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Lewis rat EAN is suppressed by the 21–aminosteroid tirilazad mesylate (U–74006F)
Author(s) -
Feasby T. E.,
Hahn A. F.,
Lovgren D.,
Wilkie L.
Publication year - 1994
Publication title -
neuropathology and applied neurobiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.538
H-Index - 95
eISSN - 1365-2990
pISSN - 0305-1846
DOI - 10.1111/j.1365-2990.1994.tb00984.x
Subject(s) - mesylate , medicine , pharmacology , chemistry , organic chemistry
Lewis rat experimental allergic neuritis (EAN) was treated with the 21–aminosteroid, tirilazad mesylate (U–74006F). High doses of tirilazad mesylate, begun just before the onset of clinical signs, reduced the clinical and pathological severity of the disease. In rats immunized with a high dose of myelin, axonal degeneration was a major pathological feature. Tirilazad mesylate reduced the amount of axonal degeneration but had little effect on the other pathological features of EAN, such as inflammation and demyelination. Tirilazad mesylate may block axonal degeneration by inhibiting lipid peroxidation of axonal membranes. Inhibition of axonal degeneration is an important goal in the treatment of human neuropathies.