目的：探讨丁苯酞（Dl-3-n-丁基苯酞，NBP）促进急性缺血性卒中小鼠神经功能恢复的作用及机制。方 法：①构建大脑中动脉阻断（middle cerebral artery occlusion，MCAO）小鼠模型，设Sham、MCAO及MCAO+ NBP组，采用行为学测评、免疫荧光染色、透射电镜方法探究NBP对血脑屏障和神经功能的保护作用；②体 外建立脑微血管内皮细胞氧糖剥夺/复氧模型，给予NBP干预，采用迁移、成管、屏障通透试验、CCK 8试剂盒 检测、碘化丙啶染色及细胞爬片荧光探针染色探究其对内皮功能和线粒体状态的调控效应。结果：①与 MCAO组相比，NBP干预显著上调内皮细胞紧密连接蛋白Claudin-5、ZO-1、Occludin表达，减少血浆渗透蛋 白albumin与fibrinogen渗漏，降低线粒体DNA氧化损伤标记物8-OHdG水平，并改善神经功能（P＜0.05）。 ②体外给予 NBP 处理后，内皮细胞迁移与成管能力增强，通透性降低，活性提高，DNA损伤减少，同时线粒 体活性、膜电位和氧化应激状态显著改善（P＜0.05）。结论：对急性缺血性卒中，NBP可通过抑制线粒体氧化 应激，保护脑内皮细胞功能，修复血脑屏障结构，进而促进神经功能恢复。

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.