Explore the vast range of titles available.

Background Skin radiance represents both healthy and esthetic aspects of human skin, usually influenced by a compromised barrier and the aging process. The reduction of the stratum corneum by chemical peels is a prevalent procedure employed to enhance facial radiance, but peeling is not suitable for compromised skin. Objectives Prinsepia utilis Royle polysaccharides (PURP) is a natural extract with repairing properties, which has been reported as a barrier repairing agent. ESETRILLQ (EQ) peptide has been recently reported as a novel antiaging bioactive peptide. This study aims to investigate the combined efficacy of these two ingredients on skin radiance enhancement. Methods Reconstructed human full‐thickness skin models were subjected to UVA exposure, followed by treatment with 1000 ppm PURP, 20 ppm EQ9, and their combinations: PUR9‐1 (1000 ppm PURP + 10 ppm EQ9) and PUR9‐2 (1000 ppm PURP + 20 ppm EQ9). Transcriptomic profiling was performed as a preliminary study to define the synergistic effect. RT‐qPCR was performed assessing the regulation of skin barrier‐related genes. Thirty‐three Chinese sensitive skin individuals were enrolled in a placebo‐controlled split‐face clinical research for 2 weeks to evaluate a PUR9‐2 containing lotion. Instrument measurement and expert evaluation were conducted to evaluate the parameters of glossiness and skin tone at baseline, Day 7, and Day 14. Skin glossiness was determined by VISIA 7, Glossymeter, and Translucency Meter. TEWL was determined by Tewameter Hex. Wrinkel number and area were obtained by VISIA 7. Results Transcriptomic profiling identified PUR9‐2 to regulate significantly different genes distinct from PURP and EQ9. The combination increased the gene expression levels of TNFAIP3 and CRNN. PUR9‐2 also increased the expression of FLG, LOR, and DSG1on UVA‐irradiated skin model. PUR9‐2 containing lotion significantly decreased TEWL by 16.96%. Clinical evaluations demonstrated a statistically significant 22.32% (Glossymeter) and 35.56% (VISIA 7) improvement in skin glossiness on the PUR9‐2 lotion‐treated side by Day 14 compared to baseline. Translucency demonstrated a statistically significant 13.06% increase of K value, which all aligned with the expert evaluation of skin radiance enhancement. Conclusion PCA analysis revealed PUR9‐2 uniquely modulated gene expression compared to PURP and EQ9. Functional enrichment analysis based on Gene Ontology (GO) demonstrated PUR9‐2 restored UVA‐suppressed TNFAIP3 and CRNN gene. The results of RT–PCR also indicated that PUR9‐2 enhanced skin barrier integrity in 3D models via upregulated expression of FLG, LOR, and DSG1. The Chou‐Talalay method further validated PUR9‐2's synergistic potency (CI < 1) in accelerating keratinocyte scratch wound closure. The clinical research demonstrated protective effects of PUR9‐2 on compromised skin barrier and enhanced both glossiness of the sensitive skin surface and translucency within the skin structure. This study provides a potential solution for improving the radiance and overall conditions of compromised skin.

Prinsepia utilis Royle (PUR) exhibits moisturizing, antioxidative, and antibacterial properties, supporting skin barrier integrity. Nevertheless, the molecular mechanisms underlying these effects remain unclear. This study investigates the role of polysaccharide from PUR (PUR-P) in keratinocyte differentiation, lipid metabolism, tight junction, and skin barrier repair, focusing on PPARα involvement. Cytotoxicity of PUR-P in keratinocytes was assessed using CCK-8, EdU staining, and flow cytometry. Marker expression associated with differentiation (K1 and K10), proliferation (K16 and K17), sebum synthesis (CERS3, FAS and HMGCS2), and tight junction (ZO-1, Occludin and Claudin-1) were measured via western blot and qRT-PCR. The FulKutis skin model was used to assess the effects of PUR-P and PPARα on the skin barrier. PUR-P induced cytotoxicity in keratinocytes above 10 mg/mL (48 h) and 5 mg/mL (72 h). At 10 mg/mL, PUR-P upregulated K1, K10, CERS3, FAS, ZO-1, Occludin, Claudin-1, PPARα, and PPARβ/δ at both mRNA and protein levels. These effects were mediated by PPARα, as inhibition by Norathyriol or PPARα shRNA lentiviruses reduced PUR-P’s efficacy. In the FulKutis skin model, PUR-P mitigated sodium lauryl sulfate-induced stratum corneum damage, restoring transepithelial electrical resistance, reducing FITC-Dextran permeability, and improving protein expression levels, effects dependent on PPARα. PUR-P enhances skin barrier integrity by promoting keratinocyte differentiation, lipid metabolism, and tight junctions, which is associated with PPARα up-regulated K1, K10, K16, K17, CERS3, FAS, HMGCS2, ZO-1, Occludin, Claudin-1, FLG, INV, and LOR expression. These findings underscore the potential of PUR-P as a therapeutic agent for skin barrier-related disorders.