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目的:研究丁基苯酞(NBP)对局灶性脑缺血再灌注引起的血脑屏障(BBB)破坏的保护作用。方法:尼龙线栓塞法造成大鼠局灶性脑缺血模型,尼龙线抽出进行再灌。BBB的通透性以结合有伊文氏蓝染料的血浆蛋白外渗进入脑组织的量以及免疫组化和电镜方法进行了测定。结果:脑缺血3h再灌注3h可使结合有血浆蛋白的伊文氏蓝在缺血皮层含量明显增加;免疫球蛋白IgG在大脑皮层中的表达明显增加;皮层组织中毛细血管内皮细胞膜上有微小孔洞的形成,内皮细胞中线粒体空泡化。NBP 5,10,和20mg·kg~(-1)可使皮层中染料含量分别下降33.3％,46.7％和50.7％;缺血皮层中IgG的表达减少;毛细血管超微结构的损伤也有一定程度的减轻。NBP20mg·kg~(-1)亦可使脑缺血再灌后脑水肿程度明显减轻。结论:NBP可减轻局灶性脑缺血再灌引起的BBB损伤。
Objective: To study the protective effect of butylphthalide (NBP) on the destruction of the blood-brain barrier (BBB) induced by focal cerebral ischemia-reperfusion. Methods: The model of focal cerebral ischemia induced by nylon thread embolism was withdrawn by nylon thread for reperfusion. The permeability of BBB was measured by the amount of extravasation of plasma proteins that incorporated Evans blue dye into brain tissue as well as by immunohistochemistry and electron microscopy. Results: The reperfusion at 3h after cerebral ischemia resulted in a significant increase in the amount of Evans blue with plasma protein in the ischemic cortex. The expression of immunoglobulin IgG in the cerebral cortex was significantly increased. The cortical tissue with small capillary endothelial cell membrane The formation of holes, mitochondria in endothelial cells vacuolization. NBP 5, 10, and 20 mg · kg -1 could decrease the dye content in the cortex by 33.3%, 46.7% and 50.7%, respectively. The expression of IgG decreased in the ischemic cortex and the damage of capillary ultrastructure to a certain degree The reduction. NBP20mg · kg ~ (-1) can also make cerebral edema after cerebral ischemia and reperfusion extent significantly reduced. Conclusion: NBP can reduce the damage of BBB induced by focal cerebral ischemia and reperfusion.