Introducing molecular imprinting onto nanozymes: toward selective catalytic analysis.

The discovery of enzyme-like catalytic characteristics in nanomaterials triggers the generation of nanozymes and their multifarious applications. As a class of artificial mimetic enzymes, nanozymes are widely recognized to have better stability and lower cost than natural bio-enzymes, but the lack of catalytic specificity hinders their wider use. To solve the problem, several potential strategies are explored, among which molecular imprinting attracts much attention because of its powerful capacity for creating specific binding cavities as biomimetic receptors. Attractively, introducing molecularly imprinted polymers (MIPs) onto nanozyme surfaces can make an impact on the latter's catalytic activity. As a result, in recent years, MIPs featuring universal fabrication, low cost, and good stability have been intensively integrated with nanozymes for biochemical detection. In this critical review, we first summarize the general fabrication of nanozyme@MIPs, followed by clarifying the potential effects of molecular imprinting on the catalytic performance of nanozymes in terms of selectivity and activity. Typical examples are emphatically discussed to highlight the latest progress of nanozyme@MIPs applied in catalytic analysis. In the end, personal viewpoints on the future directions of nanozyme@MIPs are presented, to provide a reference for studying the interactions between MIPs and nanozymes and attract more efforts to advance this promising area.

Purple sweet potato color attenuated NLRP3 inflammasome by inducing autophagy to delay endothelial senescence.

Autophagy is a vital negative factor regulating cellular senescence. Purple sweet potato color (PSPC), one type of flavonoid, has been demonstrated to suppress endothelial senescence and restore endothelial function in diabetic mice by inhibiting the nucleotide-binding oligomerization domain, leucine rich repeat and pyrin domain containing protein 3 (NLRP3) inflammasome. However, the roles of autophagy in the inflammatory response during endothelial senescence are unknown. Here, we found that PSPC augmented autophagy to restrict high-glucose-induced premature endothelial senescence. In addition, PSPC administration impaired endothelium aging in diabetic mice by increasing autophagy. Inhibition of autophagy accelerated endothelial senescence, while enhancement of autophagy delayed senescence. Moreover, deactivation of the NLRP3 inflammasome triggered by PSPC was autophagy-dependent. Autophagy receptor microtubule-associated protein 1 light chain 3 and p62 interacted with the inflammasome component NLRP3, suggesting that autophagosomes target the NLRP3 inflammasome and deliver it to the lysosome for degradation. Altogether, PSPC amplified cellular autophagy, subsequently attenuated NLRP3 inflammasome activity and finally delayed endothelial senescence to ameliorate cardiovascular complication. These results suggest a potential therapeutic target in senescence-related cardiovascular diseases.