Tang Nou-Ying, Lin Yi-Wen, Ho Tin-Yun, Cheng Chin-Yi, Chen Chao-Hsiang, Hsieh Ching-Liang
School of Chinese Medicine, College of Chinese Medicine, China Medical University, Taichung 40402, Taiwan.
School of Post-Baccalaureate Chinese Medicine, College of Chinese Medicine, China Medical University, Taichung 40402, Taiwan.
Evid Based Complement Alternat Med. 2017;2017:9732854. doi: 10.1155/2017/9732854. Epub 2017 Feb 23.
Epileptic seizures are crucial clinical manifestations of recurrent neuronal discharges in the brain. An imbalance between the excitatory and inhibitory neuronal discharges causes brain damage and cell loss. Herbal medicines offer alternative treatment options for epilepsy because of their low cost and few side effects. We established a rat epilepsy model by injecting kainic acid (KA, 12 mg/kg, i.p.) and subsequently investigated the effect of (UR) and its underlying mechanisms. Electroencephalogram and epileptic behaviors revealed that the KA injection induced epileptic seizures. Following KA injection, S100B levels increased in the hippocampus. This phenomenon was attenuated by the oral administration of UR and valproic acid (VA, 250 mg/kg). Both drugs significantly reversed receptor potentiation for advanced glycation end product proteins. Rats with KA-induced epilepsy exhibited no increase in the expression of metabotropic glutamate receptor 3, monocyte chemoattractant protein 1, and chemokine receptor type 2, which play a role in inflammation. Our results provide novel and detailed mechanisms, explaining the role of UR in KA-induced epileptic seizures in hippocampal CA1 neurons.
癫痫发作是大脑中神经元反复放电的关键临床表现。兴奋性和抑制性神经元放电之间的失衡会导致脑损伤和细胞丢失。草药因其成本低、副作用少，为癫痫提供了替代治疗选择。我们通过注射 kainic 酸（KA，12mg/kg，腹腔注射）建立了大鼠癫痫模型，随后研究了（UR）的作用及其潜在机制。脑电图和癫痫行为显示，注射 KA 可诱发癫痫发作。注射 KA 后，海马体中 S100B 水平升高。口服 UR 和丙戊酸（VA，250mg/kg）可减轻这种现象。两种药物均显著逆转了晚期糖基化终产物蛋白的受体增强作用。KA 诱导的癫痫大鼠在代谢型谷氨酸受体 3、单核细胞趋化蛋白 1 和 2 型趋化因子受体的表达上没有增加，这些在炎症中起作用。我们的结果提供了新颖而详细的机制，解释了 UR 在 KA 诱导的海马 CA1 神经元癫痫发作中的作用。
