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近年来，许多研究的结果显示，兴奋性氨基酸谷氨酸、天冬氨酸等通过其受体介导了缺氧、缺血性脑损伤，同时兴奋性氨基酸受体拮抗剂对缺氧、缺血性脑损伤有一定的保护作用。本文研究了离体培养的小鼠皮层神经细胞的缺氧模型，并观察缺氧和兴奋性氨基酸受体激动剂Ｎ－甲基－Ｄ－天冬氨酸（ＮＭＤＡ）对神经细胞的损伤作用，同时应用兴奋性氨基酸ＮＭＤＡ受体拮抗剂ＣＰＰ、Ｋｅｔ，及非ＮＭＤＡ受体拮抗剂ＮＢＱＸ观察其对缺氧及ＮＭＤＡ毒性损伤的保护作用。结果表明：（１）兴奋性氨基酸ＮＭＤＡ受体参与介导了缺氧引起的神经元损伤，（２）ＮＭＤＡ受体拮抗剂ＣＰＰ、Ｋｅｔ和非ＮＭＤＡ拮抗剂ＮＢＱＸ对缺氧引起的神经元损伤均有良好的保护作用。研究结果提示，兴奋性氨基酸受体拮抗剂有望成为临床脑缺血治疗的一个很有价值的途径。
In recent years, many studies have shown that excitatory amino acids glutamic acid, aspartic acid and so on through its receptor mediated hypoxia, ischemic brain injury, while excitatory amino acid receptor antagonists on hypoxia, lack Bloody brain injury have a protective effect. In this paper, the hypoxia model of cultured mouse cortical neurons was studied and the injury of neurons by hypoxia and excitatory amino acid receptor agonist N-methyl-D-aspartate (NMDA) At the same time, excitatory amino acid NMDA receptor antagonist CPP, Ket, and non-NMDA receptor antagonist NBQX were used to observe their protective effects on hypoxic and NMDA toxicity. The results showed that: (1) The excitatory amino acid NMDA receptor was involved in the hypoxia-induced neuronal injury; (2) Both hypoxic-induced neuronal damage was induced by NMDA receptor antagonist CPP, Ket and non-NMDA antagonist NBQX Have a good protective effect. The results suggest that excitatory amino acid receptor antagonists are expected to become a valuable method of clinical treatment of cerebral ischemia.