Hashemi Paria, Moloudi Mohammad Raman, Vahabzadeh Zakaria, Izadpanah Esmael
Cellular and Molecular Research Center, Research Institute for Health Development, Kurdistan University of Medical Sciences, Sanandaj, Iran.
Neurosciences Research Center, Research Institute for Health Development, Kurdistan University of Medical Sciences, Sanandaj, Iran.
Neurochem Res. 2023 Jul;48(7):2187-2195. doi: 10.1007/s11064-023-03897-w. Epub 2023 Mar 1.
Temporal lobe epilepsy (TLE) is the most common form of partial and drug-resistant epilepsy, characterized by recurrent seizures originating from temporal lobe structures like the hippocampus. Hippocampal sclerosis and oxidative stress are two important factors in the pathogenesis of TLE that exacerbate epileptic seizures in this form of epilepsy. Recently, royal jelly (RJ) shown to have neuroprotective and antioxidant activities in several neurodegenerative models. Therefore, the aim of the present study was to investigate the pretreatment effect of RJ on epileptic seizures, hippocampal neuronal loss, and oxidative stress in the rat model of kainic acid (KA)-induced TLE. To this aim, 40 male Wistar rats weighing 200-250 g were divided into 4 groups, including control, vehicle, KA, and RJ + KA. Rats received RJ (150 mg/kg/day) for 14 days before induction of TLE with KA. Epileptic behaviors were evaluated according to Racine's scale. Oxidative stress markers including, malondialdehyde (MDA), total oxidant status (TOS) and total antioxidant capacity (TAC) as well as neuronal loss in the CA1 region of the hippocampus (using Nissl staining) were evaluated in all groups. Our findings showed that RJ pretreatment significantly reduced the seizure score and increased the latency to the first seizure. RJ also reduced MDA and TOS while increasing TAC. In addition, RJ reversed neuronal damage in the hippocampal CA1 and CA3 areas. In conclusion, our results suggest that RJ has anticonvulsant and neuroprotective effects in KA induced TLE via its antioxidative properties.
颞叶癫痫（TLE）是最常见的部分性和耐药性癫痫形式，其特征是源自海马等颞叶结构的反复发作性癫痫。海马硬化和氧化应激是TLE发病机制中的两个重要因素，它们会加剧这种癫痫形式中的癫痫发作。最近，蜂王浆（RJ）在几种神经退行性模型中显示出具有神经保护和抗氧化活性。因此，本研究的目的是探讨RJ对海藻酸（KA）诱导的TLE大鼠模型中癫痫发作、海马神经元损失和氧化应激的预处理作用。为此，将40只体重200 - 250克的雄性Wistar大鼠分为4组，包括对照组、溶剂组、KA组和RJ + KA组。在用KA诱导TLE前14天，大鼠接受RJ（150毫克/千克/天）。根据Racine量表评估癫痫行为。在所有组中评估氧化应激标志物，包括丙二醛（MDA）、总氧化状态（TOS）和总抗氧化能力（TAC）以及海马CA1区的神经元损失（使用尼氏染色）。我们的研究结果表明，RJ预处理显著降低了癫痫发作评分并延长了首次发作的潜伏期。RJ还降低了MDA和TOS，同时增加了TAC。此外，RJ逆转了海马CA1和CA3区的神经元损伤。总之，我们的结果表明，RJ通过其抗氧化特性在KA诱导的TLE中具有抗惊厥和神经保护作用。
