摘要： 目的 探讨艾地苯醌（IDBN）对癫痫大鼠海马神经元损伤的预防性保护作用及其作用机制。方法 共48只Wistar大鼠随机分为正常对照组、IDBN预防组（预防组）、癫痫组和IDBN 25 mg组、50 mg组、100 mg组，观察不同处理组大鼠治疗前后行为学变化，检测海马组织超氧化物歧化酶（SOD）、谷胱甘肽过氧化物酶（GSH-Px）活性和丙二醛（MDA）含量，观察海马组织学形态及神经元线粒体超微结构。结果 不同处理组大鼠海马组织SOD、GSH-Px和MDA表达水平差异具有统计学意义（均P=0.000）。IDBN不同剂量组以100 mg组SOD和GSH-Px活性最强、MDA含量最低：SOD和GSH-Px活性高于癫痫组（P=0.000，0.000）、IDBN 25 mg组（P=0.000，0.000）和50 mg组（P=0.004，0.005），MDA含量低于癫痫组（P=0.000）、IDBN 25 mg组（P=0.000）和50 mg组（P=0.002）。与正常对照组和预防组相比，癫痫组大鼠海马神经元出现不同程度损伤，经艾地苯醌处理后损伤减轻且随剂量的增加其程度逐渐减轻；癫痫组大鼠海马神经元线粒体结构破坏明显，可见变形、肿胀，部分线粒体呈空泡化；经艾地苯醌处理后损伤减轻，且随剂量的增加其程度逐渐减轻。结论 艾地苯醌可通过抑制癫痫大鼠体内氧化应激损伤作用保护海马神经元结构及功能。

关键词: 苯醌类, 癫痫, 海马, 细胞凋亡, 超氧化物歧化酶, 谷胱甘肽过氧化酶, 丙二醛, 疾病模型,动物

Abstract: Objective To investigate the protective effect of idebenone (IDBN) on hippocampal neuron injury in epileptic rats and its mechanism. Methods Forty-eight Wistar rats were randomly divided into normal control group, IDBN prevention group (prevention group), epilepsy group, IDBN 25, 50 and 100 mg groups. Behavioral changes of rats in different treatment groups before and after treatment with IDBN were observed. The activity of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) and the content of malondialdehyde (MDA) in hippocampal were detected. The ultrastructural changes of hippocampal neurons and mitochondria were observed. Results The expression levels of SOD, GSH-Px and MDA in different treatment groups were significantly different (P=0.000, for all). The activity of SOD and GSH-Px was the highest and the content of MDA was the lowest in IDBN 100 mg group. The activity of SOD and GSH-Px in IDBN 100 mg group were higher than those in epilepsy group (P=0.000, 0.000), IDBN 25 mg group (P=0.000, 0.000) and 50 mg group (P=0.004, 0.005), while the content of MDA was lower than that in epilepsy group (P=0.000), IDBN 25 mg group (P=0.000) and 50 mg group (P=0.002). Compared with normal control group and prevention group, hippocampal neurons in epilepsy group showed different degrees of damage, which was relieved after treatment with IDBN and gradually decreased with the increase of dose. In epilepsy group, the mitochondrial structure of hippocampal neurons was damaged obviously, with deformation and swelling, and some mitochondria were vacuolated. After treatment with IDBN, the damage was relieved, and the 100 mg group had the least damage. Conclusions IDBN can protect hippocampal neuron structure and function by inhibiting oxidative stress injury in epileptic rats.

Key words: Benzoquinones, Epilepsy, Hippocampus, Apoptosis, Superoxide dismutase, Glutathione peroxidase, Malondialdehyde, Disease models, animal