Edaravone (Eda) is a free radical scavenger used in clinical trials for the treatment of ischemic stroke and amyotrophic lateral sclerosis. However, how Eda exerts its neuroprotective effects remains to be elucidated. We investigated the neuroprotective effects of Eda in cultured hippocampal neurons and in a mouse model of AlCl₃/D-galactose-induced cognitive impairment. Eda protected hippocampal neurons by eliminating H₂O₂ or glutamate-induced toxicity, leading to decreased cell viability and neurite shortening. Consistently, Eda restored impaired levels of BDNF, FGF2 and their associated signaling axes (including TrkB, p-Akt and Bcl-2) to attenuate neuronal death. In a mouse model of chemically-induced cognitive impairment, Eda restored the levels of BDNF, FGF2 and TrkB/Akt signaling axis to attenuate neuronal apoptosis, thereby ameliorating cognitive impairment. Meanwhile, the pro-inflammation was eliminated due to the restoration of pro-inflammatory factors such as TNF-α, IL-6, IL-1β, and NOS2. In summary, Eda is an effective drug for protecting neurons from neurotoxic injury. BDNF, FGF2, and their regulated pathways may be potential therapeutic targets for neuroprotection.

依达拉奉 (Eda) 是一种自由基清除剂，在临床试验中用于治疗缺血性中风和肌萎缩性侧索硬化症。然而，Eda 如何发挥其神经保护作用仍有待阐明。我们研究了 Eda 在培养的海马神经元和 AlCl ₃ /D-半乳糖诱导的认知障碍小鼠模型中的神经保护作用。_{Eda 通过消除 H 2} O ₂保护海马神经元或谷氨酸诱导的毒性，导致细胞活力降低和神经突缩短。始终如一地，Eda 恢复受损水平的 BDNF、FGF2 及其相关信号轴（包括 TrkB、p-Akt 和 Bcl-2）以减轻神经元死亡。在化学诱导的认知障碍小鼠模型中，Eda 恢复了 BDNF、FGF2 和 TrkB/Akt 信号轴的水平，以减轻神经元凋亡，从而改善认知障碍。同时，由于促炎因子如TNF-α、IL-6、IL-1β和NOS2的恢复，促炎作用被消除。总之，Eda是一种保护神经元免受神经毒性损伤的有效药物。BDNF、FGF2 及其调节途径可能是神经保护的潜在治疗靶点。