Dieckol Isolated from Eisenia bicyclis Ameliorates Wrinkling and Improves Skin Hydration via MAPK/AP-1 and TGF-β/Smad Signaling Pathways in UVB-Irradiated Hairless Mice

Abstract

Repetitive exposure to ultraviolet B (UVB) is one of the main causes of skin photoaging. We previously reported that dieckol isolated from Eisenia bicyclis extract has potential anti-photoaging effects in UVB-irradiated Hs68 cells. Here, we aimed to evaluate the anti-photoaging activity of dieckol in a UVB-irradiated hairless mouse model. In this study, hairless mice were exposed to UVB for eight weeks. At the same time, dieckol at two doses (5 or 10 mg/kg) was administered orally three times a week. We found that dieckol suppressed UVB-induced collagen degradation and matrix metalloproteinases (MMPs)-1, -3, and -9 expression by regulating transforming growth factor beta (TGF-β)/Smad2/3 and mitogen-activated protein kinases (MAPKs)/activator protein-1 (AP-1) signaling. In addition, dieckol rescued the production of hyaluronic acid (HA) and effectively restored the mRNA expression of hyaluronan synthase (HAS)-1/-2 and hyaluronidase (HYAL)-1/-2 in UVB-irradiated hairless mice. We observed a significant reduction in transepidermal water loss (TEWL), epidermal/dermal thickness, and wrinkle formation in hairless mice administered dieckol. Based on these results, we suggest that dieckol, due to its anti-photoaging role, may be used as a nutricosmetic ingredient for improving skin health.

Myconoside and Calceolarioside E Restrain UV-Induced Skin Photoaging by Activating NRF2-Mediated Defense Mechanisms

“…Photoaging is characterized by a loss of skin elasticity with the depletion of collagen, elastin, and hyaluronan content, resulting in coarse wrinkling and dysregulated pigmentation [1][2][3][4][5][6][7][8]. In the present study, UVA/UVB irradiation was used to mimic the exposure close to the solar spectrum that is mostly associated with skin photoaging induction.…”

“…Collectively, the data from the gene expression analysis suggest that both MYC and CAL modulate signaling pathways related to the UVR-induced photodamage response. The Wnt/β-catennin signaling governs cell proliferation, migration, and cellular regeneration following UVR-induced skin damage [7,8,10]. The gene expression data indicated that MYC, but not HRE or CAL, positively regulated the mRNA expression of WNT5a and CTNNB1.…”

“…Skin tissue has a complex photo-sensing molecular network as the first line of defense that protects the human body from the harmful effects of environmental stimuli, including ultraviolet radiation (UVR) [1][2][3][4]. Prolonged excessive exposure to solar radiation causes photodamage associated with accelerated skin aging, impairment, oxidative stress, burns, inflammation, erythema, and the breakdown of the extracellular matrix (ECM), as well as visible changes such as wrinkles and dysregulated pigmentation [3,[5][6][7][8].…”

Comparison of five retinoids for anti‐photoaging therapy: Evaluation of anti‐inflammatory and anti‐oxidative activities in vitro and therapeutic efficacy in vivo

“…The chronic exposure to UVB often induces an inflammatory response, resulting in the upregulated expression of proinflammatory cytokines, such as IL-1, IL-6 and TNF-α in the skin, contributing to the development of skin photoaging. 41 The excessive ROS produced by UVB exposure induces cellular oxidative stress, 42 leading to inflammatory damage, and accelerates photoaging of the skin by regulating the expression of certain key genes. In this study, we observed that RPalm, RP, HPR and ROL functioned to simultaneously and significantly alleviate UVB-irradiation induced inflammation and oxidative stress, revealing important molecular mechanisms underlying these retinoids' anti-photoaging activity.…”

“…The chronic exposure to UVB often induces an inflammatory response, resulting in the upregulated expression of proinflammatory cytokines, such as IL‐1, IL‐6 and TNF‐α in the skin, contributing to the development of skin photoaging 41 . The excessive ROS produced by UVB exposure induces cellular oxidative stress, 42 leading to inflammatory damage, and accelerates photoaging of the skin by regulating the expression of certain key genes.…”