ArticleBiomaterials2021
Antioxidant thioether core-crosslinked nanoparticles prevent the bilateral spread of secondary injury to protect spatial learning and memory in a controlled cortical impact mouse model of traumatic brain injury.
Article in Biomaterials, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
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The trial behind it
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Who cites it
22 citing papers in PubMed, 56 citations in OpenAlex.
- Thiol-Based Neuroprotective Copolymers Acutely Restore Redox Metabolism and Mediate Vasogenic Edema in a Mouse Model of Traumatic Brain Injury.Macromolecular bioscience · 2026Article
- Immunoaffinity-Mimetic Assembly of Peptide-Aptamer Conjugates and Stem Cell-Derived Exosomes into Hierarchical Microgels for Spinal Cord Injury Repair.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Neuroprotective effects of cobalt oxide nanoparticles through mitigating oxidative stress and reactive glial responses in traumatic brain injury.Materials today. Bio · 2025Article
- Advances in research on biomaterials and stem cell/exosome-based strategies in the treatment of traumatic brain injury.Acta pharmaceutica Sinica. B · 2025Review
- Stimuli-Responsive Nanomedicines for the Treatment of Non-cancer Related Inflammatory Diseases.ACS nano · 2025Review
- Optimal Timing of Exercise for Enhanced Learning and Memory: Insights From CA1 and CA3 Regions in Traumatic Brain Injury Model in Male Rats.Brain and behavior · 2025Article
- Claudin-1 impairs blood-brain barrier by downregulating endothelial junctional proteins in traumatic brain injury.Tissue barriers · 2025Article
- Deferoxamine Induces Autophagy Following Traumatic Brain Injury via TREM2 on Microglia.Molecular neurobiology · 2024Article
- Ring Opening Functionalization of Thiolactone Homopolymers for ROS Scavenging.Journal of polymer science (2020) · 2024Article
- Nicotine suppresses crystalline silica-induced astrocyte activation and neuronal death by inhibiting NF-κB in the mouse hippocampus.CNS neuroscience & therapeutics · 2024Article
- Applications of hydrogels and nanoparticles in the treatment of traumatic brain injury.Frontiers in bioengineering and biotechnology · 2024Review
- Antioxidant theranostic copolymer-mediated reduction in oxidative stress following traumatic brain injury improves outcome in a mouse model.Advanced therapeutics · 2023Article
- Cellular Antioxidant, Anti-Inflammatory, and Antiproliferative Activities from the Flowers, Leaves and Fruits ofMolecules (Basel, Switzerland) · 2023Article
- An updated Barnes maze protocol for assessing the outcome of controlled cortical impact mouse models of traumatic brain injury.Journal of neuroscience methods · 2023Article
- Sex-based differences of antioxidant enzyme nanoparticle effects following traumatic brain injury.Journal of controlled release : official journal of the Controlled Release Society · 2023Article
- Nanoparticle-based drug delivery for the treatment of traumatic brain injury.Expert opinion on drug delivery · 2023Review
- Integrated printed BDNF-stimulated HUCMSCs-derived exosomes/collagen/chitosan biological scaffolds with 3D printing technology promoted the remodelling of neural networks after traumatic brain injury.Regenerative biomaterials · 2023Article
- The Potential Role of mAntioxidants (Basel, Switzerland) · 2022Review
- Insulin-incubated palladium clusters promote recovery after brain injury.Journal of nanobiotechnology · 2022Article
- Theranostic Copolymers Neutralize Reactive Oxygen Species and Lipid Peroxidation Products for the Combined Treatment of Traumatic Brain Injury.Biomacromolecules · 2022Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
The secondary phase of traumatic brain injury (TBI) is partly caused by the release of excess reactive oxygen species (ROS) from the primary injury. However, there are currently no therapies that have been shown to reduce the secondary spread of injury beyond the primary insult. Nanoparticles offer the ability to rapidly accumulate and be retained in injured brain for improved target engagement. Here, we utilized systemically administered antioxidant thioether core-cross-linked nanoparticles (NP1) that scavenge and inactivate ROS to reduce this secondary spread of injury in a mild controlled cortical impact (CCI) mouse model of TBI. We found that NP1 treatment protected CCI mice from injury induced learning and memory deficits observed in the Morris water maze (MWM) test at 1-month post-CCI. This protection was likely a result of NP1-mediated reduction in oxidative stress in the ipsilateral hemisphere as determined by immunofluorescence imaging of markers of oxidative stress and the spread of neuroinflammation into the contralateral hippocampus as determined by immunofluorescence imaging of activated microglia and neuron-astrocyte-microglia triad formation. These data suggest NP1-mediated reduction in post-traumatic oxidative stress correlates with the reduction in the spread of injury to the contralateral hippocampus to protect spatial memory and learning in CCI mice. Therefore, these materials may offer an improved treatment strategy to reduce the secondary spread of TBI.
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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.