Cerebrovascular disease is a common disease which continually occurs in clinic work. It has become one of the three main causes for adult death and the chief cause for deformity. The incidence, CFR and mutilation of it are much higher than ever. Ischemic cerebrovascular disease happens much frequently. Reperfusion treatment is the main measure to treat ICVD. Reperfusion following focal cerebral ischemia exacerbates the level of brain edema. Changes in Blood-brain barrier permeability are responsible for the brain edema associated with reperfusion after cerebral ischemia. So it is essential to further study the change of BBB.BBB is a complicated system including endothelial cell, tight junction, astrocyte, pericyte, microglia and basement membrane. Then endothelial cell plays the role of barrier. Nuclear factor-kappa is one kind of pleiotropia transcription factors that generally exists in several kinds of cells and viruses. It has the function of transmitting information exterior and interior nuclear that is involved in immunity, stress, inflammation and apoptosis. It is certified recently that NF-κB exists in the cell such as endothelial cell, astrocyte and neuron. It can be activated by central nervous system damage. The purpose of this experiment is to study the activation of NF-κB and relation with the permeability of BBB in rats after cerebral ischemia-reperfusion, further analyze the mechanism of BBB damage and provide rationale for treatment.









  The MCAO/R model was induced using intraluminal suture technique first described by Longa with a little modification. Male Wistar rats were divided into sham-operation group, ischemia- reperfusion group. Each group was respectively further divided into 5 subgroups: I2hR3h (ischemia for 2 hours and reperfusion for 3 hour), I2hR6h, I2hR12h, I2hR24h and I2hR48h .We observed the changes in permeability of BBB by measuring the amount of EB in brain and the morphologu of brain through HE stain by microscope,then detected the expression of NF-κB in endothelial cell by immumohistochemical technique. Ischemia-reperfusion group and PDTC-treament group were done at one point of the peak of permeability of BBB and another point of the peak of the expression of NF-κB, we analyzed the amount of EB in brain and the expression of NF-κB.









  The results showed:①At 3h of reperfusion after cerebral ischemia for 2h, the permeability of BBB began to increase, reached the peak at 24h of reperfusion and was still elevated at 48h, and afterwards began to decrease.②HE stain: necrotic cells extensively existed in the center of ischemia. Ischemic tissue confused, neurons shrinkage or collapsed with peripheral edema, astrocytes swelled. Ischemic penumbra was intact, changed little. In PDTC-treatment group necrotic cells were fewer, a few small vessels hemorrhage and astrocyte reaction can be seen. There were few inflammatory cells near the needle tunnel.③NF-κB little expressed in sham-operation group, mainly in the apical lobe subcortex and corpus striatum symmetrically. Obvious positive expression cell of NF-κB can be 02seen in ischemic cerebral hemisphere and distributed in the ischemic penumbra. We can observe the positive expression in endothelial cell, neuron, astrocyte, ventricle cliff, choroids plexus cell, and smooth muscle cell. The process of the expression of NF-κB is dynamic. At 3h of reperfusion after cerebral ischemia for 2h, the expression began to increase, reached the peak at 6h of reperfusion and was still elevated at 48h, and afterwards began to decrease.④At 6h and 24h of reperfusion after cerebral ischemia for 2h, PDTC were applied. PDTC can inhibit the expression of NF-κB, the amount of EB lowed.









  According to the result, we can conclude: NF-κB was activated after focal cerebral-reperfusion, then the permeability of BBB began to increase; PDTC, the inhibitor of NF-κB, can depress the expression of NF-κB, meanwhile the permeability of BBB reduced. The activation of NF-κB can affect the permeability of BBB.