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观察了ｅｂｓｅｌｅｎ对超氧阴离子Ｏ·－２和羟自由基·ＯＨ诱发的体外培养大鼠皮层神经元乳酸脱氢酶（ｌａｃｔｉｃｄｅｈｙｄｒｏｇｅｎａｓｅ，ＬＤＨ）释放，和ＴＢＡＲＳ（ｔｈｉｏｂａｒｂｉｔｕｒｉｃａｃｉｄｒｅａｃｔｉｖｅｓｕｂｓｔａｎｃｅ）含量升高及制备的皮层线粒体ＴＢＡＲＳ含量升高的影响。结果表明：超氧阴离子和羟自由基引起了培养神经元和线粒体明显的损伤。浓度在５～５０μｍｏｌ·Ｌ－１之间，ｅｂｓｅｌｅｎ能剂量依赖性地抑制ＬＤＨ释放和ＴＢＡＲＳ含量的增加，对线粒体的ＴＢＡＲＳ含量升高也有显著的抑制作用。但浓度为０．２～５０μｍｏｌ·Ｌ－１时，药物无直接清除超氧阴离子和羟自由基的活性。因此，ｅｂｓｅｌｅｎ对氧自由基诱发的神经元脂质过氧化损伤有拮抗作用，这种作用与直接清除自由基无关。
The effects of ebselen on the release of lactic dehydrogenase (LDH) and TBARS (thiobarbituric acid reactive antigen) in cultured rat cortical neurons induced by superoxide anion O · -2 and hydroxyl radical · OH were observed and the cortical mitochondria Effect of elevated TBARS content. The results showed that superoxide anion and hydroxyl radical caused obvious damage of cultured neurons and mitochondria. The concentration of 5 ~ 50μmol·L-1, ebselen dose-dependently inhibited the release of LDH and TBARS content increased mitochondrial TBARS content also significantly inhibited. But the concentration of 0.2 ~ 50μmol·L-1, the drug does not directly scavenge superoxide anion and hydroxyl radical activity. Therefore, ebselen antagonizes oxygen free radicals induced neuronal lipid peroxidation injury, this role has nothing to do with the direct scavenging of free radicals.