Epilepsy is one of the most frequent neurological disorders characterized by an enduring predisposition to generate epileptic seizures. Oxidative stress is believed to directly participate in the pathways of neurodegenerations leading to epilepsy. Approximately, one-third of the epileptic patients who suffer from seizures do not receive effective medical treatment. Sodium valproate (SVP) is a commonly used antiepileptic drug (AED); however, it has toxic effects. Lutein (L), a carotenoid, has potent antioxidant and anti-inflammatory properties. The aim of this study was to determine the neuroprotective effect of sodium valproate (SVP) and lutein (L) in a rat model of pilocarpine- (PLC-) induced epilepsy. To achieve this aim, fifty rats were randomly divided into five groups. Group I: control, group II: received PLC (400 mg/kg intraperitoneally), group III: received PLC + SVP (500 mg/kg orally), group IV: received PLC + SVP + L (100 mg/kg orally), and group V: received (PLC + L). Racine Scale (RC) and latency period to onset seizure were calculated. After eight weeks, the hippocampus rotarod performance and histological investigations were performed. Oxidative stress was investigated in hippocampal homogenates. Results revealed that SVP and L, given alone or in combination, reduced the RC significantly, a significant delay in latency to PLC-kindling onset, and improved rotarod performance of rats compared with the PLC group. Moreover, L was associated with a reduction of oxidative stress in hippocampal homogenate, a significant decrease in serum tumor necrosis factor-alpha (TNF-α) level, and inhibition of cerebral injury and displayed antiepileptic properties in the PLC-induced epileptic rat model. Data obtained from the current research elucidated the prominent neuroprotective, antioxidant, and anti-inflammatory activities of lutein in this model. In conclusion, lutein cotreatment with AEDs is likely to be a promising strategy to improve treatment efficacy in patients suffering from epilepsy.

中文翻译：

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丙戊酸钠和叶黄素对毛果芸香碱白化大鼠癫痫模型神经保护作用的组织病理学和生化评估

癫痫是最常见的神经系统疾病之一，其特征是持久易发生癫痫发作。氧化应激被认为直接参与导致癫痫的神经变性途径。大约有三分之一的癫痫患者没有得到有效的治疗。丙戊酸钠（SVP）是一种常用的抗癫痫药（AED）；然而，它有毒性作用。叶黄素 (L) 是一种类胡萝卜素，具有强大的抗氧化和抗炎特性。本研究的目的是确定丙戊酸钠 (SVP) 和叶黄素 (L) 在毛果芸香碱 (PLC-) 诱发的癫痫大鼠模型中的神经保护作用。为了达到这个目的，五十只大鼠被随机分成五组。I组：对照，II组：接受PLC（腹膜内400mg/kg），III 组：接受 PLC + SVP（500 mg/kg 口服），IV 组：接受 PLC + SVP + L（100 mg/kg 口服），V 组：接受（PLC + L）。计算拉辛量表 (RC) 和癫痫发作的潜伏期。八周后，进行海马旋转杆性能和组织学研究。在海马匀浆中研究氧化应激。结果表明，与 PLC 组相比，SVP 和 L，单独或联合给药，显着降低了 RC，显着延迟了 PLC 点燃开始的潜伏期，并改善了大鼠的旋转棒性能。此外，L 与海马匀浆中氧化应激的减少、血清肿瘤坏死因子-α (TNF- 收到（PLC + L）。计算拉辛量表 (RC) 和癫痫发作的潜伏期。八周后，进行海马旋转杆性能和组织学研究。在海马匀浆中研究氧化应激。结果表明，与 PLC 组相比，SVP 和 L，单独或联合给药，显着降低了 RC，显着延迟了 PLC 点燃开始的潜伏期，并改善了大鼠的旋转棒性能。此外，L 与海马匀浆中氧化应激的减少、血清肿瘤坏死因子-α (TNF- 收到（PLC + L）。计算拉辛量表 (RC) 和癫痫发作的潜伏期。八周后，进行海马旋转杆性能和组织学研究。在海马匀浆中研究氧化应激。结果表明，与 PLC 组相比，SVP 和 L，单独或联合给药，显着降低了 RC，显着延迟了 PLC 点燃开始的潜伏期，并改善了大鼠的旋转棒性能。此外，L 与海马匀浆中氧化应激的减少、血清肿瘤坏死因子-α (TNF- 在海马匀浆中研究氧化应激。结果表明，与 PLC 组相比，SVP 和 L，单独或联合给药，显着降低了 RC，显着延迟了 PLC 点燃开始的潜伏期，并改善了大鼠的旋转棒性能。此外，L 与海马匀浆中氧化应激的减少、血清肿瘤坏死因子-α (TNF- 在海马匀浆中研究氧化应激。结果表明，与 PLC 组相比，SVP 和 L，单独或联合给药，显着降低了 RC，显着延迟了 PLC 点燃开始的潜伏期，并改善了大鼠的旋转棒性能。此外，L 与海马匀浆中氧化应激的减少、血清肿瘤坏死因子-α (TNF-α ) 水平，抑制脑损伤并在 PLC 诱导的癫痫大鼠模型中显示出抗癫痫特性。从当前研究中获得的数据阐明了叶黄素在该模型中的显着神经保护、抗氧化和抗炎活性。总之，叶黄素与 AED 联合治疗可能是提高癫痫患者治疗效果的一种有前景的策略。