Dexamethasone attenuates low-frequency brainwave disturbances following acute seizures induced by pentylenetetrazol in Wistar rats

IF 4.6 Q2 MATERIALS SCIENCE, BIOMATERIALS
Rafaella Marques Ribeiro , Esther Padilha da Silveira , Vitoria Corrêa Santos , Leonan Lima Teixeira , Gisely Santiago Santos , Izabela Nascimento Galvão , Maria Klara Otake Hamoy , Allan Carlos da Silva Tiago , Daniella Bastos de Araújo , Nilton Akio Muto , Dielly Catrina Favacho Lopes , Moisés Hamoy
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Abstract

Seizures are neurological disorders triggered by an imbalance in the activity of excitatory and inhibitory neurotransmitters in the brain. When triggered chronically, this imbalance can lead to epilepsy. Critically, many of the affected individuals are refractory to treatment. Given this, anti-inflammatory drugs, in particular glucocorticoids, have been considered as a potential antiepileptogenic therapy. Glucocorticoids are currently used in the treatment of refractory patients, although there have been contradictory results in terms of their use in association with antiepileptic drugs, which reinforces the need for a more thorough investigation of their effects. In this context, the present study evaluated the effects of dexamethasone (DEX, 0.6 mg/kg) on the electroencephalographic (EEG) and histopathological parameters of male Wistar rats submitted to acute seizure induced by pentylenetetrazol (PTZ). The EEG monitoring revealed that DEX reduced the total brainwave power, in comparison with PTZ, in 12 h after the convulsive episode, exerting this effect in up to 36 h (p < 0.05 for all comparisons). An increase in the accommodation of the oscillations of the delta, alpha, and gamma frequencies was also observed from the first 12 h onwards, with the accommodation of the theta frequency occurring after 36 h, and that of the beta frequency 24 h after the seizure. The histopathological analyses showed that the CA3 region and hilum of the hippocampus suffered cell loss after the PTZ-induced seizure (control vs. PTZ, p < 0.05), although DEX was not able to protect these regions against cell death (PTZ vs. DEX + PTZ, p > 0.05). While DEX did not reverse the cell damage caused by PTZ, the data indicate that DEX has beneficial properties in the EEG analysis, which makes it a promising candidate for the attenuation of the epileptiform wave patterns that can precipitate refractory seizures.

地塞米松可减轻戊四唑诱发 Wistar 大鼠急性癫痫发作后出现的低频脑电波紊乱
癫痫发作是由大脑中兴奋性和抑制性神经递质活动失衡引发的神经系统疾病。当这种失衡长期触发时,就会导致癫痫。重要的是,许多患者对治疗产生耐药性。有鉴于此,抗炎药物,特别是糖皮质激素,被认为是一种潜在的抗癫痫疗法。糖皮质激素目前被用于治疗难治性患者,但其与抗癫痫药物联合使用的结果却相互矛盾,因此更有必要对其效果进行更深入的研究。在此背景下,本研究评估了地塞米松(DEX,0.6 毫克/千克)对戊四氮唑(PTZ)诱导急性癫痫发作的雄性 Wistar 大鼠脑电图(EEG)和组织病理学参数的影响。脑电图监测显示,与 PTZ 相比,DEX 在惊厥发作后 12 小时内降低了脑电波的总功率,这种作用持续了 36 小时(所有比较均小于 0.05)。从最初的 12 小时开始,还观察到δ、α和γ频率振荡的容纳性增加,θ频率的容纳性发生在 36 小时之后,β频率的容纳性发生在癫痫发作后 24 小时。组织病理学分析表明,PTZ诱导的癫痫发作后,海马CA3区和海马尾部细胞丢失(对照组与PTZ相比,< 0.05),尽管DEX不能保护这些区域免受细胞死亡(PTZ与DEX + PTZ相比,0.05)。虽然DEX并不能逆转PTZ造成的细胞损伤,但这些数据表明DEX在脑电图分析中具有有益的特性,这使它成为减弱可诱发难治性癫痫发作的痫样波形的一个有希望的候选药物。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
ACS Applied Bio Materials
ACS Applied Bio Materials Chemistry-Chemistry (all)
CiteScore
9.40
自引率
2.10%
发文量
464
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