依达拉奉
肌萎缩侧索硬化
SOD1
自由基清除剂
脊髓
医学
兴奋毒性
百草枯
氧化应激
硝基酪氨酸
神经保护
药理学
麻醉
化学
内科学
生物化学
谷氨酸受体
疾病
一氧化氮
精神科
受体
一氧化氮合酶
作者
Hidefumi Ito,Reika Wate,Jianhua Zhang,Shizuo Ohnishi,Satoshi Kaneko,Hisashi Itô,Satoshi Nakano,Hirofumi Kusaka
标识
DOI:10.1016/j.expneurol.2008.07.017
摘要
Edaravone is a free-radical scavenger, an agent being widely used for cerebral ischemia in Japan. To evaluate its efficacy for possible treatment of amyotrophic lateral sclerosis (ALS), we performed a randomized blind trial in ALS model mice. After identification of the clinical onset in each female G93A mutant SOD1 transgenic mouse, we intraperitoneally administered multiple doses of edaravone to the mice and observed their motor symptoms. We also counted the number of lumbar motoneurons, determined the 3-nitrotyrosine/tyrosine ratio, and evaluated the abnormal SOD1 aggregation in the spinal cord at the 10th day after the edaravone injection. Edaravone significantly slowed the motor decline of the transgenic mice. The remaining motoneurons were significantly preserved in the higher-dose edaravone-administered group, and the 3-nitrotyrosine/tyrosine ratios were reduced dose-dependently. Intriguingly, the area of abnormal SOD1 deposition in the spinal cord was significantly decreased in the higher-dose edaravone-administered group. Our results indicate that edaravone was effective to slow symptom progression and motor neuron degeneration in the ALS model mice. These favorable actions might be attributable to the yet unidentified mechanism responsible for reducing the deposition of mutant SOD1.
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