Niobium Carbide Protects Myocardial Ischemia/Reperfusion Injury by Scavenging Reactive Oxygen Species and Improving Mitochondrial Function

Abstract

Myocardial ischemia/reperfusion (IR) injury is a significant annual clinical threat. Reperfusion injury exacerbates this issue by causing an excessive overload of reactive oxygen species (ROS) due to heme degradation and dysfunction in mitochondrial complexes. Subsequently, this surge in ROS leads to mitochondrial damage, further compromising cardiomyocyte mitochondrial function and eventually causing cell death. Given its pivotal role, targeting ROS has emerged as a viable strategy for treating myocardial ischemic injury. One promising therapeutic intervention involves the use of nanomaterials to eliminate ROS. In this study, we synthesized a polyvinylpyrrolidone-modified ultrathin niobium carbide (Nb 2 C) MXene, which effectively alleviated myocardial IR injury by scavenging ROS and enhancing mitochondrial function. Nb 2 C demonstrated multiple enzymatic-like abilities, including catalase and superoxide dismutase, which offered effective protection against myocardial ischemic injury by neutralizing superoxide anions and hydrogen peroxide. Furthermore, in the IR mice treated with Nb 2 C, mitochondrial injury was significantly reduced, and mitochondrial function was notably improved. Intravenous administration of Nb 2 C resulted in substantial recovery of cardiac function in IR mice and a marked reduction in the infarct area. This research offers insights into the potential of Nb 2 C MXene as a treatment for myocardial IR injury.