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.
Jae-Min KimKyung-Sook ChungYoung-Seo YoonSeo-Yun JangSo-Won HeoGeonha ParkYoung Pyo JangHye-Shin AhnYu-Kyoung ShinSun-Hee LeeKyung Tae LeePublished in: Marine drugs (2022)
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.
Keyphrases
- transforming growth factor
- epithelial mesenchymal transition
- hyaluronic acid
- wound healing
- mouse model
- high fat diet induced
- signaling pathway
- induced apoptosis
- oxidative stress
- healthcare
- public health
- transcription factor
- type diabetes
- high glucose
- cell death
- pi k akt
- clinical trial
- binding protein
- adipose tissue
- metabolic syndrome
- risk assessment
- toll like receptor
- human health
- inflammatory response
- endothelial cells
- tissue engineering