川芎嗪对内毒素脂多糖诱导的体外血脑屏障模型通透性增高的保护作用及其机制

Protective effect and its mechanism of liguistrazine on blood brain barrier permeability induced by lipopolysaccharide in vitro

目的:探讨川芎嗪对内毒素脂多糖(LPS)诱导的体外血脑屏障模型通透性增高的保护作用及其调控机制。方法:利用脑微血管内皮细胞与星型胶质细胞共培养建立体外大鼠血脑屏障模型,随机分为正常对照组、川芎嗪对照组、LPS干预组和川芎嗪治疗组。采用γ计数仪检测^(125)I-BSA通透量观察体外血脑屏障模型通透性的改变,Western印迹法检测紧密连接蛋白(zonula occludens-1,ZO-1)表达量的变化。结果:LPS使体外血脑屏障模型对^(125)I-BSA的通透量明显增加,脑微血管内皮细胞ZO-1蛋白表达下降,川芎嗪治疗组能明显拮抗LPS的上述作用。结论:川芎嗪对LPS诱导的体外血脑屏障通透性增高具有保护作用,其机制与它能影响血脑屏障紧密连接蛋白ZO-1表达有关。

Objective： To understand the protective effect and possible mechanism of liguistrazine on BBB （blood brain barrier） permeability induced by lipopolysaccharide （LPS） in vitro. Methods： The BBB model was established by coculturing allogenic brain microvascular eudothelial cell （BMEC） and astrocyte and divided randomly into the normal control group, liguistrazine control group, LPS pretreatment group and liguistrazine treatment group. The protective effect of liguistrazine on LPS-induced BBB permeability was measured by Gamma radioimmunoassay counter and the alterations in expression of ZO-1 was determined by Western blot. Results： The Gamma radioimmunoassay indicated that the pea meated, ^125 I-BSA in the BBB model in vitro was significant in restriction after liguistrazine treatment compare with LPS groups （P〈0.01）. At the same time, the Western blot results showed increased expression in ZO-1 conpared with the LPS group （P〈0. 01）. Conclusion： The results suggested that liguistrazine has protective effects on BBB permeability induced by LPS in vitro, and is involved in regulation of expression of ZO-1 protein.