Anticonvulsant effect of a natural compound 𝞪,β-epoxy-carvone and its action on the nerve excitability.

• Autor(a) principal: ALMEIDA, Reinaldo Nóbrega de.
• Data de Publicação: 2008
• Outros Autores: SOUSA, Damião Pergentino de., NÓBREGA, Franklin Ferreira de Farias., CLAUDINO, Fladmir de Sousa., ARAÚJO, Demétrius Antonio Machado., LEITE, José Roberto., MATTEI, Rita.
• Tipo de documento: Artigo
• Idioma: eng
• Título da fonte: Biblioteca Digital de Teses e Dissertações da UFCG
• Texto Completo: http://dspace.sti.ufcg.edu.br:8080/jspui/handle/riufcg/37238
• topic: 𝞪,β-epoxy-carvone; Anticonvulsant effect - 𝞪,β-epoxy-carvone; Nerve excitability; Convulsions induced; Anticonvulsant activity; Essential oils; Monoterpene; Epilepsy; Isolated nerve; Compound action potential; Antioxidant; Efeito anticonvulsivante - 𝞪,β-epoxy-carvone; Excitabilidade nervosa; Convulsões induzidas; Atividade anticonvulsivante; Óleos essenciais; Monoterpeno; Epilepsia; Nervo isolado; Potencial de ação do composto; Antioxidante; Farmácia.; Química.

The anticonvulsant effect of 𝞪,β-epoxy-carvone (EC), a monoterpene monocyclic, was investigated in three animal models. EC at 300 or 400 mg/kg promoted protection of 75% and 87.5%, respectively, against convulsions induced chemically by pentylenetetrazole (PTZ) and it was efficient in prevents the tonic convulsions induced by maximal electroshock (MES) in doses of 200, 300 or 400 mg/kg, resulting in 25%, 25% and 100% of protection, respectively. This monoterpene was also capable to promote an increase of latency for development of convulsions induced by picrotoxin (PIC) at 300 or 400 mg/kg and presented a significant protection against convulsions at doses of 200, 300 or 400 mg/kg, resulting in 12.5%, 12.5% and 100% of protection, respectively. On the other hand, the anticonvulsant effect of EC, was not affected by pretreatment with flumazenil (FLU), a selective antagonist of benzodiazepine site of GABAA receptor. Additionally was observed that EC treatment reduced the levels of in vitro lipoperoxidation and decreased (21.2%) the amplitude of compound action potential after 30 min of incubation. The present results clearly indicate the ability of EC to modulate the anticonvulsant and antioxidant effects. However, our data sug- gests that the action mechanisms are not due a direct activation of the GABAA benzodiazepine receptors, but could be associated with the reduction of isolated nerve excitability, possibly involving a voltage-gated Na+ channels blockade.