BMC Neuroscience最新文献

{"title":"Gut Microbiome rewiring via fecal transplants: Uncovering therapeutic avenues in Alzheimer's disease models.","authors":"Prabhat Upadhyay, Sudhir Kumar, Anurag Tyagi, Aayush Raj Tyagi, Tarun Barbhuyan, Sarika Gupta","doi":"10.1186/s12868-025-00953-9","DOIUrl":"10.1186/s12868-025-00953-9","url":null,"abstract":"<p><strong>Background: </strong>Emerging evidence implicates the gut microbiome in Alzheimer's disease (AD) pathogenesis, yet the underlying mechanisms remain elusive. This study elucidates the bidirectional relationship between gut microbiota and AD using fecal microbiota transplantation (FMT) in a mouse model.</p><p><strong>Result: </strong>Through meticulous experimentation, we conducted reciprocal FMT between AD (5xFAD) and healthy (C57BL/6) mice to unravel the impact of gut microbiome alterations on cognitive function and neuroinflammation. FMT from 5xFAD to C57BL/6 mice induced profound memory impairment and cognitive deficits, accompanied by elevated inflammatory cytokine levels, oxidative stress markers, and systemic inflammation, as evidenced by increased plasma cytokines. Conversely, transplanting healthy microbiota into 5xFAD mice yielded remarkable behavioral improvements, including enhanced spatial memory performance in the Morris water maze, directly correlating with cognitive recovery. Our findings underscore the pivotal role of the gut microbiome in AD pathogenesis and offer a promising therapeutic avenue.</p><p><strong>Conclusion: </strong>Targeted modulation of the gut microbiome through strategies like FMT may offer potential benefits in Alzheimer's disease by influencing neuroinflammation, oxidative stress, and cognitive function. This comprehensive study provides novel insights into the gut-brain axis dynamics and paves the way for innovative microbiome-based interventions in AD management.</p>","PeriodicalId":9031,"journal":{"name":"BMC Neuroscience","volume":"26 1","pages":"39"},"PeriodicalIF":2.4,"publicationDate":"2025-07-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12231717/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144564255","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Zebrafish mecp2 null-mutation increases anxiety and cortisol levels but no change in adult social preference and larval chemically-induced hyperlocomotion.","authors":"Soaleha Shams, Pierre Cronell, Jenny Landin, Thomas Pietri, Adrian Ekehorn Gimdal, Petronella Kettunen, Lars Westberg","doi":"10.1186/s12868-025-00946-8","DOIUrl":"10.1186/s12868-025-00946-8","url":null,"abstract":"<p><strong>Background: </strong>Methyl CpG binding protein 2 (MECP2) is an essential global modulator of transcription and mutations in MECP2 are the most common cause of Rett syndrome, an X-linked neurodevelopmental disorder. Patients diagnosed with Rett syndrome have increased risk for epilepsy as well as problems with anxiety and social communication. Using the zebrafish mecp2^Q63X line, this study aimed to increase our understanding of the role of Mecp2 function in regulation of pharmacologically-induced hyperlocomotion, developmental social preference, and adult socialization, anxiety-related behaviour, and baseline cortisol levels. To determine responses of mecp2^-/- zebrafish to a stimulating convulsant, general locomotor activity was measured at 5 days post-fertilization (dpf) in sibling mecp2^+/+, mecp2^+/-, and mecp2^-/- fish after treatment with a GABA_A receptor antagonist pentylenetetrazol (PTZ) at varying concentrations. Responses to social stimulus were investigated in juvenile (21 dpf) and adult mecp2^-/- and mecp2^+/+ fish. Anxiety responses to a novel tank and whole-body cortisol levels were also measured in adult mecp2^-/- and control mecp2^+/+ zebrafish.</p><p><strong>Results: </strong>The behavioural tests showed that mecp2^-/- zebrafish displayed hypolocomotion at the larval stage, along with increased freezing time and thigmotaxis, and higher whole-body cortisol levels in adulthood. However, the hyper-locomotion response to PTZ at 5 dpf and social preference for visual social stimulus at 21 dpf and in adulthood were not affected by the lack of functional Mecp2.</p><p><strong>Conclusions: </strong>Functional Mecp2 modulated larval locomotion and behavioural anxiety at different ages and adult cortisol levels, but mecp2 null-mutation did not alter adult locomotion and socialization, and developmental sociability and PTZ-induced hyperlocomotion in zebrafish. Given the variability reported in patients and in rodent Mecp2 knockout models, studies using zebrafish can explore vital elements of MECP2's role across development and improve our understanding of neural mechanisms underlying neurodevelopmental disorders.</p>","PeriodicalId":9031,"journal":{"name":"BMC Neuroscience","volume":"26 1","pages":"38"},"PeriodicalIF":2.4,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12220008/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144538428","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Shikonin inhibits epithelial-mesenchymal transition in glioblastoma cells by upregulating p53 and promoting miR-361-5p level to suppress ZEB1 expression.","authors":"Fengying Zhang, Zhiyi Liu, Yingbin Wang, Lin Zuo, Sicong Xu, Yin Liu, Hao Liang, Yixue Xue","doi":"10.1186/s12868-025-00956-6","DOIUrl":"10.1186/s12868-025-00956-6","url":null,"abstract":"<p><strong>Objective: </strong>Shikonin, an active compound from the rhizome of Lithospermum erythrorhizon, exerts anti-tumor effects in various cancers, including glioblastoma multiforme (GBM). This study explored the mechanism of Shikonin for inhibiting the migration and invasion of GBM cells, providing a rationale for developing novel glioma therapies.</p><p><strong>Methods: </strong>The effects of Shikonin on GBM cell proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT) were detected by CCK-8, scratch wound-healing, Transwell, and Western blot assays. The effect of Shikonin on miR-361-5p expression in GBM cells was examined by RT-qPCR and the effect of miR-361-5p inhibitor transfection on proliferation, migration, invasion, and EMT in Shikonin-treated GBM cells was examined. Shikonin's target genes were identified and validated using dual luciferase reporter gene assay and chromatin immunoprecipitation (ChIP) assay, focusing on its induction of miR-361-5p expression. The downstream target genes of miR-361-5p were also identified and validated under Shikonin action. A GBM cell nude mouse xenograft tumor was established to confirm the regulatory role of Shikonin.</p><p><strong>Results: </strong>Shikonin inhibited cell proliferation, migration, invasion, and EMT and upregulated miR-361-5p expression in GBM cells. Shikonin upregulated the glioma-associated protein p53, which promoted miR-361-5p transcription. miR-361-5p inhibited ZEB1 expression. Therefore, Shikonin inhibited GBM cell proliferation, migration, invasion, and EMT via p53/ miR-361-5p/ ZEB1 axis in vitro and in vivo.</p><p><strong>Conclusion: </strong>Shikonin suppresses glioma cell proliferation, migration, invasion, and EMT by inhibiting ZEB1 expression through the p53/miR-361-5p axis.</p>","PeriodicalId":9031,"journal":{"name":"BMC Neuroscience","volume":"26 1","pages":"37"},"PeriodicalIF":2.4,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12210478/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144538427","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Memantine mitigates methamphetamine-induced impairments in social and recognition memories in rats.","authors":"Mehdi Khodamoradi, Yasaman Allameh, Melika Sarani, Shahab A Zarei, Sara Faaliat, Hamed Ghazvini","doi":"10.1186/s12868-025-00955-7","DOIUrl":"10.1186/s12868-025-00955-7","url":null,"abstract":"<p><strong>Background: </strong>Methamphetamine (METH) is a widely abused neurotoxic substance that can lead to neurocognitive disabilities. Recent studies have shown that memantine (MEM), an NMDA receptor antagonist, can improve cognitive function across various disorders. Given that previous studies have revealed that exposure to METH leads to several social and cognitive impairments, this research aimed to investigate the effects of MEM on social memory, social behavior, and novel object recognition impairments caused by chronic METH exposure. Adult male Wistar rats received a regimen of METH, which causes neurotoxicity (four injections of 6 mg/kg, s.c., at 2-h intervals). After one week, the effects of MEM (5 mg/kg, i.p.) on novel object recognition memory and social behaviors in the experimental groups were examined.</p><p><strong>Results: </strong>Animals exposed to the METH regimen exhibited significant impairments in the acquisition, consolidation, and retrieval stages of novel object recognition memory. However, treatment with MEM ameliorated the detrimental effects of METH on the acquisition, consolidation, and retrieval, but not the reconsolidation, of novel object recognition memory. Additionally, the results revealed that METH-triggered deficits in social interaction and behavior were improved by MEM treatment.</p><p><strong>Conclusions: </strong>In conclusion, this study demonstrated that MEM administration effectively ameliorated memory impairments induced by chronic METH exposure. These findings provide valuable insights into the neuroprotective effects of MEM on novel object memory, social memory, and social behaviors.</p>","PeriodicalId":9031,"journal":{"name":"BMC Neuroscience","volume":"26 1","pages":"36"},"PeriodicalIF":2.4,"publicationDate":"2025-06-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12143046/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144233018","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pro-cognitive efficacy of Prospekta in a rat model of age-associated cognitive impairment.","authors":"Elena Kardash, Nataliya Petrova, Ksenia Ganina, Sergey Tarasov, Oleg Epstein","doi":"10.1186/s12868-025-00958-4","DOIUrl":"10.1186/s12868-025-00958-4","url":null,"abstract":"<p><strong>Background: </strong>Ageing is associated with lower levels of cognitive performance, and novel therapeutics are warranted to correct this defect. Aged rats represent a favourable model of human ageing. The aim of the present study is to examine the effect of a novel neurotropic S100B-targeted drug, Prospekta, on the parameters of delayed alternation in the aged rats compared to responses in the young animals.</p><p><strong>Methods: </strong>A spatial working memory task in an operant chamber, where aged and young animals (21 and 2 months old, respectively) needed to alternate between two retractable levers on a trial-by-trial basis to receive a food reward, was tested. We also assessed the Prospekta's effect on expression of some biomarkers of ageing by measuring their levels in the brains of aged rats using Western blot.</p><p><strong>Results: </strong>Treatment with Prospekta ameliorated cognitive functions, which resulted in a significant reduction of simple and choice reaction times for aged rats. The drug also decreased the number of omission errors at the beginning of the acquisition phase, which indicated the influence of treatment on attention and decision-making process. At the same time, Prospekta did not affect the majority of parameters measured in young animals. The analysis of ageing biomarker expression did not reveal any significant differences between aged rats treated with Prospekta or placebo.</p><p><strong>Conclusions: </strong>The findings of this study underscore the potential of Prospekta as a promising pro-cognitive agent for the treatment of age-related cognitive decline. However, further research is imperative to elucidate the precise mechanisms underlying its therapeutic effects and validate its efficacy in vivo.</p><p><strong>Clinical trial number: </strong>Not applicable.</p>","PeriodicalId":9031,"journal":{"name":"BMC Neuroscience","volume":"26 1","pages":"35"},"PeriodicalIF":2.4,"publicationDate":"2025-06-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12139154/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144224207","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Eosinophils differentially affect early and delayed neurological deterioration after mechanical thrombectomy in stroke.","authors":"Shuhong Yu, Jinping Yang, Xiaoting Han, Jijun Shi, Guodong Xiao, Zhiliang Guo","doi":"10.1186/s12868-025-00954-8","DOIUrl":"10.1186/s12868-025-00954-8","url":null,"abstract":"<p><strong>Background: </strong>To investigate the effect of eosinophils on early (END) and delayed neurological deterioration (DND) after mechanical thrombectomy (MT) in patients with acute ischemic stroke (AIS).</p><p><strong>Methods: </strong>A total of 442 consecutive AIS patients experiencing MT between May 2017 and January 2023 were analyzed. END and DND were defined as a rise of ≥ 2 points on the National Institutes of Health Stroke Scale (NIHSS) or a fall of ≥ 1 point on the Glasgow Coma Scale or death from baseline to 24 h and from 24 to 72 h, respectively. Multivariate regression analysis, generalize additive models and mediation analysis were used to assess the effect of eosinophils on END and DND and the underlying mechanisms.</p><p><strong>Results: </strong>113 (25.17%) and 47 (10.63%) patients had END and DND, respectively. Eosinophils was independently associated with END after adjusting potential confounders (odds ratio, 0.00; 95% CI, 0.00-0.80; P = 0.0441), which is consistent with the result of eosinophils (dichotomous) as a categorical variable (odds ratio, 0.40; 95% CI, 0.24-0.68; P = 0.0006). In assessing the relationship between eosinophils and DND, the inflection point was found to be 0.02, and eosinophils were independently correlated with DND at less than 0.02 (odds ratio, 0.00, 95% CI: 0.00-0.00, P = 0.0038); however, eosinophils ceased to be independently correlated with DND after exceeding 0.02 (P = 0.3519). Mediation analyses confirmed that eosinophils contribute to END in patients through symptomatic intracranial hemorrhage (indirect effect: -0.463; 95%CI: -0.902-0.19; P < 0.001).</p><p><strong>Conclusions: </strong>The effects of eosinophils on END and DND are not identical.</p>","PeriodicalId":9031,"journal":{"name":"BMC Neuroscience","volume":"26 1","pages":"34"},"PeriodicalIF":2.4,"publicationDate":"2025-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12131365/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144214814","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction to: Association between apolipoprotein E Ε4 status and the risk of Alzheimer's disease: a meta-analysis.","authors":"Zijun Ren, Zhenting Guan, Qingliang Guan, Hongjian Guan, Huiying Che","doi":"10.1186/s12868-025-00952-w","DOIUrl":"10.1186/s12868-025-00952-w","url":null,"abstract":"","PeriodicalId":9031,"journal":{"name":"BMC Neuroscience","volume":"26 1","pages":"32"},"PeriodicalIF":2.4,"publicationDate":"2025-05-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12105348/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144149305","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The short-term spinal cord stimulation improves the rates of tracheal decannulation in patients of brain injury with disorders of consciousness.","authors":"Guanlin Huang, Dong Wang, Qiang Chen, Qi Zhong, Weilong Huang, Xiaoping Zhou, Qiuhua Jiang","doi":"10.1186/s12868-025-00951-x","DOIUrl":"10.1186/s12868-025-00951-x","url":null,"abstract":"<p><strong>Objective: </strong>To evaluate the efficacy of short-term spinal cord stimulation (stSCS) in promoting tracheal decannulation among patients with brain injury-induced disorders of consciousness(DoC).</p><p><strong>Methods: </strong>A retrospective cohort study was conducted on 81 tracheotomized brain injury patients with DoC treated at Ganzhou People's Hospital between June 2021 and June 2022.Patients were divided into two groups: the stSCS group (n = 46) receiving stSCS intervention and the control group (n = 35) receiving standard care. Decannulation success rates were compared using chi-square tests.</p><p><strong>Results: </strong>The stSCS group demonstrated a significantly higher decannulation rate compared to the control group (50.0%vs.25.7%, χ²=5.24, p = 0.022).</p><p><strong>Conclusion: </strong>stSCS significantly enhances tracheal decannulation success in brain injury patients with DoC, suggesting its potential as a therapeutic neuromodulation strategy.</p><p><strong>Clinical trial number: </strong>Not applicable.</p>","PeriodicalId":9031,"journal":{"name":"BMC Neuroscience","volume":"26 1","pages":"33"},"PeriodicalIF":2.4,"publicationDate":"2025-05-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12107863/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144149271","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The role of the contralesional primary motor cortex in upper limb recovery after stroke: a scoping review following PRISMA-ScR guidelines.","authors":"Peerapat Suputtitada, Valton Costa, Felipe Fregni","doi":"10.1186/s12868-025-00950-y","DOIUrl":"10.1186/s12868-025-00950-y","url":null,"abstract":"<p><strong>Background: </strong>Stroke often results in motor impairments, with recovery involving complex interactions between the lesioned (ipsilesional) and non-lesioned (contralesional) hemispheres. This scoping review investigates the role of the contralesional primary motor cortex (M1) in motor recovery of the paretic upper limb following stroke, examining its structural and functional changes and compensatory roles.</p><p><strong>Methods: </strong>A systematic search for scoping review was conducted in PubMed, Embase, Web of Science, and Google Scholar following PRISMA-ScR guidelines. Studies examining contralesional M1 contributions to upper limb recovery in humans and animal models were included. Data were extracted, synthesized qualitatively, and assessed for risk of bias using SYRCLE and Cochrane tools.</p><p><strong>Results: </strong>A total of 38 studies were included in the analysis, consisting of 34 focused on stroke patients and 4 utilizing animal models. The findings revealed the dual and task-specific role of the contralesional primary motor cortex (M1) in upper limb recovery after stroke. In patients with severe motor impairments, contralesional M1 supported recovery through compensatory mechanisms, such as increased neuronal recruitment and functional reorganization. However, in cases with mild impairments, its activation was associated with inhibitory effects on ipsilesional reorganization, potentially delaying optimal recovery. Animal studies provided evidence of structural and functional plasticity, including dendritic remodeling and enhanced neuronal connectivity, which paralleled improvements in motor function. In human studies, contralesional M1 activation was task-dependent, with pronounced engagement during demanding tasks and unimanual movements. Ipsilateral motor deficits, including reduced dexterity, strength, and coordination, were commonly reported and underscored the disrupted interhemispheric dynamics influencing recovery. Neuromodulation techniques showed promise in modulating interhemispheric interactions and enhancing motor outcomes. These results emphasize the complex interplay between compensatory and inhibitory processes mediated by contralesional M1 in stroke recovery.</p><p><strong>Conclusion: </strong>The contralesional M1 plays a complex, task-specific role in upper limb recovery after stroke, acting as both a compensatory resource and a potential inhibitory factor. Future research should stratify patients by impairment severity to refine therapeutic approaches.</p><p><strong>Clinical trial number: </strong>Not applicable.</p>","PeriodicalId":9031,"journal":{"name":"BMC Neuroscience","volume":"26 1","pages":"31"},"PeriodicalIF":2.4,"publicationDate":"2025-05-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12105408/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144141411","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Body weight-supported treadmill training reduces glial scar overgrowth in SCI rats by decreasing the reactivity of astrocytes during the subacute phase.","authors":"Jili Cai, Yu Wang, Chenyuan Zhai, Kunmao Jiang, Zun Wang, Lu Fang, Xiangzhe Li, Chenchen Zhu, Wentao Liu, Tong Wang, Qi Wu","doi":"10.1186/s12868-025-00947-7","DOIUrl":"https://doi.org/10.1186/s12868-025-00947-7","url":null,"abstract":"<p><strong>Background: </strong>Spinal cord injury is followed by glial scar formation, which was long seen mainly as a physical barrier preventing axonal regeneration. Glial scar astrocytes lead to glial scar formation and produce inhibitory factors to prevent axons from growing through the scar, while inhibiting the conversion of reactive astrocytes into glial scar-forming astrocytes may represent an ideal treatment for CNS injury. Exercise is a non-invasive and effective therapeutic intervention for clinical rehabilitation of spinal cord injury. However, its precise therapeutic mechanisms still need to be continuously explored.</p><p><strong>Methods: </strong>30 rats were randomly assigned to three groups (Sham, SCI, SCI + BWSTT; n = 10 rats per group). In this study, we employed the BBB scales and gait analysis system to examine the behavioral functions of the rats in each group. Furthermore, we utilized immunoblotting of spinal cord tissue at the injury site, in addition to histological staining and immunofluorescence staining, to explore glial scar aggregation and axonal regeneration in each group of rats.</p><p><strong>Results: </strong>Our results revealed that hindlimb motor function was significantly improved in SCI rats after a sustained subacute period of BWSTT, accompanied by the promotion of histological repair and nerve regeneration. Subsequent immunofluorescence staining and immunoblotting showed diminished astrocyte reactivity in the region surrounding the spinal cord injury as well as reduced expression and distribution of collagen fibers near the lesion after BWSTT. Additionally, a significant decrease in the expression of MMP-2/9, which is closely related to astrocyte migration, was observed in the vicinity of spinal cord tissue lesions.</p><p><strong>Conclusion: </strong>Our study demonstrates that a sustained BWSTT intervention during the subacute phase of spinal cord injury can effectively reduce astrocyte reactivity and glial scarring overgrowth, thereby facilitating functional recovery after SCI.</p>","PeriodicalId":9031,"journal":{"name":"BMC Neuroscience","volume":"26 1","pages":"30"},"PeriodicalIF":2.4,"publicationDate":"2025-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12039159/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143966112","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}