ArticleBiological trace element research2026
Toxicity Validation of Cerium Oxide Nanoparticles and Mechanism of Action in the Treatment of Cerebral Ischemia-reperfusion Injury.
Article in Biological trace element research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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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.
The trial behind it
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Who cites it
1 citing paper in PubMed.
- Hydrogen Sulfide Protects Against Cerebral Ischemia-Reperfusion Injury in Rats via S-Sulfhydrating NAMPT to Enhance Mitochondrial Function and Autophagy in Cerebrovascular Endothelial Cells.Pharmaceuticals (Basel, Switzerland) · 2026Article
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Authors and funding
8 authors.
Funding
Abstract
Cerebral ischemia-reperfusion injury is a prevalent complication following blood flow restoration in ischemic stroke, which induces severe neurological dysfunction via intricate oxidative stress and inflammatory cascades. Cerium oxide nanoparticles (CeO₂NPs), endowed with unique Ce³⁺/Ce⁴⁺ valence transition properties, exhibit mimetic activities of superoxide dismutase and catalase, enabling efficient scavenging of reactive oxygen species and attenuation of inflammatory responses. This study aimed to investigate the protective effects and underlying molecular mechanisms of CeO₂NPs against cerebral ischemia-reperfusion injury. First, the physicochemical properties and toxicity of CeO₂NPs were systematically characterized: dynamic light scattering (DLS) showed a polydispersity index (PDI) of 0.28 and a ζ-potential of -24.9 mV; transmission electron microscopy (TEM) confirmed a particle size range of 2-6 nm; X-ray photoelectron spectroscopy (XPS) quantification demonstrated 100% Ce coverage on the particle surface. The Morris water maze test indicated no significant neurotoxicity at a dose of 0.4 mg/kg. Subsequently, the therapeutic efficacy was evaluated using a MCAO mouse model. Behavioral assessments revealed that 24 h after reperfusion, the CeO₂NPs-treated group exhibited behavioral performance more comparable to the normal group. Combined with histopathological analysis of brain tissues, these findings confirmed that CeO₂NPs significantly improved neurological function and alleviated brain tissue damage. Proteomics analysis further uncovered that CeO₂NPs mitigate oxidative damage and inflammation primarily by regulating the mitochondrial-mediated apoptotic pathway and superoxide dismutase-related oxidative stress responses. In conclusion, 2-6 nm CeO₂NPs hold great promise as an effective neuroprotective agent for the treatment of cerebral ischemia-reperfusion injury, with their mechanism of action involving multiple cellular protective pathways.
Indexed as
Identifiers
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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 Socratic graph.