The Effect of Butylphthalide on the Brain Edema, Blood-Brain Barrier of Rats After Focal Cerebral Infarction and the Expression of Rho A

The aim of this study was to explore the effect of butylphthalide on the brain edema, blood-brain barrier of rats of rats after focal cerebral infarction and the expression of Rho A. A total of 195 sprague-dawley male rats were randomly divided into control group, model group, and butylphthalide group (40 mg/kg, once a day, by gavage). The model was made by photochemical method. After surgery 3, 12, 24, 72, and 144 h, brain water content was done to see the effect of butylphthalide for the cerebral edema. Evans blue extravasation method was done to see the changes in blood-brain barrier immunohistochemistry, and Western blot was done to see the expression of Rho A around the infarction. Compared with the control group, the brain water content of model group and butylphthalide group rats was increased, the permeability of blood-brain barrier of model group and butylphthalide group rats was increased, and the Rho A protein of model group and butylphthalide group rats was increased. Compared with the model group, the brain water content of butylphthalide group rats was induced (73.67 +/- A 0.67 vs 74.14 +/- A 0.46; 74.89 +/- A 0.57 vs 75.61 +/- A 0.52; 77.49 +/- A 0.34 vs 79.33 +/- A 0.49; 76.31 +/- A 0.56 vs 78.01 +/- A 0.48; 72.36 +/- A 0.44 vs 73.12 +/- A 0.73; P < 0.05), the permeability of blood-brain barrier of butylphthalide group rats was induced (319.20 +/- A 8.11 vs 394.60 +/- A 6.19; 210.40 +/- A 9.56 vs 266.40 +/- A 7.99; 188.00 +/- A 9.22 vs 232.40 +/- A 7.89; 288.40 +/- A 7.86 vs 336.00 +/- A 6.71; 166.60 +/- A 6.23 vs 213.60 +/- A 13.79; P < 0.05), and the Rho A protein of butylphthalide group rats was decreased (western blot result: 1.2230 +/- A 0.0254 vs 1.3970 +/- A 0.0276; 1.5985 +/- A 0.0206 vs 2.0368 +/- A 0.0179; 1.4229 +/- A 0.0167 vs 1.7930 +/- A 0.0158;1.3126 +/- A 0.0236 vs 1.5471 +/- A 0.0158; P < 0.05). The butylphthalide could reduce the brain edema, protect the blood-brain barrier, and decrease the expression of Rho A around the infarction.