Background Research has demonstrated the anti-photoaging properties of glabridin and bakuchiol. Methods The impact of glabridin, glabridin + bakuchiol, and bakuchiol on the levels of tumor necrosis factor alpha (TNF-α) and interleukin-1 beta (IL-1β) in mice skin fibroblasts was observed. Furthermore, we investigated the potential roles of fibronectin (FN), interferon-γ (IFN-γ), interleukin-22 (IL-22), and transforming growth factor-β (TGF-β) in the tissues, and evaluated their impact on the enzymatic levels in the skin. In conjunction with transcriptomic analysis, metabolomic profiling, and network pharmacology, all samples underwent comprehensive metabolomic and principal component analysis. The Venny2.1 method was utilized to identify variances in shared metabolites between the treatment group and the UVB group, as well as between the UVB group and the control group. Subsequently, a cluster heat map was generated to forecast and analyze metabolic pathways and targets. Results The outcomes from the hematoxylin and eosin and toluidine blue staining revealed that glabridin and bakuchiol markedly decreased dermal thickness and suppressed mast cell infiltration in photoaged mice. Immunohistochemistry and Elisa analysis revealed that glabridin and bakuchiol effectively attenuated the levels of pro-inflammatory factors, including IL-1β, tumor necrosis factor-α, IL-22, and IFN-γ. Furthermore, an increase in the levels of anti-inflammatory factors such as FN and TGF-β was also observed. The determination of the contents of superoxide dismutase, hydroxypropyltransferase and malondialdehyde in mice dorsal skin revealed that glabridin and bakuchiol not only elevated the levels of superoxide dismutase and hydroxyproline, but also reduced malondialdehyde content. Due to the limited number of shared differential metabolites exclusively within Kyoto Encyclopedia of Genes and Genomes, comprehensive pathway enrichment analysis was not feasible. Conclusion This study demonstrates that glabridin and bakuchiol effectively impede photoaging and alleviate skin inflammation in mice.

Background: Retinol, an important bioactive substance with multiple physiological functions such as promoting collagen synthesis, inhibiting matrix metalloproteinase activity, alleviating oxidative stress, regulating gene expression, and promoting epidermal cell proliferation, has a significant effect on skin damage recovery. Hydroxyasiaticoside, a triterpenoid saponin derived from Centella asiatica (L.) Urb., is closely related to the secretion of collagen types I and III, and possesses multiple biological activities, including moisturizing, antioxidants, anti-apoptosis, neuroprotection, anti-inflammation, and the promotion of wound healing. It plays a particularly prominent role in reducing oxidative stress in wounds and inducing vasodilatation. Objective: The aim of this study was to investigate the therapeutic efficacy of retinol combined with hydroxyasiaticoside in histamine-induced atopic dermatitis. Materials and Methods: The experiment was carried out using three different concentrations of a retinol and hydroxyasiaticoside mixed solution: low, medium, and high concentrations. After inducing atopic dermatitis in mice through histamine administration, these solutions were applied to the skin surface of the mice, and a comparative analysis was conducted with both the control group and the model group. The effect of combination therapy on atopic dermatitis was evaluated through histopathology, immunohistochemistry, and transcriptomic analysis. Results: The combination of retinol and hydroxyasiaticoside significantly attenuated histamine-induced scratching behaviors, alleviated the phenomenon of epidermal hyperplasia, and effectively reduced the proliferation, infiltration, and degranulation of mast cells. In addition, the combination inhibited the expression of relevant pro-inflammatory cytokines. Quantitative RNA-seq analysis revealed that the gene expression patterns were similar in different concentration groups. However, the medium dose group may be able to regulate skin inflammation by regulating upstream genes to inhibit autophagy-related pathways. Further GO analysis revealed that the low-dose group mainly affected metabolism-related genes, the medium-dose group affected more genes related to body systems, and the high-dose group was dominated by genes related to human diseases.

This study aimed to investigate the protective effects of Naematelia aurantialba ethanol extract (NAAE) against skin photoaging. Furthermore, we sought to elucidate the underlying repair mechanisms and related pathways. The results indicated that NAAE treatment significantly enhanced cell viability and proliferation under UV stress, while exerting potent antioxidant effects by effectively reducing intracellular reactive oxygen species (ROS) accumulation and mitigating oxidative damage. Furthermore, NAAE accelerated the migration capacity of damaged cells and promoted skin repair. In animal models, NAAE inhibited UV-induced skin injuries in a concentration-dependent manner and facilitated tissue regeneration. Further investigations revealed that NAAE exerted photoprotective effects by modulating several key metabolic pathways and biological processes, including fatty acid metabolism and nuclear receptor activity. Moreover, NAAE positively influenced the skin microbiota by reducing the abundance of harmful bacteria and promoting the proliferation of beneficial bacteria, potentially enhancing skin barrier function through the cross-system mechanism of the "gut-skin axis." This study provides a theoretical basis for the use of NAAE in preventing and repairing skin photoaging and offers new insights for the development of natural plant-derived skincare products.

Climate change plays a critical role in shaping the geographical distribution and ecological dynamics of plant species. Amomum Roxb., a genus with importan