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Platelet-activating factor (PAF) was a lipid mediator that aggravated brain injury after cerebral ischemia and reperfusion.The aim of this study was to investigate the effect of PAF on blood brain barrier (BBB).Brain edema, Evans blue (EB) leakage, and 125 I-albumin uptake were used to quantify BBB dysfunction both in vivo and in vitro.The results indicated that intravenous drip of PAF (10 and 5 μg · kg-1) induced acute and reversible BBB disruption in vivo, such as brain edema and EB leakage.PAF (1 μmol· L-1) incubated with rat brain microvessel endothelial cells (rBMECs) for 12 h and 24 h mediated significantly increasing of 125I-albumin uptake across the rBMECs monolayer.Furthermore, PAF (5 μg· kg-1) evidently declined rat cerebral blood flow (rCBF), increased passive transport of Edaravone across BBB, and up regulated Matrix metalloproteinase-9 (MMP-9) expression.The injury above could be reversed by PAF antagonist Ginkgolide B (GB).In vitro western blot assay, MMP-9 expression was enhanced remarkable after rBMECs was incubated with PAF (1 μmol·L-1) for 12 h and 24 h.But when drug transport protein P-glycoprotein (P-gp) expression was concerned, there were no evident difference between PAF treated groups and control group both in vivo and in vitro.The current research demonstrated that intravenous drip of PAF mediated BBB disruption, and the possible mechanisms including destroy of microvessel endothelial cells tight junction and up regulation of MMP-9.