Thiamine Protects Glioblastoma Cells against Glutamate Toxicity by Suppressing Oxidative/Endoplasmic Reticulum Stress

Thiamine (vitamin B1), which is synthesized only in bacteria, fungi and plants humans should take with diet, participates basic biochemical physiological processes a versatile way its deficiency associated neurological problems accompanied by cognitive dysfunctions. The rat glioblastoma (C6) model was used, exposed to limited environment toxicity glutamate. cells were stressed exposure glutamate the presence absence of thiamine. difference cell proliferation evaluated XTT assay. Oxidative stress (OS) markers malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT) levels, as well endoplasmic reticulum (ER) 78-kDa glucose-regulated protein (GRP78), activating transcription factor-4 (ATF-4), C/EBP homologous (CHOP) measured commercial kits. Apoptosis determined flow cytometry confirmed 4',6-diamidino-2-phenylindole (DAPI) staining. At all concentrations, thiamine protects increased viability against glutamate-induced toxicity. also significantly decreased levels MDA, while increasing SOD CAT levels. Moreover, reduced ER proteins' it lessened apoptotic amount enhanced live-cell percentage DAPI As result, may be beneficial nutritional support for individuals predisposition neurodegenerative disorders due protective effect on cytotoxicity suppressing OS stress.