Abstract

Japanese red pine (Pinus densiflora) is widely present in China, Japan, and Korea. Its green pine leaves have traditionally been used as a food as well as a coloring agent. After being shed, pine leaves change their color from green to brown within two years, and although the brown pine leaves are abundantly available, their value has not been closely assessed. In this study, we investigated the potential anti-photoaging properties of brown pine leaves for skin. Brown pine leaf extract (BPLE) inhibited UVB-induced matrix metalloproteinase-1 (MMP-1) expression to a greater extent than pine leaf extract (PLE) in human keratinocytes and a human skin equivalent model. HPLC analysis revealed that the quantity of trans-communic acid (TCA) and dehydroabietic acid (DAA) significantly increases when the pine leaf color changes from green to brown. BPLE and TCA elicited reductions in UVB-induced MMP-1 mRNA expression and activator protein-1 (AP-1) transactivation by reducing DNA binding activity of phospho-c-Jun, c-fos and Fra-1. BPLE and TCA also inhibited UVB-induced Akt phosphorylation, but not mitogen activated protein kinase (MAPK), known regulators of AP-1 transactivation. We additionally found that BPLE and TCA inhibited phosphoinositide 3-kinase (PI3K), the upstream kinase of Akt, in vitro. In summary, both BPLE and its active component TCA exhibit protective effects against UVB-induced skin aging. Taken together, these findings underline the potential for BPLE and TCA to be utilized as anti-wrinkling agents and cosmetic ingredients, as they suppress UVB-induced MMP-1 expression.

Highlights

  • Human skin acts as an interface between the environment and our body [1]

  • Brown pine leaf extract (BPLE) and pine leaf extract (PLE) were tested for their inhibitory effect against UVB-induced matrix metalloproteinase-1 (MMP-1) expression in HaCaT cells within the range of concentration which did notexhibit cytotoxicity

  • The results indicated that BPLE inhibits UVB-induced matrix metalloproteinase (MMP)-1 expression in a dose-dependent manner while not affecting MMP-2

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Summary

Introduction

Chronic ultraviolet (UV) exposure causes detrimental physiological changes to skin including epidermal inflammation, hyperpigmentation, immunosuppression and photoaging [2,3,4,5]. UVB is the major source of skin damage and an etiological factor for many diseases and extrinsic skin aging as it has much higher intrinsic energy than UVA [8]. Photoaging, an extrinsic skin aging process, is characterized by pigmentary changes and severe wrinkle formation [9]. Exposure to UVB alters biological processes that promote matrix metalloproteinase (MMP) expression, decrease procollagen synthesis, and increase connective tissue damage [3, 9, 10]. Collagen breakdown by collagenase is a major cause of wrinkle formation. MMP-1 is a critical enzyme for type-1 and type-3 collagen degradation in human skin [4, 8]. Preventing unbalanced collagen degradation via inhibition of MMP-1 expression represents a potential strategy for antiphotoaging

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