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尼莫地平对匹罗卡品诱导癫痫发作后幼鼠的抗氧化作用。

Antioxidant effect of nimodipine in young rats after pilocarpine-induced seizures.

作者信息

Nascimento Viviane S, D'alva Márcia S, Oliveira Aline A, Freitas Rivelilson M, Vasconcelos Silvânia M M, Sousa Francisca C F, Fonteles Marta M F

机构信息

Department of Physiology and Pharmacology, Laboratory of Neuropharmacology, School of Medicine, Federal University of Ceará. Rua Cel. Nunes de Melo 1127, 60431-270, Fortaleza, CE, Brazil.

出版信息

Pharmacol Biochem Behav. 2005 Sep;82(1):11-6. doi: 10.1016/j.pbb.2005.07.001. Epub 2005 Aug 22.

Abstract

Nimodipine (ND) is a centrally active calcium antagonist that blocks the voltage-dependent L-type channels. Its antiepileptic properties have been proved in various animal models, including pilocarpine-induced seizures in adult rats. In order to investigate protective effects of the ND (10 (ND10) and 30 mg/kg (ND30), i.p.), young male rats (21-day-old) received ND injections before pilocarpine administration (400 mg/kg, s.c., pilocarpine group (P400)). The pretreatment with ND10 and ND30 prolonged the latencies of seizures and death on this seizure model. ND pretreatment in two doses decreased the levels of lipid peroxidation when compared to pilocarpine group. The P400 administration increased the striatal catalase activity. However, the administration of ND, in dose of 30 mg/kg, 30 min before pilocarpine, preserved catalase activity in normal levels. On the other hand, no change was detected in the animals treated with the dose of 10 mg/kg. Our results confirm the neuroprotective effect of ND on the seizures in young rats, suggesting that this drug acts positively on lipid peroxidation. Our observations shows that nimodipine cannot induces these effects via blockade of Ca(2+)-channel.

摘要

尼莫地平(ND)是一种具有中枢活性的钙拮抗剂,可阻断电压依赖性L型通道。其抗癫痫特性已在各种动物模型中得到证实,包括成年大鼠匹罗卡品诱导的癫痫发作。为了研究ND(10mg/kg(ND10)和30mg/kg(ND30),腹腔注射)的保护作用,年轻雄性大鼠(21日龄)在给予匹罗卡品(400mg/kg,皮下注射,匹罗卡品组(P400))之前接受ND注射。ND10和ND30预处理延长了该癫痫模型中癫痫发作和死亡的潜伏期。与匹罗卡品组相比,两种剂量的ND预处理均降低了脂质过氧化水平。P400给药增加了纹状体过氧化氢酶活性。然而,在匹罗卡品给药前30分钟给予30mg/kg剂量的ND可使过氧化氢酶活性保持在正常水平。另一方面,用10mg/kg剂量治疗的动物未检测到变化。我们的结果证实了ND对幼鼠癫痫发作的神经保护作用,表明该药物对脂质过氧化有积极作用。我们的观察结果表明,尼莫地平不能通过阻断Ca(2 +)通道诱导这些效应。

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