Vinpocetine ameliorates neuronal injury after cold-induced traumatic brain injury in mice

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dc.contributor.authorYelkenci, Hayriye Ecem
dc.contributor.authorDeğirmenci, Zehra
dc.contributor.authorKoç, Halil İbrahim
dc.contributor.authorBayırlı, Sevban
dc.contributor.authorBaltacı, Saltuk Buğra
dc.contributor.authorAltunay, Serdar
dc.contributor.authorÖztekin, Nevin
dc.contributor.authorKoçak, Mehmet
dc.contributor.authorKılıç, Ertuğrul
dc.contributor.authorBeker, Mustafa Çağlar
dc.date.accessioned2025-09-22T08:29:37Z
dc.date.available2025-09-22T08:29:37Z
dc.date.issued2025
dc.departmentİstanbul Medipol Üniversitesi, Rektörlük, Rejeneratif ve Restoratif Tıp Araştırmaları Merkezi (REMER)
dc.departmentİstanbul Medipol Üniversitesi, Rektörlük, Sağlık Bilim ve Teknolojileri Araştırma Enstitüsü
dc.departmentİstanbul Medipol Üniversitesi, Tıp Fakültesi, Temel Tıp Bilimleri Bölümü, Fizyoloji Ana Bilim Dalı
dc.departmentİstanbul Medipol Üniversitesi, Uluslararası Tıp Fakültesi, Temel Tıp Bilimleri Bölümü, Biyoistatistik ve Tıp Bilişimi Ana Bilim Dalı
dc.description.abstractTraumatic brain injury (TBI), also known as intracranial injury, is a common condition with the highest incidence rate among neurodegenerative disorders and poses a significant public health burden. Various methods are used in the treatment of TBI, but the effects of cold-induced traumatic brain injury have not been thoroughly studied. In this context, vinpocetine (VPN), derived from Vinca minor, exhibits notable anti-inflammatory and antioxidant properties. VPN is known for its neuroprotective role and is generally utilized for treating various neurodegenerative disorders. However, the function of VPN after cold-induced TBI needs to be studied in more detail. This study aims to investigate the neuroprotective effects of VPN at varying doses (5 mg/kg or 10 mg/kg) after cold-induced TBI. C57BL/6 mice were sacrificed 2 or 28 days after cold-induced TBI. Results indicate that VPN administration significantly reduces brain infarct volume, brain swelling, blood–brain barrier disruption, and DNA fragmentation in a dose-dependent manner. Additionally, VPN enhances neuronal survival in the ipsilesional cortex. In the long term, VPN treatment (5 mg/kg/day or 10 mg/kg/day, initiated 48 h post-TBI) improved locomotor activity, cell proliferation, neurogenesis, and decreased whole brain atrophy, specifically motor cortex atrophy. We performed liquid chromatography-tandem mass spectrometry (LC–MS/MS) to elucidate the underlying mechanisms to profile proteins and signaling pathways influenced by prolonged VPN treatment post-TBI. Notably, we found that 192 different proteins were significantly altered by VPN treatment, which is a matter of further investigation for the development of therapeutic targets. Our study has shown that VPN may have a neuroprotective role in cold-induced TBI.
dc.description.sponsorshipTürkiye Bilimsel ve Teknolojik Araştırma Kurumu (TÜBİTAK) ; Turkish Academy of Sciences
dc.identifier.citationYelkenci, H. E., Değirmenci, Z., Koç, H. İ., Bayırlı, S., Baltacı, S. B., Altunay, S. ... Beker, M. Ç. (2025). Vinpocetine ameliorates neuronal injury after cold-induced traumatic brain injury in mice. Molecular Neurobiology, 62(3), 3956-3972. http://dx.doi.org/10.1007/s12035-024-04515-8
dc.identifier.doi10.1007/s12035-024-04515-8
dc.identifier.endpage3972
dc.identifier.issn0893-7648
dc.identifier.issn1559-1182
dc.identifier.issue3
dc.identifier.pmid39361199
dc.identifier.scopus2-s2.0-85205592349
dc.identifier.scopusqualityQ1
dc.identifier.startpage3956
dc.identifier.urihttp://dx.doi.org/10.1007/s12035-024-04515-8
dc.identifier.urihttps://hdl.handle.net/20.500.12511/13050
dc.identifier.volume62
dc.identifier.wosWOS:001325697400001
dc.identifier.wosqualityQ1
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.institutionauthorYelkenci, Hayriye Ecem
dc.institutionauthorDeğirmenci, Zehra
dc.institutionauthorKoç, Halil İbrahim
dc.institutionauthorBayırlı, Sevban
dc.institutionauthorBaltacı, Saltuk Buğra
dc.institutionauthorAltunay, Serdar
dc.institutionauthorKoçak, Mehmet
dc.institutionauthorBeker, Mustafa Çağlar
dc.institutionauthorid0000-0003-0285-1362
dc.institutionauthorid0000-0001-5428-1109
dc.institutionauthorid0000-0002-9752-7508
dc.institutionauthorid0000-0002-4051-2559
dc.institutionauthorid0000-0002-3386-1734
dc.institutionauthorid0000-0002-9476-8488
dc.language.isoen
dc.relation.ispartofMolecular Neurobiology
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.relation.tubitakinfo:eu-repo/grantAgreement/TUBITAK/SOBAG/218S453
dc.rightsinfo:eu-repo/semantics/embargoedAccess
dc.subjectCold-Induced TBI
dc.subjectNeuroprotection
dc.subjectProteomics
dc.subjectTraumatic Brain Injury
dc.subjectVinpocetine
dc.titleVinpocetine ameliorates neuronal injury after cold-induced traumatic brain injury in mice
dc.typeArticle

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