Secondary metabolites are important for the pathogenesis of the fungus Aspergillus fumigatus which causes lethal Aspergillosis. Expressing groups of A. fumigatus genes in the fungus Aspergillus nidulans reveals new A. fumigatus secondary metabolites.

Synsepalum dulcificum (Schumach. & Thonn.) Daniell (Miracle fruit) is used in food, pharmaceutical, and cosmetic applications. Its leaves are rich in bioactive secondary metabolites which contribute to various therapeutic and cosmetic benefits. However, previous studies mainly focused on phenolic constituents, leaving the saponin composition largely unexplored. Molecular networking analysis revealed saponins as major metabolites in n-butanol fraction, leading to the isolation of 28 compounds, containing 16 saponins with 8 previously undescribed ones (1, 5-7, 9, 11, 12, 15). Compounds 2–3, 6, and 8-15 exhibited cytotoxic effects against multiple cancer cell (IC₅₀ values from 7.96 - 38.83 μM). Compound 6 induced apoptosis through Bcl-2 inhibition, indicating mitochondrial pathway involvement. Additionally, saponins 12–16 inhibited NF-κB activation in skin cells stimulated by TNF-α, demonstrating notable anti-inflammatory potential. This study elucidates the saponin profile of S. dulcificum leaves and supports their potential use in anticancer and skin anti-inflammatory formulations.

Background : Exosomes (Exos) derived from immune cells are emerging as potent drug delivery vectors. However, their biodistribution in clinically relevant lung cancer models remains underexplored. This study aimed to evaluate the lung-homing ability of NK cell Exos (NK-Exos) compared to mesenchymal stem cell Exos (MSC-Exos) in an orthotopic lung cancer model. Methods: Male SCID mice were orthotopically injected with luciferase-tagged A549 cells into the left lung to establish the tumor model. Mice were randomized into four groups: G1 (Healthy Control), G2 (Tumor Control + PBS), G3 (Tumor + DiR-labeled NK-Exos; 5 µM DiR + 5–7 × 10⁹ Exo particles/100 μL/mouse), and G4 (Tumor + DiR-labeled MSC-Exos; 5 µM DiR + 5–7 × 10⁹ Exo particles/100 μL/mouse). Six hours (15 min, 1 h, 2 h, 4 h, 6 h) post-intravenous injection, ex vivo biodistribution was assessed using the MILabs Spectrum imaging system. Results: Umbilical cord blood-NK-Exos (UCB-NK-Exos; G3) exhibited superior accumulation in lung tissues compared to UCB-MSC-Exos (G4), suggesting enhanced pulmonary retention. Intra-pulmonary analysis revealed an asymmetric distribution, with significantly higher radiant efficiency in the right lung (non-tumor bearing) compared to the left lung (tumor injection site) across Exo-treated groups. Conclusions: UCB-NK-Exos demonstrate distinct lung-targeting properties superior to MSC-Exos, supporting their potential as therapeutic carriers.

Delayed re-epithelialization caused by persistent inflammation and impaired keratinocyte function is a major obstacle in chronic wound healing. Resolvin E1 (RvE1), an omega-3 fatty acid-derived specialized pro-resolving mediator, is known for its anti-inflammatory actions. However, its direct effects on keratinocyte-mediated wound repair remain largely unknown. In this study, we investigated whether RvE1 promotes cutaneous wound healing by modulating keratinocyte proliferation, migration, and repair-associated signaling pathways. RvE1 significantly enhanced HaCaT keratinocyte proliferation, accompanied by increased phosphorylation of AKT, mTOR, and eIF4EBP1, as well as upregulation of cyclin D1, indicating activation of the AKT/mTOR pathway and cell cycle progression. RvE1 also accelerated scratch wound closure and induced an epithelial–mesenchymal transition-like phenotype, characterized by reduced E-cadherin expression and increased Snail and Twist protein levels. RNA sequencing (RNA-seq) revealed that RvE1 upregulated genes associated with wound healing, cell migration, epithelial–mesenchymal transition, and skin formation, including WNT3A, TRPV1, TXNIP, and KRT10. Furthermore, RvE1 activated Wnt/β-catenin signaling. Pharmacological inhibition of AKT, mTOR, or Wnt signaling abolished RvE1-induced keratinocyte proliferation and/or migration, confirming the functional involvement of these pathways. In addition, RvE1 reduced intracellular oxidative stress in keratinocytes. Topical administration of RvE1 accelerated wound closure in streptozotocin (STZ)-induced diabetic mice. Collectively, these findings demonstrate that RvE1 directly promotes keratinocyte proliferation, migration, and re-epithelialization through AKT/mTOR and Wnt/β-catenin signaling, supporting its therapeutic potential for chronic wound repair.