Simultaneous Elimination of Reactive Oxygen Species and Activation of Nrf2 by Ultrasmall Nanoparticles to Relieve Acute Kidney Injury.
Bolin BaoHanghang LiuYaobao HanLiyao XuWei XingZhen LiPublished in: ACS applied materials & interfaces (2023)
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 Cu 2- 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.
Keyphrases
- reactive oxygen species
- acute kidney injury
- oxidative stress
- cardiac surgery
- nuclear factor
- dna damage
- clinical practice
- toll like receptor
- cell death
- poor prognosis
- diabetic rats
- ischemia reperfusion injury
- induced apoptosis
- human health
- iron oxide
- stem cells
- mass spectrometry
- risk assessment
- anti inflammatory
- mesenchymal stem cells