Ferroptosis and neuroinflammation play a crucial role in the pathogenesis of Alzheimer’s disease (AD), and Edaravone (EDA) has been demonstrated to have anti-inflammatory, antioxidant and neuroprotective effects in neurodegenerative diseases. However, the relationship between EDA and ferroptosis in AD is unidentified. This research aimed to elucidate the mechanism of EDA in AD with Aβ 1-42-induced HT22 cells as in vitro cell model. The results showed that EDA could significantly reduce Aβ_1-42-induced apoptosis of HT22 cells and formation of pro-inflammatory factors TNF-α, IL-1β and IL-6, prevent the activation of TLR4/NF-κB /NLRP3 signaling pathway, and inhibit ferroptosis and lipid peroxidation. Taken together, EDA contributes to inhibiting neuroinflammatory injury and ferroptosis in Aβ 1-42-induced HT22 cells, and thus may be a potential candidate for the treatment of AD.

铁死亡和神经炎症在阿尔茨海默病 (AD) 的发病机制中起着至关重要的作用，依达拉奉 (EDA) 已被证明在神经退行性疾病中具有抗炎、抗氧化和神经保护作用。然而，EDA 与 AD 铁死亡之间的关系尚不清楚。本研究旨在以Aβ1-42诱导的HT22细胞为体外细胞模型，阐明EDA在AD中的作用机制。结果表明，EDA可显着降低Aβ _1-42-诱导HT22细胞凋亡和促炎因子TNF-α、IL-1β和IL-6的形成，阻止TLR4/NF-κB/NLRP3信号通路的激活，抑制铁死亡和脂质过氧化。总之，EDA 有助于抑制 Aβ1-42 诱导的 HT22 细胞的神经炎症损伤和铁死亡，因此可能成为治疗 AD 的潜在候选药物。