神经炎症
SOD1
神经保护
肌萎缩侧索硬化
转基因小鼠
脊髓
实验性自身免疫性脑脊髓炎
细胞因子
医学
免疫学
神经科学
炎症
转基因
生物
病理
疾病
生物化学
基因
作者
Yiheng Xie,Patrick Weydt,David Howland,Michel Kliot,Thomas Möller
出处
期刊:Neuroreport
[Ovid Technologies (Wolters Kluwer)]
日期:2004-11-01
卷期号:15 (16): 2513-2516
被引量:38
标识
DOI:10.1097/00001756-200411150-00016
摘要
Amyotrophic lateral sclerosis (ALS) is a devastating motor neuron disease. One mechanism involved in ALS pathology is neuroinflammation. Neuroinflammation is mediated by soluble pro-inflammatory molecules such as cytokines, prostaglandins and nitric oxide. Studies on transgenic mice demonstrated the expression of pro-inflammatory mediators in early stages of murine ALS. Recently a transgenic rat model became available. Since species differences in regard to cytokine expression have been reported in other disease models we set out to validate the neuroinflammatory hypothesis in the ALS-transgenic rat. We investigated the expression of inflammatory mediators and growth factors in the spinal cord by semi-quantitative RT-PCR. We found that several pro-inflammatory mediators are up-regulated at asymptomatic and end-stages, whereas VEGF, a neuroprotective factor was down-regulated.
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