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–x
Se 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.
P-NMR spectra, which demonstrate that they have the same structure and the successful grafting of phosphate groups. GPC analysis demonstrates the monodisperse molecular weight distributions of BP n with different DPs (Figure 1c). Furthermore,
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