The neurotoxicity caused by cadmium (Cd) is well known in humans and experimental animals. However, there is no effective treatment for its toxicity. In this study, we established Cd toxicity models in cultured cells or mice to investigate the detoxification effect of edaravone (Eda). We found that Eda protected GL261 cells from Cd toxicity and prevented the loss of cell viability. In Cd-exposed mice, liver, kidney and testicular damage, as well as cognitive dysfunction were observed. Oxidative stress and inflammatory responses, such as decreased SOD and CAT, increased LDH and MDA, and abnormal changes in the inflammatory factors TNF-α, IL-1β, IL-6 and IL-10 were detected in serum and brain tissue. Eda protected mice from Cd-induced toxicity and abrogated oxidative stress and inflammatory responses. Also, Eda prevented inflammatory activation of microglia and astrocytes and was accompanied by restoration of the neuronal marker protein MAP2, indicating restoration of neuronal function. In addition, the BDNF-TrkB/Akt and Notch/HES-1 signaling axes were involved in the response of Eda to the elimination of Cd toxicity. In conclusion, Eda does contribute to the clearance of Cd-induced toxicity.

镉 (Cd) 引起的神经毒性在人类和实验动物中是众所周知的。然而，对其毒性没有有效的治疗方法。在这项研究中，我们在培养的细胞或小鼠中建立了镉毒性模型，以研究依达拉奉（Eda）的解毒作用。我们发现 Eda 保护 GL261 细胞免受镉毒性并防止细胞活力丧失。在暴露于镉的小鼠中，观察到肝脏、肾脏和睾丸损伤，以及认知功能障碍。在血清和脑组织中检测到氧化应激和炎症反应，如 SOD 和 CAT 降低，LDH 和 MDA 升高，炎症因子 TNF-α、IL-1β、IL-6 和 IL-10 异常变化。Eda 保护小鼠免受镉诱导的毒性并消除氧化应激和炎症反应。还，Eda 阻止了小胶质细胞和星形胶质细胞的炎症激活，并伴随着神经元标记蛋白 MAP2 的恢复，表明神经元功能的恢复。此外，BDNF-TrkB/Akt 和 Notch/HES-1 信号轴参与了 Eda 对消除 Cd 毒性的反应。总之，Eda 确实有助于清除 Cd 诱导的毒性。