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首页> 外文期刊>BioFactors >Partial IGF-1 deficiency induces brain oxidative damage and edema, which are ameliorated by replacement therapy
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Partial IGF-1 deficiency induces brain oxidative damage and edema, which are ameliorated by replacement therapy

机译：IGF-1的部分缺乏会引起脑部氧化损伤和水肿，替代疗法可改善这种情况

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Insulin-like growth factor 1 (IGF-1) induces multiple cytoprotective effects on every tissue, including the brain. Since the mechanisms by which IGF-1 produces neuroprotection are not fully understood, the aim of this work was to delve into the underlying mechanisms. IGF-1 deficient mice (Hz) were compared with wild type (WT) and Hz mice treated with low doses of IGF-1 (2 mu g/100 g body weight/day) for 10 days (Hz+IGF). Gene expression, quantitative PCR, histology, and magnetic resonance imaging were performed in the three groups. IGF-1 deficiency induced increased oxidative damage determined by markers of lipid peroxidation and hypoxia, as well as gene expression of heat shock proteins, antioxidant enzymes, and molecules involved in inflammation, apoptosis, and mitochondrial protection. These changes correlated with edema and learning impairment in Hz mice. IGF-1 therapy improved all these alterations. In conclusion, IGF-1 deficiency is responsible for increased brain oxidative damage, edema, and impaired learning and memory capabilities which are rescued by IGF-1 replacement therapy. (c) 2016 BioFactors, 42(1):60-79, 2016
机译：胰岛素样生长因子1（IGF-1）对包括大脑在内的每个组织都具有多种细胞保护作用。由于尚未完全了解IGF-1产生神经保护的机制，因此这项工作的目的是深入研究潜在的机制。将IGF-1缺陷小鼠（Hz）与野生型（WT）和以低剂量IGF-1（2μg/ 100 g体重/天）处理10天（Hz + IGF）的Hz小鼠进行比较。在三组中进行基因表达，定量PCR，组织学和磁共振成像。 IGF-1缺乏引起脂质过氧化和缺氧的标志物以及热休克蛋白，抗氧化酶和涉及炎症，细胞凋亡和线粒体保护的分子的基因表达确定的氧化损伤增加。这些变化与Hz小鼠的水肿和学习障碍有关。 IGF-1疗法改善了所有这些改变。总之，IGF-1缺乏会导致脑部氧化损伤，水肿和学习记忆能力减退，而IGF-1替代疗法可以挽救这些缺陷。 （c）2016年生物因子，42（1）：60-79，2016

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