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目的探讨大鼠上矢状窦闭塞后基质金属蛋白酶-9(matrix metalloproteinase-9,MMP-9)与血脑屏障(blood brain barrier,BBB)紧密连接的关系。方法 2015年5月选择健康雄性Wistar大鼠50只,对其编号后采用随机表法分为对照组和实验组,实验组大鼠参照Schaller等方法进行额顶部开颅处理,并在显微镜下行结扎处理,同时进行常规喂养;对照组大鼠除最后不结扎外步骤同前;同时对两组大鼠进行BBB通透性测定及MMP-9和Claudin-3检测,研究大鼠上矢状窦闭塞后MMP-9与BBB紧密连接的关系。计量资料采用t检验,相关性采用Pearson检验。P<0.05为差异有统计学意义。结果脑组织伊文氏蓝(Evan’s blue,EB)含量在上矢状窦闭塞3 h后即开始增加并持续升高,在第24 h达到高峰后逐渐回落,实验组EB含量在6、12、24 h及3 d[(7.81±0.50)、(11.96±0.63)、(16.66±0.84)、(13.65±0.73)μg/g]与对照组[(6.64±0.53)μg/g]比较,差异均有统计学意义(均P<0.05);与对照组相比,上矢状窦闭塞6 h的MMP-9表达开始升高,24 h达到高峰,后逐渐下降;Claudin-3表达从12 h开始下降,至24 h下降到最低。MMP-9与EB含量各时间点的呈正相关关系。MMP-9与Claudin-3各时间点的呈高度负相关关系。结论上矢状窦闭塞后MMP-9通过降解Claudin-3破坏BBB的紧密连接,使其通透性增加,在血管源性脑水肿形成中发挥重要作用。
Objective To investigate the relationship between matrix metalloproteinase-9 (MMP-9) and blood brain barrier (BBB) tight junction in the superior sagittal sinus. Methods Fifty healthy male Wistar rats were selected in May, 2015. After random numbering, they were divided into control group and experimental group. The rats in experimental group were treated by Schaller’s method and were surgically removed by microscope. At the same time, BBB permeability and MMP-9 and Claudin-3 were detected in both groups to study the superior sagittal sinus occlusion The relationship between MMP-9 and BBB tight junctions. Measurement data using t test, correlation using Pearson test. P <0.05 for the difference was statistically significant. Results Evan’s blue (EB) content in brain tissue began to increase 3 h after the occlusion of the superior sagittal sinus and continued to increase, and then gradually decreased after reaching the peak at 24 h. The content of EB in the experimental group was 6, 12, 24 h and 3 d [(7.81 ± 0.50) and (11.96 ± 0.63) and (16.66 ± 0.84) and (13.65 ± 0.73) μg / g, respectively, compared with that in the control group [(6.64 ± 0.53) μg / g] (P <0.05). Compared with the control group, the expression of MMP-9 in the superior sagittal sinus began to increase at 6 h, reached the peak at 24 h, then decreased gradually. The expression of Claudin-3 decreased from 12 h , To 24 h down to the lowest. There was a positive correlation between MMP-9 and EB content at each time point. MMP-9 and Claudin-3 at each time point was highly negative correlation. Conclusions MMP-9 can disrupt the tight junction of BBB through the degradation of Claudin-3, resulting in its increased permeability. It plays an important role in the formation of vasogenic brain edema.