Xuefei Li, Jiahui Chen, Tingting Li, Ayang Zhao, Wenzhi Li
{"title":"运动通过增强脑卒中大鼠神经可塑性和脊髓代偿促进神经系统恢复。","authors":"Xuefei Li, Jiahui Chen, Tingting Li, Ayang Zhao, Wenzhi Li","doi":"10.1097/WNR.0000000000002201","DOIUrl":null,"url":null,"abstract":"<p><strong>Purpose of the research: </strong>This study aimed to explore the effects of exercise on sensorimotor recovery after stroke, neuroplasticity changes in the brain and spinal cord, and spinal cord compensation mechanisms.</p><p><strong>Methods: </strong>A rat model of ischemic stroke was induced using the middle cerebral artery occlusion/reperfusion method. A T10 spinal cord injury (SCI) model was induced using a modified Allen procedure. The animals were randomly assigned into: Sham group (S), stroke group (M), stroke+SCI group (MS), stroke+exercise+SCI group (MSI), and stroke+SCI group (MI). Neurological function was assessed poststroke using the modified Neurological Severity Score (mNSS) and Garcia scores. Infarct volumes were evaluated using triphenyl tetrazolium chloride staining, and neuronal damage was assessed using Nissl staining. Tumor necrosis factor-α (TNF-α), interleukin (IL)-10, and IL-1β levels were measured using ELISA. Neuroplasticity markers [GAP43, PSD-95, synapsin I, and brain-derived neurotrophic factor (BDNF)] levels were analyzed using WB, IHC, and ELISA.</p><p><strong>Results: </strong>Exercise improved neurological function in stroke rats, as evidenced by the enhanced mNSS and Garcia scores in the MS group compared to the M group. Exercise also alleviated neuronal damage, with the MS group showing higher neuron counts and more intact Nissl bodies than the M group. Exercise in the MS group downregulated inflammation (TNF-α down, IL-10 up) compared to the M group. Furthermore, exercise upregulated neuroplasticity markers and BDNF in both the brain and spinal cord. The beneficial effects of exercise on neurological recovery were diminished in the presence of SCI, as evidenced by the impaired recovery in the MSI group.</p><p><strong>Conclusions: </strong>Exercise enhances stroke recovery by improving neuroplasticity, reducing inflammation, and highlighting the spinal cord's role in compensation. These findings suggest spinal cord-targeted therapies may improve rehabilitation outcomes.</p>","PeriodicalId":19213,"journal":{"name":"Neuroreport","volume":"36 14","pages":"796-806"},"PeriodicalIF":1.7000,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Exercise promotes neurological recovery by enhancing neuroplasticity and the spinal cord compensation in stroke-affected rats.\",\"authors\":\"Xuefei Li, Jiahui Chen, Tingting Li, Ayang Zhao, Wenzhi Li\",\"doi\":\"10.1097/WNR.0000000000002201\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Purpose of the research: </strong>This study aimed to explore the effects of exercise on sensorimotor recovery after stroke, neuroplasticity changes in the brain and spinal cord, and spinal cord compensation mechanisms.</p><p><strong>Methods: </strong>A rat model of ischemic stroke was induced using the middle cerebral artery occlusion/reperfusion method. A T10 spinal cord injury (SCI) model was induced using a modified Allen procedure. The animals were randomly assigned into: Sham group (S), stroke group (M), stroke+SCI group (MS), stroke+exercise+SCI group (MSI), and stroke+SCI group (MI). Neurological function was assessed poststroke using the modified Neurological Severity Score (mNSS) and Garcia scores. Infarct volumes were evaluated using triphenyl tetrazolium chloride staining, and neuronal damage was assessed using Nissl staining. Tumor necrosis factor-α (TNF-α), interleukin (IL)-10, and IL-1β levels were measured using ELISA. Neuroplasticity markers [GAP43, PSD-95, synapsin I, and brain-derived neurotrophic factor (BDNF)] levels were analyzed using WB, IHC, and ELISA.</p><p><strong>Results: </strong>Exercise improved neurological function in stroke rats, as evidenced by the enhanced mNSS and Garcia scores in the MS group compared to the M group. Exercise also alleviated neuronal damage, with the MS group showing higher neuron counts and more intact Nissl bodies than the M group. Exercise in the MS group downregulated inflammation (TNF-α down, IL-10 up) compared to the M group. Furthermore, exercise upregulated neuroplasticity markers and BDNF in both the brain and spinal cord. The beneficial effects of exercise on neurological recovery were diminished in the presence of SCI, as evidenced by the impaired recovery in the MSI group.</p><p><strong>Conclusions: </strong>Exercise enhances stroke recovery by improving neuroplasticity, reducing inflammation, and highlighting the spinal cord's role in compensation. These findings suggest spinal cord-targeted therapies may improve rehabilitation outcomes.</p>\",\"PeriodicalId\":19213,\"journal\":{\"name\":\"Neuroreport\",\"volume\":\"36 14\",\"pages\":\"796-806\"},\"PeriodicalIF\":1.7000,\"publicationDate\":\"2025-10-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Neuroreport\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1097/WNR.0000000000002201\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2025/7/21 0:00:00\",\"PubModel\":\"Epub\",\"JCR\":\"Q4\",\"JCRName\":\"NEUROSCIENCES\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Neuroreport","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1097/WNR.0000000000002201","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2025/7/21 0:00:00","PubModel":"Epub","JCR":"Q4","JCRName":"NEUROSCIENCES","Score":null,"Total":0}
Exercise promotes neurological recovery by enhancing neuroplasticity and the spinal cord compensation in stroke-affected rats.
Purpose of the research: This study aimed to explore the effects of exercise on sensorimotor recovery after stroke, neuroplasticity changes in the brain and spinal cord, and spinal cord compensation mechanisms.
Methods: A rat model of ischemic stroke was induced using the middle cerebral artery occlusion/reperfusion method. A T10 spinal cord injury (SCI) model was induced using a modified Allen procedure. The animals were randomly assigned into: Sham group (S), stroke group (M), stroke+SCI group (MS), stroke+exercise+SCI group (MSI), and stroke+SCI group (MI). Neurological function was assessed poststroke using the modified Neurological Severity Score (mNSS) and Garcia scores. Infarct volumes were evaluated using triphenyl tetrazolium chloride staining, and neuronal damage was assessed using Nissl staining. Tumor necrosis factor-α (TNF-α), interleukin (IL)-10, and IL-1β levels were measured using ELISA. Neuroplasticity markers [GAP43, PSD-95, synapsin I, and brain-derived neurotrophic factor (BDNF)] levels were analyzed using WB, IHC, and ELISA.
Results: Exercise improved neurological function in stroke rats, as evidenced by the enhanced mNSS and Garcia scores in the MS group compared to the M group. Exercise also alleviated neuronal damage, with the MS group showing higher neuron counts and more intact Nissl bodies than the M group. Exercise in the MS group downregulated inflammation (TNF-α down, IL-10 up) compared to the M group. Furthermore, exercise upregulated neuroplasticity markers and BDNF in both the brain and spinal cord. The beneficial effects of exercise on neurological recovery were diminished in the presence of SCI, as evidenced by the impaired recovery in the MSI group.
Conclusions: Exercise enhances stroke recovery by improving neuroplasticity, reducing inflammation, and highlighting the spinal cord's role in compensation. These findings suggest spinal cord-targeted therapies may improve rehabilitation outcomes.
期刊介绍：
NeuroReport is a channel for rapid communication of new findings in neuroscience. It is a forum for the publication of short but complete reports of important studies that require very fast publication. Papers are accepted on the basis of the novelty of their finding, on their significance for neuroscience and on a clear need for rapid publication. Preliminary communications are not suitable for the Journal. Submitted articles undergo a preliminary review by the editor. Some articles may be returned to authors without further consideration. Those being considered for publication will undergo further assessment and peer-review by the editors and those invited to do so from a reviewer pool.
The core interest of the Journal is on studies that cast light on how the brain (and the whole of the nervous system) works.
We aim to give authors a decision on their submission within 2-5 weeks, and all accepted articles appear in the next issue to press.
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