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Complement inhibitor prevents disruption of sodium channel clusters in a rabbit model of Guillain-Barré syndrome.
- Source :
-
Journal of neuroimmunology [J Neuroimmunol] 2008 Dec 15; Vol. 205 (1-2), pp. 101-4. Date of Electronic Publication: 2008 Oct 29. - Publication Year :
- 2008
-
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.
- Subjects :
- Animals
Benzamidines
Complement C3 metabolism
Complement Inactivating Agents therapeutic use
Disease Models, Animal
Guanidines therapeutic use
Guillain-Barre Syndrome drug therapy
Guillain-Barre Syndrome physiopathology
Infusion Pumps, Implantable
Rabbits
Random Allocation
Ranvier's Nodes metabolism
Complement Inactivating Agents pharmacology
Guanidines pharmacology
Guillain-Barre Syndrome pathology
Ranvier's Nodes drug effects
Sodium Channels metabolism
Subjects
Details
- Language :
- English
- ISSN :
- 0165-5728
- Volume :
- 205
- Issue :
- 1-2
- Database :
- MEDLINE
- Journal :
- Journal of neuroimmunology
- Publication Type :
- Academic Journal
- Accession number :
- 18973956
- Full Text :
- https://doi.org/10.1016/j.jneuroim.2008.09.016