Oxidative stress is one of the principal causes of hypoxia-induced kidney injury. The ceria nanoparticle (CNP) is known to exhibit free radical scavenger and catalytic activities. When zirconia is attached to CNPs (CZNPs), the ceria atom tends to remain in a Ce³⁺ form and its efficacy as a free radical scavenger thus increases. We determined the effectiveness of CNP and CZNP antioxidant activities against hypoxia-induced acute kidney injury (AKI) and observed that these nanoparticles suppress the apoptosis of hypoxic HK-2 cells by restoring autophagy flux and alleviating mitochondrial damage. In vivo experiments revealed that CZNPs effectively attenuate hypoxia-induced AKI by preserving renal structures and glomerulus function. These nanoparticles can successfully diffuse into HK-2 cells and effectively counteract reactive oxygen species (ROS) to block hypoxia-induced AKI. This suggests that these particles represent a novel approach to controlling this condition.

中文翻译：

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二氧化铈-氧化锆抗氧化剂纳米颗粒通过恢复自噬通量和减轻线粒体损伤来减轻低氧引起的急性肾脏损伤。

氧化应激是缺氧引起的肾脏损伤的主要原因之一。已知二氧化铈纳米颗粒（CNP）具有自由基清除剂和催化活性。当氧化锆连接到CNP（CZNP）上时，二氧化铈原子倾向于以Ce ^3+的形式保留，因此其作为自由基清除剂的功效会增强。我们确定了CNP和CZNP抗氧化剂活性对缺氧诱导的急性肾损伤（AKI）的有效性，并观察到这些纳米颗粒通过恢复自噬通量和减轻线粒体损伤来抑制缺氧HK-2细胞的凋亡。体内实验表明，CZNPs通过保留肾脏结构和肾小球功能来有效减弱缺氧诱导的AKI。这些纳米粒子可以成功扩散到HK-2细胞中，并有效抵消活性氧（ROS），从而阻断缺氧诱导的AKI。这表明这些颗粒代表了一种控制这种状况的新颖方法。