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Alpha‐tocopherol protects against memory impairment caused by L ‐NAME and modulates the injury marker and blood coagulant parameters
Author(s) -
Murad Leonardo Borges,
Guimarães Marcela Rodrigues Moreira,
Vianna Lucia Marques
Publication year - 2011
Publication title -
biofactors
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.204
H-Index - 94
eISSN - 1872-8081
pISSN - 0951-6433
DOI - 10.1002/biof.171
Subject(s) - medicine , stroke (engine) , platelet , fibrinogen , nitric oxide , lactate dehydrogenase , anesthesia , biochemistry , chemistry , mechanical engineering , engineering , enzyme
Cerebrovascular disease studies have shown similarity between humans and spontaneously hypertensive rats stroke‐prone rats in the development of spontaneous stroke and transitory ischemic attacks (TIA). In addition, nitric oxide (NO) suppression by L ‐arginine methyl ester ( L ‐NAME) can precipitate several vascular diseases including TIA and strokes. On the other hand, alpha‐tocopherol (AT) has been associated with beneficial effects on vascular disorders. Four groups were tested to evaluate AT effects on NO inhibition: AT, control (C), AT + L ‐NAME, and L ‐NAME. During 4 weeks, all groups had their physiologic parameters evaluated and were submitted to neurological tests. After the sacrifice of the animals, total L ‐lactate dehydrogenase, fibrinogen levels, and platelet counts were measured. Our results demonstrated improvement in memory function and sensory–motor function of the rats treated with AT. The AT treatment also demonstrated a significant difference on the injury identifier, fibrinogen levels, and platelet count between the treated groups and the L ‐NAME group. In conclusion, AT reversed damaging L ‐NAME neurological effects and could be considered as a possible protective agent in neurological diseases.