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首页> 外文期刊>Journal of Neuroscience Research >Chronic systemic D-galactose exposure induces memory loss, neurodegeneration, and oxidative damage in mice: protective effects of R-alpha-lipoic acid.
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Chronic systemic D-galactose exposure induces memory loss, neurodegeneration, and oxidative damage in mice: protective effects of R-alpha-lipoic acid.

机译：慢性全身性D-半乳糖暴露会引起小鼠记忆力减退，神经变性和氧化损伤：R-α-硫辛酸的保护作用。

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Chronic systemic exposure of mice, rats, and Drosophila to D-galactose causes the acceleration of senescence and has been used as an aging model. The underlying mechanism is yet unclear. To investigate the mechanisms of neurodegeneration in this model, we studied cognitive function, hippocampal neuronal apoptosis and neurogenesis, and peripheral oxidative stress biomarkers, and also the protective effects of the antioxidant R-alpha-lipoic acid. Chronic systemic exposure of D-galactose (100 mg/kg, s.c., 7 weeks) to mice induced a spatial memory deficit, an increase in cell karyopyknosis, apoptosis and caspase-3 protein levels in hippocampal neurons, a decrease in the number of new neurons in the subgranular zone in the dentate gyrus, a reduction of migration of neural progenitor cells, and an increase in death of newly formed neurons in granular cell layer. The D-galactose exposure also induced an increase in peripheral oxidative stress, including an increase in malondialdehyde, a decrease in total anti-oxidative capabilities (T-AOC), total superoxide dismutase (T-SOD), and glutathione peroxidase (GSH-Px) activities. A concomitant treatment with lipoic acid ameliorated cognitive dysfunction and neurodegeneration in the hippocampus, and also reduced peripheral oxidative damage by decreasing malondialdehyde and increasing T-AOC and T-SOD, without an effect on GSH-Px. These findings suggest that chronic D-galactose exposure induces neurodegeneration by enhancing caspase-mediated apoptosis and inhibiting neurogenesis and neuron migration, as well as increasing oxidative damage. In addition, D-galactose-induced toxicity in mice is a useful model for studying the mechanisms of neurodegeneration and neuroprotective drugs and agents.
机译：小鼠，大鼠和果蝇对D-半乳糖的长期系统性暴露会导致衰老加速，并已被用作衰老模型。潜在的机制尚不清楚。为了研究该模型中神经变性的机制，我们研究了认知功能，海马神经元凋亡和神经发生，外周氧化应激生物标志物以及抗氧化剂R-α-硫辛酸的保护作用。 D-半乳糖（100 mg / kg，皮下注射，sc，7周）的慢性全身暴露导致空间记忆缺陷，海马神经元细胞核固缩，细胞凋亡和caspase-3蛋白水平增加，新数目减少齿状回中亚颗粒区的神经元，神经祖细胞迁移的减少，以及颗粒细胞层中新形成的神经元死亡的增加。 D-半乳糖暴露还引起外周氧化应激增加，包括丙二醛增加，总抗氧化能力（T-AOC），总超氧化物歧化酶（T-SOD）和谷胱甘肽过氧化物酶（GSH-Px）降低。 ）活动。硫辛酸的伴随治疗可减轻海马的认知功能障碍和神经变性，并通过减少丙二醛和增加T-AOC和T-SOD减少外周氧化损伤，而对GSH-Px无影响。这些发现表明，慢性D-半乳糖暴露可通过增强caspase介导的细胞凋亡，抑制神经发生和神经元迁移以及增加氧化损伤来诱导神经变性。此外，D-半乳糖对小鼠的毒性作用是研究神经退行性疾病和神经保护药物及制剂的有用模型。

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