GLGZG improves post-stroke spastic paralysis in rats through regulating BDNF/TrkB signaling

Stroke is the second leading cause of disability and death worldwide and imposes a significant burden on society. Post-stroke spastic paralysis (PSP) is one of the most common sequelae of stroke, severely affecting patients' limb function and rehabilitation and reducing their quality of life. This study aimed to evaluate the neuroprotective and synaptic plasticity-improving effects of Gualou Guizhi Spasmolysis Granules (GLGZG) in PSP rats and to explore the possible involvement of the brain-derived neurotrophic factor (BDNF)/tropomyosin receptor kinase B (TrkB) signaling pathway. PSP rat models were established by middle cerebral artery occlusion. Neurological deficits and limb spasticity were assessed by the Modified Neurological Severity Score (MNSS) and Modified Ashworth Scale (MAS), respectively. Immunohistochemistry and Western blot analysis were used to detect related proteins. Results showed that low-, middle-, and high-dose GLGZG significantly reduced MNSS and MAS scores and alleviated limb spasticity (all ***P < 0.001). Middle-dose GLGZG increased BDNF, TrkB, cyclic-AMP response element-binding protein (CREB), growth-associated protein 43 (GAP43), and p38 mitogen-activated protein kinase (p38 MAPK), decreased KCC2 expression, and partially reversed K252a-related changes (all indicated comparisons ***P < 0.001). These findings suggest that the therapeutic effects of GLGZG in PSP rats are associated with BDNF/TrkB signaling and enhanced synaptic plasticity.