Phytomedicine : international journal of phytotherapy and phytopharmacology · 2026
Arisaematis Rhizoma protects against refractory status epilepticus via inhibiting caspase-1-mediated neuroinflammation.
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Zhang Shuo, Guo Xiongfeng, Wang Rui, Ye Junxiu, Ye Huimin, Yan Mengqi, Shan Qiyuan, Sun Minjuan, Gong Yiwei, Wu Zhangyi, Han Fang, Du Yu, Liang Jingjia, Jin Qianxing, Xie Shengyang, Tang Yingying, Chen Zhong, Xu Cenglin
Аннотация
BACKGROUND: Status epilepticus (SE), the most severe form of epilepsy, is frequently refractory to first-line diazepam (DZP) therapy. Activation of neuroinflammation is closely associated with the development of refractory SE. AR, a traditional Chinese medicine, reportedly possesses anti-neuroinflammatory properties.
PURPOSE: This study aimed to investigate the effects of AR extract in two animal models of refractory SE and explore its underlying mechanisms.
METHODS: The main components of AR were identified by LC-MS. Pilocarpine- and kainic acid (KA)-induced refractory SE models were established to evaluate AR efficacy. Neuronal protection was assessed via NeuN staining. Network pharmacology and molecular docking were applied to predict therapeutic targets and active components. Potential mechanisms were verified by WB, immunohistochemistry, in vitro electrophysiology, and caspase-1⁻/⁻ mice.
RESULTS: AR extract attenuated acute seizures in pentylenetetrazol and KA models. Co-administration of AR with DZP effectively terminated refractory SE induced by pilocarpine or KA. AR also conferred neuroprotection against SE-induced hippocampal neuronal loss. Network analysis indicated involvement of inflammatory pathways, particularly caspase-1/IL-1β signaling. Immunohistochemistry confirmed that AR suppressed caspase-1 upregulation in refractory SE mice. It also directly inhibited caspase-1-mediated increases in neuronal excitability and excitatory synaptic transmission; these effects were absent in caspase-1⁻/⁻ mice, where AR lost its efficacy. Finally, schaftoside, a key active component of AR, replicated AR's therapeutic effects and exhibited strong binding affinity to caspase-1.
CONCLUSION: Our findings reveal that AR terminates refractory SE by inhibiting caspase-1, suggesting its potential as a therapeutic strategy for this neurological emergency.
PURPOSE: This study aimed to investigate the effects of AR extract in two animal models of refractory SE and explore its underlying mechanisms.
METHODS: The main components of AR were identified by LC-MS. Pilocarpine- and kainic acid (KA)-induced refractory SE models were established to evaluate AR efficacy. Neuronal protection was assessed via NeuN staining. Network pharmacology and molecular docking were applied to predict therapeutic targets and active components. Potential mechanisms were verified by WB, immunohistochemistry, in vitro electrophysiology, and caspase-1⁻/⁻ mice.
RESULTS: AR extract attenuated acute seizures in pentylenetetrazol and KA models. Co-administration of AR with DZP effectively terminated refractory SE induced by pilocarpine or KA. AR also conferred neuroprotection against SE-induced hippocampal neuronal loss. Network analysis indicated involvement of inflammatory pathways, particularly caspase-1/IL-1β signaling. Immunohistochemistry confirmed that AR suppressed caspase-1 upregulation in refractory SE mice. It also directly inhibited caspase-1-mediated increases in neuronal excitability and excitatory synaptic transmission; these effects were absent in caspase-1⁻/⁻ mice, where AR lost its efficacy. Finally, schaftoside, a key active component of AR, replicated AR's therapeutic effects and exhibited strong binding affinity to caspase-1.
CONCLUSION: Our findings reveal that AR terminates refractory SE by inhibiting caspase-1, suggesting its potential as a therapeutic strategy for this neurological emergency.