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目的：研究乙基４－（３－氧－１，２－苯并异硒吡咯－２－基）－α－甲基－苯乙酸盐（ＥＯＢＭＢ）对培养神经元缺氧损伤的保护作用及机制。方法：培养大鼠皮质神经元通以９５％Ｎ２＋５％ＣＯ２造成缺氧模型；体外产生的超氧阴离子和羟自由基刺激培养神经元；测定培养上清乳酸脱氢酶（ＬＤＨ）活性和硫代巴比妥酸反应活性物质（ＴＢＡＲＳ）含量；观察ＥＯＢＭＢ对超氧阴离子和羟自由基特征显色反应的影响；测定谷胱甘肽过氧化物酶（ＧＳＨ－Ｐｘ）拟似活性。结果：ＥＯＢＭＢ能抑制缺氧和自由基诱发的培养神经元的ＬＤＨ释放和ＴＢＡＲＳ含量的增加。体外无直接灭活超氧阴离子和羟自由基的活性，但表现一定的ＧＳＨ－Ｐｘ活性。结论：ＥＯＢＭＢ对神经元缺氧损伤具有保护作用，作用机制主要通过发挥ＧＳＨ－Ｐｘ活性，抑制自由基的脂质过氧化。
Objective: To study the protective effect of ethyl 4- (3-oxo-1,2-benzisoseptanil-2-yl) -α-methyl-phenylacetate (EOBMB) mechanism. METHODS: Cultured rat cortical neurons were exposed to 95% N2 + 5% CO2 for hypoxia. Neurons were stimulated by superoxide anion and hydroxyl radical generated in vitro. The activities of lactate dehydrogenase (LDH) and thio The effect of EOBMB on the characteristic color reaction of superoxide anion and hydroxyl radical was observed. The quasi-glutathione peroxidase (GSH-Px) activity was measured. Results: EOBMB can inhibit the LDH release and the increase of TBARS in cultured neurons induced by hypoxia and free radicals. No in vitro direct inactivation of superoxide anion and hydroxyl radical activity, but showed some GSH-Px activity. CONCLUSION: EOBMB has a protective effect on neuronal hypoxia. The mechanism of action is to inhibit the lipid peroxidation of free radicals by exerting GSH-Px activity.