Unveiling the Mechanism of Alleviating Ischemia Reperfusion Injury via a Layered Double Hydroxide-Based Nanozyme

Oxidative stress after ischemia reperfusion can cause irreversible brain damage. Thus, it is vital to timely consume excessive reactive oxygen species (ROS) and conduct molecular imaging monitoring on the brain injury site. However, previous studies have focused on how to scavenge ROS while ignoring the mechanism of relieving the reperfusion injury. Herein, we reported a layered double hydroxide (LDH)-based nanozyme (denoted as ALDzyme), which was fabricated by the confinement of astaxanthin (AST) with LDH. This ALDzyme can mimic natural enzymes, which include superoxide dismutase (SOD) and catalase (CAT). Furthermore, the SOD-like activity of ALDzyme is 16.3 times higher than that of CeO2 (a typical ROS scavenger). Based on these enzyme-mimicking properties, this one-of-a-kind ALDzyme offers strong anti-oxidative properties as well as high biocompatibility. Importantly, this unique ALDzyme can establish an efficient magnetic resonance imaging platform, thus guiding the in vivo details. As a result, the infarct area can be reduced by 77% after reperfusion therapy, and the neurological impairment score can be lowered from 3–4 to 0–1. Density functional theory computations can reveal more about the mechanism of this ALDzyme’s significant ROS consumption. These findings provide a method for unraveling the neuroprotection application process in ischemia reperfusion injury using an LDH-based nanozyme as a remedial nanoplatform.