ArticleStroke2024
Effects of Haptoglobin on Early Brain Injury, Vasospasm, and Lymphatic Drainage After Subarachnoid Hemorrhage in Mice.
Article in Stroke, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- M2 macrophage-derived exosomes delivering haptoglobin and interleukin-10 plasmids for synergistic therapy of intracerebral hemorrhage.Bioactive materials · 2026Article
- Possible Impact of Lymphatic Drainage on Brain Injury After Aneurysmal Subarachnoid Hemorrhage.International journal of molecular sciences · 2026Review
- Haptoglobin and Hemopexin Redirect Heme-Driven Oxidative Stress and Neurotoxicity in Organotypic Brain Slices.ACS chemical neuroscience · 2026Article
- The role of glymphatic system in brain injury after subarachnoid hemorrhage.Frontiers in immunology · 2026Review
- Cerebrospinal fluid haptoglobin levels and outcome after aneurysmal subarachnoid haemorrhage: Evidence from Mendelian randomization.PloS one · 2025Article
- Astrocyte-microglia crosstalk in subarachnoid hemorrhage: mechanisms and treatments.Frontiers in immunology · 2025Review
- When headache meets visual disturbance: An evidence-based review of common and critical entities.Science progressReview
- Sex-specific differences in basilar artery vasospasm after subarachnoid hemorrhage: evidence from a rabbit model.Frontiers in neurologyArticle
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundErythrolysis releases free Hb (hemoglobin), which is one of the most upstream and important molecules causing early brain injury and cerebral vasospasm after subarachnoid hemorrhage (SAH). The purpose of this study was to investigate if a Hb scavenger protein Hp (haptoglobin) supplementation prevents early brain injury and cerebral vasospasm and influences the lymphatic drainage mechanism in an established SAH model of mice by a blood injection into the prechiasmatic cistern.
methodsThis study consisted of 4 parts, with a total of 317 C57BL/6 male mice undergoing sham or SAH modeling, randomly followed by 24-hour intracerebroventricular infusion of no vehicle, 30.1 mg/mL BSA, 30.1 mg/mL Hp (100%; a mixture of Hp1-1, Hp2-1, and Hp2-2), 50% Hp, 25% Hp, and 12.5% Hp solutions from 30 minutes postmodeling. The effects were evaluated at 24 and 48 hours postmodeling.
resultsThe 100%Hp decreased mortality and brain edema until 48 hours post-SAH and suppressed post-SAH neurological impairments, Hb infiltrations into the perivascular spaces and brain tissues, fibrinogen-positive microthrombi formation, microglial activation, and caspase-dependent neuronal apoptosis, as well as large-vessel vasospasm on India-ink angiography at 24 hours compared with vehicle-treated SAH mice. The Hp solutions up to 50% concentrations also prevented post-SAH neurological impairments, and those up to 25% concentrations suppressed post-SAH neuronal apoptosis and vasospasm development until 48 hours. Immunohistochemical staining of deep cervical and mandibular lymph nodes demonstrated that Hb was increased in the lymphatic sinus after SAH and was further increased by Hp administration in SAH animals.
conclusionsThis study first showed that an Hp concentrate prevented early brain injury and cerebral vasospasm by inhibiting Hb penetration into brain tissues and increasing lymphatic drainage of free Hb in an established SAH model of mice.
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