目的 研究千叶素A对缺氧损伤下血脑屏障通透性的影响及其调控机制。方法 利用原代培养大鼠脑微血管内皮细胞（BMEC）建立体外血脑屏障模型，缺氧诱导损伤。荧光分光光度法检测千叶素A对BMEC异硫氰酸荧光素（FITC）-葡聚糖的荧光强度，观察其对体外血脑屏障模型通透性的影响；RT-PCR法检测千叶素A对BMEC紧密连接蛋白ZO-1、claudin-1基因表达的影响，Cell-Based ELISA法检测千叶素A对BMEC中ZO-1蛋白表达的影响。结果 缺氧使体外血脑屏障模型对FITC-葡聚糖的通透量明显增加，脑微血管内皮细胞ZO-1基因和蛋白表达下调；千叶素A能明显拮抗缺氧造成的上述损伤。结论 千叶素A对缺氧损伤体外血脑屏障具有保护作用，其机制与其影响ZO-1表达有关。

Objective To study the protective effect of oroxylin A on blood-brain barrier (BBB) permeability induced by hypoxic injury and its possible mechanism. Methods The BBB model in vitro was established by primarily culturing brain microvascular endothelial cells (BMEC), and the hypoxic injury was induced. To observe the changes of BBB permeability, fluorospectrophotometry was used to detect the fluorescence intensity of oroxylin A on fluorescein isothiocyanate (FITC)-dextran in BMEC. The effects of oroxylin A on the mRNA expression of ZO-1 and claudin-1 were assayed by RT-PCR, and the effect on the ZO-1 protein expression was measured by Cell-Based ELISA. Results Hypoxia significantly increased FITC-dextran permeability, decreased the expression of ZO-1 mRNA and protein, while oroxylin A could antagonize these effects caused by hypoxia. Conclusion Oroxylin A has a protective effect on BBB permeability induced by hypoxia in vitro, and the mechanism is involved in the regulation of ZO-1 expression.

高等学校博士学科点专项科研基金（20121210120005）；天津市科技创新体系及条件平台建设（10SYSYJC28900）