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本文引用的文献

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Emerging links between type 2 diabetes and Alzheimer's disease.2 型糖尿病与阿尔茨海默病之间新出现的联系。
World J Diabetes. 2015 Jun 10;6(5):744-51. doi: 10.4239/wjd.v6.i5.744.
2
Pre-treatment with metformin activates Nrf2 antioxidant pathways and inhibits inflammatory responses through induction of AMPK after transient global cerebral ischemia.在短暂性全脑缺血后，用二甲双胍预处理可激活Nrf2抗氧化途径，并通过诱导AMPK来抑制炎症反应。
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Modulation of the oxidative stress by metformin in the cerebrum of rats exposed to global cerebral ischemia and ischemia/reperfusion.二甲双胍对全脑缺血及缺血/再灌注大鼠大脑氧化应激的调节作用
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H₂S attenuates cognitive deficits through Akt1/JNK3 signaling pathway in ischemic stroke.硫化氢通过Akt1/JNK3信号通路减轻缺血性中风中的认知缺陷。
Behav Brain Res. 2014 Aug 1;269:6-14. doi: 10.1016/j.bbr.2014.04.027. Epub 2014 Apr 23.
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Chronic metformin treatment improves post-stroke angiogenesis and recovery after experimental stroke.慢性二甲双胍治疗可改善实验性中风后的血管生成和恢复。
Eur J Neurosci. 2014 Jun;39(12):2129-38. doi: 10.1111/ejn.12556. Epub 2014 Mar 21.
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Quercetin improves hypoxia-ischemia induced cognitive deficits via promoting remyelination in neonatal rat.槲皮素通过促进新生大鼠髓鞘再生改善缺氧缺血诱导的认知缺陷。
Brain Res. 2014 Mar 17;1553:31-40. doi: 10.1016/j.brainres.2014.01.035. Epub 2014 Jan 28.
7
Metformin increases mitochondrial energy formation in L6 muscle cell cultures.二甲双胍可增加 L6 肌细胞培养物中线粒体的能量生成。
J Biol Chem. 2013 Jul 12;288(28):20369-77. doi: 10.1074/jbc.M113.482646. Epub 2013 May 29.
8
Revisiting the mechanisms of metformin action in the liver.重新探讨二甲双胍在肝脏中的作用机制。
Ann Endocrinol (Paris). 2013 May;74(2):123-9. doi: 10.1016/j.ando.2013.03.006. Epub 2013 Apr 10.
9
Long-term post-stroke changes include myelin loss, specific deficits in sensory and motor behaviors and complex cognitive impairment detected using active place avoidance.长期的卒中后变化包括髓鞘丢失、感觉和运动行为的特定缺陷，以及使用主动回避来检测的复杂认知障碍。
PLoS One. 2013;8(3):e57503. doi: 10.1371/journal.pone.0057503. Epub 2013 Mar 7.
10
Metformin: an old but still the best treatment for type 2 diabetes.二甲双胍：一种古老但仍然是治疗 2 型糖尿病的最佳药物。
Diabetol Metab Syndr. 2013 Feb 15;5(1):6. doi: 10.1186/1758-5996-5-6.

二甲双胍通过改善再髓鞘化来减轻缺氧缺血新生大鼠的认知障碍。

Metformin Attenuates Cognitive Impairments in Hypoxia-Ischemia Neonatal Rats via Improving Remyelination.

机构信息

Medicine Intensive Care Unit, Xuzhou Children Hospital, Xuzhou, 221000, Jiangsu, People's Republic of China.

Xiangya Hospital of Centre-South University Pediatric Teaching and Research Section, 87 Xiangya Road, Changsha, 410008, Hunan, People's Republic of China.

出版信息

Cell Mol Neurobiol. 2017 Oct;37(7):1269-1278. doi: 10.1007/s10571-016-0459-8. Epub 2016 Dec 29.

DOI:10.1007/s10571-016-0459-8
PMID:28035478
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11482152/
Abstract

Perinatal hypoxia-ischemia (H/I) causes brain injury and myelination damage. Finding efficient methods to restore myelination is critical for the recovery of brain impairments. By applying an H/I rat model, we demonstrate that metformin (Met) treatment significantly ameliorates the loss of locomotor activity and cognition of H/I rat in the Morris water maze and open field task tests. After administration of Met to H/I rat, the proliferation of Olig2+ oligodendrocyte progenitor cells and the expression of myelin basic protein are obviously increased in the corpus callosum. Additionally, the myelin sheaths are more compact and the impairments are evidently attenuated. These data indicate that Met is beneficial for the amelioration of H/I-induced myelination and behavior deficits.

摘要

围产期缺氧缺血（H/I）可导致脑损伤和髓鞘损伤。寻找有效的方法来恢复髓鞘对于脑损伤的恢复至关重要。通过应用 H/I 大鼠模型，我们证明二甲双胍（Met）治疗可显著改善 H/I 大鼠在 Morris 水迷宫和旷场任务测试中运动活动和认知能力的丧失。在给予 Met 后，胼胝体中 Olig2+少突胶质前体细胞的增殖和髓鞘碱性蛋白的表达明显增加。此外，髓鞘更致密，损伤明显减轻。这些数据表明 Met 有利于改善 H/I 诱导的髓鞘形成和行为缺陷。