BLOOD-BRAIN BARRIER--IN VITRO CEREBROVASCULAR ENDOTHELIAL PERMEABILITY

游离脂肪酸从细胞膜中的释放已经 参与减弱血脑屏障（BBB） 病理条件下的渗透性。 这种持续的研究 涉及的是阐明与 花生四烯酸诱导的增加渗透性 体外培养微血管内皮细胞模型的建立 由培养的内皮细胞组成， 微血管 调查的重点是 内皮细胞膜的“流动性”与内皮细胞膜的通透性之间存在着一定的联系。 细胞暴露于单独的AA或AA和H2O2。 这些研究 表明AA修饰内皮膜“流动性” 并不影响这些细胞的渗透性。 相反， 没有增加的膜“流动性”和增加的TBA 内皮细胞的通透性与AA和H2O2有关 治疗 这些发现支持了这样的论点，即释放 花生四烯酸从细胞膜在病理条件下 可能通过改变膜的“流动性”， 或细胞渗透性。

The release of free fatty acids from cellular membranes has been implicated in attenuating the blood-brain barrier (BBB) permeability under pathological conditions. This continuous study is concerned with elucidation of mechanisms involved with an arachidonate inducible increase permeability of cerebromicrovascular endothelium using a model system in vitro consisting of cultured endothelial cells derived from cerebral microvessels. The investigations focused on the relationship between the "fluidity" of endothelial membrane and permeability of cells exposed to AA alone or to AA and H202. These studies demonstrate that AA modification of endothelial membrane "fluidity" does not affect the permeability of those cells. Conversely, an absence of increased membrane "fluidity" and an augmented TBA permeability of endothelium is associated with AA and H202 treatment. These findings support the contention that the release of arachidonate from cellular membrane under pathological conditions may alter BBB function by changing either the membrane "fluidity" or cellular permeability.