DL-3-n-Butylphthalide Attenuates Mitochondrial Oxidative Stress and Improves Blood-Brain Barrier Function After Strok

Neural Injury and Functional Reconstruction ›› 2025, Vol. 20 ›› Issue (8) : 435-440.

PDF(6592 KB)
中国科技核心期刊
美国《化学文摘》CAS数据库收录
日本科学技术振兴机构数据库收录
湖北省优秀期刊
中国知网网络首发期刊
PDF(6592 KB)
Neural Injury and Functional Reconstruction ›› 2025, Vol. 20 ›› Issue (8) : 435-440.

DL-3-n-Butylphthalide Attenuates Mitochondrial Oxidative Stress and Improves Blood-Brain Barrier Function After Strok

Author information +
History +

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

Cite this article

Download Citations
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
PDF(6592 KB)

Accesses

Citation

Detail

Sections
Recommended

/