Similar to fullerenes, carbon nanotubes and graphene, carbon dots (CDs) are causing a lot of research work in their own right. CDs are a type of surface-passivated quantum dot that contain carbon atoms. Their distinctive characteristics, such as luminescent emission that varies with size and wavelength, resistance to photobleaching, easy biological binding, lack of toxicity, and economical production without the need for intricate synthetic processes, have led to a noteworthy surge in attention within the research community. Different techniques can be utilized to create these CDs, spanning from basic candle burning to laser ablation. This review article delves into the principles of fluorescence technology, providing insights into how different synthesis methods of quantum dots impact their luminescent properties. Additionally, it highlights the latest applications of quantum dots in catalysis and biomedical fields, with special emphasis on the current status of luminescent properties in biology and chemistry. Towards the end, the article discusses the limitations of quantum dots in current practical applications, pointing out that CDs hold promising potential for future applications.

Dimethyl fumarate (DMF), a therapeutic agent for relapsing-remitting multiple sclerosis, has cytoprotective and antioxidant effects. Ferroptosis, a pathological cell death process, is recently shown to play a vital part in ischemia-reperfusion injury (IRI). This study aimed to unveil the suppressive role of DMF on ferroptosis in liver IRI. The anti-ferroptosis effect of DMF on hepatic IRI was investigated using a liver IRI mouse model and a hypoxia-reoxygenation injury (HRI) model in alpha mouse liver (AML12) cells. Serum transaminase concentrations reflected liver function. Hematoxylin and eosin staining was used to assess liver damage. Cell viability was evaluated utilizing the CCK-8 assay. Malondialdehyde (MDA), the reduced glutathione/oxidized glutathione (GSH/GSSG) ratio, and BODIPY 581/591C11 were measured to estimate the injury caused by lipid peroxidation. Western blotting and real-time polymerase chain reaction (RT-PCR) were performed to explore the underlying molecular mechanisms. We demonstrated the anti-ferroptosis effects of DMF both in vivo and in vitro. DMF treatment ameliorated hepatic IRI. KEGG enrichment analysis and transmission electron microscopy revealed a close relationship between ferroptosis and liver IRI. Furthermore, DMF protected against HRI by inhibiting ferroptosis via activating the nuclear factor E2-related factor 2 (NRF2) pathway. Interestingly, NRF2 knockdown notably decreased the expression of SLC7A11 and HO-1 and blocked the anti-ferroptosis effects of DMF. DMF inhibits ferroptosis by activating the NRF2/SLC7A11/HO-1 axis and exerts a protective effect against hepatic IRI.