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首页> 外文期刊>Journal of neurosurgery. >Reduction of brain edema and expression of aquaporins with acute ethanol treatment after traumatic brain injury Laboratory investigation
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Reduction of brain edema and expression of aquaporins with acute ethanol treatment after traumatic brain injury Laboratory investigation

机译：急性乙醇治疗脑外伤后减轻脑水肿和水通道蛋白的表达实验室研究

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摘要

Object. Previous studies have demonstrated that traumatic brain injury (TBI) causes brain edema by allowing excessive water passage through aquaporin (AQP) proteins. To establish the potential neuroprotective properties of ethanol as a post-TBI therapy, in the present study the authors determined the effect of ethanol on brain edema, AQP expression, and functional outcomes in a post-TBI setting.Methods. Adult male Sprague-Dawley rats weighing between 425 and 475 g received a closed head TBI in which Maramarou's impact-acceleration method was used. Animals were given a subsequent intraperitoneal injection of 0.5 g/kg or 1.5 g/kg ethanol at 60 minutes post-TBI and were killed 24 hours after TBI. Brains were subsequently examined for edema along with AQP mRNA and protein expression. Additional animals treated with either 0.5 g/kg or 1.5 g/kg ethanol at 60 minutes post-TBI were designated for cognitive and motor testing for 3 weeks.Results. Ethanol administration post-TBI led to significantly (p < 0.05) lower levels of brain edema as measured by brain water content. This downregulation in brain edema was associated with significantly (p < 0.05) reduced levels of AQP mRNA and protein expression as compared with TBI without treatment. These findings concur with cognitive studies in which ethanol-treated animals exhibited significantly (p < 0.05) faster radial maze completion times. Motor behavioral testing additionally demonstrated significant (p < 0.05) beneficial effects of ethanol, with treated animals displaying improved motor coordination when compared with untreated animals.Conclusions. The present findings suggest that acute ethanol administration after a TBI decreases AQP expression, which may lead to reduced cerebral edema. Ethanol-treated animals additionally showed improved cognitive and motor outcomes compared with untreated animals.
机译：目的。先前的研究表明，创伤性脑损伤（TBI）通过使水通过水通道蛋白（AQP）蛋白质过多而引起脑水肿。为了确定乙醇作为TBI后治疗的潜在神经保护特性，在本研究中，作者确定了TBI后环境中乙醇对脑水肿，AQP表达和功能结局的影响。体重在425至475 g之间的成年雄性Sprague-Dawley大鼠接受了封闭的头部TBI，其中使用了Maramarou的冲击加速方法。在TBI后60分钟对动物进行腹膜内注射0.5g / kg或1.5g / kg乙醇，并在TBI后24小时处死动物。随后检查大脑的水肿以及AQP mRNA和蛋白质表达。在TBI后60分钟用0.5 g / kg或1.5 g / kg乙醇治疗的其他动物被指定进行3周的认知和运动测试。 TBI后的乙醇给药导致脑水肿水平显着降低（p <0.05），如脑水含量所测。与未经治疗的TBI相比，脑水肿的这种下调与AQP mRNA和蛋白质表达水平显着降低（p <0.05）有关。这些发现与认知研究一致，在认知研究中，以乙醇处理的动物表现出明显的（p <0.05）更快的径向迷宫完成时间。运动行为测试还显示了乙醇的显着（p <0.05）有益作用，与未治疗的动物相比，治疗的动物表现出更好的运动协调性。本研究结果表明，TBI后急性乙醇给药会降低AQP表达，这可能导致脑水肿减轻。与未治疗的动物相比，乙醇治疗的动物还表现出改善的认知和运动结果。

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