| Literature DB >> 18973956 |
Vongsavanh Phongsisay1, Keiichiro Susuki, Kenjiro Matsuno, Takuyu Yamahashi, Saori Okamoto, Kei Funakoshi, Koichi Hirata, Motoo Shinoda, Nobuhiro Yuki.
Abstract
Complement-mediated disruption of voltage-gated sodium channels at the nodes of Ranvier acts in the development of acute motor axonal neuropathy. Nafamostat mesilate, a synthetic serine protease inhibitor, used in clinical practice for more than 20 years, has anti-complement activity. Acute motor axonal neuropathy rabbits obtained by GM1 ganglioside sensitization were or were not given nafamostat mesilate intravenously. Complement deposition and sodium channel disruption in the spinal anterior roots were significantly less frequent in the treated rabbits than in the controls. Nafamostat mesilate inhibited complement deposition and prevented sodium channel disruption. This provided the rationale for a clinical trial.Entities:
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Year: 2008 PMID： 18973956 DOI： 10.1016/j.jneuroim.2008.09.016
Source DB: PubMed Journal: J Neuroimmunol ISSN： 0165-5728 Impact factor: 3.478