Abstract
Acute kidney injury (AKI), as a common oxidative stress‐related renal disease, causes high mortality in clinics annually, and many other clinical diseases, including the pandemic COVID‐19, have a high potential to cause AKI, yet only rehydration, renal dialysis, and other supportive therapies are available for AKI in the clinics. Nanotechnology‐mediated antioxidant therapy represents a promising therapeutic strategy for AKI treatment. However, current enzyme‐mimicking nanoantioxidants show poor biocompatibility and biodegradability, as well as non‐specific ROS level regulation, further potentially causing deleterious adverse effects. Herein, the authors report a novel non‐enzymatic antioxidant strategy based on ultrathin Ti3C2‐PVP nanosheets (TPNS) with excellent biocompatibility and great chemical reactivity toward multiple ROS for AKI treatment. These TPNS nanosheets exhibit enzyme/ROS‐triggered biodegradability and broad‐spectrum ROS scavenging ability through the readily occurring redox reaction between Ti3C2 and various ROS, as verified by theoretical calculations. Furthermore, both in vivo and in vitro experiments demonstrate that TPNS can serve as efficient antioxidant platforms to scavenge the overexpressed ROS and subsequently suppress oxidative stress‐induced inflammatory response through inhibition of NF‐κB signal pathway for AKI treatment. This study highlights a new type of therapeutic agent, that is, the redox‐mediated non‐enzymatic antioxidant MXene nanoplatforms in treatment of AKI and other ROS‐associated diseases.
Highlights
The transmission electron microscopy (TEM) image displays the ultrathin Ti3C2 nanosheets with a lateral dimension of ≈200 nm (Figure 1c), and the preserved hexagonal symmetry structure was confirmed by selected area electron diffraction (SAED) pattern
The X-ray diffraction (XRD) patterns further prove the formation of delaminated Ti3C2 nanosheets as evidenced by leftward shift of the (002) peak and the disappeared characteristic peaks of Ti3AlC2 (Figure 1e)
A novel artificial non-enzymatic antioxidant MXenebased nanoplatform for effective Acute Kidney Injury (AKI) therapy in living animals was presented in this work
Summary
During the progression of AKI, toxic reactive oxygen species (ROS) generated in excess react with a few biomolecules to cause. For maintaining the intracellular redox homeostasis in human body, endogenous antioxidant defense system, mainly composed of enzymes (e.g., superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx), etc.) and non-enzymatic antioxidants (e.g., glutathione (GSH), etc.), can eliminate excess ROS to prevent or reduce progressive oxidative damage.[15] these endogenous antioxidants work out well under normal physiological conditions, they are normally insufficient to offset excessive ROS generation under pathological conditions.[16] Inspired by the natural antioxidant defense system, numerous exogenous antioxidative nanomaterials have recently attracted great attention as a new type of antioxidant due to their improved stability, broad-spectrum antioxidant capabilities, and higher ROS scavenging efficiency.[17,18] Typically, a plethora of synthetic enzyme-mimicking nanomaterials (nanozymes),[19,20,21] such as metal nanoparticles,[22] metal oxide nanoparticles,[18,23,24,25] carbon-based nanomaterials,[26] biomolecules,[27,28] and quantum dots,[29,30] have demonstrated multiple ROS scavenging capability and admirable antioxidant activity.[31] For example, to obtain enzyme-mimicking nanoparticles with good biocompatibility and quick renal clearance, Deng et al.[22] prepared ultrasmall Cu5.4O nanoparticles with multiple enzyme-mimicking and broad-spectrum ROS scavenging ability, which exhibited cytoprotective effects against ROS-mediated damage and significantly improved treatment outcomes in AKI and ROS-related diseases. This study introduces an interesting and effective way to alleviate AKI via non-enzymatic antioxidative protection of 2D MXene
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