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 Fe 2+ and Fe 3+ in vitro along with scavenging free radicals. Cur-PDA NPs were found to efficiently mitigate reactive oxygen species, reduce Fe 2+ 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.
Keyphrases
- cell death
- oxidative stress
- cell cycle arrest
- reactive oxygen species
- ischemia reperfusion injury
- oxide nanoparticles
- dna damage
- iron deficiency
- diabetic rats
- metal organic framework
- magnetic nanoparticles
- aqueous solution
- fatty acid
- squamous cell
- cerebral ischemia
- squamous cell carcinoma
- young adults
- brain injury
- heat shock
- childhood cancer
- heat shock protein