Gallic acid showed neuroprotection against endoplasmic reticulum stress in rats

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dc.authoridTuncer, Mehmet Cudi/0000-0001-7317-5467
dc.authoridkaraaslanli, abdulmutalip/0009-0005-1046-3484
dc.contributor.authorKaraaslanli, Abdulmutalip
dc.contributor.authorTuncer, Mehmet Cudi
dc.contributor.authorAsir, Firat
dc.contributor.authorKorak, Tugcan
dc.date.accessioned2025-02-22T14:08:46Z
dc.date.available2025-02-22T14:08:46Z
dc.date.issued2025
dc.departmentDicle Üniversitesien_US
dc.description.abstractPurpose: We aimed to investigate the role of gallic acid treatment on spinal cord tissues after spinal cord injury (SCI) and its relationship with endoplasmic reticulum (ER) stress by histochemical, immunohistochemical, and in-silico techniques. Methods: Thirty female Wistar albino rats were divided into three groups: sham, SCI, and SCI+gallic acid. SCI was induced by dropping a 15-g weight onto the exposed T10-T11 spinal cord segment. The SCI+gallic acid group received 25 mg/kg of gallic acid intraperitoneally daily for one week. Histopathological, immunohistochemical, and silico analyses were performed. Results: Histological analysis revealed improved neural cell survival and tissue integrity in the SCI+gallic acid group compared to the SCI group. Caspase-12 expression was significantly increased in the SCI group, indicating elevated ER stress and apoptosis. Gallic acid treatment resulted in a marked reduction in caspase-12 expression in neurons, neuroglia, and endothelial cells, suggesting decreased ER stress. Conclusion: Gallic acid exhibits significant neuroprotective effects against ER stress and cellular damage in a rat model of SCI. The in-silico analysis revealed apoptotic and immune-related pathways in which gallic acid showed neuroprotective effects by regulating caspase-12. These results suggest that gallic acid may be a promising therapeutic agent for mitigating secondary damage post-SCI.en_US
dc.identifier.doi10.1590/acb400925
dc.identifier.issn0102-8650
dc.identifier.issn1678-2674
dc.identifier.pmid39813535en_US
dc.identifier.scopus2-s2.0-85216002653en_US
dc.identifier.scopusqualityQ2en_US
dc.identifier.urihttps://doi.org/10.1590/acb400925
dc.identifier.urihttps://hdl.handle.net/11468/29634
dc.identifier.volume40en_US
dc.identifier.wosWOS:001399852000001
dc.identifier.wosqualityQ3
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoenen_US
dc.publisherActa Cirurgica Brasileiraen_US
dc.relation.ispartofActa Cirurgica Brasileiraen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.snmzKA_WOS_20250222
dc.subjectGallic Aciden_US
dc.subjectCaspasesen_US
dc.subjectEndoplasmic Reticulum Stressen_US
dc.subjectSpinal Cord Injuriesen_US
dc.titleGallic acid showed neuroprotection against endoplasmic reticulum stress in ratsen_US
dc.typeArticleen_US

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