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Saccharin enhances neurite extension by regulating organization of the microtubules

机译：糖精通过调节微管的组织增强神经突的延伸

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Aims In the present study, we found that saccharin, an artificial calorie-free sweetener, promotes neurite extension in the cultured neuronal cells. The purposes of this study are to characterize the effect of saccharine on neurite extension and to determine how saccharin enhances neurite extension. Main methods The analyses were performed using mouse neuroblastoma N1E-115 cells and rat pheochromocytoma PC12 cells. Neurite extension was evaluated by counting the cells bearing neurites and measuring the length of neurites. Formation, severing and transportation of the microtubules were evaluated by immunostaining and western blotting analysis. Key findings Deprivation of glucose increased the number of N1E-115 cells bearing long processes. And the effect was inhibited by addition of glucose. Saccharin increased the number of these cells bearing long processes in a dose-dependent manner and total neurite length and longest neurite length in each cell. Saccharin also had a similar effect on NGF-treated PC12 cells. Saccharin increased the amount of the microtubules reconstructed after treatment with nocodazole, a disruptor of microtubules. The effect of saccharin on microtubule reconstruction was not influenced by dihydrocytochalasin B, an inhibitor of actin polymerization, indicating that saccharin enhances microtubule formation without requiring actin dynamics. In the cells treated with vinblastine, an inhibitor of microtubule polymerization, after microtubule reorganization, filamentous microtubules were observed more distantly from the centrosome in saccharin-treated cells, indicating that saccharin enhances microtubule severing and/or transportation. Significance These results suggest that saccharin enhances neurite extension by promoting microtubule organization.
机译：目的在本研究中，我们发现糖精是一种人造无卡路里的甜味剂，可促进培养的神经元细胞中的神经突延伸。这项研究的目的是表征糖精对神经突延伸的影响，并确定糖精如何增强神经突延伸。主要方法使用小鼠神经母细胞瘤N1E-115细胞和大鼠嗜铬细胞瘤PC12细胞进行分析。通过计数带有神经突的细胞并测量神经突的长度来评估神经突的延伸。通过免疫染色和免疫印迹分析评估微管的形成，切断和运输。关键发现葡萄糖的缺乏增加了经历长时间过程的N1E-115细胞的数量。并且通过添加葡萄糖抑制了该作用。糖精以剂量依赖性方式增加了这些经历长时间过程的细胞的数量，并增加了每个细胞的总神经突长度和最长神经突长度。糖精对NGF处理的PC12细胞也有类似作用。糖精增加了用诺考达唑（一种微管的破坏剂）治疗后重建的微管的数量。糖精对微管重建的影响不受肌动蛋白聚合抑制剂Dihydrocytochalasin B的影响，表明糖精增强了微管的形成而无需肌动蛋白动力学。在微管重组抑制剂长春碱处理的细胞中，微管重组后，在用糖精处理过的细胞中观察到丝状微管与中心体的距离更远，表明糖精增强了微管的切断和/或转运。意义这些结果表明糖精通过促进微管组织增强神经突的延伸。

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