ArticleMolecular and cellular biochemistry2016
Role of hepcidin and its downstream proteins in early brain injury after experimental subarachnoid hemorrhage in rats.
Article in Molecular and cellular biochemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 34 citations in OpenAlex.
- Iron-driven secondary injury after intracranial hemorrhage: mitochondrial dysfunction and ferroptosis.Frontiers in neuroscience · 2026Review
- Serum Hepcidin Levels are Associated with Poor Outcomes of Patients with Severe Traumatic Brain Injury: A Two-Center Observational Analytical Study.International journal of general medicine · 2026Article
- Iron Hemostasis in Patients With Subarachnoid Hemorrhage and the Role of Early CSF Drainage.Neurology · 2025Review
- Acupuncture Alleviates Blood-Brain Barrier Damage After Delayed rtPA Thrombolysis for Acute Ischemic Stroke by Regulating Ferroptosis.Brain and behavior · 2025Article
- Hepcidin and Tissue-Specific Iron Regulatory Networks.Advances in experimental medicine and biology · 2025Review
- Iron Metabolism and Ferroptosis in Early Brain Injury after Subarachnoid Haemorrhage.Molecular neurobiology · 2024Review
- Ferroptosis in early brain injury after subarachnoid hemorrhage: review of literature.Chinese neurosurgical journal · 2024Review
- Hepcidin deficiency impairs hippocampal neurogenesis and mediates brain atrophy and memory decline in mice.Journal of neuroinflammation · 2024Article
- Iron homeostasis and post-hemorrhagic hydrocephalus: a review.Frontiers in neurology · 2023Review
- Ferroptosis and Its Multifaceted Roles in Cerebral Stroke.Frontiers in cellular neuroscience · 2021Review
- Hepcidin Promoted Ferroptosis through Iron Metabolism which Is Associated with DMT1 Signaling Activation in Early Brain Injury following Subarachnoid Hemorrhage.Oxidative medicine and cellular longevity · 2021Article
- Involvement of Hepcidin in Cognitive Damage Induced by Chronic Intermittent Hypoxia in Mice.Oxidative medicine and cellular longevity · 2021Article
- Genetic Variability in the Iron Homeostasis Pathway and Patient Outcomes After Aneurysmal Subarachnoid Hemorrhage.Neurocritical care · 2020Observational
- Article
- Genetic Variability and Trajectories of DNA Methylation May Support a Role for HAMP in Patient Outcomes After Aneurysmal Subarachnoid Hemorrhage.Neurocritical care · 2020Observational
- Deciphering the Iron Side of Stroke: Neurodegeneration at the Crossroads Between Iron Dyshomeostasis, Excitotoxicity, and Ferroptosis.Frontiers in neuroscience · 2019Review
- Hepcidin, an emerging and important player in brain iron homeostasis.Journal of translational medicine · 2018Review
- The Dual Role of Hepcidin in Brain Iron Load and Inflammation.Frontiers in neuroscience · 2018Review
- Brain iron overload following intracranial haemorrhage.Stroke and vascular neurology · 2016Review
- A review of studies on vascular dementia and iron metabolism.Science progressReview
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Early brain injury (EBI) is a major cause of mortality from subarachnoid hemorrhage (SAH). We aimed to study the pathophysiology of EBI and explore the role of hepcidin, a protein involved in iron homeostatic regulation, and its downstream proteins. One hundred and thirty-two male Sprague-Dawley rats were assigned into groups (n = 24/group): sham, SAH, SAH + hepcidin, SAH + hepcidin-targeting small interfering ribonucleic acid (siRNA), and SAH + scramble siRNA. Three hepcidin-targeting siRNAs and one scramble siRNA for hepcidin were injected 24 h before hemorrhage induction, and hepcidin protein was injected 30 min before induction. The rats were neurologically evaluated at 24 h and euthanized at 72 h. Hepcidin, ferroportin-1, and ceruloplasmin protein expression were measured by immunohistochemistry and Western blotting. Brain water content, blood-brain barrier (BBB) leakage, non-heme tissue iron and Garcia scale were evaluated. Hepcidin expression increased in the cerebral cortex and hippocampus after experimental SAH (P < 0.05 compared to sham), while ferroportin-1 and ceruloplasmin decreased (P < 0.05). Hepcidin injection lowered the expression of ferroportin-1 and ceruloplasmin further but siRNA reduced the levels of hepcidin (P < 0.05 compared to SAH) resulting in recovery of ferroportin-1 and ceruloplasmin levels. Apoptosis was increased in SAH rats compared to sham (P < 0.05) and increased slightly more by hepcidin, but decreased by siRNA (P < 0.05 compared to SAH). SAH rats had lower neurological scores, high brain water content, BBB permeability, and non-heme tissue iron (P < 0.05). In conclusion, downregulation of ferroportin-1 and ceruloplasmin caused by hepcidin enhanced iron-dependent oxidative damage and may be the potential mechanism of SAH.
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