大鼠局灶性脑缺血再灌注损伤周围带黏结合蛋白多糖-1的表达

目的研究黏结合蛋白多糖-1(syndecan-1)在大鼠急性局灶性脑缺血再灌注损伤周围带不同时相点的变化及意义.方法采用线栓法制作大鼠大脑中动脉缺血再灌注损伤模型.利用HE染色、免疫组织化学方法,观察正常对照组、假手术组及脑缺血2 h再灌注4、24、72 h和7 d的syndecan-1阳性细胞的分布部位、数量及缺血脑组织的病理变化.结果正常对照组和假手术组syndecan-1免疫活性在皮质部位和皮质下结构表达明显;脑缺血2 h再灌注4 h可见梗死核心区的syndecan-1表达开始减少,24 h明显减少达高峰,72 h和7 d梗死核心区未见syndecan-1表达;脑缺血2 h再灌注4 h周围带的syndecan-1表达开始减少,24 h减少达高峰,到72 h脑梗死周围带的syndecan-1表达增加,7 d时梗死区周围带syndecan-1表达基本恢复;syndecan-1的表达和脑梗死周围带炎性细胞的浸润有一定的关系.结论脑缺血再灌注损伤周围带syndecan-1表达减少,可能是炎性细胞浸润的诱发因素.

Syndecan-1 expression in perilesional zone of cerebral ischemia/reperfusion rat

Objective To explore the expression of syndecan-1 in different intervals following focal cerebral ischemia/reperfusion in rat and the relationship between syndecan-1 and inflammatory cells in the rat brain.Methods The rat model of middle cerebral artery occlusion(MACO) was performed by using the intraluminal filament occlusion for 2 h,then released.The rat brain were cut in the coronal planes at the levels of the hippocampus as the templates.The immunohistochemical staining and HE staining were used to observe the distribution and the quantity of syndecan-1 and inflammatory cell expression in the normal control group,sham operation group and the MCAO groups at 4,24,72 h and 7 d after reperfusion.Results The expression of syndecan-1 was mainly in the cortex and the subcortex in the rats of normal control group and sham operation group.The immunoreactivity of syndecan-1 in the infarcted core and perilesional infarcted zone started decreasing at 4 h after ischemia/reperfusion,reached the lowest at 24 h.The expression of syndecan-1 in the perilesional infarcted zone was up-regulated at 72 h and recovered at 7 d.The relationship between syndecan-1 and inflammatory cells was of negative correlation.Conclusion The decreasing of syndecan-1 may contribute to inflammatory response in the cerebral infarction region after focal cerebral ischemia/reperfusion.