Department of Anesthesiology, The Affiliated Hospital of Dalian Medical University, Dalian, 116023, Liaoning, China.
Cell Biochem Biophys. 2014 Jun;69(2):363-8. doi: 10.1007/s12013-013-9808-0.
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 ± 0.67 vs 74.14 ± 0.46; 74.89 ± 0.57 vs 75.61 ± 0.52; 77.49 ± 0.34 vs 79.33 ± 0.49; 76.31 ± 0.56 vs 78.01 ± 0.48; 72.36 ± 0.44 vs 73.12 ± 0.73; P < 0.05), the permeability of blood-brain barrier of butylphthalide group rats was induced (319.20 ± 8.11 vs 394.60 ± 6.19; 210.40 ± 9.56 vs 266.40 ± 7.99; 188.00 ± 9.22 vs 232.40 ± 7.89; 288.40 ± 7.86 vs 336.00 ± 6.71; 166.60 ± 6.23 vs 213.60 ± 13.79; P < 0.05), and the Rho A protein of butylphthalide group rats was decreased (western blot result: 1.2230 ± 0.0254 vs 1.3970 ± 0.0276; 1.5985 ± 0.0206 vs 2.0368 ± 0.0179; 1.4229 ± 0.0167 vs 1.7930 ± 0.0158;1.3126 ± 0.0236 vs 1.5471 ± 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.
本研究旨在探讨丁基苯酞对大鼠局灶性脑梗死后脑水肿、血脑屏障及 RhoA 表达的影响。将 195 只雄性 Sprague-Dawley 大鼠随机分为对照组、模型组和丁基苯酞组（40mg/kg，每天 1 次，灌胃）。采用光化学法造模。术后 3、12、24、72、144h 测量脑水含量，观察丁基苯酞对脑水肿的作用。采用伊文思蓝渗出法观察血脑屏障的变化，免疫组化法检测 RhoA 表达。与对照组相比，模型组和丁基苯酞组大鼠脑水含量增加，血脑屏障通透性增加，RhoA 蛋白表达增加。与模型组相比，丁基苯酞组大鼠脑水含量降低（73.67±0.67 比 74.14±0.46；74.89±0.57 比 75.61±0.52；77.49±0.34 比 79.33±0.49；76.31±0.56 比 78.01±0.48；72.36±0.44 比 73.12±0.73；P<0.05），血脑屏障通透性降低（319.20±8.11 比 394.60±6.19；210.40±9.56 比 266.40±7.99；188.00±9.22 比 232.40±7.89；288.40±7.86 比 336.00±6.71；166.60±6.23 比 213.60±13.79；P<0.05），RhoA 蛋白表达降低（western blot 结果：1.2230±0.0254 比 1.3970±0.0276；1.5985±0.0206 比 2.0368±0.0179；1.4229±0.0167 比 1.7930±0.0158；1.3126±0.0236 比 1.5471±0.0158；P<0.05）。丁基苯酞可减轻脑水肿，保护血脑屏障，降低梗死周围 RhoA 的表达。
