Vasogenic edema in terms of blood-brain barrier

我们研究了匹伐他汀对体外血脑屏障（BBB）模型的屏障功能的影响与原代培养的大鼠脑毛细血管内皮细胞（RBEC）。匹伐他汀增加跨内皮电阻（TEER），内皮间紧密连接（TJ）的屏障紧密性的指数，在10-8 M的浓度，并降低荧光素钠通过RBEC单层的内皮渗透性。在类异戊二烯香叶基香叶基焦磷酸的存在下，TEER的增加显着减少，而焦磷酸法呢酯对TEER没有影响。我们的免疫细胞化学和蛋白质印迹分析表明，匹伐他汀治疗增强了紧密连接蛋白-5，一个主要的功能蛋白的TJ的表达。我们的数据表明，匹伐他汀加强RBEC原代培养物的屏障完整性。匹伐他汀的BBB稳定作用可能部分通过抑制甲羟戊酸途径和随后上调claudin-5的表达来介导。在10年的时间里，5例（3男2女，17-68岁）创伤性CCF在长崎大学医院接受治疗。由于引流至上级眼静脉，他们表现为眼部症状，1例皮质返流患者发生颅内出血。所有病例均采用血管内弹簧圈栓塞治疗（3例动静脉分流闭塞，2例载瘤动脉闭塞）。

We investigated the effect of pitavastatin on barrier functions of an in vitro blood-brain barrier (BBB) model with primary cultures of rat brain capillary endothelial cells (RBEC). Pitavastatin increased the transendothelial electrical resistance (TEER), an index of barrier tightness of interendothelial tight junctions (TJs), at a concentration of 10-8 M, and decreased the endothelial permeability for sodium fluorescein through the RBEC monolayer. The increase in TEER was significantly reduced in the presence of isoprenoid geranylgeranyl pyrophosphate, whereas farnesyl pyrophosphate had no effect on TEER. Our immunocytochemical and Western blot analyses revealed that treatment with pitavastatin enhanced the expression of claudin-5, a main functional protein of TJs. Our data indicate that pitavastatin strengthens the barrier integrity in primary cultures of RBEC. The BBB-stabilizing effect of pitavastatin may be mediated partly through inhibition of the mevalonate pathway and subsequent up-regulation of claudin-5 expression.During a 10-year period, five cases (three men and two women, 17-68 years) of traumatic CCF were treated at the Nagasaki University hospital. They represented ophthalmic symptoms because of drainage to the superior ophthalmic vein, and one case with cortical reflux developed intracranial hemorrhage. All cases were managed with endovascular coil embolization (three arteriovenous shunt occlusion, two parent artery occlusion).