Introduction: Lung injury, a common complication of sepsis, arises from elevated reactive oxygen species (ROS), mitochondrial dysfunction, and cell death driven by inflammation. In this study, a novel class of ultrasmall nanoparticles (Cu4.5O USNPs) was developed to address sepsis-induced lung injury (SILI).
Methods: The synthesized nanoparticles were thoroughly characterized to assess their properties. In vitro experiments were conducted to determine the biologically effective concentration and elucidate the anti-inflammatory mechanism of action. These findings were further supported by in vivo studies, showcasing the material's efficacy in mitigating SILI.
Results: The Cu4.5O USNPs demonstrated remarkable scavenging capabilities for hydrogen peroxide (H2O2), superoxide anions (O2 -), and hydroxyl radicals (·OH), attributed to their catalase (CAT)- and superoxide dismutase (SOD)-like activities. Additionally, the nanoparticles exhibited strong anti-inflammatory effects, preserved mitochondrial homeostasis through potent ROS scavenging, and significantly reduced cell death. In vivo studies on mice further validated their protective role against SILI.
The conclusion: This study highlights the therapeutic potential of Cu4.5O USNPs in treating sepsis-induced lung injury by effectively scavenging ROS and reducing cell death. These findings provide compelling evidence for the future use of copper-based nanoparticles as antioxidant therapeutics.
Keywords: anti-inflammation; lung injury; mitochondria; reactive oxygen species scavenging; ultrasmall copper-based nanoparticles.
© 2024 Li et al.