Abstract
Cherry blossom (Prunus yedoensis) petals are used as ingredients in many cosmetics. However, despite their use in numerous products, the exact function of cherry blossom petals in cosmetics is unclear. Therefore, we need evidence-based studies to support the labeling claims that are made in cherry blossom products in the cosmetics industry. We investigated the skin anti-aging potential of non-enzymatic softening cherry blossom extract (NES-CBE) in this study. The extract desalinated, to improve its quality such that it can be used as a functional material for the skin. The anti-wrinkle effect of NES-CBE was investigated on human keratinocytes (HaCaT cells) under solar UV (sUV) light exposure. We found that NES-CBE reduced the sUV-induced matrix metalloproteinase (MMP)-1 expression and modulated the transactivation of the activator protein (AP)-1. Furthermore, NES-CBE suppressed the phosphorylation of MEK1/2 and ERK proteins, indicating its regulation of sUV-induced MAPK signaling. Additionally, we observed NES-CBE reduced MMP-1 protein expression in a human skin equivalent model. Taken together, these results suggest that NES-CBE reduces sUV-induced MMP-1 protein expression through reducing AP-1 transactivation via regulation of the MEK1/2-ERK pathway.
Highlights
Solar ultraviolet light irradiation plays a major factor in aging, with an estimated 80% of facial skin photoaging caused by sUV light [1,2]
Skin wrinkles are mainly caused by sUV that increase matrix metalloproteinase (MMP)-1 protein expression and oxidative stress and deplete collagen in the skin [6]. sUV-induced MMP-1 regulation directly impacts the skin wrinkling process [12]
Previous studies have shown that UV-activated MAP kinase pathways, including JNK and p38, lead to activator protein (AP)-1 activation, which subsequently enhances MMP-1 expression. sUV activates mitogen-activated protein kinase (MAPK) and Akt pathways [6]
Summary
Solar ultraviolet (sUV) light irradiation plays a major factor in aging, with an estimated 80% of facial skin photoaging caused by sUV light [1,2]. SUV is divided into a wavelength spectrum that comprises three subtypes including UVA (320–400 nm), UVB (280–320 nm), and UVC (200–280 nm). SUV irradiation consisting of about 94.5% UVA and 5.5% UVB usually causes skin wrinkles and chronic exposure causes skin damage and aging [5]. Among them are three enzymes that degrade collagen: MMP-1, 8, and 13. MMP-1 is known as a rate limiting enzyme in the decomposition of collagen caused by sUV in the skin. MMP-1 plays critical roles in degrading types I and III collagens, which are structural components of the ECM [4]
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