{"title":"Silencing IncRNA BACE1-AS alleviates neuronal injury and neurological deficits after ischemic stroke via targeting miR-103a-3p.","authors":"Kaijie Yu, Fang Liu, Tianrui Yu, Yanping Ding, Juyao Liu, Lianlian Lv","doi":"10.1080/01616412.2025.2568025","DOIUrl":null,"url":null,"abstract":"<p><strong>Objective: </strong>To investigate the role of lncRNA BACE1-AS in neuronal injury and neurological deficits after ischemic stroke and explore its underlying molecular mechanism.</p><p><strong>Methods: </strong>MCAO rat model and OGD/R cell model were established. BACE1-AS expression was detected by RT-qPCR. Neurological function was evaluated by mNSS and MWM test. Inflammatory factors (TNF-α, IL-6, IL-10), neuronal injury markers (NSE, GFAP), and apoptosis-related markers (Bcl-2, Bax, Caspase-3) were detected by ELISA and RT-qPCR. Bioinformatics analysis, dual-luciferase reporter assay, and RIP assay were used to validate the targeting relationship between BACE1-AS and miR-103a-3p.</p><p><strong>Results: </strong>BACE1-AS was significantly upregulated in both MCAO rats and OGD/R-treated SH-SY5Y cells. Silencing BACE1-AS alleviated neurological deficits, reduced pro-inflammatory cytokine levels, and inhibited neuronal apoptosis. Mechanistically, BACE1-AS targeted miR-103a-3p, and inhibiting miR-103a-3p reversed the neuroprotective effects of BACE1-AS silencing in vivo and in vitro.</p><p><strong>Conclusion: </strong>Silencing BACE1-AS mitigates neuronal injury and neurological deficits after ischemic stroke by targeting miR-103a-3p, providing a novel therapeutic target for ischemic stroke.</p>","PeriodicalId":19131,"journal":{"name":"Neurological Research","volume":" ","pages":"1375-1385"},"PeriodicalIF":1.9000,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Neurological Research","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1080/01616412.2025.2568025","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2025/10/30 0:00:00","PubModel":"Epub","JCR":"Q3","JCRName":"CLINICAL NEUROLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
Objective: To investigate the role of lncRNA BACE1-AS in neuronal injury and neurological deficits after ischemic stroke and explore its underlying molecular mechanism.
Methods: MCAO rat model and OGD/R cell model were established. BACE1-AS expression was detected by RT-qPCR. Neurological function was evaluated by mNSS and MWM test. Inflammatory factors (TNF-α, IL-6, IL-10), neuronal injury markers (NSE, GFAP), and apoptosis-related markers (Bcl-2, Bax, Caspase-3) were detected by ELISA and RT-qPCR. Bioinformatics analysis, dual-luciferase reporter assay, and RIP assay were used to validate the targeting relationship between BACE1-AS and miR-103a-3p.
Results: BACE1-AS was significantly upregulated in both MCAO rats and OGD/R-treated SH-SY5Y cells. Silencing BACE1-AS alleviated neurological deficits, reduced pro-inflammatory cytokine levels, and inhibited neuronal apoptosis. Mechanistically, BACE1-AS targeted miR-103a-3p, and inhibiting miR-103a-3p reversed the neuroprotective effects of BACE1-AS silencing in vivo and in vitro.
Conclusion: Silencing BACE1-AS mitigates neuronal injury and neurological deficits after ischemic stroke by targeting miR-103a-3p, providing a novel therapeutic target for ischemic stroke.
期刊介绍:
Neurological Research is an international, peer-reviewed journal for reporting both basic and clinical research in the fields of neurosurgery, neurology, neuroengineering and neurosciences. It provides a medium for those who recognize the wider implications of their work and who wish to be informed of the relevant experience of others in related and more distant fields.
The scope of the journal includes:
•Stem cell applications
•Molecular neuroscience
•Neuropharmacology
•Neuroradiology
•Neurochemistry
•Biomathematical models
•Endovascular neurosurgery
•Innovation in neurosurgery.