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目的探讨氢氧化铝致猫运动区癫痫模型的制作方法及SOD、MDA在猫运动区癫痫模型中的作用。方法在猫的左侧大脑乙状前回注入氢氧化铝乳剂或生理盐水50μl。术后观察猫的行为学变化,皮层脑电图变化,20周后取材检测致痫区脑组织SOD、MDA的含量。结果氢氧化铝组于术后11～14周时发现临床癫痫发作;氢氧化铝组于8周时检测到皮层棘波放电,12周时放电次数最明显,持续到20周仍有棘波放电,且趋于稳定;氢氧化铝组致痫区脑组织SOD含量明显低于生理盐水组,MDA含量明显高于生理盐水组。结论成功制成氢氧化铝癫痫模型,其发病机制与SOD含量减少及MDA含量增多有关。
Objective To explore the method of making aluminum hydroxide-induced epilepsy in cat’s motor area and the role of SOD and MDA in cat’s epilepsy model. Methods In the cat’s left brain before the retrograde infusion of aluminum hydroxide emulsion or saline 50μl. Postoperative observation of cat behavior changes, cortical EEG changes, 20 weeks after the detection of epileptic seizures area brain tissue SOD, MDA content. Results The aluminum hydroxide group showed clinical seizures at 11-14 weeks after operation. In the aluminum hydroxide group, the cortical spike discharge was detected at 8 weeks, and the discharge was most obvious at 12 weeks. The spike wave was still discharged after 20 weeks , And tended to be stable. The content of SOD in the brain tissue of epileptogenic zone of aluminum hydroxide group was significantly lower than that of saline group, and the content of MDA was significantly higher than that of saline group. Conclusion The aluminum hydroxide epilepsy model was successfully established. Its pathogenesis was related to the decrease of SOD and the increase of MDA content.