锰暴露可致神经损伤，但其损害机制尚未阐明。研究表明非编码RNA对细胞增殖、分化和凋亡具有重要调控作用，且mTOR信号通路的激活是神经损伤重要机制之一。预实验显示lncRNA-nov-1 通过 miRNA-nov-1调控Dhrs3这一新线索，结合锰可引起N27细胞凋亡，且与mTOR信号通路相关。研究拟以锰致N27细胞凋亡为切入点，lncRNA-nov-1通过miRNA-nov-1/Dhrs3调控mTOR信号通路为轴线，设计细胞实验的质粒转染上调或下调lncRNA/miRNA，shRNA技术敲除mTOR及其关键分子；动物实验采用siRNA技术验证细胞实验结果，探讨提出的科学假说：lncRNA-nov-1通过miRNA-nov-1/Dhrs3调控mTOR信号通路在锰致多巴胺能神经元凋亡中发挥了重要作用。本研究有助于拓展锰致神经毒性研究思路，进一步阐明其毒性分子机制，为防治神经损伤提供研究基础。

Manganese exposure can cause nerve damage, but the mechanism is not yet clear. Studies have shown that non-coding RNA plays an important regulatory role in cell proliferation, differentiation and apoptosis，and the activation of mTOR signaling pathway is one of the important mechanisms of nerve injury. Our preliminary experiment results showed that lncRNA-nov-1 regulates Dhrs3 through miRNA-nov-1, which is a new clue. Combining with manganese can not only cause N27 cells apoptosis, but also be related to mTOR signling pathway. Therefore, our study will start from the apoptosis of N27 cells caused by manganese, lncRNA-nov-1 regulates the mTOR signaling pathway through miRNA-nov-1/Dhrs3 as the axis of it. In accordance with this idea, we will design plasmid transfection to up-regulate or down-regulate lncRNA/miRNA, mTOR and its key molecules will be knocked out by shRNA technology in cell experiments. siRNA technology will be made animal models to further verify the results of cell experiments. We explore and propose a scientific hypothesis that lncRNA-nov-1 plays an important role in mTOR signaling pathway through miRNA-nov-1/Dhrs3 in apoptosis of Dopaminergic neuron induced by manganese. This study is helpful to expand the research ideas of manganese-induced neurotoxicity, further clarify the molecular mechanism of its toxicity, and provide a research basis for the prevention and treatment of nerve injury.