ArticleNeurochemical research2012
Poloxamer-188 attenuates TBI-induced blood-brain barrier damage leading to decreased brain edema and reduced cellular death.
Article in Neurochemical research, 2012. 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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Who cites it
36 citing papers in PubMed, 2 syntheses or guidelines pooled it, 70 citations in OpenAlex.
- Application of Aquaporins as Markers in Forensic Pathology: A Systematic Review of the Literature.International journal of molecular sciences · 2024Pooled it
- Poloxamer 188 (P188), A Potential Polymeric Protective Agent for Central Nervous System Disorders: A Systematic Review.Current neuropharmacology · 2022Pooled it
- Unlocking therapeutic potential in traumatic brain injury: exploring microenvironmental targets, signaling pathways and translational hurdles.Inflammopharmacology · 2025Review
- Cardioprotection by poloxamer 188 is mediated through increased endothelial nitric oxide production.Scientific reports · 2025Article
- Bundle-specific tractography approach for identifying white matter microstructural changes following traumatic brain injury in rats: An EpiBioS4Rx study.Imaging neuroscience (Cambridge, Mass.) · 2025Article
- Effects of poloxamer 188 on traumatic brain injury.Brain, behavior, & immunity - health · 2024Review
- Vepoloxamer improves functional recovery in rat after traumatic brain injury: A dose-response and therapeutic window study.Neurochemistry international · 2024Article
- Pluronic P85 decreases the delivery of phenytoin to the brain in drug-resistant rats with P-glycoprotein overexpressed chronic mesial temporal lobe epilepsy.IBRO neuroscience reports · 2023Article
- Review
- Consequences of poly(ethylene oxide) and poloxamer P188 on transcription in healthy and stressed myoblasts.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Poloxamer-Based Scaffolds for Tissue Engineering Applications: A Review.Gels (Basel, Switzerland) · 2022Review
- Aquaporin 4 in Traumatic Brain Injury: From Molecular Pathways to Therapeutic Target.Neurochemical research · 2022Review
- Poloxamer-188 Exacerbates Brain Amyloidosis, Presynaptic Dystrophies, and Pathogenic Microglial Activation in 5XFAD Mice.Current Alzheimer research · 2022Article
- Low blood caspase-8 levels in survivor patients of traumatic brain injury.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2021Observational
- Poloxamer 188 Exerts Direct Protective Effects on Mouse Brain Microvascular Endothelial Cells in an In Vitro Traumatic Brain Injury Model.Biomedicines · 2021Article
- Evaluation of In Vitro Neuronal Protection by Postconditioning with Poloxamer 188 Following Simulated Traumatic Brain Injury.Life (Basel, Switzerland) · 2021Article
- Microenvironmental Variations After Blood-Brain Barrier Breakdown in Traumatic Brain Injury.Frontiers in molecular neuroscience · 2021Review
- Pharmacological Approach for Neuroprotection After Cardiac Arrest-A Narrative Review of Current Therapies and Future Neuroprotective Cocktail.Frontiers in medicine · 2021Review
- Poloxamer 188 Attenuates Ischemia-Reperfusion-Induced Lung Injury by Maintaining Cell Membrane Integrity and Inhibiting Multiple Signaling Pathways.Frontiers in pharmacology · 2021Article
- Poloxamer 188 Protects Isolated Adult Mouse Cardiomyocytes from Reoxygenation Injury.Pharmacology research & perspectives · 2020Article
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Plasmalemma permeability plays an important role in the secondary neuronal death induced by traumatic brain injury (TBI). Previous works showed that Poloxamer 188 (P188) could restore the intactness of the plasma membrane and play a cytoprotective action. However, the roles of P188 in blood-brain barrier (BBB) integrity and TBI-induced neural cell death are still not clear. In this study, mice were induced TBI by controlled cortical impact (CCI), and cerebral water content was measured to explore the profile of brain edema after CCI. Further, the regimen of P188 in mouse CCI models was optimized. The neurological test and BBB integrity assessment were performed, and the numbers of TBI-induced neural cell death were counted by propidium iodide (PI) labeling. The expression of apoptotic pathway associated proteins (Bax, cyt-c, caspase-8, caspase-9, caspase-3, P53) and aquaporin-4 (AQP4) was assessed by RT-PCR or immunoblotting. The data showed that the brain edema peaked at 24 h after TBI in untreated animals. Tail intravenous injection of P188 (4 mg/ml, 100 μl) 30 min before TBI or within 30 min after TBI could attenuate TBI-induced brain edema. P188 pre-treatment restored BBB integrity, suppressed TBI-induced neural cell death, and improved neurological function. TBI induced an up-regulation of Bax, cyt-c, caspase-8, caspase-9, caspase-3, and the expression of p53 was down-regulated by P188 pre-treatment. AQP4 mainly located on endothelial cells and astrocytes, and its expression was also regulated by P188 pretreatment. All these results revealed that P188 attenuates TBI-induced brain edema by resealing BBB and regulating AQP4 expression, and suppressed apoptosis through extrinsic or intrinsic pathway. Plasmalemma permeability may be a potential target for TBI treatment.
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