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二甲双胍可减轻大脑缺血/再灌注大鼠模型中的神经元损伤,并促进神经母细胞的增殖与分化。

Metformin reduces neuronal damage and promotes neuroblast proliferation and differentiation in a cerebral ischemia/reperfusion rat model.

作者信息

Yuan Rui, Wang Yu, Li Qingyun, Zhen Fei, Li Xinyu, Lai Qingwei, Hu Peng, Wang Xiao, Zhu Yansha, Fan Hongbin, Yao Ruiqin

机构信息

Xuzhou Key Laboratory of Neurobiology, Jiangsu Key Laboratory of New Drug Research and Clinical Pharmacy, Department of Cell Biology and Neurobiology, Xuzhou Medical University.

Department of Neurology, Shanxi Provincial People's Hospital, Xian, People's Republic of China.

出版信息

Neuroreport. 2019 Feb 6;30(3):232-240. doi: 10.1097/WNR.0000000000001190.

DOI:10.1097/WNR.0000000000001190
PMID:30614910
Abstract

According to the previous research, metformin, a medication utilized for type 2 diabetes management, inhibits neural aging and reduces infarct size by enhancing angiogenesis in a mouse stroke model. What is more, metformin administration also promotes neural precursor cells proliferation, migration, as well as differentiation for newborn mice with hypoxia-ischemia brain injury. However, whether metformin regulates neurogenesis in an adult rat ischemia/reperfusion (I/R) model remains unclear. The current research found that metformin administration reduced neuronal damage in the CA1 area of hippocampus in a rat model of I/R. The number of neuronal nuclei positive neuron was significantly increased and glial fibrillary acidic protein positive astrocyte became obviously declined in the CA1 region in I/R rats treated with metformin. It was further demonstrated that metformin promoted neuroblasts proliferation and neuronal differentiation in the subgranular zone of the dentate gyrus and inhibited the formation of astrocyte. Our study indicates that activation of endogenous neuroblasts using metformin will become a favorable target in therapeutic intervention of cerebral ischemia injury models.

摘要

根据先前的研究,二甲双胍是一种用于治疗2型糖尿病的药物,在小鼠中风模型中,它通过促进血管生成来抑制神经衰老并减小梗死面积。此外,二甲双胍给药还能促进缺氧缺血性脑损伤新生小鼠神经前体细胞的增殖、迁移以及分化。然而,二甲双胍是否能在成年大鼠缺血/再灌注(I/R)模型中调节神经发生仍不清楚。当前研究发现,在I/R大鼠模型中,给予二甲双胍可减少海马CA1区的神经元损伤。在用二甲双胍治疗的I/R大鼠中,CA1区神经元核阳性神经元数量显著增加,胶质纤维酸性蛋白阳性星形胶质细胞明显减少。进一步证明,二甲双胍促进齿状回颗粒下区神经母细胞的增殖和神经元分化,并抑制星形胶质细胞的形成。我们的研究表明,使用二甲双胍激活内源性神经母细胞将成为脑缺血损伤模型治疗干预的一个有利靶点。

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Cell Biochem Biophys. 2025 Feb 26. doi: 10.1007/s12013-025-01687-5.
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Novel mechanistic insights of the potential role of gasotransmitters and autophagy in the protective effect of metformin against hepatic ischemia/reperfusion injury in rats.气体递质与自噬在二甲双胍对大鼠肝脏缺血/再灌注损伤保护作用中的潜在作用的新机制见解
Naunyn Schmiedebergs Arch Pharmacol. 2025 Feb 6. doi: 10.1007/s00210-025-03837-1.
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