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依地酸二钠钙对匹罗卡品诱导的癫痫发作的神经保护作用:对大鼠海马抗氧化状态、DNA 损伤和 Na(+)、K (+)-ATP 酶活性的调节。

Neuroprotective effects of idebenone against pilocarpine-induced seizures: modulation of antioxidant status, DNA damage and Na(+), K (+)-ATPase activity in rat hippocampus.

机构信息

Department of Pharmacology and Toxicology, Faculty of Pharmacy, Misr University for Science and Technology, 6th of October City, Egypt,

出版信息

Neurochem Res. 2014 Feb;39(2):394-402. doi: 10.1007/s11064-014-1236-z. Epub 2014 Jan 11.

Abstract

The current study investigated the neuroprotective activity of idebenone against pilocarpine-induced seizures and hippocampal injury in rats. Idebenone is a ubiquinone analog with antioxidant, and ATP replenishment effects. It is well tolerated and has low toxicity. Previous studies reported the protective effects of idebenone against neurodegenerative diseases such as Friedreich's ataxia and Alzheimer's disease. So far, the efficacy of idebenone in experimental models of seizures has not been tested. To achieve this aim, rats were randomly distributed into six groups. Two groups were treated with either normal saline (0.9 %, i.p., control group) or idebenone (200 mg/kg, i.p., Ideb200 group) for three successive days. Rats of the other four groups (P400, Ideb50 + P400, Ideb100 + P400, and Ideb200 + P400) received either saline or idebenone (50, 100, 200 mg/kg, i.p.) for 3 days, respectively followed by a single dose of pilocarpine (400 mg/kg, i.p.). All rats were observed for 6 h post pilocarpine injection. Latency to the first seizure, and percentages of seizures and survival were recorded. Surviving animals were sacrificed, and the hippocampal tissues were separated and used for the measurement of lipid peroxides, total nitrate/nitrite, glutathione and DNA fragmentation levels, in addition to catalase and Na(+), K(+)-ATPase activities. Results revealed that in a dose-dependent manner, idebenone (100, 200 mg/kg) prolonged the latency to the first seizure, elevated the percentage of survival and diminished the percentage of pilocapine-induced seizures in rats. Significant increases in lipid peroxides, total nitrate/nitrite, DNA fragmentation levels and catalase activity, in addition to a significant reduction in glutathione level and Na(+), K(+)-ATPase activity were observed in pilocarpine group. Pre-administration of idebenone (100, 200 mg/kg, i.p.) to pilocarpine-treated rats, significantly reduced lipid peroxides, total nitrate/nitrite, DNA fragmentation levels, and normalized catalase activity. Moreover, idebenone prevented pilocarpine-induced detrimental effects on brain hippocampal glutathione level, and Na(+), K(+)-ATPase enzyme activity in rats. Data obtained from the current investigation emphasized the critical role of oxidative stress in induction of seizures by pilocarpine and elucidated the prominent neuroprotective and antioxidant activities of idebenone in this model.

摘要

本研究旨在探讨艾地苯醌对匹罗卡品诱导的大鼠癫痫发作和海马损伤的神经保护作用。艾地苯醌是一种具有抗氧化和 ATP 补充作用的泛醌类似物。它具有良好的耐受性和低毒性。先前的研究报道了艾地苯醌对弗里德里希共济失调和阿尔茨海默病等神经退行性疾病的保护作用。迄今为止,艾地苯醌在癫痫实验模型中的疗效尚未得到检验。为了达到这个目的,大鼠被随机分为六组。两组分别用生理盐水(0.9%,ip,对照组)或艾地苯醌(200mg/kg,ip,Ideb200 组)连续 3 天处理。其他四组(P400、Ideb50+P400、Ideb100+P400 和 Ideb200+P400)分别接受生理盐水或艾地苯醌(50、100、200mg/kg,ip)3 天,随后单次腹腔注射匹罗卡品(400mg/kg)。所有大鼠在匹罗卡品注射后 6 小时内观察。记录首次癫痫发作的潜伏期、癫痫发作的百分比和存活率。存活的动物被处死,分离海马组织,用于测量脂质过氧化物、总硝酸盐/亚硝酸盐、谷胱甘肽和 DNA 片段化水平,以及过氧化氢酶和 Na(+)、K(+)-ATP 酶活性。结果表明,艾地苯醌(100、200mg/kg)以剂量依赖的方式延长了首次癫痫发作的潜伏期,提高了存活率,减少了匹罗卡品诱导的大鼠癫痫发作的百分比。在匹罗卡品组中观察到脂质过氧化物、总硝酸盐/亚硝酸盐、DNA 片段化水平和过氧化氢酶活性显著增加,谷胱甘肽水平和 Na(+)、K(+)-ATP 酶活性显著降低。预先给予艾地苯醌(100、200mg/kg,ip)可显著降低匹罗卡品处理大鼠的脂质过氧化物、总硝酸盐/亚硝酸盐、DNA 片段化水平,并使过氧化氢酶活性正常化。此外,艾地苯醌可防止匹罗卡品对大鼠海马组织谷胱甘肽水平和 Na(+)、K(+)-ATP 酶活性的有害影响。本研究获得的数据强调了氧化应激在匹罗卡品诱导癫痫发作中的关键作用,并阐明了艾地苯醌在该模型中的突出的神经保护和抗氧化作用。

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