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机构地区:[1]湖南中医药大学第一附属医院,中国湖南长沙410007 [2]中南大学湘雅医院,中国湖南长沙410008
出 处:《生命科学研究》2017年第6期519-522,共4页Life Science Research
基 金:国家自然科学基金资助项目(81570776)
摘 要:为探索高糖培养对原代海马神经元形态损伤和神经退行性相关蛋白β-淀粉样蛋白前体(amyloid β-protein precursor,APP)含量的影响,分离胎龄16 d的大鼠海马神经元,分别使用含有25 mmol/L、50 mmol/L、75 mmol/L和100 mmol/L葡萄糖浓度的Neurobasal培养基进行原代培养干预,Western-blot检测APP蛋白水平,光学显微镜下观察不同浓度葡萄糖作用后海马神经元形态的变化。结果发现:高糖培养后,胎鼠海马神经元突触变短,胞体肿胀,同时APP水平随着葡萄糖浓度的递增逐渐升高。以上信息提示高糖引发的神经元形态破坏与APP高水平有关,控制血糖可能有利于保护神经元细胞,使其免受损伤。Abstract: Amyloid β-protein precursor (APP) is a major molecule inducing neurodegeneration in diabetic patients. To explore the effects of high-glucose cultivation on the injury of primary hippocampal neurons and the expression of APP, the primary hippocampal neurons were separated from the embryonic day 16 (E16) SD rats and then cultured in the presence of 25 mmol/L, 50 mmol/L, 75 mmol/L and 100 mmol/L glucose, respectively. The cell morphology was observed with an inverted microscope and the expression of APP protein was detected by Western-blot. The results indicated that, following exposure to high concentrations of glucose, the axons of hippocampal neurons became swelling and the synapses gradually grew shorter, while the expression of APP increased. The results suggested that APP might play important roles in high glucose-induced hippocampal neuron damage and that glycemic control would be potentially beneficial for the protection of neuronal cells.
关 键 词:β-淀粉样蛋白前体(APP) 高血糖 神经退行性疾病 大鼠海马神经元
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