statistically significant(F=3.089,P>0.05); the differences in liver MRI T2 value among the three groups were not statistically significant(F=0.131,P>0.05),There were significant differences in heart iron load MRI T2 values among the three groups((34.27 ± 6.30)ms vs.(23 ± 2.79)ms vs.(21.8 ± 2.20)ms,F=39.54,P<0.05) .Conclusion Deferoxamine,deferiprone and deferasirox can effectively alleviate the iron load in patients with thalassemia major.in terms of cardiac iron overload,the curative effects of deferiprone treatment in patients with thalassemia is superior than desferrioxamine and deferasirox treatment,it is worthy of clinical promotion.
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Iron is the most abundant metal element to support the body's physiological activities and play crucial roles in the central nervous system. Iron homeostasis is under strict control in normal circumstances, and some diseases will occur once the homeostasis was disrupted. Numerous researches suggest that iron homeostasis disruptes in Alzheimer's disease (AD) and the homeostasis disruption interacts with AD's hallmarks. Dispute still exists on how iron plays a role in AD despite of the great number of researches. This article will focus on iron metabolism, normal function in the brain and recent therapies of AD based on iron chelation.
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BACKGROUND/AIMS: The treatment of chronic myeloid leukemia (CML) has achieved impressive success since the development of the Bcr-Abl tyrosine kinase inhibitor, imatinib mesylate. Nevertheless, resistance to imatinib has been observed, and a substantial number of patients need alternative treatment strategies. METHODS: We have evaluated the effects of deferasirox, an orally active iron chelator, and imatinib on K562 and KU812 human CML cell lines. Imatinib-resistant CML cell lines were created by exposing cells to gradually increasing concentrations of imatinib. RESULTS: Co-treatment of cells with deferasirox and imatinib induced a synergistic dose-dependent inhibition of proliferation of both CML cell lines. Cell cycle analysis showed an accumulation of cells in the subG1 phase. Western blot analysis of apoptotic proteins showed that co-treatment with deferasirox and imatinib induced an increased expression of apoptotic proteins. These tendencies were clearly identified in imatinib-resistant CML cell lines. The results also showed that co-treatment with deferasirox and imatinib reduced the expression of BcrAbl, phosphorylated Bcr-Abl, nuclear factor-kappaB (NF-kappaB) and beta-catenin. CONCLUSIONS: We observed synergistic effects of deferasirox and imatinib on both imatinib-resistant and imatinib-sensitive cell lines. These effects were due to induction of apoptosis and cell cycle arrest by down-regulated expression of NF-kappaB and beta-catenin levels. Based on these results, we suggest that a combination treatment of deferasirox and imatinib could be considered as an alternative treatment option for imatinib-resistant CML.
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Humanos , Antineoplásicos/farmacología , Apoptosis/efectos de los fármacos , Proteínas Reguladoras de la Apoptosis/metabolismo , Benzoatos/farmacología , Proliferación Celular/efectos de los fármacos , Relación Dosis-Respuesta a Droga , Resistencia a Antineoplásicos/efectos de los fármacos , Puntos de Control de la Fase G1 del Ciclo Celular/efectos de los fármacos , Mesilato de Imatinib/farmacología , Quelantes del Hierro/farmacología , Células K562 , Leucemia Mielógena Crónica BCR-ABL Positiva/tratamiento farmacológico , Inhibidores de Proteínas Quinasas/farmacología , Transducción de Señal/efectos de los fármacos , Triazoles/farmacologíaRESUMEN
Objective: To evaluate the efficacy of deferiprone (DFP), 1-(N-acetyl-6-aminohexyl)-3-hydroxy-2-methylpyridin-4-one (CM1) or green tea extract (GTE) in enhancing expression of hepatic hepcidin1 (Hamp1) mRNA and relieving iron overload in β-globin knockout thalassemic mice. Methods: The β-globin knockout thalassemic mice were fed with a ferrocene-supplemented diet for 2 months and oral administration of deionized water, DFP (50 mg/kg), CM1 (50 mg/kg), GTE (50 mg epigallocatechin 3-gallate equivalent/kg), GTE along with DFP (50 mg/kg), and GTE along with CM1 (50 mg/kg) every day for 3 months. Levels of hepatic Hamp1 mRNA, plasma non-transferrin bound iron, plasma alanine aminotransferase activity and tissue iron content were determined. Results: All chelation treatments could reduce plasma non-transferrin bound iron concentrations. Additionally, hepatic Hamp1 mRNA expression was significantly up-regulated in the mice in a GTE + DFP combined treatment, correlating with a decrease in the plasma alanine aminotransferase activity and tissue iron deposition. Conclusions: The GTE + DFP treatment could ameliorate iron overload and liver oxidative damage in non-transfusion dependent β-thalassemic mice, by chelating toxic iron in plasma and tissues, and increasing hepcidin expression to inhibit duodenal iron absorption and iron release from hepatocytes and macrophages in the spleen. There is probably an advantage in giving GTE with DFP when treating patients with iron overload.
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Objective:To examine the efficacy of 1-(N-acetyl-6-aminohexyl)-3-hydroxy-2-methylpyridin-4-one (CM1) iron chelator and green tea extract (GTE) as anti-malarial activity in Plasmodium berghei (P. berghei ) infected mice. Methods:The CM1 (0–100 mg/kg/day) and GTE (0–100 mg (-)-epigallocatechin 3-gallate equivalent/kg/day) were orally administered to P. berghei infected mice for consecutive 4 days. Parasitized red blood cells (PRBC) were enumerated by using Giemsa staining microscopic method. Results: CM1 lowered percentage of PRBC in dose-dependent manner with an ED50 value of 56.91 mg/kg, when compared with pyrimethamine (PYR) (ED50=0.76 mg/kg). GTE treatment did not show any inhibition of the malaria parasite growth. In combined treatment, CM1 along with 0.6 mg/kg PYR significantly inhibited the growth of P. berghei in mice while GTE did not enhance the PYR anti-malarial activity. Conclusions: CM1 would be effective per se and synergize with PYR in inhibiting growth of murine malaria parasites, possibly by limiting iron supply from plasma transferrin and host PRBC cytoplasm, and chelating catalytic iron constitutive in parasites’ mitochondrial cytochromes and cytoplasmic ribonucleotide reductase. CM1 would be a promising adjuvant to enhance PYR anti-malarial activity and minimize the drug resistance.
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Objective: To examine the efficacy of 1-(N-acetyl-6-aminohexyl)-3-hydroxy-2-methylpyridin-4-one (CM1) iron chelator and green tea extract (GTE) as anti-malarial activity in Plasmodium berghei ( P. berghei) infected mice. Methods: The CM1 (0-100 mg/kg/day) and GTE (0-100 mg (-)-epigallocatechin 3-gallate equivalent/kg/day) were orally administered to P. berghei infected mice for consecutive 4 days. Parasitized red blood cells (PRBC) were enumerated by using Giemsa staining microscopic method. Results: CM1 lowered percentage of PRBC in dose-dependent manner with an ED
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Aims: The aim of this study is to report an oral iron chelator phytic acid (PA), on blood samples from different types of thalassaemic patients of various age groups and physical conditions. Study Design: The In vitro iron chelating effect was evaluated by ferritin assay using ELISA. Methodology: Blood from the iron-overloaded 30 Thalassaemic patients of different age groups, body weights and heights were collected and the serum was separated. Patients without any history of blood transfusion and chelation therapy were taken as control group. The ELISA based ferritin assay was performed with standard phytic acid (40% water solution, Fluka), using Desferrioxamine (DFO) as control (0.5g Deferoxamine mesylate USP, Novartis, USA). The serum ferritin levels were recorded in two different conditions (treated with DFO and PA) at different time intervals (10, 30 and 60 min) by measuring absorbance at 450 nm. Results: The Kolmogorov-Smirnov test of patient samples in two different conditions showed that the ferritin concentration, treated by DFO and PA, was significantly decrease in PA treated group compared to DFO, when used in equivalent concentrations, at intervals of 10 min (P=0.760),30 min (P=0.537) and 60 min (P=0.055). Conclusion: The common iron chelators DFO or Deferiprone used as monotherapy may lead to transient and incomplete removal of iron, while PA showed a more complete and sustained removal of ferritin due to specific chemical binding at a wider pH range. However, further trial is required to establish its maintenance dose, comparative efficacy and mechanism of action.
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<p><b>OBJECTIVE</b>To evaluate the iron-chelating properties and free-radical scavenging activities of 1-(N-acetyl-6-aminohexyl)-3-hydroxy-2-methylpyridin-4-one (CM1) treatment in chronic iron-loaded β-thalassemic (BKO) mice.</p><p><b>METHODS</b>The BKO mice were fed with a ferrocene-rich diet and were orally administered with CM1 [50 mg/(kg.day)] for 6 months. Blood levels of non-transferrin bound iron, labile plasma iron, ferritin (Ft) and malondialdehyde were determined.</p><p><b>RESULTS</b>The BKO mice were fed with an iron diet for 8 months which resulted in iron overload. Interestingly, the mice showed a decrease in the non-transferrin bound iron, labile plasma iron and malondialdehyde levels, but not the Ft levels after continuous CM1 treatment.</p><p><b>CONCLUSIONS</b>CM1 could be an effective oral iron chelator that can reduce iron overload and lipid peroxidation in chronic iron overload β-thalassemic mice.</p>
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Objective: To evaluate the iron-chelating properties and free-radical scavenging activities of 1-(N-acetyl-6-aminohexyl)-3-hydroxy-2-methylpyridin-4-one (CM1) treatment in chronic iron-loaded β-thalassemic (BKO) mice. Methods: The BKO mice were fed with a ferrocene-rich diet and were orally administered with CM1 [50 mg/(kg.day)] for 6 months. Blood levels of non-transferrin bound iron, labile plasma iron, ferritin (Ft) and malondialdehyde were determined. Results: The BKO mice were fed with an iron diet for 8 months which resulted in iron overload. Interestingly, the mice showed a decrease in the non-transferrin bound iron, labile plasma iron and malondialdehyde levels, but not the Ft levels after continuous CM1 treatment. Conclusions: CM1 could be an effective oral iron chelator that can reduce iron overload and lipid peroxidation in chronic iron overload β-thalassemic mice.
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La sobrecarga de hierro es una complicación frecuente en un número importante de enfermedades hematológicas que cursan con anemia y requieren transfusiones sanguíneas como parte de su terapia. Entre ellas se destacan la talasemia, la drepanocitosis, los síndromes mielodisplásicos, la anemia de Blackfan-Diamond, la anemia de Fanconi y la deficiencia de piruvato quinasa, La sobrecarga de hieroo tambiún se presenta en otras enfermedades tales como la hemocromatosis hereditaria, la hepatitis viral, el síndrome metabólico y determinados trastornos neurovegetativos. El diagnóstico de sobrecarga suele hacerse mediante la determinación del hierro sérico no unido a la transferrina, la ferritina sérica y un aumento de la concentración hepática de hierro. Las consecuencias más importantes del efecto tóxico de un exceso de hierro son las disfunciones cardíacas y endocrinas, debidas al efecto oxidante del hierro sobre las membranas celulares, con el consiguiente daño celular. Tales alteraciones contribuyen al incremento de la morbilidad y la mortalidad en estos pacientes. El tratamiento consiste básicamente en el usode agentes quelantes de hierro que facilitan la excreción del exceso del metal y reducen su efecto tóxico, Entre tales agentes se cuentan la deferrioxamina (de uso intravenoso). y móa recientemente el deferiprone (ambos de uso orak)
Iron overload is a frequent complication in patients with hematological diseases which develop anemía and require blood transfusion as a therapeutic measure. Thalassemia, drepanocytosis, myelodisplastic syndromes, Blackfan-Diamond anemia, Franconi anemia and pyruvate kinase deficiency are the most common of these diseases. Iron overload is the hallmark of hereditary hemochromatosis, and also complicates diseases such as viral hepatitis, the metabolic syndrome, and certain neurovegetative disfunctions. The diagnosis of iron overload is commonly established through the evaluation of serum iron, transferrin saturation, serum ferritin and liver iron concentration. Cardiac and endocrine dysfunctions are the most important consequences of the toxic efffect of iron accumulation; these are due to the oxidixing effect of iron upon the cellular membranes, followed by cellular damage. Such alterations contribute to the increased morbility and mortality rates in these patients. The treatment of iron overload is based mainly on the use of iron chelators which facilitate the excretion of iron excess and reduce its toxic effect. Deferrioxamine (for intravenous use), and more recently deferiprone and deferasirox (both for oral administration) are the drugs of choice
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Humanos , Masculino , Femenino , Anemia/genética , Enfermedades Hematológicas/complicaciones , Sobrecarga de Hierro/patología , Sobrecarga de Hierro/sangre , Hemocromatosis/etiología , Talasemia/etiología , Transfusión Sanguínea/métodosRESUMEN
There is an unmet need in progressive neurodegenerative diseases such as Parkinson's and Alzheimer's diseases. The present therapeutics for these diseases at best is symptomatic and is not able to delay disease or possess disease modifying activity. Thus an approach to drug design should be made to slow or halt progressive course of a neurological disorder by interfering with a disease-specific pathogenetic process. This would entail the ability of the drug to protect neurons by blocking the common pathway for neuronal injury and cell death and the ability to promote regeneration of neurons and restoration of neuronal function. We have now developed a number of multi target drugs which possess neuroprotective, and neurorestorative activity as well as being able to active PGC-1alpha (peroxisome proliferator-activated receptor gamma coactivator-1alpha), SIRT1 (NAD-dependent deacetylase protein) and NTF (mitochondrial transcription factor) that are intimately associated with mitochondrial biogenesis.
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Muerte Celular , Diseño de Fármacos , Enfermedades del Sistema Nervioso , Enfermedades Neurodegenerativas , Neuronas , Enfermedad de Parkinson , Regeneración , Células Madre , Biogénesis de OrganelosRESUMEN
Objective: Seven to eight days germinated plants of Triticum aestivum (wheat grass) are a rich source of vitamin A, C, calcium, magnesium, phosphorus, potassium, sodium, sulphur, cobalt, zinc and protein. Traditionally the aqueous extract of T. aestivum was reported to be used as a health tonic in folk and ayurvedic medicine. We previously reported that aqueous extract of T. aestivum was found to reduce the blood transfusion requirement in iron overloaded Thalassemia and Myelodysplastic syndrome patients. Our objective was to extract and purify active ingredients from wheat grass and study their mode of action in stabilizing hemoglobin level in those patients. Design and Method: Active ingredients of wheat grass were extracted and purified by cation exchange column chromatography followed by High Performance Liquid Chromatography. In vitro experiments with phenylhydrazine treated red blood cell hemolysate were carried out before and after treatment of purified fraction of T. aestivum to study iron chelating activity. Result: Purified fraction of T. aestivum treated red blood cell showed significant inhibition of free reactive iron production and formation of thio-barbituric acid reactive substances when compared to desferrioxamine treated hemolysate. Conclusion: Iron chelating activity of purified fraction of T. aestivum, an inexpensive, easily available source, is very promising for further clinical trial and development of oral iron chelator drug for Thalassemia, Myelodysplastic syndrome and other iron overloaded diseases.
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Intracerebral hemorrhage (ICH) is a common nervous system disease, its mortality and disability are very high. However, the mechanisms of brain injury after ICH have not yet been fully explained. "[he latest studies have suggested that iron overloading plays an important role in the brain injury after ICH. This article reviews the advances in research on the distribution and function of iron in the brain, the mechanisms of brain injury caused by iron overloading after ICH as well as the use of iron chelator.
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A series of pathophysiologic changes in brain tissues will occur after intracerebral hemorrhage, including the enlargement of hematoma, metabolism abnormality in perihematoma tissues, and formation of cerebral edema. Recent researches have demonstrated that iron ions play an important role in the secondary brain injury after intracerebral hemorrhage. Iron chelator can block iron-induced injury process by specifically binding iron ions. This article reviews the changes of iron metabolism, iron-related mechanisms of brain injury, and the neuroprotective effect of iron chelator.