LAUSR

ABSTRACT Glutamate excitotoxicity plays a crucial role in the pathogenesis behind the development and progression of several neurodegenerative diseases. The study aimed to investigate the neuroprotective activity of Gallic acid (GA) against glutamate‐induced neurotoxicity in primary rat cortex neurons (RCN). Treated the RCNs with GA 25 & 50 &mgr;g/ml for 2 h and later treated the cells with 100 &mgr;M glutamate (GLU) and incubated for 24 h at 37 °C. The results demonstrated that, the GA improved the antioxidant profile in the cortex neurons and inhibited the production of the proinflammatory cytokine. GA also maintained the Ca2+ homeostasis, IGF‐1 expression, and protected the neurons from glutamate‐induced neuronal toxicity. The neuroprotective activity of GA has further confirmed from the results of N‐acetylaspartate and expression of microtubule‐associated protein‐2 expression. The reports suggest that, GA is significantly attenuated the glutamate‐induced neurotoxicity and protected neurons from various chemical events that are involved in the pathogenesis of neurotoxicity. HighlightsGlutamate excitotoxicity is a major pathogenesis behind the development and progression of neurodegenerative diseases.Glutamate‐induced neurotoxicity in RCN is mediated through the formation of free radicles and proinflammatory cytokine.Glutamate treatment also caused an alteration in Ca2+ homeostasis and decline in IGF‐1 level.Observed a down‐regulation of MAP‐2 expression and NAA concentration in glutamate treated rat cortex neurons.Treatment with GA improved the antioxidant status in neurons and inhibited proinflammatory cytokine production.GA also maintained the Ca2+ homeostasis, IGF‐1 expression, and protected neurons from glutamate‐induced neuronal toxicity.