The protective effect of Kaempferia parviflora extract on UVB-induced skin photoaging in hairless mice.

BACKGROUND: Chronic skin exposure to ultraviolet (UV) light increases reactive oxygen species (ROS) and stimulates the expression of matrix metalloproteinases (MMPs) through c-Jun and c-Fos activation. These signaling cascades induce the degradation of extracellular matrix (ECM) components, resulting in photoaging. METHODS: This study evaluated the preventive effect of the ethanol extract of Kaempferia parviflora Wall. ex. Baker (black ginger) on UVB-induced photoaging in vivo. To investigate the antiphotoaging effect of K. parviflora extract (KPE), UVB-irradiated hairless mice administered oral doses of KPE (100 or 200 mg/kg/day) for 13 weeks. RESULTS: In comparison to the UVB control group, KPE significantly prevented wrinkle formation and the loss of collagen fibers with increased type I, III, and VII collagen genes (COL1A1, COL3A1, and COL7A1). The decrease in wrinkle formation was associated with a significant reduction in the UVB-induced expression of MMP-2, MMP-3, MMP-9, and MMP-13 via the suppression of c-Jun and c-Fos activity. KPE also increased the expression of catalase, which acts as an antioxidant enzyme in skin. In addition, expression of inflammatory mediators, such as nuclear factor kappa B (NF-κB), interleukin-1ß (IL-1ß), and cyclooxygenase-2 (COX-2), was significantly reduced by KPE treatment. CONCLUSION: The results show that oral administration of KPE significantly prevents UVB-induced photoaging in hairless mice, suggesting its potential as a natural antiphotoaging material.

Effects of macelignan isolated from Myristica fragrans (Nutmeg) on expression of matrix metalloproteinase-1 and type I procollagen in UVB-irradiated human skin fibroblasts.

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 ß (TGF-ß)/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-ß/Smad signaling, suggesting its potential as an efficacious antiphotoaging agent.

Panduratin A, an activator of PPAR-α/δ, suppresses the development of oxazolone-induced atopic dermatitis-like symptoms in hairless mice.

AIMS: Panduratin A isolated from Boesenbergia pandurata (Roxb.) has been reported to have antioxidant, anti-inflammatory, and anti-allergic activities. However, the effect of panduratin A on atopic dermatitis (AD) has not been studied. In the present study, we investigated the efficacy of panduratin A, an activator of peroxisome proliferator-activated receptors (PPAR) α/δ, using oxazolone-induced AD-like model in hairless mice. MAIN METHODS: To determine PPARα/δ activation of panduratin A, HaCaT, Hs68, and COS-7 cells were treated with panduratin A, then PPARα/δ and PPAR response element (PPRE) activities were assessed with a reporter gene assay. For the in vivo study, oral administration of panduratin A was performed for 4weeks, with oxazolone treatment every other day. The efficacy of panduratin A on parameters of oxazolone-induced AD was assessed physiologically, morphologically, and immunologically. KEY FINDINGS: Panduratin A increased PPARα/δ and PPRE activation both in vitro and in vivo. Panduratin A attenuated dermatitis-associated barrier damage as demonstrated by transepidermal water loss, erythema, and filaggrin expression. Furthermore, infiltration of inflammatory cells and epidermal thickness in the skin were decreased. Panduratin A decreased serum immunoglobulin (Ig) E and interleukin-4 levels but increased IgG2a and interferon-γ levels. In addition, panduratin A decreased inflammation-associated molecules in the skin. Panduratin A also decreased Th2-associated molecules and increased Th1/regulatory T cell (Treg)-associated molecules in the spleen. SIGNIFICANCE: Panduratin A showed a beneficial effect on AD by modulating Th1/Th2/Treg-associated immune response and is a potential candidate for treating AD.

Effects of Collagen Tripeptide Supplement on Photoaging and Epidermal Skin Barrier in UVB-exposed Hairless Mice.

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.