Anticonvulsant effect of a natural compound α,β-epoxy-carvone and its action on the nerve excitability
Anticonvulsant effect of a natural compound α,β-epoxy-carvone and its action on the nerve excitability
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DOI：
10.1016/j.neulet.2008.07.037
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发表时间：
2008-09-26
影响因子：
2.5
通讯作者：
Mattei, Rita
中科院分区：
文献类型：
--
作者：
de Almeida, Reinaldo Nobrega;de Sousa, Damiao Pergentino;Mattei, Rita
用3种动物模型研究了单萜单环化合物α，β-环氧香芹酮(EC)的抗惊厥作用。300或400 mg/kg的EC对小鼠的保护率分别为75%和87.5%。对戊四氮(PTZ)化学性惊厥和200、300、400 mg/kg最大电休克(MES)所致的强直性惊厥均有较好的保护作用，保护率分别为25%、25%和100%。该单萜还能促进300或400 mg/kg印防己毒素(PIC)引起的惊厥潜伏期的延长，并对200、300和400 mg/kg剂量的惊厥有明显的保护作用，分别为12.5%、12.5%和100%。而预先给予GABA(A)受体的苯二氮卓类受体拮抗剂氟马西尼(Flu)则不影响EC的抗惊厥作用。此外，还观察到EC处理降低了体外脂质过氧化水平，并在孵育30min后使复合动作电位的幅度降低了21.2%。目前的结果清楚地表明EC具有调节抗惊厥和抗氧化作用的能力。然而，我们的数据表明，这种作用机制不是由于GABAA苯二氮卓类受体的直接激活，而可能与降低分离的神经兴奋性有关，可能涉及电压门控Na+通道阻断。皇冠版权所有(C)2008由爱思唯尔爱尔兰有限公司出版。保留所有权利。
The anticonvulsant effect of alpha,beta-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 GABA(A) 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 suggests 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. Crown Copyright (C) 2008 Published by Elsevier Ireland Ltd. All rights reserved.