Journal of ethnopharmacology · 2025
Anticonvulsant effect of Stachydrine on pentylenetetrazole-induced kindling seizure mouse model via Notch and NMDAR signaling pathways.
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Li Qifa, Li Ruipeng, Ge Biying, Luo Xiaoqin, Xu Jing, Fu Lei, Kong Yue, Yang Jin-Yi, Li Shao
Аннотация
ETHNOPHARMACOLOGICAL RELEVANCE: Stachydrine (STA), the principal bioactive alkaloid of Leonurus japonicus (Motherwort/"Yi Mu Cao"), may derive its ethnopharmacological relevance for epilepsy management from the botanical origin-Motherwort's documented traditional use in treating seizures and other neurological cardiovascular diseases.
AIM OF THE STUDY: To validate STA's ethnomedicinal claim an anticonvulsant by mechanistically interrogating its dual modulation of Notch1-driven neuroinflammation and NMDA receptor-mediated excitotoxicity, which are two key hallmarks of chronic epileptogenesis.
MATERIALS AND METHODS: Male C57BL/6 mice were divided into three groups to evaluate the neuroprotective and an anticonvulsant effects of STA in the PTZ-induced seizure model: Control group, PTZ group, and PTZ + STA group. Behavioral seizure scoring and cognitive tests were integrated with EEG recordings to assess neuronal synchronization. Molecular mechanisms were dissected via hippocampal immunohistochemistry and Western blotting.
RESULTS: Our results showed that daily oral administration of STA for a duration of 25 days significantly reduced seizure scores. EEG recordings indicated that STA treatment resulted in a notable reduction in both total brainwave power and firing amplitude within the groups receiving STA. Furthermore, STA administration provided cognitive protection against kindling-associated deficits, as demonstrated by improved alteration behavior and recognition index in Y-maze and object recognition tests. STA administration reduced neuronal loss and glial cell activation. Additionally, significant downregulation of NMDA receptor subunits, CAMK2, caspase-3, Notch1, and Hes1 expression levels was observed following STA administration.
CONCLUSION: These findings suggest that STA provides neuroprotection against PTZ-induced epilepsy by modulating the Notch and NMDA receptor pathways, thus addressing neuroinflammation and apoptosis resulting from excitotoxicity.
AIM OF THE STUDY: To validate STA's ethnomedicinal claim an anticonvulsant by mechanistically interrogating its dual modulation of Notch1-driven neuroinflammation and NMDA receptor-mediated excitotoxicity, which are two key hallmarks of chronic epileptogenesis.
MATERIALS AND METHODS: Male C57BL/6 mice were divided into three groups to evaluate the neuroprotective and an anticonvulsant effects of STA in the PTZ-induced seizure model: Control group, PTZ group, and PTZ + STA group. Behavioral seizure scoring and cognitive tests were integrated with EEG recordings to assess neuronal synchronization. Molecular mechanisms were dissected via hippocampal immunohistochemistry and Western blotting.
RESULTS: Our results showed that daily oral administration of STA for a duration of 25 days significantly reduced seizure scores. EEG recordings indicated that STA treatment resulted in a notable reduction in both total brainwave power and firing amplitude within the groups receiving STA. Furthermore, STA administration provided cognitive protection against kindling-associated deficits, as demonstrated by improved alteration behavior and recognition index in Y-maze and object recognition tests. STA administration reduced neuronal loss and glial cell activation. Additionally, significant downregulation of NMDA receptor subunits, CAMK2, caspase-3, Notch1, and Hes1 expression levels was observed following STA administration.
CONCLUSION: These findings suggest that STA provides neuroprotection against PTZ-induced epilepsy by modulating the Notch and NMDA receptor pathways, thus addressing neuroinflammation and apoptosis resulting from excitotoxicity.