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.

Accurately detecting dynamic changes in bioactive small molecules in real-time is very challenging. In this study, a hemin-based peptide assembly was rationally designed for the colorimetric detection of active small molecules. Hemin-functionalized peptide nanotubes were obtained through the direct incubation of hemin (hemin@PNTs) and peptide nanotubes (PNTs) or were coassembled with the heptapeptide Ac-KLVFFAL-NH₂ via electrostatic, π–π stacking, and hydrophobic interactions (hemin-PNTs). This new substance is significant because it exhibits the benefits of both hemin and PNTs as well as some special qualities. First, hemin-PNTs exhibited higher intrinsic peroxidase-like activity, which, in the presence of H₂O₂, could catalyze the oxidation of the substrate 3,3',5,5'-tetramethylbenzidine (TMB) to yield a typical blue solution after 10 min at 25 ℃. Second, hemin-PNTs showed significantly higher activity than that of hemin, PNTs alone, or hemin@PNTs. Hemin-PNTs with a 20.0% hemin content may cooperate to improve catalytic activity. The catalytic activity was dependent on the reaction temperature, pH, reaction time, and H₂O₂ concentration. The nature of the TMB-catalyzed reaction may arise from the production of hydroxyl radicals. Fluorescence analysis was used to demonstrate the catalytic mechanism. According to this investigation, a new highly selective and sensitive colorimetric technique for detecting glutathione (GSH), L-cysteine, and glucose was established. The strategy demonstrated excellent sensitivity for GSH in the range of 1 to 30 μM with a 0.51 μM detection limit. Importantly, this glucose detection technique, which employs glucose oxidase and hemin-PNTs, is simple and inexpensive, with a 0.1 μM to 1.0 mM linear range and a 15.2 μM detection limit. Because of their low cost and high catalytic activity, hemin-PNTs are an excellent choice for biocatalysts in a diverse range of potential applications, including applications in clinical diagnostics, environmental chemistry, and biotechnology.

Background: Parkinson's disease (PD) is the second most prevalent neurodegenerative disorder, characterized by the degeneration of dopamine (DA) neurons in the substantia nigra (SN) of the midbrain. Recent studies have highlighted the role of ferroptosis in neuronal death, with elevated peroxide levels being a hallmark of this process. Resveratrol (RSV), a natural compound, has shown promise as a neuroprotective agent. This study explores the potential of RSV in mitigating ferroptosis in PD and elucidates its mechanisms. Methods: Network pharmacology was employed to predict the interactions between RSV, ferroptosis, and PD‐related targets. Cytoscape protein‐protein interaction (PPI) analysis identified key potential targets, while Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses provided insights into the probable mechanisms linking RSV, ferroptosis, and PD. Subsequently, in vitro experiments were conducted to validate these findings, followed by in vivo studies to confirm the therapeutic efficacy of RSV in PD. Results: Network pharmacology results indicated that RSV, PD and ferroptosis interact at multiple biological levels. Compared to the PD group, RSV upregulated the expression of SIRT1 and NRF2 and alleviated MPTP‐induced motor deficits in mice. Furthermore, RSV reduced levels of MDA, ROS, lipid peroxidation, and cellular iron, while upregulating ferroptosis‐negative regulators such as GPX4 and FTH1, as well as pathway indicators like SIRT1 and NRF2. Inhibition of SIRT1 and NRF2 resulted in a decrease in the expression of GPX4/FTH1 and the SIRT1/NRF2 signaling pathway. Conclusions: Our findings demonstrate that RSV alleviates motor dysfunction in PD by inhibiting ferroptosis through SIRT1/NRF2 activation, providing novel mechanistic insights into its therapeutic potential for neurodegenerative diseases.