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Article Abstract
Objective: This study aims to explore the neuroprotective effects of Dl-3-n-Butylphthalide (NBP) against cerebral ischemia-reperfusion injury (CIRI), with a focus on NBP's underlying molecular mechanism.
Methods: A CIRI rat model was established, followed by treatment with NBP with/without microRNA-20a-5p (miR-20a-5p) mimic or negative control. Neurological deficits, brain infarct size, and histopathological changes were assessed. In vitro, an oxygen-glucose deprivation/reoxygenation (OGD/R)-induced PC12 cell model was developed, followed by cell viability and apoptosis evaluation. miR-20a-5p, X-linked inhibitor of apoptosis protein (XIAP), and apoptosis-related protein levels were detected. A dual-luciferase reporter assay was performed to confirm the interaction between miR-20a-5p and XIAP.
Results: NBP treatment significantly restored neurological function, reduced infarct size, and inhibited neuronal apoptosis. Mechanistically, NBP downregulated miR-20a-5p and upregulated XIAP. The protective effects of NBP were abolished by miR-20a-5p overexpression.
Conclusion: NBP exerts neuroprotective effects against CIRI by modulating the miR-20a-5p/XIAP axis. NBP may serve as a therapeutic agent for CIRI.
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