丁苯酞对氯化锂-匹鲁卡品诱发的癫痫大鼠海马神经元损伤的作用

目的〓〖HTK〗探讨丁苯酞对颞叶癫痫大鼠海马神经元的保护作用。 〖HTW〗方法〓〖HTK〗随机将30只雄性成年Wistar大鼠分为丁苯酞组、癫痫组和空白对照组。丁苯酞组和癫痫组先分别给予丁苯酞80mg/kg、等量生理盐水腹腔注射，再分别给予氯化锂、匹鲁卡品建立癫痫模型，在癫痫发作终止后3、24h时将动物处死，分别取出海马在光镜和电镜下观察，并检测超氧化物歧化酶活力及丙二醛含量。 〖HTW〗结果〓〖HTK〗丁苯酞组能明显延长癫痫发作的潜伏期，增加超氧化物歧化酶的活力（P＜0.01，P＜0.05），降低丙二醛的含量（P＜0.05，P＜0.01），细胞结构基本正常，但核仁有边聚、间隙肿胀，部分线粒体膜有断裂和嵴缺失现象。癫痫组细胞肿胀、破裂，神经元数目明显减少, 胞质中线粒体变形、肿胀, 线粒体嵴缺失。 〖HTW〗结论〓〖HTK〗丁苯酞能减轻颞叶癫痫对海马神经元造成的损伤，其作用机制可能与丁苯酞对神经元线粒体的保护有关。

Butyphthalide inhibits hippocampal neuron injury induced by lithium chloride-pilocarpine in epileptic rats

Objective To explore the protective effect of butyphthalide on hippocampus neurons in epileptic rats.Methods 30 adult male Wistar rats were randomly divided into three groups: the intervention group,the epilepsy group and the control group.The intervention group was given 80 mg/Kg butyphthalide via i.p injection and the epilepsy group was given 80 mg/Kg 0.9%NaCl the same way. Rats were killed 3 or 24hours after the end of lesion,and then the hippocampus was taken out and observed by light microscopy and electron microscopy and the levels of superoxide dismutase(SOD) and malonadialdehyde(MDA) were determined.Results The epileptic paroxysm latent period of the intervention group was significantly prolonged,the results of HE staining and electron microscopy showed that there was less cellular swelling and plasmatorrhexis,and there were few neurons in the intervention group.Bioblasts were deformed,crista mitochondriales disappeared,and cavitation and membranous bodies were found in the kytoplasm.In the butyphthalide intervention group,cellular construction was roughly normal,but the nucleoli were collected aside,and the construction of the chondriosomes was still integrated.There were few membranous bodies,but the membrane broke and cristae mitochondriale depletion still appeared in some of the neurons.Zymology showed butyphthalide can raise the activation of SOD(P<0.01,P<0.05) and decrease the quantity of MDA(P<0.05,P<0.01).Conclusion Butyphthalide can decrease hippocampus neuron damage caused by temporal epilepsy,which is related to the protective effect of butyphthalide on chondrosomes.