ArticleMolecular neurobiology2016
Effect Comparison of Both Iron Chelators on Outcomes, Iron Deposit, and Iron Transporters After Intracerebral Hemorrhage in Rats.
Article in Molecular neurobiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 54 citations in OpenAlex.
- Ironing out mechanisms of ferroptotic death to tailor new stroke therapies.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2026Review
- Ferroptosis associated with secondary brain damage induced by hypertensive underlying biological processes in intracerebral hemorrhage and therapeutic prospects.European journal of medical research · 2026Review
- Quercetin carbon quantum dots: dual-target therapy for intracerebral hemorrhage in mice.Molecular brain · 2025Article
- Nasal exudate for diagnosis of stroke: fundamental studies through iron fractionation, total iron, and targeted protein determinations.Analytical and bioanalytical chemistry · 2024Article
- Advancing stroke recovery: unlocking the potential of cellular dynamics in stroke recovery.Cell death discovery · 2024Review
- DMT1 ubiquitination by Nedd4 protects against ferroptosis after intracerebral hemorrhage.CNS neuroscience & therapeutics · 2024Article
- Amelioration of nephrotoxicity by targeting ferroptosis: role of NCOA4, IREB2, and SLC7a11 signaling.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2024Article
- Targeting Pro-Oxidant Iron with Exogenously Administered Apotransferrin Provides Benefits Associated with Changes in Crucial Cellular Iron Gate Protein TfR in a Model of Intracerebral Hemorrhagic Stroke in Mice.Antioxidants (Basel, Switzerland) · 2023Article
- Neuroprotection of NRF2 against Ferroptosis after Traumatic Brain Injury in Mice.Antioxidants (Basel, Switzerland) · 2023Article
- Review
- Minimally Invasive Surgery for ICH Evacuation Combined With Deferoxamine Treatment Increased Perihematomal Claudin-5 and ZO-1 Expression Levels and Decreased BBB Permeability in Rabbits.Frontiers in neurology · 2022Article
- Elucidating the progress and impact of ferroptosis in hemorrhagic stroke.Frontiers in cellular neuroscience · 2022Review
- Spatial-temporal changes of iron deposition and iron metabolism after traumatic brain injury in mice.Frontiers in molecular neuroscience · 2022Article
- Electroacupuncture Reduces Cerebral Hemorrhage Injury in Rats by Improving Cerebral Iron Metabolism.Mediators of inflammation · 2022Article
- Neuronal ferroptosis after intracerebral hemorrhage.Frontiers in molecular biosciences · 2022Review
- Oxidative Stress Following Intracerebral Hemorrhage: From Molecular Mechanisms to Therapeutic Targets.Frontiers in immunology · 2022Review
- Long non-coding RNA H19 protects against intracerebral hemorrhage injuries via regulating microRNA-106b-5p/acyl-CoA synthetase long chain family member 4 axis.Bioengineered · 2021Article
- Regenerative Potential of Hydrogels for Intracerebral Hemorrhage: Lessons from Ischemic Stroke and Traumatic Brain Injury Research.Advanced healthcare materials · 2021Article
- Targeting NRF2 to suppress ferroptosis in brain injury.Histology and histopathology · 2021Review
- Deferiprone Treatment in Aged Transgenic Tau Mice Improves Y-Maze Performance and Alters Tau Pathology.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2021Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Iron overload plays a key role in brain injury after intracerebral hemorrhage (ICH). We explored the roles of ferric iron chelator-deferiprone (DFP)-and ferrous iron chelator-clioquinol (CQ)-in ICH rats through the outcomes, iron deposits, reactive oxygen species (ROS), brain water content, and related iron transporters. One hundred eight Sprague-Dawley rats received intra-striatal infusions of 0.5 U of type IV collagenase to establish ICH models. The rats were randomly assigned to the sham, vehicle, DFP, and CQ groups. We evaluated the outcomes, iron levels, brain water content, and ROS; meanwhile, immunohistochemistry and real-time quantitative polymerase chain reaction (RT-qPCR) were utilized to determine ferritin, transferrin, transferrin receptor, divalent metal transport 1 (DMT1), and ferroportin at 48 and 72 h, 7 and 14 days after surgery. Our results showed ICH induced iron overload, brain edema, ROS formation, and neurological deficits. Both iron chelators decreased iron levels; CQ improved the neurological outcome, attenuated brain edema, and ROS production. DFP reduced iron contents but not brain water content and ROS generation. DFP failed to improve the outcome. ICH initiated endogenous iron chelators and transporters, both exogenous iron chelators enhanced expression of transferrin and transferrin receptor. CQ enhanced expression of ferroportin but not DMT1, while DFP enhanced expression of DMT1 but not ferroportin. Ferrous iron contributed to brain injury, and binding ferrous iron can modestly improve outcome after ICH in rats. The exogenous ferrous iron chelator possibly functioned via endogenous ferrous iron transporters on ICH. Therefore, ferrous iron may be a promising target for ICH in future.
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