Investıgatıon of The Amelıoratıve Effects of Gallic Acid Agaınst Neurotoxicity Caused by Glutamate in C6 Cells
Effect of gallic acid on Glutamate-Induced neurotoxicity
DOI:
https://doi.org/10.5281/zenodo.11471554Keywords:
Gallic acid, Glutamate, Oxidative stress, caspase-3, C6 glioma cellsAbstract
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.
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