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Citation |
Wu W, Tian R, Hao S, Xu F, Mao X, Liu B. Br. J. Neurosurg. 2014; 28(6): 739-745. |
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Affiliation |
Department of Neurosurgery, Beijing Tiantan Hospital, Capital Medical University , Beijing , P. R. China. |
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Copyright |
(Copyright © 2014, Informa - Taylor and Francis Group) |
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DOI |
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PMID |
24814385 |
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Abstract |
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 hypoxia-inducible factor-1α (HIF-1α). 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-1α, 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-1α 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-1α 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-1α and AQP4 might be involved. Language: en |