中文摘要：

目的 探讨吸入麻醉药七氟烷对APP/PS1双转基因小鼠海马组织神经元蛋白质损伤和聚集的影响.方法 12月龄APP/PS1双转基因小鼠随机分为两组各30只：对照组小鼠给予2 L/min氧气吸入4 h;七氟烷组小鼠给予2%七氟烷吸入麻醉4 h.部分小鼠麻醉后6 h应用末端脱氧核苷酸转移酶（TUNEL）法检测海马神经元凋亡情况,应用二氯荧光黄双乙酸盐（DCFH-DA）检测活性氧（ROS）水平;部分小鼠麻醉后24 h应用免疫组织化学法（IHC）和Western印迹法检测海马神经元内氧化损伤蛋白质（蛋白羰基化合物、硝基化酪氨酸蛋白和Aβ42）的表达,应用TEM观察海马神经元内蛋白质聚集物.结果 七氟烷组小鼠海马神经元凋亡率、ROS水平、蛋白羰基化合物、硝基化酪氨酸蛋白和Aβ42的表达水平均高于对照组,蛋白质聚集物增多（P〈0.05）.结论 12月龄APP/PS1双转基因小鼠给予2%七氟烷麻醉4 h,能够加剧其海马神经元氧化应激损伤,促进蛋白质损伤和聚集,诱导海马神经元凋亡,加重阿尔茨海默病（AD）的神经病理损害.

英文摘要：

Objective To investigate the effects of the neuronal protein damage and aggregation induced by inhaled anesthetic sevoflurane in the APP/PS1 transgenic mice hippocampus.Methods 60 APP/PS1 transgenic mice were randomly divided into control and sevoflurane groups.TUNEL and DCFH-DA were applied to detect the hippocampal neuronal apoptosis and ROS level respectively,immunohistochemical method and Western blot were applied to detect Aβ42 level,carbonyl compounds and nitrotyrosine,TEM was applied to observe the protein aggregation.Results Compared with those of control group,the neuronal apoptosis rate,expression levels of ROS,Aβ42,oxidative protein carbonyl compounds and nitrotyrosine were significantly increased in sevoflurane group（P〈0.05）.Conclusions 2% sevoflurane exposure for 4 hours significantly aggravates the oxidative-stress injury of hippocampal neuron,hippocampal protein damage and aggregation,guides neuronal apoptosis,exacerbates neuropathology injury.