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冷却与α-硫辛酸的抗惊厥作用比较:一项神经化学研究。

The anticonvulant effect of cooling in comparison to α-lipoic acid: a neurochemical study.

机构信息

Medical Division, Medical Physiology Department, National Research Center, El-Bohouth St., P.O. 12622, Giza, Egypt.

出版信息

Neurochem Res. 2013 May;38(5):906-15. doi: 10.1007/s11064-013-0995-2. Epub 2013 Feb 7.

Abstract

Brain cooling has pronounced effects on seizures and epileptic activity. The aim of the present study is to evaluate the anticonvulsant effect of brain cooling on the oxidative stress and changes in Na(+), K(+)-ATPase and acetylcholinesterase (AchE) activities during status epilepticus induced by pilocarpine in the hippocampus of adult male rat in comparison with α-lipoic acid. Rats were divided into four groups: control, rats treated with pilocarpine for induction of status epilepticus, rats treated for 3 consecutive days with α-lipoic acid before pilocarpine and rats subjected to whole body cooling for 30 min before pilocarpine. The present findings indicated that pilocarine-induced status epilepticus was accompanied by a state of oxidative stress as clear from the significant increase in lipid peroxidation (MDA) and superoxide dismutase (SOD) and significant decrease in reduced glutathione and nitric oxide (NO) levels and the activities of catalase, AchE and Na(+), K(+)-ATPase. Pretreatment with α-lipoic acid ameliorated the state of oxidative stress and restored AchE to nearly control activity. However, Na(+), K(+)-ATPase activity showed a significant decrease. Rats exposed to cooling for 30 min before the induction of status epilepticus revealed significant increases in MDA and NO levels and SOD activity. AchE returned to control value while the significant decrease in Na(+), K(+)-ATPase persisted. The present data suggest that cooling may have an anticonvulsant effect which may be mediated by the elevated NO level. However, brain cooling may have drastic unwanted insults such as oxidative stress and the decrease in Na(+), K(+)-ATPase activity.

摘要

脑冷却对癫痫发作和癫痫活动有明显的影响。本研究的目的是评估脑冷却对匹鲁卡品诱导的成年雄性大鼠海马癫痫持续状态下氧化应激以及 Na(+)、K(+)-ATP 酶和乙酰胆碱酯酶 (AchE) 活性变化的抗惊厥作用,并与α-硫辛酸进行比较。大鼠分为四组:对照组、匹鲁卡品诱导癫痫持续状态组、匹鲁卡品前连续 3 天给予α-硫辛酸组和匹鲁卡品前全身冷却 30 分钟组。本研究结果表明,匹鲁卡品诱导的癫痫持续状态伴随着氧化应激状态,表现为脂质过氧化 (MDA) 和超氧化物歧化酶 (SOD) 显著增加,还原型谷胱甘肽和一氧化氮 (NO) 水平以及过氧化氢酶、AchE 和 Na(+)、K(+)-ATP 酶活性显著降低。α-硫辛酸预处理可改善氧化应激状态,并使 AchE 恢复接近正常活性。然而,Na(+)、K(+)-ATP 酶活性显著下降。在诱导癫痫持续状态前 30 分钟进行冷却的大鼠显示 MDA 和 NO 水平以及 SOD 活性显著增加。AchE 恢复到对照值,而 Na(+)、K(+)-ATP 酶活性显著下降。本研究数据表明,冷却可能具有抗惊厥作用,其机制可能与升高的 NO 水平有关。然而,脑冷却可能会产生严重的不良影响,如氧化应激和 Na(+)、K(+)-ATP 酶活性下降。

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