ArticleStroke2019
Complement Inhibition Attenuates Early Erythrolysis in the Hematoma and Brain Injury in Aged Rats.
Article in Stroke, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
36 citing papers in PubMed, 47 citations in OpenAlex.
- Lipid metabolism, microglia, and stroke.Neural regeneration research · 2026Article
- Microglia‑mediated neuroinflammation in intracerebral hemorrhage: Pathological mechanisms and implications for therapeutic development (Review).International journal of molecular medicine · 2026Review
- The Glymphatic System and Meningeal Lymphatics: Current Understandings and Future Perspectives.MedComm · 2026Review
- The Interaction of Neutrophil Extracellular Traps and Complement in Intracerebral Hemorrhage.Cellular and molecular neurobiology · 2026Review
- Red Blood Cell-Derived Exosomes Deliver Complement C5 to Exacerbate Neuroinflammation and Neuronal Injury after Intracerebral Hemorrhage.Inflammation · 2026Article
- Recent research progress and future directions of intracerebral hemorrhage.Frontiers in immunology · 2026Review
- Potential Therapeutic Targets and Emerging Strategies to Promote Hematoma Resolution in Intracerebral Hemorrhage.Revista de neurologia · 2025Review
- The Role of Complement C1qa in Experimental Intracerebral Hemorrhage.Translational stroke research · 2025Article
- Complement Inhibition Reduces Early Erythrolysis, Attenuates Brain Injury, Hydrocephalus, and Iron Accumulation after Intraventricular Hemorrhage in Aged Rats.Translational stroke research · 2025Article
- Unraveling cell death mechanisms in traumatic brain injury: dynamic roles of ferroptosis and necroptosis.Molecular biology reports · 2025Review
- Inclusion Complex of Nimodipine with Sulfobutylether-β-cyclodextrin: Preparation, Characterization, In Vitro and In Vivo Evaluation.AAPS PharmSciTech · 2025Article
- The Role of the Complement System in Synaptic Pruning after Stroke.Aging and disease · 2024Review
- Attenuation of ventriculomegaly and iron overload after intraventricular hemorrhage by membrane attack complex inhibition.Journal of neurosurgery · 2024Article
- The complement system in neurodegenerative diseases.Clinical science (London, England : 1979) · 2024Article
- Neuroinflammation in Acute Ischemic and Hemorrhagic Stroke.Current neurology and neuroscience reports · 2023Review
- Animal models for the study of intracranial hematomas (Review).Experimental and therapeutic medicine · 2023Review
- The Critical Role of Erythrolysis and Microglia/Macrophages in Clot Resolution After Intracerebral Hemorrhage: A Review of the Mechanisms and Potential Therapeutic Targets.Cellular and molecular neurobiology · 2023Review
- Therapeutic strategies to recover ependymal barrier after inflammatory damage: relevance for recovering neurogenesis during development.Frontiers in neuroscience · 2023Review
- High plasma complement C4 levels as a novel predictor of clinical outcome in intracerebral hemorrhage.Frontiers in aging neuroscience · 2023Article
- Brain edema formation and therapy after intracerebral hemorrhage.Neurobiology of disease · 2023Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Background and Purpose- Early erythrolysis in the hematoma contributes to brain injury after intracerebral hemorrhage (ICH). This study investigated the effects of N-acetylheparin, a complement inhibitor, and aurin tricarboxylic acid, a membrane attack complex inhibitor, on early erythrolysis, brain iron deposition, and brain injury in aged rats. Methods- There were 3 parts in the study. First, aged (18 months old) male Fischer 344 rats had an ICH. The time course of erythrolysis in the hematoma was determined by T2* weighted magnetic resonance imaging, and the expression of CD163 was examined. Second, aged rats had an ICH with N-acetylheparin or vehicle. Rats were euthanized at days 1, 3, and 28 after magnetic resonance imaging (T2-, T2*-weighted, and T2* array) and behavioral tests. Brains were used for immunohistochemistry. Third, aged rats had an ICH with avaurin tricarboxylic acid or vehicle. The rats had magnetic resonance imaging and behavioral tests and were euthanized at day 3. Brains were used for immunohistochemistry. Results- Early erythrolysis occurred within the clot in aged F344 rats. There were increased numbers of CD163-positive cells after ICH. Almost all perihematomal CD163-positive cells were microglia/macrophages, while positive neurons were found more distant from the hematoma. Coinjection of N-acetylheparin attenuated erythrolysis, iron accumulation, CD163 expression, microglia activation, brain swelling, and neuronal death in the acute phase, as well as reducing brain atrophy and neurological deficits in the chronic phase. Coinjection of aurin tricarboxylic acid also reduced erythrolysis and ICH-induced brain injury. Conclusions- Inhibiting complement activation resulted in less erythrolysis and brain injury after ICH.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.