Efeito do ácido rosmarínico sobre as crises epilépticas e alterações comportamentais em diferentes modelos experimentais de epilepsia

Detalhes bibliográficos
Ano de defesa: 2016
Autor(a) principal: Grigoletto, Jéssica
Orientador(a): Não Informado pela instituição
Banca de defesa: Não Informado pela instituição
Tipo de documento: Dissertação
Tipo de acesso: Acesso aberto
Idioma: por
Instituição de defesa: Universidade Federal de Santa Maria
Brasil
Farmacologia
UFSM
Programa de Pós-Graduação em Farmacologia
Centro de Ciências da Saúde
Programa de Pós-Graduação: Não Informado pela instituição
Departamento: Não Informado pela instituição
País: Não Informado pela instituição
Palavras-chave em Português:
Link de acesso: http://repositorio.ufsm.br/handle/1/17987
Resumo: Epilepsy is a chronic neurological disease characterized by recurrent seizures. Current anticonvulsant drugs are ineffective in nearly one third of patients and may cause significant adverse effects. Rosmarinic acid is a naturally-occurring substance which displays several biological effects including antioxidant, anti inflammatory and neuroprotective activity. Since oxidative stress, inflammation and excitotoxicity play a role in the pathophysiology of seizures, we aimed the present study to test the hypothesis that rosmarinic acid displays anticonvulsant effects in different experimental models. Our results demonstrate that rosmarinic acid at the dose of 30 mg/kg increased the latencies to myoclonic and generalized seizures induced by PTZ and myoclonic seizures induced by pilocarpine. These data were confirmed by encephalographic recordings. Furthermore, the anticonvulsant dose of rosmarinic acid was anxiolytic, since it increased the number of crossings and the time of exploration in the center of open field. In the forced swimming test rosmarinic acid increased the immobility time. In another set of experiments, we evaluated the effects of sub-chronic treatment of rosmarinic acid (30 mg/kg) on epileptic seizures and behavioral changes in epilepsy model induced by pilocarpine. However, the treatment with rosmarinic acid caused no significant changes in the frequency of seizures nor in the behavioral comorbities evaluated. These results probably reflect the GABAergic action of rosmarinic acid, by inhibiting the enzyme GABA- transaminase, since it was anticonvulsant and anxiolytic activity in the acute protocols. However, anticonvulsant effect and/or disease-modifying effects were seen in the chronic model of epilepsy. Further studies are needed to investigate the clinical implications of these findings and their underlying mechanisms.