Seon Min Oh

Cannabis sativa L. (C. sativa), commonly known as hemp, is widely recognized for its diverse range of bioactive compounds with therapeutic potential in medicinal, industrial, and nutritional applications. This study investigates the use of adventitious roots (ARs) derived from C. sativa as a scalable platform for producing bioactive metabolites with immunomodulatory and anti-inflammatory properties. We first isolated extracts from C. sativa ARs (CS-AR) using various solvents: methanol (MeOH-E), chloroform (CHCl₃-E), and hexane (Hexane-E), and explored their effects on dendritic cell (DC) maturation, a key process involved in immune responses. Notably, MeOH-E demonstrated strong anti-inflammatory effects without inducing cytotoxicity in DCs, distinguishing it from the other extracts. Metabolomic analysis of these extracts annotated the presence of cannabinoid derivatives and metabolites, including cannabinoid glycoside derivatives, cannabigerolic acid-O-acetate (CBGA-O-acetate), cannabidiol diacetate derivatives, and cannabidiol mono-acetate mono-benzoate. Among these, cannabinoid glycoside derivatives and CBGA-O-acetate were found to be present at higher levels in MeOH-E. Further investigation into the functional properties of MeOH-E revealed that it could suppress the expression of key surface molecules and antigen-presenting ability in mature DCs, alongside attenuating mitogen-activated protein kinase (MAPK) signaling pathways as well as nuclear factor kappa-B (NF-κB) signaling. Additionally, MeOH-E inhibited T cell proliferation and activation. These findings underscore the CS-AR system as a promising, reproducible biotechnological platform for producing therapeutic bioactive compounds for inflammatory diseases, with significant potential for application in the pharmaceutical and nutraceutical industries.

Daphne kiusiana is a naturally occurring plant in East Asia belonging to the Thymelaeaceae family. While its biological properties have been explored, its potential role in wound healing remains largely unknown. This study investigated the effects of Daphne kiusiana extracts on keratinocyte migration and the underlying mechanisms. The crude extract and its fractions was tested in vitro at various concentrations to evaluate their ability to promote keratinocyte migration, and a cytotoxicity assay was conducted to assess cell viability. The results demonstrated that Daphne kiusiana significantly enhanced keratinocyte migration without inducing notable cytotoxicity at tested concentrations. Mechanistically, this effect was mediated through the modulation of matrix metalloproteinase-9 (MMP-9) via extracellular signal-regulated kinase (ERK) signaling, which plays a crucial role in keratinocyte migration. These findings suggest that Daphne kiusiana may serve as a potential therapeutic agent for enhancing keratinocyte migration in wound healing. However, further investigations, including clinical studies, are necessary to confirm its efficacy and safety. To our knowledge, this is the first study to report the potential of Daphne kiusiana in promoting keratinocyte migration, offering new insights into wound healing therapies.

The recently defined type of cell death ferroptosis has garnered significant attention as a potential new approach to cancer treatment owing to its more immunogenic nature when compared with apoptosis. Ferroptosis is characterized by the depletion of glutathione (GSH)/glutathione peroxidase-4 (GPx4) and iron-dependent lipid peroxidation. Diplacone (DP), a geranylated flavonoid compound found in Paulownia tomentosa fruit, has been identified to have anti-inflammatory and anti-radical activity. In this study, the potential anticancer activity of DP was explored against A549 human lung cancer cells. It was found that DP induced a form of cytotoxicity distinct from apoptosis, which was accompanied by extensive mitochondrial-derived cytoplasmic vacuoles. DP was also shown to increase mitochondrial Ca²⁺ influx, reactive oxygen species (ROS) production, and mitochondrial permeability transition (MPT) pore-opening. These changes led to decreases in mitochondrial membrane potential and DP-induced cell death. DP also induced lipid peroxidation and ATF3 expression, which are hallmarks of ferroptosis. The ferroptosis inhibitors ferrostatin-1 and liproxstatin-1 were effective in counteracting the DP-mediated ferroptosis-related features. Our results could contribute to the use of DP as a ferroptosis-inducing agent, enabling studies focusing on the relationship between ferroptosis and the immunogenic cell death of cancer cells.