地塞米松处理和戊四氮点燃动物的氧化应激参数和行为。

Journal of epilepsy research Pub Date : 2021-12-31 eCollection Date: 2021-12-01 DOI:10.14581/jer.21017
Edson Fernando Muller Guzzo, Gabriel de Lima Rosa, Rafael Padilha Bremm, Caroline Paula Meska, Carmen Regla Vargas, Adriana Simon Coitinho
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引用次数: 1

摘要

背景和目的:氧化应激(OS)被定义为活性氧的过量产生,不能被抗氧化剂的作用中和,也可以作为细胞氧化还原平衡的改变。OS和癫痫之间的关系尚不完全清楚。本研究的目的是评价地塞米松对戊四唑点燃模型大鼠OS水平和记忆的影响。方法:将大鼠分为6组:不给药对照组、给药组、地西泮组、地塞米松组(1、2、4 mg/kg)。治疗动物隔天服用戊四唑,共15天。2 h后进行抑制回避试验,动物祭祀后评价OS。结果:在地塞米松治疗方面,与对照组相比,在抑制性回避测试方面无显著差异。在OS水平下,海马中过氧化氢酶活性水平降低,海马中硫代巴比妥酸活性物质和谷胱甘肽过氧化物酶水平升高。结论:地塞米松的抗惊厥作用尚不确定。随着细胞因子和炎症介质的释放,免疫机制似乎是这一过程的关键。产生OS的机制可能与所发现的抗惊厥作用有关。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Parameters of Oxidative Stress and Behavior in Animals Treated with Dexametasone and Submitted to Pentylenetetrazol Kindling.

Parameters of Oxidative Stress and Behavior in Animals Treated with Dexametasone and Submitted to Pentylenetetrazol Kindling.

Parameters of Oxidative Stress and Behavior in Animals Treated with Dexametasone and Submitted to Pentylenetetrazol Kindling.

Parameters of Oxidative Stress and Behavior in Animals Treated with Dexametasone and Submitted to Pentylenetetrazol Kindling.

Background and purpose: Oxidative stress (OS) is defined as an excessive production of reactive oxygen species that cannot be neutralized by the action of antioxidants, but also as an alteration of the cellular redox balance. The relationship between OS and epilepsy is not yet fully understood. The objective of this study was to evaluate the effect of dexamethasone on OS levels and memory in the kindling model induced by pentylenetetrazole.

Methods: The animals were divided in six groups: control group that received no treatment, vehicle group treated with vehicle, diazepam group, and groups treated with dexamethasone (1, 2 and 4 mg/kg). Treated animals received pentylenetetrazole in alternated days for 15 days. Inhibitory avoidance test was conducted in 2 hours and OS was evaluated after animal sacrifice.

Results: Regarding the treatment with dexamethasone, there was no significant difference when compared to the control groups in relation to the inhibitory avoidance test. On OS levels, there was a decrease in catalase activity levels in the hippocampus and an increase in thiobarbituric acid reactive substances and glutathione peroxidase levels in the hippocampus.

Conclusions: The anticonvulsant effect of dexametasone remains uncertain. Immunological mechanisms, with the release of cytokines and inflammatory mediators, seem to be the key to this process. The mechanisms that generate OS are probably related to the anticonvulsant effects found.

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