Chronic Low-Dose Alcohol Consumption Promotes Cerebral Angiogenesis in Mice.
Chronic Low-Dose Alcohol Consumption Promotes Cerebral Angiogenesis in Mice.
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DOI：
10.3389/fcvm.2021.681627
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发表时间：
2021
影响因子：
3.6
通讯作者：
Sun H
中科院分区：
文献类型：
--
作者：
Li J;Li C;Loreno EG;Miriyala S;Panchatcharam M;Lu X;Sun H
长期饮酒剂量依赖性地影响缺血性卒中的发病率和预后。我们确定了生理条件下和缺血性中风后慢性饮酒对脑血管生成的影响。在体外研究中，急性暴露于低浓度乙醇显着增加血管生成能力和上调血管内皮生长因子A（VEGF-A）和血管内皮生长因子受体2（VEGFR 2）在C57 BL/6 J小鼠脑微血管内皮细胞（MBMVECs）。在VEGFR 2抑制剂的存在下，血管生成能力的增加被消除。此外，增加的血管生成能力和上调的VEGF-A和VEGFR 2保持在长期低浓度乙醇暴露的MBMVECs。在体内研究中，在生理条件下，用低剂量乙醇灌胃8周显著增加了大脑皮层中的血管密度和血管分支，并上调了VEGF-A和VEGFR 2。此外，血管密度，血管分支，VEGF-A和VEGFR 2在梗死周围皮质的表达显着更大的低剂量乙醇喂养小鼠在72小时的再灌注。虽然低剂量乙醇并没有改变脑血管反应性和局部脑血流量（rCBF）之前或在缺血，它显着增强缺血后再灌注期间充血。相反，暴露于高浓度乙醇和8周灌胃高剂量乙醇仅对血管生成能力和脑血管生成有轻度抑制作用。我们的结论是，大量饮酒可能不会显着改变脑血管生成，而轻度饮酒显着促进脑血管生成。
Chronic alcohol consumption dose-dependently affects the incidence and prognosis of ischemic stroke. We determined the influence of chronic alcohol consumption on cerebral angiogenesis under physiological conditions and following ischemic stroke. In in vitro studies, acute exposure to low-concentration ethanol significantly increased angiogenic capability and upregulated vascular endothelial growth factor A (VEGF-A) and vascular endothelial growth factor receptor 2 (VEGFR2) in C57BL/6J mouse brain microvascular endothelial cells (MBMVECs). The increased angiogenic capability was abolished in the presence of a VEGFR2 inhibitor. In addition, the increased angiogenic capability and upregulated VEGF-A and VEGFR2 remained in chronically low-concentration ethanol-exposed MBMVECs. In in vivo studies, 8-week gavage feeding with low-dose ethanol significantly increased vessel density and vessel branches and upregulated VEGF-A and VEGFR2 in the cerebral cortex under physiological conditions. Furthermore, vessel density, vessel branches, and expression of VEGF-A and VEGFR2 in the peri-infarct cortex were significantly greater in low-dose ethanol-fed mice at 72 h of reperfusion. Although low-dose ethanol did not alter cerebral vasoreactivity and regional cerebral blood flow (rCBF) either before or during ischemia, it significantly augmented post-ischemic hyperemia during reperfusion. In contrast, exposure to high-concentration ethanol and 8-week gavage feeding with high-dose ethanol only had a mild inhibitory effect on angiogenic capability and cerebral angiogenesis, respectively. We conclude that heavy alcohol consumption may not dramatically alter cerebral angiogenesis, whereas light alcohol consumption significantly promotes cerebral angiogenesis.
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影响因子：
5.6
作者：
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通讯作者：
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影响因子：
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作者：
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