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首页> 外文期刊>British journal of neurosurgery >A pre-injury high ethanol intake in rats promotes brain edema following traumatic brain injury
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A pre-injury high ethanol intake in rats promotes brain edema following traumatic brain injury

机译：大鼠受伤前高乙醇摄入会导致脑外伤后脑水肿

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摘要

Drinking is a risk factor for traumatic brain injury (TBI), and ethanol can aggravate the outcome by promoting brain edema. The mechanism involved is not fully understood. It has been confirmed that aquaporin-4 (AQP4) and vascular endothelial growth factor (VEGF) play pivotal roles in cytotoxic/vasogenic brain edema individually, and both of these proteins are downstream regulatory factors of hypoxiainducible factor-1 alpha (HIF-1 alpha). In this study, we used a fluid percussion injury (FPI) model in rats to determine the effects of acute ethanol intake on the expression levels of HIF-1 alpha, AQP4, and VEGF prior to FPI. The animals were sacrificed 1, 2, 3, and 4 days post-injury. We found that the expression levels of HIF-1 alpha and AQP4 were significantly upregulated in the ethanol-pretreated groups, whereas the VEGF expression level was not. In addition, there was a positive correlation between HIF-1 alpha and AQP4. The results of this study indicate that cytotoxic brain edema may play an important role in the early stage of FPI in ethanol-pre-treated animals and that HIF-1 alpha and AQP4 might be involved.
机译：饮酒是发生脑外伤（TBI）的危险因素，乙醇可通过促进脑水肿而加重结局。所涉及的机制尚未完全了解。已经证实水通道蛋白4（AQP4）和血管内皮生长因子（VEGF）在细胞毒性/血管源性脑水肿中分别起关键作用，并且这两种蛋白都是低氧诱导因子1α（HIF-1 alpha）的下游调节因子。 ）。在这项研究中，我们在大鼠中使用了流体打击伤害（FPI）模型来确定急性乙醇摄入对FPI之前HIF-1α，AQP4和VEGF表达水平的影响。在受伤后1、2、3和4天处死动物。我们发现，在乙醇预处理组中，HIF-1α和AQP4的表达水平显着上调，而VEGF表达水平则没有。此外，HIF-1 alpha与AQP4之间存在正相关。这项研究的结果表明，在乙醇预处理的动物中，细胞毒性脑水肿可能在FPI的早期发挥重要作用，并且可能涉及HIF-1 alpha和AQP4。

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