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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 |
| Hits 191 Download times 65 Received:November 25, 2025 |
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| DOI
10.11656/j.issn.1672-1519.2026.02.12 |
| Key Words
Rongchang Capsule;catamenial epilepsy;neuronal model of catamenial epileptic;NMDA pathway;antiepileptic mechanism |
| Author Name | Affiliation | | YAN Haihong | Children's Hospital of Shanxi, Taiyuan 030009, China | | GUO Ting | The First Affiliated Hospital of Henan University of Chinese Medicine, Zhengzhou 450000, China | | CHEN Haipeng | Dongfang Hospital Beijing University of Chinese Medicine, Beijing 100078, China | | ZHANG Xilian | First Teaching Hospital of Tianjin University of Traditional Chinese Medicine, Tianjin 300381, China
National Clinical Research Center for Chinese Medicine, Tianjin 300381, China | | RONG Ping | First Teaching Hospital of Tianjin University of Traditional Chinese Medicine, Tianjin 300381, China
National Clinical Research Center for Chinese Medicine, Tianjin 300381, China | | LI Ruiben | First Teaching Hospital of Tianjin University of Traditional Chinese Medicine, Tianjin 300381, China
National Clinical Research Center for Chinese Medicine, Tianjin 300381, China | | FU Qianfang | First Teaching Hospital of Tianjin University of Traditional Chinese Medicine, Tianjin 300381, China
National Clinical Research Center for Chinese Medicine, Tianjin 300381, China | | MA Rong | First Teaching Hospital of Tianjin University of Traditional Chinese Medicine, Tianjin 300381, China
National Clinical Research Center for Chinese Medicine, Tianjin 300381, China |
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| Abstract
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| [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. |
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