铝进入脑细胞蓄积可产生严重的中枢神经系统毒性，表现为认知功能障碍等症状。研究表明，ROS可能与铝导致神经毒性相关。Nrf2/ARE信号通路是目前发现的最重要的体内内源性抗氧化通路，莱菔硫烷（SFN）是Nrf2/ARE的激活剂。有关Nrf2/ARE通路在铝诱导的神经毒性的抗氧化作用及SFN对铝诱导神经毒性的保护作用及其机制不清楚。本研究拟建立铝暴露认知功能障碍动物模型，初步探讨氧化应激在铝暴露致认知功能障碍中的表达变化。拟采用Nrf2-/- C57/B6小鼠和建立高表达或低表达Nrf2的人神经细胞（HCN-2）、人神经胶质细胞(HM)细胞株，验证Nrf2/ARE信号通路对铝暴露致认知功能障碍中的保护作用及其机制。进一步以该通路为靶点，探讨SFN是否通过激活Nrf2/ARE信号通路来缓解铝诱导的神经毒性。以期为临床治疗铝中毒和预防提供新的思路,同时也为SFN临床应用提供理论基础和实验依据。

As a chronic accumulation neuropoison, aluminium can enter brain cell to induce severe central nervous system toxicity which show recognition functional disturbance. Many researches showed neurotoxicity induced by aluminum are associated with the production of excessive ROS. Nrf2-ARE pathway plays an important role in the endogenous antioxidant systems. Sulforaphane(SFN) can activate the Nrf2/ARE pathway. However , the direct evidence of whether Nrf2-ARE pathway plays an important role against aluminium-induced oxidative damage and whether the antioxidative role of SFN is mediated by activating the Nrf2 signaling pathway. So in this study we will apply the Wistar mouse exposed AlCl3 and explore its relationship between Nrf2 /ARE signaling pathways and cognitive dysfunction induced by AlCl3. We will apply the Nrf2 -/- C57/B6 mice and HCN-2 cells, HM cells with high or low expression of Nrf2 to validate the protective effects of Nrf2 /ARE signaling pathways in aluminum induced neurotoxicity. We will further investigate whether the SFN alleviate the neurotoxicity induced by aluminum through activation of Nrf2 /ARE signaling pathways. The results of which will provide a new strategy for the clinical treatment of neurotoxicity induced by aluminum and also to provide a theoretical and experimental basis for SFN clinical application.