丁苯酞对局灶性脑梗死大鼠脑水肿、血脑屏障通透性和皮质RhoA表达的影响

目的 探讨丁苯酞对局灶性脑梗死大鼠脑水肿、血脑屏障通透性和皮质RhoA表达水平的影响.方法 雄性Sprague-Dawley大鼠220只,按随机数字表法分为假手术组、脑缺血组和丁苯酞组（40 mg/kg,1次/d,灌胃）.采用光化学法建立大鼠局灶性脑梗死模型.分别于模型制作后3、12、24、72和144 h时,采用干湿重法和伊文思蓝渗出法检测脑组织含水量和血脑屏障通透性.在模型制作后24 h,采用免疫组化染色和蛋白质印迹法检测梗死周围皮质RhoA蛋白表达水平.结果 与假手术组比较,脑缺血组和丁苯酞组脑组织含水量（除6h时间点外）和血脑屏障通透性均显著性增高（P均＜0.05）.免疫组化染色和蛋白质印迹分析提示,脑缺血组和丁苯酞组梗死周围皮质RhoA表达显著上调.与脑缺血组比较,丁苯酞组各时间点脑组织含水量和血脑屏障通透性均显著性降低（P均＜0.05）,RhoA表达水平也显著性降低（P＜0.05）.结论 丁苯酞可减轻局灶性脑梗死大鼠脑水肿,抑制血脑屏障的破坏,下调RhoA表达.

Effects of butylphthalide on brain edema,blood-brain barrier permeability and RhoA expression in cortex in focal cerebral infarction in rats

Objective To investigate the effects of butylphthalide on brain edema,blood-brain barrier permeability and RhoA expression in cortex in focal cerebral infarction in rats.Methods A total of 220 male Sprague Dawley rats were divided into a control,a model and a butylphthalile group （40 mg/kg,once a day,gavage） according to the random number table method.A model of rat focal cerebral infarction was induced by photochemical method.At 3,12,24,72,and 144 h after modeling,wet-dry weight method and Evans blue extravasation method were used to detect the brain water content and blood-brain barrier permeability.At 24 h after modeling,immunohistochemical staining and Western blot were used to detect the expression of RhoA protein in the periinfarction cortex.Results Compared to the control group,the brain water content （except at 6 h） and blood-brain barrier permeability in the model group and the butylphthalide group were increased significantly （all P 〈 0.05）.The immunohistochemical staining and Western blot suggested that the RhoA expression in the periinfarction cortex was upregulated significantly （all P 〈 0.05）.Compared to the model group,the brain water content and blood-brain barrier permeability at different time points in the butylphthalide group were decreased significantly （all P 〈 0.05）.The expression levels of RhoA were also decreased significantly （P 〈 0.05）.Conclusions Butylphthalide may reduce the brain edema of focal cerebral infarction in rats,inhibit disruption of the blood-brain barrier,and down-regulate the expression of RhoA.