Effect of Gallic Acid on PTZ-induced Neurotoxıcıty, Oxidative Stress and Inflammation in SH-SY5Y Neuroblastoma Cells

Abstract

Aim: The human neuroblastoma cell lines are widely used to elucidate neurotoxic substances' cellular and molecular mechanisms and to facilitate the prioritization of in vivo testing. Pentylenetetrazole (PTZ) is a tetrazole derivative. Although PTZ is the most commonly used chemical to create an in vivo and in vitro epilepsy (EP) model, its mechanism of action in neuronal cells has not been fully elucidated. Gallic acid (GA) has broad biological properties such as antioxidant, anti-microbial, and anti-inflammatory activities. The present study aimed to investigate the effect of GA on PTZ-induced neurotoxicity in neuroblastoma cells. 
 Methods: For the study, four groups were formed from SH-SY5Y neuroblastoma cells as control (Cont), GA (100 μM), PTZ (30 μM), and PTZ+GA. In the study, Total antioxidant and oxidant status (TAS and TOS), inflammatory cytokines (TNF α, IL 1β, and IL 6), lipid peroxidation levels as malondialdehyde (MDA), glutathione peroxidase (GSHPx), and glutathione (GSH) levels in the SH-SY5Y neuroblastoma cells were determined. 
 Results: The results showed that PTZ treatment caused neurotoxicity in the neuroblastoma cell line and increased TOS, TNF α, IL 1β, IL 6, and MDA levels while decreasing TAS, GSH, and GSHPx levels. This situation improved with GA treatment.
 Conclusion: As a result, it was determined that GA treatment showed a protective effect in the PTZ-induced neural toxicity model in SH-SY5Y human neuroblastoma cell lines.