Complement inhibitor prevents disruption of sodium channel clusters in a rabbit model of Guillain-Barré syndrome
Autor(es): Phongsisay Vongsavanh,Susuki Keiichiro,Matsuno Kenjiro,Yamahashi Takuyu,Okamoto Saori,Funakoshi Kei,Hirata Koichi,Shinoda Motoo,Yuki Nobuhiro
Resumo: 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.
Imprenta: Journal of Neuroimmunology, v. 205, n. 1-2, p. 101-104, 2008
Identificador do objeto digital: 10.1016/j.jneuroim.2008.09.016
Descritores: Guillain-Barre Syndrome - Biosynthesis ; Guillain-Barre Syndrome - Cell ; Guillain-Barre Syndrome - Cytopathology ; Guillain-Barre Syndrome - Proteins ; Guillain-Barre Syndrome - Public health
Data de publicação: 2008
