ArticleJournal of nanobiotechnology2025
Improving epilepsy management by targeting P2 × 7 receptor with ROS/electric responsive nanomicelles.
Article in Journal of nanobiotechnology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
2 citing papers in PubMed.
- Metabolite-neuro-immune relay in chronic pain: spatial-temporal lactate, succinate and itaconate signalling as drivers of glial reprogramming and neuronal sensitisation.Frontiers in pharmacology · 2026Review
- Transcriptomic decoding of regional cortical vulnerability to drug-resistant epilepsy using 7T MRI.Communications biology · 2025Article
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
backgroundThe intricate pathogenesis of epilepsy, characterized by abnormal neuronal discharges and neuroinflammation, underscores the critical involvement of the adenosine triphosphate (ATP)-P2X purinoceptor 7 (P2 × 7) receptor pathway in inflammation activation. To address this, a reactive oxygen species (ROS)/electric-responsive d-α-tocopheryl polyethylene glycol 1000 succinate (TPGS)-ferrocene-poloxamer nanomicelle (TFP@A) was engineered to deliver the P2 × 7 receptor antagonist A 438,079, aiming to provide a targeted therapeutic strategy for epilepsy management.
methodsThe study meticulously designed and characterized TFP@A for precise drug delivery through various techniques including transmission electron microscopy (TEM), dynamic light scattering (DLS), and high-performance liquid chromatography (HPLC). Cellular uptake and blood-brain barrier (BBB) permeability were evaluated using fluorescein isothiocyanate (FITC)-labeled TFP@A in vitro and in a brain endothelial cell line (bEnd.3) cell BBB model. In vivo distribution and safety assessments were conducted in an epilepsy mouse model. The impact of TFP@A on epilepsy was investigated through seizure analysis, electroencephalogram (EEG) recordings, and inflammatory pathway assessment.
resultsTFP@A exhibited a robust drug release profile under ROS and electrical stimulation conditions. In vitro studies demonstrated its efficacy in scavenging ROS, reducing oxidative stress, and alleviating cell apoptosis in epilepsy models. Efficient cellular uptake, BBB penetration, and in vivo accumulation in the brain were observed. Notably, TFP@A effectively modulated the P2 × 7 receptor (P2 × 7R)-nucleotide-binding oligomerization domain-like receptor family pyrin domain-containing 3 (NLRP3) pathway, inhibiting inflammatory mediators and promoting anti-inflammatory responses.
conclusionTFP@A loaded with the P2 × 7 receptor antagonist showcases potential therapeutic benefits in suppressing NLRP3 inflammasome activation, mitigating microglial-neuron crosstalk, and ameliorating epilepsy symptoms, positioning it as a promising avenue for targeted epilepsy treatment.
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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.