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重组人促红细胞生成素通过防止运动神经元死亡和炎症反应,抑制肌萎缩侧索硬化症G93A-SOD1小鼠模型的症状发作和进展。

Recombinant human erythropoietin suppresses symptom onset and progression of G93A-SOD1 mouse model of ALS by preventing motor neuron death and inflammation.

作者信息

Koh Seong-Ho, Kim Youngchul, Kim Hyun Young, Cho Goang Won, Kim Kyung Sook, Kim Seung H

机构信息

Department of Neurology, College of Medicine, Hanyang University, Seoul, Korea.

出版信息

Eur J Neurosci. 2007 Apr;25(7):1923-30. doi: 10.1111/j.1460-9568.2007.05471.x.

DOI:10.1111/j.1460-9568.2007.05471.x
PMID:17439481
Abstract

Multifactorial pathogenic mechanisms, including inflammation, attenuated survival signals and enhanced death signals, are involved in amyotrophic lateral sclerosis (ALS). Erythropoietin (EPO) has recently been highlighted as a cytokine with various potent neuroprotective effects, including reduction of inflammation, enhancement of survival signals and prevention of neuronal cell death. This study was undertaken to evaluate the effect of recombinant human EPO (rhEPO) on ALS model mice. We treated 96 ALS model mice with vehicle only, or 1, 2.5 or 5 imu of rhEPO/g of mouse once every other week after they were 60 days old. The treatment significantly prolonged symptom onset and life span, preserved more motor neurons, enhanced survival signals, and attenuated inflammatory signals in a dose-dependent manner. These data suggest that treatment with rhEPO represents a potential therapeutic strategy for ALS.

摘要

多因素致病机制,包括炎症、生存信号减弱和死亡信号增强,都与肌萎缩侧索硬化症(ALS)有关。促红细胞生成素(EPO)最近被视为一种具有多种强大神经保护作用的细胞因子,包括减轻炎症、增强生存信号和预防神经元细胞死亡。本研究旨在评估重组人促红细胞生成素(rhEPO)对ALS模型小鼠的影响。我们将96只ALS模型小鼠在60日龄后每隔一周分别给予仅溶剂、或1、2.5或5国际单位/克小鼠体重的rhEPO进行治疗。该治疗以剂量依赖的方式显著延长了症状出现时间和寿命,保留了更多运动神经元,增强了生存信号,并减弱了炎症信号。这些数据表明,rhEPO治疗是一种潜在的ALS治疗策略。

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