ArticleMetabolites2025
Metabolomics-Based Study on the Anticonvulsant Mechanism of
Article in Metabolites, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 2 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
- Correction: Chen et al. Metabolomics-Based Study on the Anticonvulsant Mechanism ofMetabolites · 2025Article
- Antiepileptic Effects ofBiology · 2025Article
Corrections and comments
- Erratum issued
Authors and funding
4 authors.
Funding
Abstract
BACKGROUND/
objectivesEpilepsy is a common chronic and recurrent neurological disorder that poses a threat to human health, and
methodsAn epileptic model of rats was established using pentylenetetrazol. The potential targets and pathways of ATS were predicted by network pharmacology. Ultra Performance Liquid Chromatography-Quadrupole-Time of Flight Mass Spectrometrynce Liquid Chromatography-Quadrupole-Time of Flight Mass Spectrometryance Liquid Chromatography-Quadrupole-Time of Flight Mass Spectrometry and statistical analyses were used to profile plasma metabolites and identify ATS's effects on epilepsy.
resultsKyoto Encyclopedia of Genes and Genomes enrichment analysis revealed that ATS was involved in regulating multiple signaling pathways, mainly including the neuroactive ligand-receptor interaction and GABAerGamma-aminobutyrate transaminaseAminobutyrate Transaminaseapse signaling pathway. ATS treatment restored 19 metabolites in epiGamma-aminobutyrate transaminaseminobutyrate Transaminase rats, affecting lysine, histidine, and purine metabolism. GABA-T was found as a new key target for treating epilepsy with ATS. The IC
conclusionsThese results improved our understanding of epilepsy and ATS treatment, potentially leading to better therapies. The identification of key metabolites and their associated pathways in this study offers potential novel therapeutic targets for epilepsy. By modulating these metabolites, future therapies could be designed to better manage the disorder. Moreover, the insights from network pharmacology can guide the development of more effective antiepileptic drugs, paving the way for improved clinical outcomes for patients.
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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.