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Maintaining a youthful appearance is a common desire among the aging population. Loss of elasticity and dermal density constitutes major causes of wrinkle formation during skin aging. In particular, periorbital wrinkles comprise the critical assessment point of skin aging. To address these issues, cosmetic industries have been making increasing efforts to develop efficient agents against wrinkle formation. Arg-Gly-Asp (RGD) is a tripeptide sequence used for surface coating because of its integrin-binding property. However, its pharmacological properties on skin have not yet been studied. Here, we synthesize the novel palmitoyl-Arg-Gly-Asp (Palm-RGD) and investigate its effects on periorbital wrinkle formation by clinical and in vitro studies. We observed that Palm-RGD cream application for 12 weeks decreased global photodamage and skin roughness (R1, R2, R3, and Ra) scores without causing skin irritation. In addition, topical application of Palm-RGD cream time-dependently increased skin elasticity and dermal density. An in vitro study using human dermal fibroblasts (HDFs) demonstrated increased type I procollagen production by Palm-RGD treatment. Furthermore, Palm-RGD suppressed MMP-1 expression in HDFs. Our results demonstrate that Palm-RGD has protective effects against wrinkle formation, likely through the activation of collagen expression and the protection against collagen degradation. Therefore, Palm-RGD could be used as a potential agent for the prevention of wrinkle formation consequent to aging.

Wrinkle formation and abnormal pigmentation are major clinical alterations associated with skin aging. As the aim of our study was to investigate the effects of palmitoyl-KVK-L-ascorbic acid on skin aging, the anti-wrinkle and depigmentation effects of palmitoyl-KVK-L-ascorbic acid were evaluated by measuring collagen expression in dermal fibroblast cells and inhibition of melanogenesis in B16F1 cells, respectively. The anti-aging effect of palmitoyl-KVK-L-ascorbic acid cream was also evaluated against a placebo cream in a clinical trial. Our results confirmed that the expression of type Ι collagen in dermal fibroblast cells treated with palmitoyl-KVK-L-ascorbic acid (0.1-4 μg/mL) increased in a dose-dependent manner. In B16F1 cells, treatment with 20 μg/mL palmitoyl-KVK-L-ascorbic acid reduced the melanin content by approximately 20% compared to alpha-melanocyte stimulating hormone treatment. In the clinical trial, application of palmitoyl-KVK-L-ascorbic acid cream led to an improvement in skin roughness and lightness in 12 and 8 weeks, respectively. Our data show that palmitoyl-KVK-L-ascorbic acid is an effective anti-aging agent that reduces wrinkles and abnormal skin pigmentation.

Ethnopharmacological Relevance: Perilla frutescens (L.) Britt. (Lamiaceae) is a traditional herb that is consumed in East Asian countries as a traditional medicine. This traditional herb has been documented for centuries to treat various diseases such as depression, allergies, inflammation and asthma. However, the effect of Perilla frutescens on skin has not been characterized well., Aim of the Study: The present study aimed to investigate the effect of Perilla frutescens leaves extract (PLE) on ultraviolet radiation-induced extracellular matrix damage in human dermal fibroblasts and hairless mice skin., Materials and Methods: Human dermal fibroblasts and Skh-1 hairless mice were irradiated with UV and treated with PLE. Protein and mRNA levels of various target molecules were analyzed by western blotting and quantitative RT-PCR, respectively. Histological changes of mouse skin were analyzed by H&E staining. To elucidate underlying mechanism of PLE, activator protein-1 (AP-1) DNA binding assay and the measurement of reactive oxygen species (ROS) were performed., Results: PLE significantly inhibited basal and UV-induced MMP-1 and MMP-3 expression dose-dependently, and also decreased UV-induced phosphorylation of extracellular signal-regulated kinases and c-Jun N-terminal kinases. This inhibitory effects of PLE on MMP-1 and MMP-3 were mediated by reduction of ROS generation and AP-1 DNA binding activity induced by UV. Furthermore, PLE promoted type I procollagen production irrespective of UV irradiation. In the UV-irradiated animal model, PLE significantly reduced epidermal skin thickness and MMP-13 expression induced by UV., Conclusion: Our results demonstrate that PLE has the protective effect against UV-induced dermal matrix damage. Therefore, we suggest that PLE can be a potential agent for prevention of skin aging., (Copyright © 2016 Elsevier Ireland Ltd. All rights reserved.)

Cacao beans contain various bioactive phytochemicals that could modify the pathogeneses of certain diseases. Here, we report that oral administration of cacao powder (CP) attenuates UVB-induced skin wrinkling by the regulation of genes involved in dermal matrix production and maintenance. Transcriptome analysis revealed that 788 genes are down- or upregulated in the CP supplemented group, compared with the UVB-irradiated mouse skin controls. Among the differentially expressed genes, cathepsin G and serpin B6c play important roles in UVB-induced skin wrinkle formation. Gene regulatory network analysis also identified several candidate regulators responsible for the protective effects of CP supplementation against UVB-induced skin damage. CP also elicited antiwrinkle effects via inhibition of UVB-induced matrix metalloproteinases-1 expression in both the human skin equivalent model and human dermal fibroblasts. Inhibition of UVB-induced activator protein-1 via CP supplementation is likely to affect the expression of matrix metalloproteinases-1. CP supplementation also downregulates the expression of cathepsin G in human dermal fibroblasts. 5-(3',4'-Dihydroxyphenyl)-γ-valerolactone, a major in vivo metabolite of CP, showed effects similar to CP supplementation. These results suggest that cacao extract may offer a protective effect against photoaging by inhibiting the breakdown of dermal matrix, which leads to an overall reduction in wrinkle formation., (Copyright © 2016 The Authors. Published by Elsevier Inc. All rights reserved.)