Corylin

Corylin is a natural flavonoid isolated from the seeds of Psoralea corylifolia L., a traditional medicinal herb historically used to treat bone-related disorders such as osteoporosis. However, its role in organismal aging and the underlying molecular mechanisms remain largely unexplored.

This study aimed to evaluate the anti-aging efficacy of corylin and elucidate the molecular basis of its action.

Using Caenorhabditis elegans (C. elegans) as a model organism, we systematically assessed the impact of corylin on lifespan and multiple aging-associated phenotypes, including locomotor capacity, muscle integrity, lipofuscin accumulation, and resistance to thermal, pathogenic, and oxidative stress. Neuroprotective potential was evaluated using transgenic models of Parkinson's and Huntington's diseases. To uncover the mechanisms involved, we analyzed the DAF-16/SKN-1 signaling axis and autophagy-related processes using transgenic reporter strains, RNA interference, and RT-qPCR.

Corylin treatment significantly extended lifespan, improved locomotor performance, and reduced lipofuscin accumulation. Furthermore, it enhanced resistance to environmental stresses and conferred neuroprotection in models of neurodegeneration. Mechanistically, corylin promoted nuclear translocation of DAF-16 and upregulated the expression of DAF-16/SKN-1 target genes. This transcriptional activation was associated with enhanced autophagic flux and improved mitochondrial quality. Crucially, the beneficial effects of corylin were abolished in daf-16 and skn-1 mutants, as well as under autophagy-deficient conditions.

Corylin exerts multifaceted anti-aging effects in C. elegans by coordinately activating the DAF-16/SKN-1 signaling axis, thereby enhancing autophagic flux and maintaining mitochondrial homeostasis. These findings identify corylin as a promising natural candidate for aging intervention.

Corylin is a bioactive extract of Psoralea corylifolia L. with reported antioxidant, anti-tumor, and anti-inflammatory effects. Its anti-tumor effects have been investigated, but mechanistic explanations are lacking. This study mainly focuses on the role and mechanism of Corylin in inducing liver cancer cell death.

The effects of Corylin on liver cancer cell proliferation were analyzed using crystal violet staining and cell counting kit-8 (CCK-8) assays. Nuclear changes were detected via Hoechst staining, while apoptosis levels were assessed using Annexin V- fluorescein isothiocyanate (FITC)/propidium iodide (PI) staining. Changes in mitochondrial membrane potential and reactive oxygen species (ROS) levels were analyzed using JC-1 and tetramethylrhodamine methyl ester (TMRM) staining combined with flow cytometry. Immunofluorescence staining and Western blot (WB) experiments assessed alterations in apoptosis- and autophagy-related proteins. Finally, the effects of Corylin on liver cancer cells in vivo were validated by establishing a subcutaneous tumor model.

In this study, we found that Corylin had a significant anti-liver cancer effect and significantly increased the apoptosis level of liver cancer cells. Additionally, Corylin was found to significantly reduce mitochondrial membrane potential and significantly increase ROS release. It was also observed that Corylin significantly influenced autophagy levels in liver cancer cells. Further analysis revealed that Corylin induced mitophagy, with the increase in autophagy levels being directly proportional to the rise in apoptosis levels. Finally, the establishment of a subcutaneous tumor-bearing model showed that Corylin also had a significant anti-liver cancer effect in vivo.

The above results demonstrated that Corylin mainly caused the death of liver cancer cells through the endogenous apoptosis and mitophagy pathway and had great potential as an anti-liver cancer drug.