SOD-like activity of CeO₂ nanoparticles (Ce NPs) is driven by Ce³⁺/Ce⁴⁺, high oxidative stress can oxidize Ce³⁺ to reduce the ratio of Ce³⁺/Ce⁴⁺, inactivating the SOD activity of Ce NPs. Herein, we found Au@Ce NPs, assembled by Au NPs and Ce NPs, exhibited high-performance of SOD mimetic enzyme activity even upon the oxidation of H₂O₂. Ce NPs supported by nano-Au can acquire the electrons from Au NPs through the enhanced localized surface plasmon resonance (LSPR), maintaining the stability of Ce³⁺/Ce⁴⁺ and SOD-like activity. Meanwhile, Au@Ce NPs retained the peroxidase function and catalase function. As a result, Au@Ce NPs effectively scavenged O₂•- and the derived ROS in AML cells, which are the important signaling source that drives AML cell proliferation and accelerates cell cycle progression. When HL-60 cells were treated by Au@Ce NPs, the removal of endogenous ROS signal significantly arrested cell cycle at G1 phase and suppressed the cell proliferation by blocking the mitogen-activated protein kinases (MAPKs) signaling and the Akt/Cyclin D1 cell cycle signaling. Importantly, this treatment strategy showed therapeutic effect for subcutaneous transplantation of AML model as well as a satisfactory result in diminishing the leukocyte infiltration of liver and spleen particularly. Thus, assembled Au@Ce NPs show the high-performance SOD-like activity, promising the potential in treating AML and regulating abnormal ROS in other diseases safely and efficiently.

CeO ₂纳米颗粒（Ce NPs）的类SOD活性受Ce ³⁺ /Ce ⁴⁺驱动，高氧化应激可氧化Ce ³⁺降低Ce ³⁺ /Ce ⁴⁺比值，使Ce的SOD活性失活NP。在此，我们发现由 Au NPs 和 Ce NPs 组装的 Au@Ce NPs 即使在 H ₂ O ₂氧化时也表现出高性能的 SOD 模拟酶活性。纳米金支持的Ce NPs可以通过增强的局域表面等离子体共振（LSPR）从Au NPs获得电子，保持Ce ³⁺ /Ce ⁴⁺的稳定性和类似 SOD 的活动。同时，Au@Ce NPs 保留了过氧化物酶功能和过氧化氢酶功能。结果，Au@Ce NPs 有效地清除了 O ₂•- 以及AML细胞中衍生的ROS，它们是驱动AML细胞增殖和加速细胞周期进程的重要信号源。当 HL-60 细胞被 Au@Ce NPs 处理时，内源性 ROS 信号的去除显着阻止了 G1 期的细胞周期，并通过阻断丝裂原活化蛋白激酶 (MAPKs) 信号和 Akt/Cyclin D1 细胞抑制细胞增殖循环信号。重要的是，该治疗策略对AML模型的皮下移植显示出治疗效果，尤其是在减少肝脏和脾脏的白细胞浸润方面取得了令人满意的结果。因此，组装的Au@Ce NPs显示出高性能的类SOD活性，有望安全有效地治疗AML和调节其他疾病中的异常ROS。