中文摘要：

目的：探讨盘状结构域受体酪氨酸激酶（discoidin domain recetor1，DDRl）蛋白在局灶性脑缺血致血脑屏障损伤中的作用机制及其病理性意义。方法：成年雄性sD大鼠80只，体重280—320g，采用随机数字表法，将其随机分为假手术组、缺血再灌注组、siRNA处理组和siRNA错配组，每组5只。采用大鼠大脑中动脉线栓法制备局灶性脑缺血再灌注模型，缺血120min再灌注24h时进行神经行为学评分，随后处死大鼠取脑，分别采用TIC（2，3，5-triphenyl tetrazolium chloride）染色法、干湿比重法、伊文思蓝法测定脑梗死体积、脑组织含水量及血脑屏障的通透性。结果：与假手术组比较，脑缺血再灌注组神经行为学评分降低（P〈0．05），脑梗死体积百分比增加，缺血侧脑组织含水量增多（P〈0．05），血脑屏障的通透性增大（P〈0．01）；与局灶性脑缺血再灌注组比较，DDR1-siRNA处理组神经行为学评分升高，脑梗死体积百分比减少，脑组织含水量减少（P〈0．05），血脑屏障通透性降低（P〈0．01）。结论：DDR1蛋白可能参与了脑缺血再灌注损伤后血脑屏障的破坏，抑制DDRl的表达可降低血脑屏障的通透性；另外，检测DDR1的表达可作为脑卒中早期诊断和判断预后的分子指标之一。

英文摘要：

Objective： To explore the effect and mechanism of discoidin domain receptor 1 （DDR1） on blood brain barrier impairment after focal cerebral ischemia-reperfusion in rats. Methods： 80 adult male SD rats, weighing 280 N 320 g, were randomly divided into the sham group, the middle cerebral artery occlusion （MCAO） group, the DDRI-siRNA group and the scramble siRNA group （ n = 5 ）. Focal cerebral ischemia was induced by MCAO in rats. At 24 h after the reperfusion following 120 min ischemia, TI＇C staining, dry/wet weight method and Evans blue dye extravasation were applied to quantify infarction volume, brain water content and blood-brain barrier impairment, respectively. Neurological deficit scores were also evaluated. Results： The neurological score was significantly lower in the MCAO group than in the sham group （ P 〈 0.05 ）. The focal cerebral infarction volume percentage, brain water content and blood-brain barrier impairment were significantly higher in the MCAO group than in the sham group（P 〈0.05, P 〈0.01 ）. Compared with the MCAO group, The focal cerebral infarction volume percentage, brain water content and blood-brain barrier impairment were significantly lower in the DDRI-siRNA group（P 〈0.05, P 〈 0.01 ） ; while the neurological score was significantly higher in the DDRI-siRNA group than in the MCAO group （ P 〈 0.05 ）. Conclusion： DDR1 may be involved in bloodbrain barrier impairment after focal cerebral ischemia-reperfusion in rats, inhibiting the expression of DDR1 can reduce the blood-brain barrier permeability. In addition, the detection of DDR1 may contribute to diagnosis for stroke in early stage and may act as one of biological indicators of prognosis.