Curcumin–polydopamine nanoparticles alleviate ferroptosis by iron chelation and inhibition of oxidative stress damage†
Abstract
Ferroptosis, characterized by elevated iron levels and lipid peroxidation (LPO), is a recently identified regulatory mechanism of cell death. Its substantial involvement in ischemic tissue injury, neurodegenerative disorders, and cancer positions ferroptosis inhibition as a promising strategy for managing these diverse diseases. In this study, we introduce curcumin–polydopamine nanoparticles (Cur–PDA NPs) as an innovative ferroptosis inhibitor. Cur–PDA NPs demonstrate remarkable efficacy in chelating both Fe2+ and Fe3+ in vitro along with scavenging free radicals. Cur–PDA NPs were found to efficiently mitigate reactive oxygen species, reduce Fe2+ accumulation, suppress LPO, and rejuvenate mitochondrial function in PC12 cells. Thus, these NPs can act as potent therapeutic agents against ferroptosis, primarily via iron chelation and reduction of oxidative stress.