A tripartite-enzyme via curcumin regarded as zymoexciter towards highly efficient relieving reperfusion injury

For alleviating ischemic reperfusion injury, reasonable design mimic multi-functional nanozyme can simulta-neously capture ROS and inhibit inflammatory factors, which plays an important role. However, the low effi-ciency of natural enzyme and their ability to capture only a single species limit their effectiveness. Therefore, additional materials to capture other ROS are highly needed. These motivates us to construct a nanozyme via hybridize/coupled curcumin (CUR) with ZnCe Layered Rare-earth Hydroxide (ZnCe-LRH) to achieve highly efficient ROS scavenging efficiency and the multiple ROS capture (denoted as CUR/ZnCe-LRH). Ce element was highly dispersed on the LRH layer, and CUR further coordinated with Zn on the layer to form a stable nanozyme structure. This mimic tripartite nanozyme can not only simulate superoxide dismutase (SOD) and catalase (CAT) activity to capture O-center dot(2)- and H2O2, but also arrest center dot OH within a short period of time, which can be regarded as the tripartite nanozyme. Density functional theory (DFT) calculations can further confirm the high efficient ROS scavenging mechanism by the CUR/ZnCe-LRH systems. In vivo results can further probe that this CUR/ZnCe-LRH can also suppress inflammation-and immune response-induced injury, thus achieving good prevention and treatment in neuroprotective therapy. The infarct area can reduce by 78% after the reperfusion therapy and the neurological deficit score can reduce from 3.50 to 0.67. This strategy provided a novel multifunctional enzyme mimetic for ischemia-reperfusion therapy and clarifies the application mechanism of neuroprotection against ischemia-reperfusion injury.

Automated summary

This study demonstrates the design of a multi-functional nanozyme CUR/ZnCe-LRH for effective removal of ROS and capture of multiple ROS to alleviate ischemic reperfusion injury. The results show promising neuroprotective therapy effects and shed light on the mechanism of neuroprotection against ischemic reperfusion injury.