Biological Effects of an Isoquercetin-Containing Formulation in Preclinical Models of Skin Aging

Background Skin aging involves oxidative stress, inflammation, extracellular matrix degradation, and glycation. Bioactive compounds targeting multiple pathways may offer mechanistic advantages in skin aging modulation. Objective This study aimed to evaluate the biological effects of a compound containing isoquercetin using preclinical in vitro and ex vivo skin models. Methods Five independent assays were conducted in human skin explants, reconstructed human epidermis enriched with peripheral blood mononuclear cells (PBMCs), and human dermal fibroblasts (HFF-1). NQO1 gene expression was quantified by quantitative real-time polymerase chain reaction (qRT-PCR). IL-6 and IL-8 levels were measured using cytometric bead array. UV radiation-induced oxidative stress was assessed by radical protein assays. Ki-67 and type I pro-collagen expression were evaluated by immunofluorescence. Antiglycation and deglycation activity were assessed through carboxymethyl-lysine (CML) quantification. Data were analyzed using Student's t-test or one-way ANOVA. Results The compound significantly increased NQO1 expression (+78%, p < 0.05) in human skin explants. In the inflammatory model, IL-6 and IL-8 levels were reduced by 45% and 50%, respectively (p < 0.001). UV radiation-induced oxidative protein markers were reduced (radical protection: 66.79%, p < 0.001). Ki-67 expression increased by 41.83% (p < 0.05), and type I pro-collagen synthesis increased 2.01-fold (p < 0.0001). In fibroblast models, antiglycation and deglycation assays demonstrated reductions in CML levels of 56.90% and 39.75%, respectively (p < 0.001). Conclusion In preclinical skin models, a compound containing isoquercetin significantly modulated oxidative stress, inflammatory response, collagen synthesis, and glycation pathways. Controlled clinical studies are required to determine whether these biological effects translate into measurable outcomes in human subjects.