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在氟代乙酰胺诱导的癫痫持续状态中,黑质网状部的坏死可通过自旋捕获剂α-苯基-N-叔丁基硝酮得到改善。

Necrosis of the substantia nigra, pars reticulate, in flurothyl-induced status epilepticus is ameliorated by the spin trap alpha phenyl-N-tert-butyl nitrone.

作者信息

He Q P, Smith M L, Li P A, Siesjö B K

机构信息

Laboratory for Experimental Brain research, University of Lund, Sweden.

出版信息

Free Radic Biol Med. 1997;22(5):917-22. doi: 10.1016/s0891-5849(96)00478-9.

Abstract

The objective of the present study was to explore whether a diffusible free radical scavenger can ameliorate the pan-neurotic lesions of the substantia nigra, pars reticulate (SNPR), which are incurred in rats subjected to status epilepticus of more than 30 min duration. Vehicle-injected animals had flurothyl seizures induced for 45 min. The seizures were then terminated and the animals were recovered for 7 d to allow histopathological evaluation of the SNPR lesions. Drug-treated animals, which were otherwise treated identically, were given either 100-800 mg/ kg of dimethylthiourea (DMTU), a diffusible hydroxyl ion scavenger, or the diffusible spin trap alpha-phenyl N-tert-butyl nitrone (PBN) in a dose of 100 mg/kg i.p.. All animals given DMTU died 2 to 8 h after status epilepticus, but PBN was tolerated well by the animals. The amount of flurothyl required to sustain the electrographic seizures was identical in the vehicle- and drug-injected groups, demonstrating that PBN did not suppress seizure activity. Vehicle-injected animals had large bilateral infarcts localized to the SNPR. Of the six animals treated with PBN, one had a small, unilateral lesions, and in all other animals the SNPR had a normal histological appearance. The results strongly suggest that the pan-necrotic lesions of the SNPR incurred during ongoing seizure activity represent a free radical-mediated lesion.

摘要

本研究的目的是探讨一种可扩散的自由基清除剂是否能改善在持续30分钟以上癫痫持续状态的大鼠中出现的黑质网状部(SNPR)的广泛性神经病变。给注射赋形剂的动物诱导氟烷惊厥45分钟。然后终止惊厥,让动物恢复7天,以便对SNPR病变进行组织病理学评估。在其他方面接受相同处理的药物治疗动物,腹腔注射100 - 800毫克/千克的二甲基硫脲(DMTU,一种可扩散的羟基离子清除剂),或100毫克/千克剂量的可扩散自旋捕捉剂α-苯基N-叔丁基硝酮(PBN)。所有给予DMTU的动物在癫痫持续状态后2至8小时死亡,但动物对PBN耐受性良好。维持脑电图癫痫发作所需的氟烷量在注射赋形剂组和注射药物组中相同,表明PBN不抑制癫痫发作活动。注射赋形剂的动物在SNPR部位有双侧大梗死灶。在接受PBN治疗的6只动物中,1只出现小的单侧病变,其他所有动物的SNPR组织学外观正常。结果强烈表明,在持续癫痫发作活动期间发生的SNPR广泛性坏死性病变是一种自由基介导的病变。

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