Temporal effects of edaravone, a free radical scavenger, on transient ischemia-induced neuronal dysfunction in the rat hippocampus
Temporal effects of edaravone, a free radical scavenger, on transient ischemia-induced neuronal dysfunction in the rat hippocampus
复制标题
DOI：
10.1016/j.ejphar.2005.01.050
复制
发表时间：
2005-04-11
影响因子：
5
通讯作者：
Yoshioka, M
中科院分区：
文献类型：
--
作者：
Otani, H;Togashi, H;Yoshioka, M
我们检测了自由基清除剂依达拉奉对缺血/再灌流诱导的大鼠海马齿状回穿通径突触长时程增强损伤的影响，以此作为短暂性全脑缺血4天(2血管闭塞，10分钟)后功能结果的衡量标准。依达拉奉(3和10 mg/kg，静脉注射)再灌流后即刻(第0天)可剂量依赖性地减轻缺血所致的长时程增强损伤，而再灌注后第1天或第4天的治疗不能挽救受损的长时程增强。第0天给予依达拉奉也能阻止脑缺血后羟基自由基形成的增加以及海马区血管内皮生长因子、碱性成纤维细胞生长因子、神经元型和诱导型一氧化氮合酶的表达。因此，依达拉奉通过治疗时间窗保护大鼠海马区免受缺血诱导的长时程增强损伤，这表明缺血/再灌注后自由基的形成是全球缺血性卒中后神经功能并发症的关键触发因素。(C)2005 Elsevier B.V.保留所有权利。
We examined the effect of a free radical scavenger edaravone on ischemia/reperfusion-induced impairment of long-term potentiation in the perforant path-dentate gyrus synapses of the rat hippocampus, as a measure of functional outcome 4 days after transient global ischemia (2-vessel occlusion, 10 min). Edaravone (3 and 10 mg/kg, i.v.) immediately after reperfusion (Day 0) alleviated ischemia-induced impairment of long-term potentiation in a dose-related manner, whereas treatment on Day 1 or 4 after reperfusion failed to rescue the impaired long-term potentiation. Edaravone administration on Day 0 also prevented the post-ischemic increase in hydroxyl radical formation and the expression of vascular endothelial growth factor, basic fibroblast growth factor and neuronal and inducible nitric oxide synthases of the hippocampus. Thus, edaravone protected the rat hippocampus from ischemia-induced long-term potentiation impairment with a therapeutic time window, suggesting that free radical formation after ischemia/reperfusion is a pivotal trigger of neurofunctional complications after global ischemic stroke. (c) 2005 Elsevier B.V. All rights reserved.