Evidence map›Paper›PMID 42201503›Full record

ArticleMolecular biology reports2026

The relationship of cucurbitacin E with epileptic seizures, circadian rhythm, and genetics in a pentylenetetrazole-induced mouse model of epilepsy.

Sinem Bebek Sarıcı, Özlem Ovayolu, Şenay Görücü Yılmaz

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Article in Molecular biology reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

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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.

2 · The registry

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

3 authors.

Sinem Bebek SarıcıFaculty of Health Science, Department of Internal Medicine, University of Gaziantep, Gaziantep, Turkey. sinem.bebek@sanko.edu.tr.ORCID http://orcid.org/0000-0003-0339-4888
Özlem OvayoluFaculty of Health Science, Department of Internal Medicine, University of Gaziantep, Gaziantep, Turkey. oucan@gantep.edu.tr.ORCID http://orcid.org/0000-0002-7335-4032
Şenay Görücü YılmazFaculty of Health Science, Department of Nutrition and Dietetics, University of Gaziantep, Gaziantep, Turkey. gorucu@gantep.edu.tr.ORCID http://orcid.org/0000-0003-0523-7819

Funding

Gaziantep Üniversitesi SBF.DT.22.06
6 · The paper itself

Abstract

backgroundEpilepsy is a chronic neurological disorder characterized by recurrent seizures resulting from abnormal neuronal electrical activity. Increasing evidence suggests that circadian clock dysfunction contributes to seizure susceptibility and neuronal excitability. Melatonin, a major regulator of circadian rhythm, possesses antioxidant and neuroprotective properties that may influence seizure regulation. Cucurbitacin E (CuE), a triterpenoid compound with potent antioxidant and anti-inflammatory activities, has emerged as a potential therapeutic agent targeting circadian and oxidative pathways. This study investigated the effects of CuE on seizure activity, oxidative balance, melatonin levels, and circadian clock gene expression in a pentylenetetrazol (PTZ)-induced epilepsy model.

methodsEighteen male C57BL/6 mice were randomly assigned to control, PTZ, and PTZ + CuE groups (baseline n = 6/group). PTZ (35 mg/kg/day, i.p.) was administered every other day for 12 days, while CuE (0.5 mg/kg/day, i.p.) was administered 30 min after PTZ injections. Two animals were excluded during the study, resulting in final group sizes of n = 6, n = 5, and n = 5, respectively. Seizure severity was assessed using Racine scoring, and locomotor activity was monitored using the LABORAS system with manual seizure validation. Serum melatonin, total antioxidant status (TAS), total oxidant status (TOS), and circadian clock gene expression (PER1, CRY1, CLOCK, BMAL1, RORA, and REV-ERBα) were analyzed.

resultsPTZ significantly increased seizure severity, oxidative stress, melatonin levels, and disrupted clock gene expression, whereas CuE markedly reduced seizures, improved oxidative balance, normalized melatonin levels, and partially restored circadian gene expression. Significant correlations were identified between melatonin levels and multiple clock genes.

conclusionThese findings demonstrate that CuE exerts anticonvulsant effects through integrated chronomodulatory and antioxidant mechanisms, supporting its potential as a multi-target therapeutic strategy for epilepsy management.

Indexed as

Circadian RhythmEpilepsySeizuresTriterpenesAnimalsAnticonvulsantsAntioxidantsCircadian ClocksDisease Models, AnimalMaleMelatoninMiceMice, Inbred C57BLOxidative StressPentylenetetrazoleAnticonvulsantsAntioxidantscucurbitacin EMelatoninPentylenetetrazoleTriterpenesAnticonvulsantCircadian clock genesCucurbitacin EMelatoninPTZSeizure

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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.