Sinapic acid alleviates glutamate-induced excitotoxicity by inhibiting neuroinflammation and endoplasmic reticulum stress pathway in C6 glioma cells

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dc.authoridOzdemir, Ercan/0000-0001-8231-1053
dc.contributor.authorOrtasoz, Ahmet Mahmut
dc.contributor.authorOzdemir, Ercan
dc.contributor.authorTaskiran, Ahmet Sevki
dc.contributor.authorOzturk, Aysegul
dc.date.accessioned2025-05-04T16:46:59Z
dc.date.available2025-05-04T16:46:59Z
dc.date.issued2025
dc.departmentSivas Cumhuriyet Üniversitesi
dc.description.abstractSinapic acid (SA) is a polyphenol compound derived from hydroxycinnamic acid found in various foods such as cereals and vegetables and has antioxidant, anti-inflammatory and neuroprotective properties. However, its effects on glutamate-induced excitotoxicity, which is important in neurodegenerative diseases, have not been fully elucidated. This study aimed to investigate the effect of SA on glutamate excitotoxicity and the possible role of proinflammatory cytokines and the endoplasmic reticulum (ER) stress pathway. In the study, C6 rat glioma cell line was used and the cells were divided into 4 groups: control, glutamate, SA and glutamate+SA. Cells were treated with 10 mM glutamate for 24 h to induce excitotoxicity. Additionally, SA was applied to cells at concentrations of 12.5 to 100 mu M to examine its effects on glutamate excitotoxicity. XTT test was used for cell viability, and apoptotic cells were determined by immunofluorescence and flow cytometry methods. Proinflammatory cytokines (tumor necrosis factor-alpha, TNF-alpha and interleukin-beta, IL-1(3), ER stress markers (glucose regulatory protein 78, GRP78; C/EBP homologous protein, CHOP and activating transcription factor-4, ATF-4) and caspase-3 was used to measure ELISA method. Findings indicated that SA (50 mu M) significantly increased cell viability against glutamate-induced excitotoxicity (p < 0.05). Also, SA caused a significant decrease in TNF-alpha, IL-1(3, GRP78, CHOP, ATF-4 and caspase-3 levels in glutamate-treated cells (p < 0.05). Flow cytometry and immunofluorescence staining results showed that SA reduced apoptosis in C6 glioma cells. In conclusion, our findings suggested that SA attenuated glutamate-induced excitotoxicity by preventing apoptosis through reducing proinflammatory cytokines and ER stress protein levels.
dc.identifier.doi10.1016/j.tiv.2024.105977
dc.identifier.issn0887-2333
dc.identifier.issn1879-3177
dc.identifier.pmid39615638
dc.identifier.scopus2-s2.0-85210383847
dc.identifier.scopusqualityQ2
dc.identifier.urihttps://doi.org/10.1016/j.tiv.2024.105977
dc.identifier.urihttps://hdl.handle.net/20.500.12418/35442
dc.identifier.volume103
dc.identifier.wosWOS:001415620700001
dc.identifier.wosqualityQ3
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoen
dc.publisherPergamon-Elsevier Science Ltd
dc.relation.ispartofToxicology in Vitro
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.snmzKA_WOS_20250504
dc.subjectSinapic acid
dc.subjectGlutamate excitotoxicity
dc.subjectPro-inflammatory cytokines
dc.subjectEndoplasmic reticulum stress
dc.subjectApoptosis
dc.titleSinapic acid alleviates glutamate-induced excitotoxicity by inhibiting neuroinflammation and endoplasmic reticulum stress pathway in C6 glioma cells
dc.typeArticle

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