ArticleMolecular neurobiology2017
Effects of Toll-Like Receptor 4 Antagonists Against Cerebral Vasospasm After Experimental Subarachnoid Hemorrhage in Mice.
Article in Molecular neurobiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 2 of them syntheses that pooled it.
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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.
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Who cites it
36 citing papers in PubMed, 2 syntheses or guidelines pooled it, 61 citations in OpenAlex.
- Meta-review on Perforation Model of Subarachnoid Hemorrhage in Mice: Filament Material as a Possible Moderator of Mortality.Translational stroke research · 2024Pooled it
- Role of Adaptor Protein Myeloid Differentiation 88 (MyD88) in Post-Subarachnoid Hemorrhage Inflammation: A Systematic Review.International journal of molecular sciences · 2021Pooled it
- Targeting the intestinal TLR4-GABAJournal of neuroinflammation · 2026Article
- Article
- Tenascin-C as a Target for Intervention in Delayed Cerebral Ischemia After Subarachnoid Hemorrhage.Acta neurochirurgica. Supplement · 2025Review
- Article
- TAK-3 Inhibits Lipopolysaccharide-Induced Neuroinflammation in Traumatic Brain Injury Rats Through the TLR-4/NF-κB Pathway.Journal of inflammation research · 2024Article
- Protective effect of IAXO-102 on renal ischemia-reperfusion injury in rats.Journal of medicine and life · 2023Article
- Review
- Roles of glutamate in brain injuries after subarachnoid hemorrhage.Histology and histopathology · 2022Review
- Astrocytic NDRG2-PPM1A interaction exacerbates blood-brain barrier disruption after subarachnoid hemorrhage.Science advances · 2022Article
- The blood-brain barrier and the neurovascular unit in subarachnoid hemorrhage: molecular events and potential treatments.Fluids and barriers of the CNS · 2022Review
- Melatonin affects hypoxia-inducible factor 1α and ameliorates delayed brain injury following subarachnoid hemorrhage via H19/miR-675/HIF1A/TLR4.Bioengineered · 2022Article
- Article
- Specific signature biomarkers highlight the potential mechanisms of circulating neutrophils in aneurysmal subarachnoid hemorrhage.Frontiers in pharmacology · 2022Article
- Inflammatory role of microglia in brain injury caused by subarachnoid hemorrhage.Frontiers in cellular neuroscience · 2022Review
- Inflammation and immune cell abnormalities in intracranial aneurysm subarachnoid hemorrhage (SAH): Relevant signaling pathways and therapeutic strategies.Frontiers in immunology · 2022Review
- Renoprotective Potential of the Ultra-Pure Lipopolysaccharide from Rhodobacter Sphaeroides on Acutely Injured Kidneys in an Animal Model.Archives of Razi Institute · 2021Article
- Toll-Like Receptor Signaling Pathways: Novel Therapeutic Targets for Cerebrovascular Disorders.International journal of molecular sciences · 2021Review
- Cerebrovascular pathophysiology of delayed cerebral ischemia after aneurysmal subarachnoid hemorrhage.Histology and histopathology · 2021Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Toll-like receptor 4 (TLR4) signaling may play a crucial role in the occurrence of cerebral vasospasm after subarachnoid hemorrhage (SAH). The main purpose of this study was to assess if selective blockage of TLR4 on cerebral arteries prevents cerebral vasospasm development and neurological impairments after SAH in mice. One hundred fourteen mice underwent endovascular perforation SAH or sham operation and were randomly divided into the following 6 groups: sham+vehicle, sham+LPS-RS ultrapure 8 μg, sham+LPS-RS ultrapure 40 μg, SAH+vehicle, SAH+LPS-RS ultrapure 8 μg, and SAH+LPS-RS ultrapure 40 μg. A selective TLR4 antagonist, LPS-RS ultrapure (8 or 40 μg), was administered intracerebroventricularly to mice at 30 min, and the effects were evaluated by neurobehavioral tests and India-ink angiography at 24-48 h, and Western blotting and immunohistochemistry on cerebral arteries at 24 h post-SAH. Higher but not lower dosages of LPS-RS ultrapure significantly prevented post-SAH neurological impairments and ameliorated cerebral vasospasm. SAH caused TLR4 activation and cyclooxygenase-1 (COX1) upregulation in the endothelial cells and smooth muscle cells of spastic cerebral arteries, both of which were significantly suppressed by LPS-RS ultrapure. Another selective TLR4 antagonist, IAXO-102, which has a different binding site from LPS-RS ultrapure, also showed similar protective effects to LPS-RS ultrapure. These findings suggest that TLR4 signaling is implicated in cerebral vasospasm development at least partly via COX1 upregulation, and that TLR4 antagonists have therapeutic potential as a new therapy against cerebral vasospasm.
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Registered trials
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