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轻度饮酒促进成年C57BL/6J小鼠缺血性中风后的早期神经发生。

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

作者信息

Li Jiyu, Li Chun, Subedi Pushpa, Tian Xinli, Lu Xiaohong, Miriyala Sumitra, Panchatcharam Manikandan, Sun Hong

机构信息

Department of Cellular Biology & Anatomy, LSUHSC-Shreveport, Shreveport, LA 71103, USA.

Department of Pharmacology, Toxicology & Neuroscience, LSUHSC-Shreveport, Shreveport, LA 71103, USA.

出版信息

Biomedicines. 2023 Apr 2;11(4):1074. doi: 10.3390/biomedicines11041074.

DOI:10.3390/biomedicines11041074
PMID:37189692
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10136277/
Abstract

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.

摘要

缺血性中风是全球范围内导致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关键作用。酒精对缺血性中风的预后有剂量依赖性影响。我们研究了轻度饮酒（LAC）在生理条件下以及缺血性中风后对神经发生的影响。将3个月大的C57BL/6J小鼠每天喂食0.7 g/kg/天的乙醇（设定为LAC）或等体积的水（设定为对照），持续8周。为了评估神经发生，在脑室下区（SVZ）、齿状回（DG）、缺血皮层和缺血纹状体中评估5-溴-2-脱氧尿苷（BrdU）/双皮质素（DCX）和BrdU/神经元核抗原（NeuN）神经元的数量。通过加速转棒试验和旷场试验测定运动活性。在生理条件下，LAC显著增加了SVZ中的BrdU/DCX和BrdU/NeuN细胞。缺血性中风显著增加了DG、SVZ、缺血皮层和缺血纹状体中的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使DG、SVZ和缺血皮层中的BrdU/NeuN细胞显著增加了约三倍。此外，LAC减少了缺血性脑损伤并改善了运动活性。因此，LAC可能通过促进神经发生来保护大脑免受缺血性中风的影响。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c06a/10136277/509dc77591f7/biomedicines-11-01074-g008.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c06a/10136277/509dc77591f7/biomedicines-11-01074-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c06a/10136277/7e1d08c62f25/biomedicines-11-01074-g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c06a/10136277/cb60a31db5a3/biomedicines-11-01074-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c06a/10136277/addc5f795a03/biomedicines-11-01074-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c06a/10136277/b633f53a48de/biomedicines-11-01074-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c06a/10136277/38c2b28f4278/biomedicines-11-01074-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c06a/10136277/509dc77591f7/biomedicines-11-01074-g008.jpg

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