Evidence map›Paper›PMID 41424426›Full record

ArticleUlusal travma ve acil cerrahi dergisi = Turkish journal of trauma & emergency surgery : TJTES2025

Neuroprotective effects of hesperidin on cerebral vasospasm after subarachnoid hemorrhage in rats: an experimental study.

Emrah Keskin, Bayram Yılmaz, Mehmet Selim Gel

Abstract read
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Article in Ulusal travma ve acil cerrahi dergisi = Turkish journal of trauma & emergency surgery : TJTES, 2025. 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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4 · The record

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5 · Who and what money

Authors and funding

3 authors.

Emrah KeskinDepartment of Neurosurgery, Zonguldak Bulent Ecevit University Faculty of Medicine, Zonguldak-Türkiye.
Bayram YılmazDepartment of Pathology, Hitit University Faculty of Medicine, Çorum-Türkiye.
Mehmet Selim GelDepartment of Neurosurgery, Trabzon Kanuni Training and Research Hospital, Trabzon-Türkiye.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundSubarachnoid hemorrhage (SAH) is a severe neurological emergency with high morbidity and mortality, primarily due to vasospasm and delayed ischemia. Hesperidin (HSP), a natural flavonoid, possesses strong antioxidant and vasoprotective properties. This experimental animal study examined HSP's neuroprotective role in oxidative stress and vascular remodeling after SAH, focusing on the extracellular regulated kinase 5-Kruppel-like factor 2-endothelial nitric oxide synthase (Erk5-KLF2-eNOS) pathway.

methodsThe study was conducted from 2021 to 2022. Forty female Wistar albino rats were divided into five groups: control (G1, n=8), sham (G2, n=8), SAH + Vehicle (G3, n=8), SAH with low-dose HSP (G4, n=8), and SAH with high-dose HSP (G5, n=8). SAH was induced using a double injection of homologous blood into the cisterna magna. Biochemical markers (superoxide dismutase [SOD], catalase [CAT], glutathione peroxidase [GPx], nitric oxide [NOS]), basilar artery morphometry, and molecular expressions (Erk5, p-Erk5, KLF2, eNOS) were evaluated 48 hours post-SAH.

resultsSAH significantly increased oxidative stress and reduced vascular lumen diameter in untreated rats (G3). Both HSP-treated groups (G4 and G5) showed improved antioxidant enzyme levels (SOD, CAT, GPx) and near-normal NOS levels. Morphometric analysis demonstrated significant preservation of basilar artery lumen diameter in treated groups, with no significant changes in wall thickness. Molecular analysis revealed upregulation of the Erk5-KLF2-eNOS pathway, suggesting a role in vasodilation and mitigation of oxidative stress.

conclusionHSP protects against SAH-induced vasospasm and oxidative damage by enhancing antioxidant capacity and modu-lating the Erk5-KLF2-eNOS pathway, suggesting its therapeutic potential.

Indexed as

HesperidinNeuroprotective AgentsSubarachnoid HemorrhageVasospasm, IntracranialAnimalsAntioxidantsDisease Models, AnimalFemaleNitric Oxide Synthase Type IIIOxidative StressRatsRats, WistarAntioxidantsHesperidinNeuroprotective AgentsNitric Oxide Synthase Type III

Identifiers

PMID41424426
PMCPMC12782706

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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.