Leontopodium alpinum is a source of raw material for food additives and skin health. The purpose of this study was to investigate the application of Leontopodium alpinum callus culture extract (LACCE) to prevent blue light damage to the skin. We screened and identified the blue light-damage-protecting activities and mechanisms of ten components of LACCE, including chlorogenic acid (A), isoquercitrin (B), isochlorogenic acid A (C), cynaroside (D), syringin (E), isochlorogenic acid (F), cynarin (G), rutin (H), leontopodic acid A (I), and leontopodic acid B (J), using a novel blue light-induced human foreskin fibroblast (HFF-1) cell injury model. The study examined the cytotoxicity of ten ingredients using the cell counting kit-8 (CCK-8) assay, and selecting concentrations of 5, 10, and 20 μM for experiments with a cell viability above 65%. We explored the effects and mechanisms of action of these LACCE components in response to blue light injury using Western blotting and an enzyme-linked immunosorbent assay. We also measured ROS secretion and Ca²⁺ influx. Our study revealed that leontopodic acid A effectively boosted COI-1 expression, hindered MMP-1 expression, curbed ROS and Ca²⁺ endocytosis, and reduced OPN3 expression. These results provide theoretical support for the development of new raw materials for the pharmaceutical and skincare industries.

Ceramides constitute approximately 50% of the lipid mass in the stratum corneum and are essential for epidermal permeability barrier function. In acne vulgaris, barrier disruption is accompanied by altered ceramide composition, yet the molecular mechanisms that connect acne-associated signals to specific changes in ceramide metabolism remain incompletely understood. This review integrates evidence from lipidomic profiling, enzymatic pathway characterization, and inflammatory signaling studies to examine how ceramide biosynthesis and turnover are modulated in acne-prone skin. Particular attention is directed to the elongation of very-long-chain fatty acids (VLCFAs) and their incorporation into ceramides by ceramide synthase 3 (CerS3). In cultured keratinocytes, Cutibacterium acnes (C. acnes)-derived short-chain fatty acids (SCFAs) have been reported to suppress CerS3 and 3-ketodihydrosphingosine reductase (KDSR) through peroxisome proliferator-activated receptor α (PPARα), limiting ultra-long-chain fatty acid (ULCFA) supply. We propose a working model in which SCFAs act via PPARα to upregulate ELOVL-family elongases while suppressing CerS3 and KDSR, reducing ULCFA-ceramides and compromising barrier integrity. The CerS3–KDSR node is a candidate regulatory point coupling microbial metabolites to barrier impairment and inflammation. However, this model rests largely on in vitro evidence and requires in vivo validation. Clarifying these regulatory relationships may inform the development of barrier-restorative strategies as adjuncts to conventional acne therapy.