Light Alcohol Consumption Promotes Early Neurogenesis Following Ischemic Stroke in Adult C57BL/6J Mice.

Light Alcohol Consumption Promotes Early Neurogenesis Following Ischemic Stroke in Adult C57BL/6J Mice.
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DOI:
10.3390/biomedicines11041074
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发表时间:
2023-04-02
期刊:
影响因子:
4.7
通讯作者:
--
中科院分区:
工程技术3区
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缺血性中风是世界范围内死亡和残疾的主要原因之一。神经发生在缺血后功能恢复中起着至关重要的作用。酒精剂量依赖性地影响缺血性卒中的预后。我们研究了生理条件下和缺血性卒中后轻度饮酒(LAC)对神经发生的影响。C57 BL/6 J小鼠(3月龄)每天喂食0.7 g/kg/天乙醇(设计为LAC)或体积匹配的水(设计为对照),持续8周。为了评价神经发生,在室下区(SVZ)、齿状回(DG)、缺血皮质和缺血纹状体中评估了5-溴-2-脱氧尿苷(BrdU)+/双皮质素(DCX)+和BrdU+/NeuN+神经元的数量。通过加速旋转杆和旷场实验测定自发活动。在生理条件下,LAC显著增加SVZ中的BrdU+/DCX+和BrdU+/NeuN+细胞。缺血性卒中显著增加DG、SVZ、缺血性皮质和缺血性纹状体中的BrdU+/DCX+和BrdU+/NeuN+细胞。与对照小鼠相比,LAC小鼠中BrdU+/DCX+细胞的增加显著更大。此外,LAC显著增加DG、SVZ和缺血皮质中的BrdU+/NeuN+细胞约3倍。此外,LAC减少缺血性脑损伤并改善运动活性。因此,LAC可能通过促进神经发生来保护脑免受缺血性卒中。
Ischemic stroke is one of the leading causes of death and disability worldwide. Neurogenesis plays a crucial role in postischemic functional recovery. Alcohol dose-dependently affects the prognosis of ischemic stroke. We investigated the impact of light alcohol consumption (LAC) on neurogenesis under physiological conditions and following ischemic stroke. C57BL/6J mice (three months old) were fed with 0.7 g/kg/day ethanol (designed as LAC) or volume-matched water (designed as control) daily for eight weeks. To evaluate neurogenesis, the numbers of 5-bromo-2-deoxyuridine (BrdU)+/doublecortin (DCX)+ and BrdU+/NeuN+ neurons were assessed in the subventricular zone (SVZ), dentate gyrus (DG), ischemic cortex, and ischemic striatum. The locomotor activity was determined by the accelerating rotarod and open field tests. LAC significantly increased BrdU+/DCX+ and BrdU+/NeuN+ cells in the SVZ under physiological conditions. Ischemic stroke dramatically increased BrdU+/DCX+ and BrdU+/NeuN+ cells in the DG, SVZ, ischemic cortex, and ischemic striatum. The increase in BrdU+/DCX+ cells was significantly greater in LAC mice compared to the control mice. In addition, LAC significantly increased BrdU+/NeuN+ cells by about three folds in the DG, SVZ, and ischemic cortex. Furthermore, LAC reduced ischemic brain damage and improved locomotor activity. Therefore, LAC may protect the brain against ischemic stroke by promoting neurogenesis.
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