Effects of butylphthalide on brain edema, blood-brain barrier permeability and RhoA expression in cortex in focal cerebral infarction in rats
10.3760/cma.j.issn.1673-4165.2013.12.005
- VernacularTitle: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
- Author:
Ying XIAO
;
Lina WANG
;
Yongliang LIU
;
Peng WANG
- Publication Type:Journal Article
- Keywords:
Brain Ischemia;
rho GTP-Binding Proteins;
Brain Edema;
Blood-Brain Barrier;
Benzofurans;
3-n-butylphthalide;
Disease Models,Animal;
Rats
- From:
International Journal of Cerebrovascular Diseases
2013;21(12):903-907
- CountryChina
- Language:Chinese
-
Abstract:
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.
