全氟辛烷磺酸盐（PFOS）具有明显神经毒性，可导致学习记忆能力下降和认知功能损伤。课题组前期预实验发现，PFOS可引起星形胶质细胞活化以及炎症因子IL-1β的分泌，进而导致神经元损伤和动物认知功能下降。基于此，课题组提出PFOS可通过引起星形胶质细胞炎性活化和神经元损伤的机制，促进中枢神经系统功能障碍的假说。课题组拟首先分析PFOS暴露对大鼠行为及学习记忆能力的影响；进而分析脑组织中胶质细胞活化和神经炎症的改变，以及炎症因子改变和神经元损伤的关联；并分析神经元损伤后，释放的Aβ对星形胶质细胞炎症激活的影响；最后在体外分析PFOS诱导星形胶质细胞活化和炎症因子IL-1β诱导神经元损伤，以及神经元释放Aβ的分子机制。本课题的开展将有助于阐明PFOS诱发神经毒性确切机制，并为全氟辛烷磺酸及其类似环境毒物引起的神经毒性疾病的预防和治疗提供理论依据。

Perfluorinated octane sulfonates (PFOS) displays significant neurotoxicity, leading to the impairment of learning, memory and cognitive function. Our preliminary data found that PFOS could cause astrocyte activation and the secretion of inflammatory factor IL-1β, potentially resulting in neuronal damage, amyloid beta (Aβ) accumulation and cognitive dysfunction. Based on these findings, the research group proposes the hypothesis that PFOS caused neuronal damage and the central nervous system dysfunction through astrocytes activation and nerve inflammation. We plan to first analyze that the effect of PFOS exposure on rat behaviors and the damage of learning and memory ability. Next, we will analyze the association between astrocyte activation and neuronal damage in brain tissue. Furthermore, our group will determine the impact of astrocyte activation on neuronal release of Aβ. Finally, using cultured astrocyte model, we will investigate the molecular mechanism underlying PFOS-induced neuronal damage through Aβ and inflammatory cytokines IL-1β. The development of this project will help clarify the precise mechanism underlying PFOS neurotoxicity, and thus benefit the prevention and therapy of PFOS-induced neurotoxicity.