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| 基于NMDA通路探讨茸菖胶囊干预月经性癫痫神经元模型的抗痫机制 |
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闫海虹1, 郭婷2, 陈海鹏3, 张喜莲4,5, 戎萍4,5, 李瑞本4,5, 付乾芳4,5, 马融4,5
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1.山西省儿童医院, 太原 030013;2.河南中医药大学第一附属医院, 郑州 450003;3.北京中医药大学东方医院, 北京 100078;4.天津中医药大学第一附属医院, 天津 300381;5.中医国家临床医学研究中心, 天津 300381
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| 摘要: |
| [目的] 观察茸菖胶囊对月经性癫痫神经元模型的N-甲基-D-天冬氨酸（NMDA）受体的影响，探讨其作用机制。[方法] 以外源性添加雌二醇（E2）的无镁诱导的癫痫神经元（月经性癫痫神经元模型）为研究对象，随机分为7组：对照组、癫痫模型组、月经性癫痫模型组、丙戊酸钠组、茸菖低剂量组、茸菖中剂量组和茸菖高剂量组。观察各组神经元形态、放电频率、静息膜电位、24 h NMDA电流变化、NMDA受体1（NR1）、NMDA受体2A（NR2A）蛋白表达情况。[结果] 与对照组相比，月经性癫痫模型组高频高幅棘波放电明显增多、神经元数目明显减少，放电频率明显增加、静息膜电位明显升高、24 h NMDA通道电流密度明显增加（P < 0.05或P < 0.01），NR1蛋白表达明显降低、NR2A蛋白表达明显升高（P < 0.05或P < 0.01）。与月经性癫痫模型组相比，丙戊酸钠组高频高幅棘波放电减少、神经元数目增多，放电频率明显减少（P < 0.05），静息膜电位未见明显降低、24 h NMDA通道电流密度未见明显降低（P>0.05），NR1、NR2A蛋白表达未见明显改变（P>0.05）；茸菖高剂量组高频高幅棘波放电明显减少、神经元数目明显增多，放电频率明显减少、静息膜电位明显降低、24 h NMDA通道电流密度明显降低（P < 0.05），NR2A蛋白表达明显降低（P < 0.05），NR1蛋白表达未见明显升高（P>0.05）。[结论] 茸菖胶囊可能通过下调NR2A蛋白表达，降低NMDA受体介导的神经的异常兴奋，从而减轻外源性添加E2的无镁癫痫神经元的异常放电，发挥抗癫痫作用。 |
| 关键词: 茸菖胶囊 月经性癫痫 神经元模型 NMDA通路 抗痫机制 |
| DOI：10.11656/j.issn.1672-1519.2026.02.12 |
| 分类号:R285.5 |
| 基金项目:国家自然科学基金项目（81574018）；山西省基础研究计划项目（202403021222477） |
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| Anti-epileptic mechanism of Rongchang Capsule intervention in the neuronal model of catamenial epilepsy was discussed based on the NMDA pathway |
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YAN Haihong1, GUO Ting2, CHEN Haipeng3, ZHANG Xilian4,5, RONG Ping4,5, LI Ruiben4,5, FU Qianfang4,5, MA Rong4,5
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1.Children's Hospital of Shanxi, Taiyuan 030009, China;2.The First Affiliated Hospital of Henan University of Chinese Medicine, Zhengzhou 450000, China;3.Dongfang Hospital Beijing University of Chinese Medicine, Beijing 100078, China;4.First Teaching Hospital of Tianjin University of Traditional Chinese Medicine, Tianjin 300381, China;5.National Clinical Research Center for Chinese Medicine, Tianjin 300381, China
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| Abstract: |
| [Objective]To observe the effect of Rongchang Capsules on N-Methyl-D-aspartic acid(NMDA)receptor in the neuronal model of catamenial epilepsy, and to explore its mechanism.[Methods]The magnesium-free epileptic neurons induced by exogenous E2(catamenial epileptic neuron model)were randomly divided into 7 groups: control group, epilepsy model group, catamenial epilepsy model group, sodium valproate group and Rongchang Capsules low dose group, Rongchang Capsules middle dose group and Rongchang Capsules high dose group. The neuronal morphology, discharge frequency, resting membrane potential, 24 h NMDA current changes, NMDA Receptor 1(NR1)and NMDA Receptor 2A(NR2A)receptor protein expression were observed.[Results]Compared with the control group, the high - frequency and high - amplitude spike discharges in the catamenial epilepsy model group were significantly increased; the number of neurons was significantly decreased; the discharge frequency was significantly increased; the resting membrane potential was significantly increased; the 24 h NMDA channel current density was significantly increased(P < 0.05 or P < 0.01);the expression of NR1 protein was significantly decreased, and the expression of NR2A protein was significantly increased(P < 0.05 or P < 0.01). Compared with the catamenial epilepsy model group, the high-frequency high-amplitude spike wave discharge in the sodium valproate group was significantly decreased; the number of neurons increased; the discharge frequency decreased significantly (P < 0.05);the resting membrane potential and the 24 h NMDA channel current density was not decreased significantly(P>0.05);the expression of NR1 and NR2A protein did not change significantly(P>0.05);the high - frequency and high - amplitude spike wave discharge in the Rongchang capsules high dose group was significantly decreased; the number of neurons was significantly increased; the discharge frequency was significantly decreased; the resting membrane potential was significantly decreased and the 24 h NMDA channel current density was significantly decreased(P < 0.05), and the expression of NR2A protein was significantly decreased(P < 0.05), and the expression of NR1 protein was not significantly increased(P>0.05).[Conclusion]Rongchang Capsules may reduce the abnormal excitability of NMDA receptor-mediated nerves by down-regulating the expression of NR2A protein, thereby reducing the abnormal discharge of magnesium-free epileptic neurons supplemented with exogenous E2, thus exerting anti-epileptic effects. |
| Key words: Rongchang Capsule catamenial epilepsy neuronal model of catamenial epileptic NMDA pathway antiepileptic mechanism |
