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 μg/ml for 2 h and later treated the cells with 100 μM 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.

谷氨酸兴奋性毒性在几种神经退行性疾病的发生和发展背后的发病机理中起着至关重要的作用。这项研究旨在调查没食子酸（GA）对谷氨酸诱导的原代大鼠皮层神经元（RCN）的神经毒性的神经保护活性。用GA 25和50μg/ ml处理RCN 2小时，然后用100μM谷氨酸（GLU）处理细胞，并在37°C下孵育24 h。结果表明，GA改善了皮层神经元的抗氧化特性，并抑制了促炎细胞因子的产生。GA还保持了Ca ²⁺稳态，IGF-1表达，并保护神经元免受谷氨酸诱导的神经元毒性。从N-乙酰天门冬氨酸和微管相关蛋白2的表达结果进一步证实了GA的神经保护活性。报告表明，GA显着减轻了谷氨酸诱导的神经毒性，并保护了神经元免受涉及神经毒性发病机理的各种化学事件的影响。