摘要砷作为一种可影响人类健康的毒性物质，过量时可引发包括认知障碍在内的多种神经功能障碍。相关流行病学调查和动物实验研究均显示，砷暴露不仅可以使人出现智力障碍，引发外周神经病变，还会使人群及动物行为出现异常。目前，砷致神经系统损伤的机制仍不明确。过氧化物酶体增殖物激活受体γ辅助活化因子α（PGC-1α）作为一种核转录辅助激活因子，能与转录因子或其他辅助激活因子相互作用，在线粒体生物发生、能量代谢等生物学过程中发挥作用。PGC-1α通过激活线粒体生物发生影响能量代谢，激活氧化应激调节因子[过氧化氢酶（CAT）、谷胱甘肽过氧化物酶（GSH-Px）、超氧化物歧化酶（SOD）等]影响氧化应激等方式，减轻砷对中枢神经系统、周围神经系统及血脑屏障（BBB）的损伤。本文总结了砷致神经系统损伤及PGC-1α在砷致神经系统损伤中作用机制的研究进展，为进一步防治因砷所致的神经系统疾病提供理论依据。

abstractsArsenic, as a toxic substance that can affect human health, can cause various neurological disorders, including cognitive impairment, when excessive. Relevant epidemiological surveys and animal experimental studies have shown that exposure to arsenic can not only cause intellectual impairment and peripheral neuropathy in humans, but also lead to abnormal behavior in humans and animals. However, so far, the mechanism of arsenic induced damage to the nervous system is still unclear. Peroxisome proliferator activated receptor γ auxiliary activation factor 1α (PGC-1α), as a nuclear transcription coactivator, can interact with transcription factors or other coactivators and plays a role in biological processes such as mitochondrial biogenesis and energy metabolism. PGC-1α, by activating mitochondrial biogenesis, affecting energy metabolism, activating oxidative stress regulatory factors [catalase (CAT), glutathione peroxidase (GSH-Px), superoxide dismutase (SOD), etc.], mitigates the damage to the central nervous system (CNS), peripheral nervous system (PNS), and blood-brain barrier (BBB) caused by arsenic. This article summarize the research progress of arsenic-induced neurological injury and the mechanism of PGC-1α's role in arsenic-induced neurological injury to provide a theoretical basis for further prevention and treatment of neurological diseases caused by arsenic.