Silencing IncRNA BACE1-AS alleviates neuronal injury and neurological deficits after ischemic stroke via targeting miR-103a-3p

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.

Keywords: Ischemic stroke; apoptosis; lncRNA BACE1-AS; miR-103a-3p; neuroinflammation.