Axonal protection using flecainide in experimental autoimmune encephalomyelitis

被引:138
作者
Bechtold, DA
Kapoor, R
Smith, KJ
机构
[1] Kings Coll London, Dept Neuroimmunol, London WC2R 2LS, England
[2] Natl Hosp Neurol & Neurosurg, London WC1N 3BG, England
关键词
D O I
10.1002/ana.20045
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Axonal degeneration is a major cause of permanent neurological deficit in multiple sclerosis (MS), but no current therapies for the disease are known to be effective at axonal protection. Here, we examine the ability of a sodium channel-blocking agent, flecainide, to reduce axonal degeneration in an experimental model of MS, chronic relapsing experimental autoimmune encephalomyelitis (CR-EAE). Rats with CR-EAE were treated with flecainide or vehicle from either 3 days before or 7 days after inoculation (dpi) until termination of the experiment at 28 to 30 dpi. Morphometric examination of neurofilament-labeled axons in the spinal cord of CR-EAE animals showed that both flecainide treatment regimens resulted in significantly higher numbers of axons surviving the disease (83 and 98% of normal) compared with controls (62% of normal). These findings indicate that flecainide and similar agents may provide a novel therapy aimed at axonal protection in MS and other neuroinflammatory disorders.
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收藏
页码:607 / 616
页数:10
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