Brain and behavior · 2026
Baishaoluoshi Decoction Mitigates Post-Stroke Spasticity by Targeting Synaptic Plasticity Through the Nogo-A/NgR Signaling Pathway.
СтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Sun Xiongxing, Zeng Shanshan, Lin Shigao, Wu Lingying, Tang Xukun, Zhu Jiajian, Zhang Yuhui, Li Lu, Chen Ziming, Deng Xinyu, Wu Dahua, Xie Le
Аннотация
OBJECTIVE: This study systematically investigated the effects and molecular mechanisms of Baishaoluoshi Decoction (BD) on synaptic plasticity in rats with post-stroke spasticity (PSS).
METHODS: A rat model of PSS was established using middle cerebral artery occlusion. Behavioral assessments, including modified neurological severity scores, rotarod tests, and the Modified Ashworth Scale, were employed. Synaptic ultrastructure was analyzed using transmission electron microscopy (TEM). The molecular mechanisms were explored using immunofluorescence and western blot analyses to evaluate protein expression (Nogo-A, Nogo receptor (NgR), RhoA, Collapsin Response Mediator Protein 2 (CRMP2), and AGG) and NgR/Olig2 colocalization. BD was also tested in combination with the NgR antagonist NEP1-40.
RESULTS: BD significantly ameliorated the neurological deficits, prolonged rotarod fall latency, and reduced spasticity. TEM revealed that BD restored the synaptic ultrastructure in the peri-infarct regions by increasing postsynaptic density (PSD) thickness and length, and narrowing synaptic clefts. BD downregulates synaptic-plasticity-related proteins (Nogo-A, NgR, RhoA, AGG, and CRMP2) and attenuates oligodendrocyte-mediated inhibitory signaling via reduced NgR/Olig2 co-localization. BD combined with NEP1-40 exhibits synergistic therapeutic efficacy.
CONCLUSION: BD alleviates PSS by enhancing synaptic plasticity and suppressing inhibitory signaling through multitarget modulation of neuron-glia interactions. These findings highlight BD as a promising therapeutic intervention for PSS, which is supported by molecular evidence of its effects on synaptic remodeling and functional recovery.
METHODS: A rat model of PSS was established using middle cerebral artery occlusion. Behavioral assessments, including modified neurological severity scores, rotarod tests, and the Modified Ashworth Scale, were employed. Synaptic ultrastructure was analyzed using transmission electron microscopy (TEM). The molecular mechanisms were explored using immunofluorescence and western blot analyses to evaluate protein expression (Nogo-A, Nogo receptor (NgR), RhoA, Collapsin Response Mediator Protein 2 (CRMP2), and AGG) and NgR/Olig2 colocalization. BD was also tested in combination with the NgR antagonist NEP1-40.
RESULTS: BD significantly ameliorated the neurological deficits, prolonged rotarod fall latency, and reduced spasticity. TEM revealed that BD restored the synaptic ultrastructure in the peri-infarct regions by increasing postsynaptic density (PSD) thickness and length, and narrowing synaptic clefts. BD downregulates synaptic-plasticity-related proteins (Nogo-A, NgR, RhoA, AGG, and CRMP2) and attenuates oligodendrocyte-mediated inhibitory signaling via reduced NgR/Olig2 co-localization. BD combined with NEP1-40 exhibits synergistic therapeutic efficacy.
CONCLUSION: BD alleviates PSS by enhancing synaptic plasticity and suppressing inhibitory signaling through multitarget modulation of neuron-glia interactions. These findings highlight BD as a promising therapeutic intervention for PSS, which is supported by molecular evidence of its effects on synaptic remodeling and functional recovery.