非药物预处理对脑缺血后兴奋毒性的调控作用

Regulatory Effect of Non-Pharmaceutical Preconditioning on Excitotoxicity after Cerebral Ischemia

兴奋性神经递质谷氨酸过量释放引起的神经毒性是脑缺血后一系列级联事件发生的主要初始病理变化。非药物预处理可通过抑制缺血后兴奋毒性减轻神经损伤。将首先梳理脑区谷氨酸代谢过程,包括谷氨酸突触前生成和释放、突触间隙重摄取以及突触后与受体结合;然后围绕谷氨酸代谢过程中的作用位点对非药物预处理在兴奋毒性方面的研究进展进行概述,为进一步研究非药物预处理对抗脑缺血后兴奋性氨基酸毒性的作用机制提供参考。

Neurotoxicity caused by the excessive release of the excitatory neurotransmitter glutamate is the main initial pathological change in a series of cascade events after cerebral ischemia.Non-pharmaceutical preconditioning can reduce ischemia-induced cerebral injury by inhibiting excitatory toxicity.This paperfirst reviewed the glutamate metabolism in brain regions,including presynaptic glutamate production and release,synaptic gap reuptakeand postsynaptic binding to receptors.And then,wesummarized the research progress of non-pharmaceutical pretreatmentin regulating excitotoxicity from progress of glutamate metabolism.Hopefully,our work could provide reference for further research on the mechanism of non-pharmaceutical pretreatment in inhibiting excitotoxicity of ischemic stroke.