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

机译:丁苯酞对局灶性脑梗死大鼠脑水肿,血脑屏障及Rho A表达的影响

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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.
机译:本研究的目的是探讨丁基苯酞对局灶性脑梗死大鼠脑水肿,血脑屏障和Rho A表达的影响。随机将195只成年鼠大鼠分为对照组。组,模型组和丁基邻苯二甲酸酯组(40 mg / kg,每天一次,通过管饲法)。通过光化学方法建立模型。分别在术后3、12、24、72和144 h进行脑含水量测试,以观察丁苯酞对脑水肿的影响。进行伊文思蓝外渗法以观察血脑屏障免疫组织化学的变化,并进行蛋白质印迹以观察Rho A在梗塞周围的表达。与对照组相比,模型组和丁基苯酞组大鼠脑含水量增加,模型组和丁基苯酞组大鼠血脑屏障通透性增加,模型组和丁基苯酞组大鼠Rho A蛋白增加。增加。与模型组相比,丁基苯酞组大鼠的脑含水量被诱导(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),可诱导丁基苯酞组大鼠的血脑屏障通透性(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),丁基苯酞组大鼠的Rho A蛋白降低(蛋白质印迹结果:1.2230±0.0254 vs 1.3970±0.0276; 1.5985±0.0206 vs 2.0368 ±0.0179; 1.4229±0.0167与1.7930±0.0158; 1.3126±0.0236与1.5471±0.0158; P <0.05)。丁基酞可以减轻脑水肿,保护血脑屏障,并降低梗塞周围Rho A的表达。

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