Investigation of neuroprotective effects of newly synthesized benzimidazolium salt against neurotoxicity in differentiated SH-SY5Y neuronal cells

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dc.contributor.authorYildiz, Fatma
dc.date.accessioned2026-01-24T12:31:07Z
dc.date.available2026-01-24T12:31:07Z
dc.date.issued2025
dc.departmentAlanya Alaaddin Keykubat Üniversitesi
dc.description.abstractNeurodegenerative diseases (ND) are a group of neurological disorders characterized by various pathological features such as selective neuronal loss, chronic inflammation, and aggregation of specific proteins. This study aimed to investigate the possible protective effects of newly synthesized benzimidazolium salt (BS) against H2O2-induced oxidative stress in differentiated SH-SY5Y cells. Firstly, retinoic acid was applied to SH-SY5Y cells to obtain mature neurons. Then, a toxicity model was created by H2O2 treatment of neuron-like differentiated SH-SY5Y (d- SH-SY5Y) cells. Survival rates of d-SH-SY5Y cells were determined using the 3-(4,5-Dimethylthiazol-2-yl)-2,5-Diphenyltetrazolium Bromide (MTT) method. In addition, pro-inflammatory cytokine (tumor necrosis factor-alpha (TNF-alpha), interleukin-1 beta (IL-1 beta), interleukin-6 (IL-6) levels were determined by ELISA method, while gene expression levels of apoptotic markers (Bax, Bcl-2, caspase-3 and caspase-8) were determined by RT-QPCR method. In addition, the effect of BS on neurite length in these cell groups was evaluated through morphological observations. According to our results, BS showed neuroprotective effect by increasing cell viability against H2O2-induced neurotoxicity in d-SH-SY5Y cells (p < 0.01). BS pretreatment provided H2O2-induced Bcl-2 up-regulation, Bax down-regulation, caspase-3 activation and caspase-8 inhibition. In addition, BS supported the decrease in TNF-alpha, IL-1 beta and IL-6 protein levels. This study demonstrated for the first time that BS exhibited potential neuroprotective effects on H2O2-induced neuronal damage by attenuating inflammation and apoptosis. These findings suggest that BS may be considered a promising candidate in preventing and treating oxidative stress-mediated neurodegenerative diseases.
dc.identifier.doi10.1016/j.bbrc.2025.152255
dc.identifier.issn0006-291X
dc.identifier.issn1090-2104
dc.identifier.pmid40580722
dc.identifier.scopus2-s2.0-105008947030
dc.identifier.scopusqualityQ2
dc.identifier.urihttps://doi.org/10.1016/j.bbrc.2025.152255
dc.identifier.urihttps://hdl.handle.net/20.500.12868/5646
dc.identifier.volume777
dc.identifier.wosWOS:001523093100002
dc.identifier.wosqualityQ3
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoen
dc.publisherAcademic Press Inc Elsevier Science
dc.relation.ispartofBiochemical and Biophysical Research Communications
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.snmzKA_WoS_20260121
dc.subjectSH-SY5Y
dc.subjectd-SH-SY5Y
dc.subjectNeurodegenerative diseases
dc.subjectBenzimidazolium salt
dc.subjectNeuroprotective effect
dc.titleInvestigation of neuroprotective effects of newly synthesized benzimidazolium salt against neurotoxicity in differentiated SH-SY5Y neuronal cells
dc.typeArticle

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