A novel mitochondria-targeted near-infrared metal-free fluorescence probe for detecting carbon monoxide in atherosclerosis

Abstract

The early stage of atherosclerosis (AS) is characterized by explosion of reactive oxygen species (ROS) in mitochondria and inflammatory reaction, and then abundant ROS further promote the progress of AS. As an endogenous signal biomolecule with antioxidant properties, carbon monoxide (CO) is enriched in mitochondria to combat oxidative stress, thereby significantly increasing during the pathogenesis of AS. However, there is currently no mitochondria-targeted near-infrared fluorescence probe for detecting CO in atherosclerosis. In this paper, we use a mitochondrion-targeting metal-free near-infrared fluorescence probe, AS-CO, for investigating AS via detecting and mapping the fluctuations of CO with enhanced sensitivity and selectivity. In addition, probe AS-CO can be positioned at mitochondria. It has also proven effective in detecting both internally and externally sourced CO in HUVEC cells. More importantly, using AS-CO, for the first time, we provided the visualization evidence of endogenous CO generation in the aorta of mice that induced AS by high-fat diet (HFD) and further investigated the protective effects of (−)-epicatechin gallate (ECG) against HFD-induced AS. The results demonstrated the feasibility of AS-CO for monitoring and evaluating personalized treatment of AS.