Abstract
Though melatonin is known to improve ultraviolet B (UVB)-induced oxidative damage and inflammatory conditions via the blockade of the nuclear factor (NF)-κB, interleukin (IL)-6, there is no report on the anti-wrinkle effect of melatonin to date. Hence in the present study, the anti-wrinkle mechanism of melatonin was elucidated in UVB treated HaCaT keratinocytes and hairless mice. Herein melatonin protected against a radical initiator tert-Butyl hydroperoxide (t-BOOH) induced reactive oxygen species (ROS) production, matrix metalloprotease 1 (MMP-1), pro-collagen and cytotoxicity in HaCaT keratinocytes. Additionally, melatonin suppressed the expression of sonic hedgehog (SHH) and GLI1 for hedgehog signaling and p-NF-κB, cyclooxygenase (COX-2), phospho-extracellular signal-regulated kinase-1 (p-ERK) for inflammatory responses in UVB treated HaCaT keratinocytes. Furthermore, melatonin protected skin from wrinkle formation, transdermal water loss in hairless mice irradiated by UVB for 8 weeks. Notably, melatonin prevented against epidermal thickness and dermal collagen degradation in UVB irradiated hairless mice by Hematoxylin and Eosin and Masson’s trichrome staining. Taken together, these findings suggest that melatonin reduces wrinkle formation via inhibition of ROS/SHH and inflammatory proteins such as NF-κB/COX-2/ERK/MMP1.
Highlights
Facial wrinkles are known as one of the most prominent features for skin aging [1]
ultraviolet B (UVB) exposure upregulates the expression of matrix metalloprotease 1 (MMP-1), -3 and -9 as well as sonic hedgehog (SHH) and GLI1 [8,9] in
Melatonin Protected Against t-BOOH Induced reactive oxygen species (ROS) Production and Cytotoxicity in HaCaT
Summary
Skin aging is usually classified as either intrinsic (chronological) and extrinsic (photoaging) aging. Extrinsic aging shows photoaged skin with rough wrinkles mainly due to exposure to sunlight including ultraviolet B, while intrinsic aging is induced by aging genetic factors with a pale and smooth wrinkle formation [2]. It is well documented that the loss of skin elasticity and degradation of elastic fibers and collagen are usually shown in aged or wrinkled skin [3,4]. Previous evidence reveals that reactive oxygen species (ROS) in dermal fibroblast and epidermal keratinocyte produce matrix metalloproteinases (MMPs) to induce collagen degradation leading to skin aging, since MMPs degrade the extracellular matrix, including collagen fibers and contributes to wrinkle formation [5]. UVB exposure upregulates the expression of MMP-1, -3 and -9 as well as sonic hedgehog (SHH) and GLI1 [8,9] in
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