Abstract
Solar ultraviolet (UV) radiation is the primary factor of cutaneous aging, resulting in coarse wrinkles and dryness. In this study, we aimed to test whether decanal, an aromatic compound found mainly in citrus fruits, inhibits UVB-mediated photoaging in human dermal fibroblasts and to explore whether its anti-photoaging effect occurs via cyclic adenosine monophosphate (cAMP) signaling. We found that decanal promotes collagen production dose-dependently. Meanwhile, it also increased the intracellular cAMP levels and decreased the number of molecules involved in the mitogen-activated protein kinase (MAPK)/activator protein 1 (AP-1) pathway, downregulating the collagen genes and upregulating the matrix metalloproteinase (MMP) genes in UVB-exposed dermal fibroblasts. Furthermore, it enhanced hyaluronic acid levels and hyaluronic acid synthase mRNA expression. Notably, the beneficial effects of decanal were lost in the presence of a cAMP inhibitor. Our results revealed the potential of decanal for preventing photoaging and suggested that its effects are cAMP-mediated in human dermal fibroblasts.
Highlights
Skin aging can be caused by intrinsic and extrinsic factors
Our results revealed the potential of decanal for preventing photoaging and suggested that its effects are Cyclic adenosine monophosphate (cAMP)-mediated in human dermal fibroblasts
Intrinsic aging is an unavoidable physiological step that leads to gradual dermal atrophy, whereas extrinsic aging is caused by environmental factors, including poor diet, stress and sun exposure, that lead to deep wrinkles, dry skin and loss of elasticity [1,2,3]
Summary
Skin aging can be caused by intrinsic and extrinsic factors. Intrinsic aging is an unavoidable physiological step that leads to gradual dermal atrophy, whereas extrinsic aging is caused by environmental factors, including poor diet, stress and sun exposure, that lead to deep wrinkles, dry skin and loss of elasticity [1,2,3]. One of the hallmarks of this UV-induced damage of the dermal tissue is increased matrix metalloproteinase (MMP) expression, which causes collagen breakdown in the dermal fibroblast and promotes subsequent skin wrinkling [4,5]. In human dermal fibroblasts, adenyl cyclase (Adcy) activator, forskolin and two other well-known cAMP-elevating agents (3-isobutyl-1-methylxanthine and dibutyryl cAMP) have been found to inhibit MMP1 expression [9]
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