ABSTRACT
Photoaging accounts for most age-related changes in skin appearance. It has been suggested that both astaxanthin, a potent antioxidant, and collagen hydrolysate can be used as antiaging modalities in photoaged skin. However, there is no clinical study using astaxanthin combined with collagen hydrolysate. We investigated the effects of using a combination of dietary astaxanthin and collagen hydrolysate supplementation on moderately photoaged skin in humans. A total of 44 healthy subjects were recruited and treated with astaxanthin (2 mg/day) combined with collagen hydrolysate (3 g/day) or placebos, which were identical in appearance and taste to the active supplementation for 12 weeks. The elasticity and hydration properties of facial skin were evaluated using noninvasive objective devices. In addition, we also evaluated the expression of procollagen type I, fibrillin-1, matrix metalloproteinase-1 (MMP-1) and -12, and ultraviolet (UV)-induced DNA damage in artificially UV-irradiated buttock skin before and after treatment. The supplement group showed significant improvements in skin elasticity and transepidermal water loss in photoaged facial skin after 12 weeks compared with the placebo group. In the supplement group, expression of procollagen type I mRNA increased and expression of MMP-1 and -12 mRNA decreased compared with those in the placebo group. In contrast, there was no significant difference in UV-induced DNA damage between groups. These results demonstrate that dietary astaxanthin combined with collagen hydrolysate can improve elasticity and barrier integrity in photoaged human facial skin, and such treatment is well tolerated.
Subject(s)
Collagen/administration & dosage , Dietary Supplements , Skin Aging/drug effects , Skin/drug effects , Adult , Antioxidants/administration & dosage , Asian People , Collagen Type I/genetics , Collagen Type I/metabolism , DNA Damage/drug effects , DNA Damage/radiation effects , Double-Blind Method , Elasticity , Female , Fibrillin-1 , Fibrillins , Humans , Matrix Metalloproteinase 1/genetics , Matrix Metalloproteinase 1/metabolism , Matrix Metalloproteinase 12/genetics , Matrix Metalloproteinase 12/metabolism , Microfilament Proteins/genetics , Microfilament Proteins/metabolism , Middle Aged , Patient Compliance , RNA, Messenger/genetics , RNA, Messenger/metabolism , Skin/metabolism , Ultraviolet Rays/adverse effects , Xanthophylls/administration & dosageABSTRACT
The consumption of flavonoid-rich Citrus extracts has been associated with multiple beneficial effects including anti-inflammatory properties, but the potential effects on the inflammatory responses in the gut have not been thoroughly investigated. We used microarrays to search for molecular changes induced in human colon fibroblasts in response to the exposure to a flavanone-rich bitter orange extract under physiologically representative conditions. Dietary nontoxic levels of the predigested extract induced moderate but significant changes in the expression of genes associated with tissue repair and inflammation. Among the top regulated genes, plasminogen activator inhibitor 1 (PAI-1) was downregulated, and the matrix metallopeptidase 12 (MMP-12) was upregulated (mRNA and protein levels). Both proteins are involved in extracellular matrix (ECM) remodeling and fibroblast migration. The extract also affected the fibroblast migration and reduced monocyte adhesion, but the response was different in unstimulated cells and in cells pretreated with TNF-alpha. Collectively, these results were indicative of a moderate activation of the colon fibroblast inflammation-related function after exposure to the extract. Further investigations are required to identify the in vivo role of this Citrus derived extract in the maintenance of the normal balance in the intestine and in the pathogenesis of inflammatory diseases.