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香根草调节实验性癫痫发作引起的大鼠大脑中的癫痫发作、氧化应激和细胞凋亡。

Vetiveria zizanioides modulates experimental epilepsy-induced seizures, oxidative stress, and apoptosis in the brain of rats.

机构信息

Department of Physiology, Faculty of Medicine, Süleyman Demirel University, Isparta, 32260, Turkey.

Department of Pathology, Faculty of Veterinary Medicine, Burdur Mehmet Akif Ersoy University, Burdur, Turkey.

出版信息

Metab Brain Dis. 2024 Nov 22;40(1):36. doi: 10.1007/s11011-024-01443-3.

DOI:10.1007/s11011-024-01443-3
PMID:39576294
Abstract

In this study, we investigated the protective actions of Vetiveria zizanioides oil (VET) against oxidative stress and apoptosis in a rat model of pentylenetetrazol (PTZ)-induced epilepsy model. Rats were divided into four groups: control (1 ml/kg saline, by gavage, 7 days + 1 ml/kg saline, i.p, single dose, 8th day), PTZ (1 ml/kg saline, by gavage, 7 days + 60 mg/kg, i.p, single dose, 8th day), PTZ + VET-200 (200 mg/kg VET, by gavage, 7 days + 60 mg/kg PTZ, i.p, single dose, 8th day), and PTZ + VET-400 (400 mg/kg VET, by gavage, 7 days + 60 mg/kg PTZ i.p, single dose, 8th day). Behavioral evaluation (Racine scale was used to classify the severity of seizures according to stages) and EEG recordings were taken. At the end of the experiment, the animals were sacrificed, and blood, hippocampus, and cerebral cortex tissues were removed for biochemical and histopathological examinations. PTZ injection increased the duration of the first epileptic spike and the total number of seizures and caused oxidative stress by increasing the total oxidant status (TOS). The treatment of PTZ induced neurodegenerative changes in the tissues such as increases of apoptosis, Bcl-2, Cyclin B1, and GABA expressions, but decreased Beta-tubulin. However, all the adverse changes of PTZ were modulated by the treatment of VET-200 and VET-400. In conclusion, these results showed that VET could ameliorate epileptic seiures, oxidative stress, and neuronal apoptosis in PTZ-induced seizures.

摘要

在这项研究中,我们调查了香根草油(VET)对戊四氮(PTZ)诱导的癫痫模型大鼠模型中氧化应激和细胞凋亡的保护作用。大鼠分为四组:对照组(1ml/kg 生理盐水,灌胃,7 天+1ml/kg 生理盐水,腹腔注射,单次剂量,第 8 天)、PTZ 组(1ml/kg 生理盐水,灌胃,7 天+60mg/kg,腹腔注射,单次剂量,第 8 天)、PTZ+VET-200 组(200mg/kg VET,灌胃,7 天+60mg/kg PTZ,腹腔注射,单次剂量,第 8 天)和 PTZ+VET-400 组(400mg/kg VET,灌胃,7 天+60mg/kg PTZ,腹腔注射,单次剂量,第 8 天)。进行行为评估(Racine 量表用于根据阶段对癫痫发作的严重程度进行分类)和脑电图记录。实验结束时,处死动物,取出血液、海马和大脑皮质组织进行生化和组织病理学检查。PTZ 注射增加了第一个癫痫棘波的持续时间和总发作次数,并通过增加总氧化剂状态(TOS)引起氧化应激。PTZ 诱导的组织神经退行性变化,如增加凋亡、Bcl-2、Cyclin B1 和 GABA 表达,但减少 Beta-微管蛋白。然而,VET-200 和 VET-400 的治疗调节了 PTZ 引起的所有不利变化。总之,这些结果表明 VET 可以改善 PTZ 诱导的癫痫发作中的癫痫发作、氧化应激和神经元凋亡。

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