Investıgatıon of The Amelıoratıve Effects of Gallic Acid Agaınst Neurotoxicity Caused by Glutamate in C6 Cells: Effect of gallic acid on Glutamate-Induced neurotoxicity


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Ahlatcı A.

Neuro-Cell Molecular Research, cilt.1, sa.1, ss.7-13, 2024 (Hakemli Dergi)

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 1 Sayı: 1
  • Basım Tarihi: 2024
  • Dergi Adı: Neuro-Cell Molecular Research
  • Derginin Tarandığı İndeksler: Other Indexes
  • Sayfa Sayıları: ss.7-13
  • Van Yüzüncü Yıl Üniversitesi Adresli: Evet

Özet

Gallic acid (GA) is present as a phenolic component of various foods and plants. GA is a molecule with broad biological properties such as antioxidant, anti-microbial, and anti-inflammatory activities. As the main excitatory neurotransmitter in the mammalian central nervous system excessive extracellular glutamate can activate the glutamate receptors and neuronal/intracellular calcium (Ca2+) overload, producing neurotoxicity, a common pathway for neuronal injury or death and is associated with neurodegenerative diseases. The present study aimed to investigate the effect of gallic acid on glutamate-induced cytotoxicity in C6 glioma cells. For the study, groups were formed from C6 cells as control, GA (100 µM, 24 h), Glutamate (10 mM, 24 h), and GA+Glutamate. In the study, Total oxidant (TOS), total antioxidant (TAS), MDA, and caspase-3 levels in the cells were determined by ELISA kit. The results showed that glutamate administration increased TOS, MDA, and caspase-3 levels by causing cytotoxicity in C6 cells (p<0.05). However, in C6 cells treated with GA before glutamate incubation, TOS, MDA, and caspase-3 levels were decreased, and TAS levels increased compared to the glutamate group (p<0.05). As a result, it was determined that GA treatment showed a protective effect in the glutamate-induced cytotoxicity model in C6 cells.