Hakimi Naeini Saghi, Rajabi-Maham Hassan, Azizi Vahid, Hosseini Abdolkarim
Department of Animal Sciences and Marine Biology, Faculty of Life Sciences and Biotechnology, Shahid Beheshti University, Tehran, Iran.
Front Pharmacol. 2024 Aug 23;15:1392325. doi: 10.3389/fphar.2024.1392325. eCollection 2024.
Epilepsy, characterized by recurrent seizures, poses a significant health challenge globally. Despite the availability of anti-seizure medications, their adverse effects and inadequate efficacy in controlling seizures propel the exploration of alternative therapeutic measures. In hypothesis, glycitin is a phytoestrogenic compound found in soybeans and due to its estrogenic properties may have anti-epileptic and neuroprotective effects. This study investigates the potential anti-epileptic properties of glycitin in the context of pentylenetetrazol (PTZ) induced seizures in male Wistar rats. The rats were pretreated with varying doses of glycitin (5, 10, and 20 mg/kg) before PTZ (35 mg/kg) administration, and assessments included behavioral observations and histological evaluation via hematoxylin and eosin (H&E) staining. Additionally, oxidative stress markers, such as malondialdehyde (MDA), glutathione peroxidase (GPx), and superoxide dismutase (SOD) levels, were quantified to examine glycitin's impact on oxidative stress. Molecular analysis was conducted to assess the activation of the Nuclear factor erythroid 2-related factor (Nrf2)/Heme oxygenase 1 (HO-1) signaling pathway. Results indicated that glycitin pretreatment effectively mitigated PTZ-induced convulsive behaviors, supported by histological findings from H&E staining. Furthermore, glycitin administration led to significant alterations in MDA, GPx, and SOD levels, suggestive of its ability to modulate oxidative stress. Notably, glycitin treatment induced activation of the Nrf2/HO-1 signaling pathway. These findings underscore the potential of glycitin as an anticonvulsant agent, elucidating its mechanism of action through histological protection, modulation of oxidative stress markers, and activation of the Nrf2/HO-1 signaling pathway.
癫痫以反复发作的癫痫发作为特征，在全球范围内构成了重大的健康挑战。尽管有抗癫痫药物可用，但它们的不良反应以及在控制癫痫发作方面的疗效不足促使人们探索替代治疗措施。理论上，大豆苷元是一种存在于大豆中的植物雌激素化合物，由于其雌激素特性，可能具有抗癫痫和神经保护作用。本研究在雄性Wistar大鼠中，研究了大豆苷元在戊四氮（PTZ）诱导的癫痫发作背景下的潜在抗癫痫特性。在给予PTZ（35mg/kg）之前，用不同剂量的大豆苷元（5、10和20mg/kg）对大鼠进行预处理，评估包括行为观察和通过苏木精和伊红（H&E）染色进行组织学评估。此外，对氧化应激标志物，如丙二醛（MDA）、谷胱甘肽过氧化物酶（GPx）和超氧化物歧化酶（SOD）水平进行定量，以检查大豆苷元对氧化应激的影响。进行分子分析以评估核因子红细胞2相关因子（Nrf2）/血红素加氧酶1（HO-1）信号通路的激活情况。结果表明，大豆苷元预处理有效地减轻了PTZ诱导的惊厥行为，H&E染色的组织学结果支持了这一点。此外，给予大豆苷元导致MDA、GPx和SOD水平发生显著变化，表明其具有调节氧化应激的能力。值得注意的是，大豆苷元治疗诱导了Nrf2/HO-1信号通路的激活。这些发现强调了大豆苷元作为抗惊厥剂的潜力，并通过组织学保护、氧化应激标志物的调节以及Nrf2/HO-1信号通路的激活阐明了其作用机制。
