ArticleJournal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism2015
TAK-242, an antagonist for Toll-like receptor 4, protects against acute cerebral ischemia/reperfusion injury in mice.
Article in Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 104 papers.
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Who cites it
104 citing papers in PubMed, 186 citations in OpenAlex.
- Review
- Neuroinflammation after stroke: initiation, amplification and therapeutic prospects.Journal of translational medicine · 2026Review
- Principal Component-Based Comprehensive Physical Health Score Associates With Long-Term Death in Patients With Ischemic Stroke.Journal of the American Heart Association · 2026Article
- Targeting the intestinal TLR4-GABAJournal of neuroinflammation · 2026Article
- Bimodal regulation and precision therapy of neutrophil extracellular traps in liver ischemia-reperfusion injury: recent advances.Frontiers in immunology · 2026Review
- Acupuncture in Cerebral Ischemia-Reperfusion Injury: A Mechanistic Narrative Review of Innate Immune Sensing and Regulated Cell Death-Related Inflammatory Amplification.International journal of general medicine · 2026Review
- Late-Stage Activation of Toll-like receptor 3 Alleviates Cognitive Impairment and Neuropathology in an Alzheimer's Disease Mouse Model.Molecular neurobiology · 2025Article
- Elucidating the association between TLR-4 expression and the clinical course of glioblastoma leptomeningeal disease.British journal of cancer · 2025Article
- IFP35, a novel DAMP, aggravates neuroinflammation following acute ischemic stroke via TLR4/NF-κB/NLRP3 signaling.Journal of neuroinflammation · 2025Article
- The opposite effect of ELP4 and ZEB2 on TCF7L2-mediated microglia polarization in ischemic stroke.Journal of cell communication and signaling · 2025Article
- The Extract ofCurrent neuropharmacology · 2025Article
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- Potential effects of Resatorvid and alpha lipoic acid on gentamicin-induced nephrotoxicity in rats.Pharmacology research & perspectives · 2024Article
- Ischemic stroke and diabetes: a TLR4-mediated neuroinflammatory perspective.Journal of molecular medicine (Berlin, Germany) · 2024Review
- Cerebroprotective Effects of the TLR4-Binding DNA Aptamer ApTOLL in a Rat Model of Ischemic Stroke and Thrombectomy Recanalization.Pharmaceutics · 2024Article
- Intracerebral hemorrhage-induced brain injury in mice: The role of peroxiredoxin 2-Toll-like receptor 4 inflammatory axis.CNS neuroscience & therapeutics · 2024Article
- Article
- Inflammatory signaling pathways in the treatment of Alzheimer's disease with inhibitors, natural products and metabolites (Review).International journal of molecular medicine · 2023Review
- The herbicide glyphosate inhibits hippocampal long-term potentiation and learning through activation of pro-inflammatory signaling.Scientific reports · 2023Article
44 more citing papers are in PubMed but not listed here.
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
Toll-like receptor 4 (TLR4) contributes to cerebral ischemia/reperfusion (I/R) injury and is a potential target for the treatment of ischemic stroke. This experiment is to evaluate the effect of an exogenous TLR4 antagonist, TAK-242, against acute cerebral I/R injury. A mouse model of cerebral I/R was induced by transient middle cerebral artery occlusion. TAK-242 (3 mg/kg body weight) was injected intraperitoneally 1 hour after ischemia. Our results showed that the concentration of TAK-242 in plasma increased to 52.0 ng/mL 3 hours after injection, was maintained at 54.1 ng/mL 8 hours after injection, and decreased to 22.6 ng/mL 24 hours after injection. The concentration of TAK-242 in brain tissue increased to 26.1 ng/mL in ischemic hemisphere and 14.2 ng/mL in nonischemic hemisphere 3 hours after injection, and was maintained at the similar levels 24 hours after injection. We found that TAK-242 significantly reduced cerebral infarction compared with vehicle control, improved neurologic function, inhibited the phosphorylation of downstream protein kinases in TLR4 signaling pathway, and downregulated the expression of inflammatory cytokines. We conclude that TAK-242 is able to cross blood-brain barrier, blocks TLR4 signaling, mediates the expression of inflammatory cytokines, and protects the brain from acute damage induced by I/R.
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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.