Neuroprotective effects of nicotine are still under debate, so further studies on its effectiveness against Parkinsonʼs disease are required. In our present study, we used primary dopaminergic cell cultures and N18TG2 neuroblastoma cells to investigate the effect of nicotine and its neuroprotective potential against rotenone toxicity. Nicotine protected dopaminergic (tyrosine hydroxylase immunoreactive) neurons against rotenone. This effect was not nAChR receptor-dependent. Moreover, the alkaloid at a concentration of 5 µM caused an increase in neurite length, and at a concentration of 500 µM, it caused an increase in neurite count in dopaminergic cells exposed to rotenone. Nicotine alone was not toxic in either cell culture model, while the highest tested concentration of nicotine (500 µM) caused growth inhibition of N18TG2 neuroblastoma cells. Nicotine alone increased the level of glutathione in both cell cultures and also in rotenone-treated neuroblastoma cells. The obtained results may be helpful to explain the potential neuroprotective action of nicotine on neural cell cultures.

中文翻译：

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重新评估尼古丁对中脑多巴胺能细胞培养物和神经母细胞瘤 N18TG2 细胞的神经毒性的影响

尼古丁的神经保护作用仍在争论中，因此需要进一步研究其对帕金森病的有效性。在我们目前的研究中，我们使用原代多巴胺能细胞培养物和 N18TG2 神经母细胞瘤细胞来研究尼古丁的作用及其对鱼藤酮毒性的神经保护潜力。尼古丁保护多巴胺能（酪氨酸羟化酶免疫反应性）神经元对抗鱼藤酮。这种作用不依赖于 nAChR 受体。此外，浓度为 5 μM 的生物碱导致神经突长度增加，而在 500 μM 浓度下，它导致暴露于鱼藤酮的多巴胺能细胞中的神经突计数增加。单独的尼古丁在两种细胞培养模型中都没有毒性，而最高测试浓度的尼古丁 (500 µM) 会抑制 N18TG2 神经母细胞瘤细胞的生长。尼古丁单独增加了两种细胞培养物中谷胱甘肽的水平，也增加了鱼藤酮处理的神经母细胞瘤细胞中的谷胱甘肽水平。获得的结果可能有助于解释尼古丁对神经细胞培养物的潜在神经保护作用。