立体定向和功能性神经外科杂志 ›› 2026, Vol. 39 ›› Issue (1): 7-14.DOI: 10.19854/j.cnki.1008-2425.2026.01.0002

• 论著 • 上一篇    下一篇

卡马西平通过NLRP3/Caspase-1/IL-1β通路减少锂-匹罗卡品诱导的慢性癫痫大鼠的细胞焦亡

彭琼, 王强, 杨萍, 卢军, 石璐, 彭红莉, 朱勇, 黄亚辉   

  1. 410007 长沙 湖南省第二人民医院(湖南省脑科医院)癫痫中心(彭琼,卢军,黄亚辉),湖南省第二人民医院(湖南省脑科医院)精神科(王强,杨萍,石璐,彭红莉),湖南省第二人民医院(湖南省脑科医院)神经外科(朱勇)
  • 收稿日期:2025-12-17 出版日期:2026-02-25 发布日期:2026-08-25
  • 通讯作者: 黄亚辉 158386302@qq.com
  • 基金资助:
    湖南省自然科学基金项目(编号:2023JJ60291,2024JJ9360),湖南省卫生健康委科研课题项目(编号:D202319017874,B202303077762),湖南省临床医学研究中心项目(编号:2023SK4020)

Carbamazepine reduces pyroptosis via the nLRP3/caspase-1/IL-1β pathway in lithium-pilocarpine-induced chronic epileptic rats

Peng Qiong1, Wang Qiang2, Yang Ping2, Lu Jun1, Shi Lu2, Peng Hongli2, Zhu Yong3, Huang Yahui1*   

  1. 1. Department of Epilepsy Center,The Second People's Hospital of Hunan Province (Hunan Brain Hospital),Changsha,Hunan 410007,China.
    2. Department of Psychiatry,The Second People's Hospital of Hunan Province (Hunan Brain Hospital),Changsha, Hunan 410007,China.
    3. Department of Neurosurgery,The Second People's Hospital of Hunan Province (Hunan Brain Hospital),Changsha,Hunan 410007,China
  • Received:2025-12-17 Online:2026-02-25 Published:2026-08-25
  • Contact: Huang Yahui 158386302@qq.com

摘要: 目的 探讨卡马西平在锂-匹罗卡品诱导的慢性自发性复发性癫痫大鼠模型中降低NLRP3/ Caspase-1/ IL-1β信号通路诱导细胞焦亡的作用机制。方法 96只大鼠随机均等分配到正常对照组、CSRS组、CSRS+CBZ50组、CSRS+CBZ100组,构建锂-匹罗卡品癫痫大鼠模型,通过免疫荧光检测海马神经元焦亡,免疫组化和ELISA检测IL-1β蛋白水平,实时PCR和Western blot检测Caspase-1、ASC-1和NLRP3的表达水平。结果 卡马西平减轻了锂-匹罗卡品诱导的癫痫发作频率,并降低了海马神经元中IL-1β水平。此外,IL-1β水平降低是通过卡马西平诱导的Caspase-1依赖性焦亡抑制实现的,而神经元焦亡减少是由于NLRP3炎症小体生成减少。结论 卡马西平降低IL-1β的作用可能是通过减少海马神经元中NLRP3/Caspase-1通路诱导的焦亡来实现的。

关键词: 卡马西平, 发作, 细胞焦亡, 白细胞介素-1β, Nod样受体蛋白3(NLRP3)

Abstract: Objective To investigate the mechanism by which carbamazepine reduces pyroptosis induced by the NLRP3/Caspase-1/IL-1β signaling pathway in a lithium-pilocarpine-induced rat model of chronic spontaneous recurrent seizures. Methods Ninety-six rats were randomly and equally assigned to four groups:normal control group,CSRS group,CSRS+CBZ50 group,and CSRS+CBZ100 group.The lithium-pilocarpine model of epileptic rats was established.Hippocampal neuronal pyroptosis was detected using immunofluorescence.IL-1β protein levels were measured by immunohistochemistry and ELISA.The expression levels of Caspase-1,ASC,and NLRP3 were detected using real-time PCR and Western blot. Results Carbamazepine alleviated the frequency of lithium-pilocarpine-induced seizures and reduced IL-1β levels in hippocampal neurons.Furthermore,the reduction in IL-1β levels was achieved through carbamazepine-induced inhibition of Caspase-1-dependent pyroptosis.The decrease in neuronal pyroptosis resulted from reduced NLRP3 inflammasome formation. Conclusion The effect of carbamazepine in reducing IL-1β may be achieved by decreasing pyroptosis induced by the NLRP3/Caspase-1 pathway in hippocampal neurons.

Key words: Carbamazepine, Seizures, Pyroptosis, IL-1β, Nod like receptor protein (NLRP3)

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