Department of Pharmacology, Acharya & B.M. Reddy College of Pharmacy, Bengaluru, 560107, Karnataka, India.
Department of Pharmacology, Acharya & B.M. Reddy College of Pharmacy, Bengaluru, 560107, Karnataka, India.
Neurochem Int. 2018 Dec;121:50-58. doi: 10.1016/j.neuint.2018.10.011. Epub 2018 Oct 17.
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 Ca 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展和进展的发病机制中起着至关重要的作用。本研究旨在探讨没食子酸（GA）对原代大鼠皮质神经元（RCN）中谷氨酸诱导的神经毒性的神经保护活性。用 25 和 50μg/ml 的 GA 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 小时。结果表明，GA 改善了皮质神经元的抗氧化谱，并抑制了促炎细胞因子的产生。GA 还维持了钙稳态、IGF-1 表达，并防止神经元免受谷氨酸诱导的神经元毒性。从 N-乙酰天冬氨酸和微管相关蛋白-2 表达的结果进一步证实了 GA 的神经保护活性。报告表明，GA 显著减弱了谷氨酸诱导的神经毒性，并保护神经元免受涉及神经毒性发病机制的各种化学事件的影响。
