Evidence map›Paper›PMID 42792207›Full record

ArticleAntioxidants (Basel, Switzerland)2026

Resveratrol's Neuroprotective Effects on the Retina in a Pentylenetetrazol-Induced Epilepsy Model in Rats: Insights into SIRT1 Signaling, Apoptosis, and Gliosis.

Omer Unal, Nilufer Akgun-Unal, Elif Gulbahce-Mutlu, Seda Simsek, Mustafa Ayyildiz

Abstract read
In one paragraph

Article in Antioxidants (Basel, Switzerland), 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

What it found

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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

5 authors.

Omer UnalDepartment of Physiology, Faculty of Medicine, Samsun University, 55080 Samsun, Türkiye.ORCID 0000-0002-4816-830X
Nilufer Akgun-UnalDepartment of Biophysics, Faculty of Medicine, Ondokuz Mayis University, 55139 Samsun, Türkiye.ORCID 0000-0001-7750-482X
Elif Gulbahce-MutluDepartment of Medical Biology, Faculty of Medicine, KTO Karatay University, 42020 Konya, Türkiye.
Seda SimsekDepartment of Histology and Embryology, Faculty of Medicine, Selcuk University, 42130 Konya, Türkiye.ORCID 0000-0003-4237-5831
Mustafa AyyildizDepartment of Physiology, Faculty of Medicine, Ondokuz Mayis University, 55139 Samsun, Türkiye.ORCID 0000-0002-6594-3080

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND/

objectivesA chronic neurological disorder known as epilepsy results in neurodegeneration, oxidative stress, and damage to the retina and the central nervous system's structure. The main objective of this research was to examine the neuroprotective benefits of Resveratrol (RES) on the retina in a model using Pentylenetetrazol (PTZ) in rats to induce kindling and to investigate the underlying molecular and biochemical mechanisms (SIRT1, GFAP, VEGF, apoptotic pathways, and oxidative stress markers [malondialdehyde (MDA) and reduced glutathione (GSH)] of this protective effect.

methodsA total of thirty-two male Wistar albino rats were randomly assigned to four distinct groups: Sham, RES (5 mg/kg/day), PTZ (35 mg/kg), and PTZ + RES (

resultsSubstantial increases in seizure scores and electrocorticogram spike counts were noted in the PTZ group, whereas RES treatment significantly reduced the total ECoG spike count by 49.6% (from 702.87 ± 145.82 in PTZ to 354.25 ± 31.22 in PTZ + RES,

conclusionsChronic epilepsy causes glial activation, oxidative damage, and apoptosis in the retina, with RES-associated retinal protection involving the restoration of redox homeostasis and the upregulation of the SIRT1 signaling pathway. These preclinical findings suggest that RES represents a promising protective strategy against epilepsy-associated retinal damage, though further clinical validation is warranted to establish its therapeutic safety and efficacy in human patients.

Indexed as

apoptosisepilepsyGFAPPTZresveratrolretinaSIRT1

Identifiers

PMID42792207
PMCPMC13603480

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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 OpenQuestion graph.