To investigate the role of GluN2A and GluN2B in neuroprotective effect of sevoflurane preconditioning against cerebral ischemia–reperfusion injury (CIRI). Rats were randomly divided into five groups as follows: control, ischemia–reperfusion (I/R) 6 h, sevoflurane preconditioning (SP), SP + amantadine, SP + NMDA. Immunoblot and immunoprecipitation were used to detect the tyrosine phosphorylation of GluN2A/GluN2B, the interaction of GluN2A/GluN2B-PSD-95-MLK3 and the expression of phosphorylation of MLK3, MKK7 and JNK3. Cresyl violet staining was employed to analyse neuronal injury in rat hippocampal CA1 subfields. Sevoflurane preconditioning inhibits the tyrosine phosphorylation of GluN2A/GluN2B, the interaction of GluN2A/GluN2B-PSD-95-MLK3 and the phosphorylation of MLK3, MKK7 and JNK3 in rat hippocampus. An N-methyl-d-aspartate receptor (NMDAR) antagonist amantadine reversed the MLK3-MKK7- JNK3 signal events. Such reversion was also realized by NMDA (60 and 80 nmol) and low doses of NMDA (0–40 nmol) could not change the inhibitory effect of sevoflurane preconditioning on MLK3-MKK7-JNK3 signal events. Finally, Cresyl violet staining also confirmed that low dose of NMDA reduced neuronal loss in rat hippocampal CA1 subfields. Sevoflurane preconditioning provides neuroprotection against CIRI by inhibiting NMDAR over-activation.

研究 GluN2A 和 GluN2B 在七氟醚预处理对脑缺血再灌注损伤 (CIRI) 的神经保护作用中的作用。大鼠随机分为以下五组：对照，缺血再灌注（I / R）6小时，七氟醚预处理（SP），SP +金刚烷胺，SP + NMDA。采用免疫印迹和免疫沉淀法检测GluN2A/GluN2B的酪氨酸磷酸化、GluN2A/GluN2B-PSD-95-MLK3的相互作用以及MLK3、MKK7和JNK3磷酸化的表达。甲酚紫染色用于分析大鼠海马 CA1 亚区的神经元损伤。七氟烷预处理抑制大鼠海马中 GluN2A/GluN2B 的酪氨酸磷酸化、GluN2A/GluN2B-PSD-95-MLK3 的相互作用以及 MLK3、MKK7 和 JNK3 的磷酸化。一个ñ甲基d天冬氨酸受体（NMDAR）拮抗剂金刚烷胺逆转MLK3-MKK7- JNK3信号事件。这种逆转也可以通过 NMDA（60 和 80 nmol）实现，低剂量的 NMDA（0-40 nmol）不能改变七氟醚预处理对 MLK3-MKK7-JNK3 信号事件的抑制作用。最后，甲酚紫染色还证实低剂量的 NMDA 减少了大鼠海马 CA1 亚区的神经元丢失。七氟烷预处理通过抑制 NMDAR 过度激活提供针对 CIRI 的神经保护。