Abstract
Excess reactive oxygen species (ROS) can induce serious acute kidney injury (AKI) to result in numerous deaths annually in clinical practice. Elimination of excess ROS by advanced nanotechnology is a very promising AKI therapy. In this Article, we report that PVP-stabilized and quercetin-functionalized ultrasmall Cu2-xSe nanoparticles (abbreviated as CSPQ NPs) can efficiently scavenge ROS and increase the expression of intracellular antioxidative enzymes by activating the nuclear factor erythroid 2-related factor 2 (Nrf2) protein, which drastically alleviates the cellular oxidative stress. Our ultrasmall nanoparticles exhibit excellent biocompatibility. They can be rapidly accumulated into the injured kidney to simultaneously eliminate ROS and activate Nrf2 to improve the renal function. This work demonstrates the great potential of simultaneous elimination of ROS and activation of intracellular Nrf2 in treatment of AKI. It also highlights the potential of CSPQ NPs in protection and prevention of AKI.
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