Abstract
To investigate the effect and mechanism of Dl-3-n-butylphthalide (NBP) on promoting
neurological function recovery in mice with acute ischemic stroke (AIS). Methods: (1) An in vivo middle
cerebral artery occlusion (MCAO) mouse model was established, with three groups: Sham, MCAO, and MCAO+
NBP. Behavioral assessments, immunofluorescence staining, and transmission electron microscopy were used to
evaluate the protective effects of NBP on blood-brain barrier (BBB) integrity and neurological function. (2) An in
vitro oxygen-glucose deprivation/reoxygenation (OGD/R) model was established in brain microvascular
endothelial cells, followed by NBP treatment. Endothelial function and mitochondrial status were assessed
through migration and tube formation assays, permeability tests, CCK-8 assay, propidium iodide staining, and
fluorescence probe staining of cell slides. Results: (1) Compared with the MCAO group, NBP treatment
significantly increased the expression of endothelial tight junction proteins Claudin-5, ZO-1, and Occludin,
reduced leakage of plasma proteins albumin and fibrinogen, decreased levels of the mitochondrial DNA oxidative
damage marker 8-OHdG, and improved neurological function (P<0.05). (2) In vitro, NBP treatment enhanced
endothelial cell migration and tube formation, reduced permeability, improved cell viability, and decreased DNA
damage. In addition, mitochondrial activity, membrane potential, and oxidative stress levels were significantly
improved (P<0.05). Conclusion: NBP exerts protective effects in AIS by attenuating mitochondrial oxidative
stress, preserving endothelial cell function, restoring BBB integrity, and thereby promoting neurological recovery.
Key words
DL-3-n-butylphthalide; acute ischemic stroke; blood-brain barrier; mitochondrial oxidative stress;
neurological recovery
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DL-3-n-Butylphthalide Attenuates Mitochondrial Oxidative Stress and Improves Blood-Brain
Barrier Function After Strok[J]. Neural Injury and Functional Reconstruction. 2025, 20(8): 435-440
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