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首页> 外文期刊>Journal of Neurochemistry: Offical Journal of the International Society for Neurochemistry >Zinc-alpha 2-glycoprotein relieved seizure-Induced neuronal glucose uptake impairment via insulin-like growth factor 1 receptor-regulated glucose transporter 3 expression
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Zinc-alpha 2-glycoprotein relieved seizure-Induced neuronal glucose uptake impairment via insulin-like growth factor 1 receptor-regulated glucose transporter 3 expression

机译：锌-α2-糖蛋白缓解癫痫发作诱导的神经元葡萄糖摄取损伤，通过胰岛素样生长因子1受体调节葡萄糖转运蛋白3表达

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摘要

Glucose hypometabolism is observed in epilepsy and promotes epileptogenesis. Glucose hypometabolism in epilepsy may be attributed to decreased neuronal glucose uptake, but its molecular mechanism remains unclear. Zinc-α2-glycoprotein (ZAG) is related to glucose metabolism and is reported to suppress seizures. The anti-epileptic effect of ZAG may be attributed to its regulation of neuronal glucose metabolism. This study explored the effect of ZAG on neuronal glucose uptake and its molecular mechanism via insulin-like growth factor 1 receptor (IGF1R)-regulated glucose transporter 3 (GLUT-3) expression. The ZAG level was modulated by lentivi-rus in primary culture neurons. Neuronal seizure models were induced by Mg2+-free artificial cerebrospinal fluid. We assessed neuronal glucose uptake by the 2-NBDG method and Glucose Uptake Colorimetric Assay Kit. IGF1R was activated by IGF1 and blocked by AXL1717. The expression and distribution of IGF1R and GLUT-3, together with IGF1R phosphorylation, were measured by western blot. The binding between ZAG and IGF1R was determined by coimmunoprecipitation. Neuronal glucose uptake and GLUT-3 expression were significantly decreased by seizure or ZAG knockdown, whereas ZAG over-expression or IGF1 treatment reversed this decrease. The effect of ZAG on neuronal glucose uptake and GLUT-3 expression was blocked by AXL1717. ZAG increased IGF1R distribution and phosphorylation possibly by binding. Additionally, IGF1R increased GLUT-3 activity by increasing GLUT-3 expression. In epilepsy/seizure, neuronal glucose uptake suppression may be attributed to a decrease in ZAG, which suppresses neuronal GLUT-3 expression by regulating the activity of IGF1R. ZAG, IGF1R, and GLUT-3 may be novel potential therapeutic targets of glucose hypometabolism in epilepsy and seizures.
机译：癫痫患者存在糖代谢低下，并促进癫痫的发生。癫痫患者葡萄糖代谢低下可能是由于神经元葡萄糖摄取减少，但其分子机制尚不清楚。锌-α2-糖蛋白（ZAG）与葡萄糖代谢有关，据报道可抑制癫痫发作。ZAG的抗癫痫作用可能与其调节神经元糖代谢有关。本研究通过胰岛素样生长因子1受体（IGF1R）调节的葡萄糖转运蛋白3（GLUT-3）表达，探讨ZAG对神经元葡萄糖摄取的影响及其分子机制。在原代培养的神经元中，ZAG水平由豆状病毒调节。用无镁人工脑脊液诱导神经元癫痫模型。我们通过2-NBDG法和葡萄糖摄取比色测定试剂盒评估神经元葡萄糖摄取。IGF1激活IGF1R，AXL1717阻断IGF1R。通过western blot检测IGF1R和GLUT-3的表达和分布，以及IGF1R的磷酸化。ZAG和IGF1R之间的结合通过共同免疫沉淀测定。癫痫发作或ZAG基因敲除可显著降低神经元葡萄糖摄取和GLUT-3表达，而ZAG过度表达或IGF1治疗可逆转这种降低。ZAG对神经元葡萄糖摄取和GLUT-3表达的影响被AXL1717阻断。ZAG可能通过结合增加IGF1R分布和磷酸化。此外，IGF1R通过增加GLUT-3表达增加GLUT-3活性。在癫痫/癫痫发作中，神经元葡萄糖摄取抑制可能归因于ZAG的减少，ZAG通过调节IGF1R的活性抑制神经元GLUT-3的表达。ZAG、IGF1R和GLUT-3可能是癫痫和癫痫发作中葡萄糖低代谢的新潜在治疗靶点。

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