Urinary Metabolic Profiling During Epileptogenesis in Rat Model of Lithium-Pilocarpine-Induced Temporal Lobe Epilepsy

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dc.contributor.authorAntmen, Fatma Merve
dc.contributor.authorMatpan, Emir
dc.contributor.authorDayanc, Ekin Dongel
dc.contributor.authorSavas, Eylem Ozge
dc.contributor.authorEken, Yunus
dc.contributor.authorAcar, Dilan
dc.contributor.authorAk, Alara
dc.date.accessioned2026-04-04T13:31:12Z
dc.date.available2026-04-04T13:31:12Z
dc.date.issued2025
dc.departmentİnönü Üniversitesi
dc.description.abstractBackground/Objectives: Temporal lobe epilepsy (TLE) often develops following an initial brain injury, where specific triggers lead to epileptogenesis-a process transforming a healthy brain into one prone to spontaneous, recurrent seizures. Although electroencephalography (EEG) remains the primary diagnostic tool for epilepsy, it cannot predict the risk of epilepsy after brain injury. This limitation highlights the need for biomarkers, particularly those measurable in peripheral samples, to assess epilepsy risk. This study investigated urinary metabolites in a rat model of TLE to identify biomarkers that track epileptogenesis progression across the acute, latent, and chronic phases and elucidate the underlying mechanisms. Methods: Status epilepticus (SE) was induced in rats using repeated intraperitoneal injections of lithium chloride-pilocarpine hydrochloride. Urine samples were collected 48 h, 1 week, and 6 weeks after SE induction. Nuclear magnetic resonance spectrometry was used for metabolomic analysis, and statistical evaluations were performed using MetaboAnalyst 6.0. Differences between epileptic and control groups were represented using the orthogonal partial least squares discriminant analysis (OPLS-DA) model. Volcano plot analysis identified key metabolic changes, applying a fold-change threshold of 1.5 and a p-value < 0.05. Results: The acute phase exhibited elevated levels of acetic acid, dihydrothymine, thymol, and trimethylamine, whereas glycolysis and tricarboxylic acid cycle metabolites, including pyruvic and citric acids, were reduced. Both the acute and latent phases showed decreased theobromine, taurine, and allantoin levels, with elevated 1-methylhistidine in the latent phase. The chronic phase exhibited reductions in pimelic acid, tiglylglycine, D-lactose, and xanthurenic acid levels. Conclusions: These findings highlight stage-specific urinary metabolic changes in TLE, suggesting distinct metabolites as biomarkers for epileptogenesis and offering insights into the mechanisms underlying SE progression.
dc.description.sponsorshipAcibadem University Scientific Research Projects Commission; [TDK-2023-79]; [118C082]
dc.description.sponsorshipThis research was funded by the Acibadem University Scientific Research Projects Commission (Grant number: TDK-2023-79). Fatma Merve Antmen is supported as a research scholar in the TUBITAK-BIDEB 2244 Industrial Ph.D. Program [Grant Number 118C082].
dc.identifier.doi10.3390/biomedicines13030588
dc.identifier.issn2227-9059
dc.identifier.issue3
dc.identifier.orcid0009-0004-3535-1801
dc.identifier.orcid0009-0009-8600-4099
dc.identifier.orcid0000-0003-0863-1547
dc.identifier.orcid0000-0003-2900-2969
dc.identifier.orcid0000-0002-8814-7351
dc.identifier.orcid0000-0002-8053-7523
dc.identifier.orcid0000-0002-6175-897X
dc.identifier.pmid40149565
dc.identifier.scopus2-s2.0-105000978665
dc.identifier.scopusqualityQ1
dc.identifier.urihttps://doi.org/10.3390/biomedicines13030588
dc.identifier.urihttps://hdl.handle.net/11616/108646
dc.identifier.volume13
dc.identifier.wosWOS:001454018700001
dc.identifier.wosqualityQ1
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoen
dc.publisherMdpi
dc.relation.ispartofBiomedicines
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/openAccess
dc.snmzKA_WOS_20250329
dc.subjectepilepsy
dc.subjecturine
dc.subjectnuclear magnetic resonance
dc.subjectmetabolomics
dc.subjectepileptogenesis
dc.subjectrat
dc.titleUrinary Metabolic Profiling During Epileptogenesis in Rat Model of Lithium-Pilocarpine-Induced Temporal Lobe Epilepsy
dc.typeArticle

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