Collagen tripeptide (CTP) is a functional food material with several biological effects such as improving dry skin and wound and bone fracture healing. This study focused on the anti-photoaging effects of CTP on a hairless mouse model. To evaluate the effects of CTP on UVB-induced skin wrinkle formation in vivo, the hairless mice were exposed to UVB radiation with oral administration of CTP for 14 weeks. Compared with the untreated UVB control group, mice treated with CTP showed significantly reduced wrinkle formation, skin thickening, and transepidermal water loss (TEWL). Skin hydration and hydroxyproline were increased in the CTP-treated group. Moreover, oral administration of CTP prevented UVB-induced MMP-3 and -13 activities as well as MMP-2 and -9 expressions. Oral administration of CTP increased skin elasticity and decreased abnormal elastic fiber formation. Erythema was also decreased in the CTP-treated group. Taken together, these results strongly suggest that CTP has potential as an anti-photoaging agent.

The results show that oral administration of KPE significantly prevents UVB-induced photoaging in hairless mice, suggesting its potential as a natural antiphotoaging material.

Exposure to ultraviolet (UV) light causes premature skin aging that is associated with upregulated matrix metalloproteinases (MMPs) and decreased collagen synthesis. Macelignan, a natural lignan compound isolated from Myristica fragrans HOUTT. (nutmeg), has been reported to possess antioxidant and antiinflammatory activities. This study assessed the effects of macelignan on photoaging and investigated its mechanisms of action in UV-irradiated human skin fibroblasts (Hs68) by reverse transcription-polymerase chain reaction, Western blot analysis, 2′,7′-dichlorofluorescein diacetate assay, and enzyme-linked immunosorbent assay. Our results show that macelignan attenuated UV-induced MMP-1 expression by suppressing phosphorylation of mitogen-activated protein kinases (MAPKs) induced by reactive oxygen species. Macelignan also increased type I procollagen expression and secretion through transforming growth factor β (TGF-β)/Smad signaling. These findings indicate that macelignan regulates the expression of MMP-1 and type I procollagen in UV-irradiated human skin fibroblasts by modulating MAPK and TGF-β/Smad signaling, suggesting its potential as an efficacious antiphotoaging agent.Key words macelignan; matrix metalloproteinase-1; type I procollagen; mitogen-activated protein kinase; UV irradiation; reactive oxygen species Skin aging, which causes wrinkling, sagging and roughness, can be divided into two distinct processes: intrinsic aging and photoaging. Photodamage and premature skin aging is caused by ultraviolet (UV) irradiation, which increases the synthesis of matrix metalloproteinases (MMPs).1) MMP upregulation in skin fibroblasts accelerates the degradation of dermal collagen, which confers tensile strength.2) Skin aging is characterized by reductions in type I collagen, the primary component of the extracellular matrix (ECM), which provides structural support to the skin dermis.3) Therefore, natural compounds that decrease the MMP production and increase procollagen synthesis may have potential for the prevention and treatment of photoaging. Most are secreted as inactive proenzymes (proMMPs) that are activated primarily by proteolytic cascades, generally catalyzed by neutral proteinases. MMP-1 is primarily responsible for degradation of ECM. 4)UV irradiation also leads to the generation of reactive oxygen species (ROS), direct or indirect DNA damage, and inflammatory response and damage to ECM integrity. 5)

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