Abstract

Recently, there has been much effort to find effective ingredients which can prevent or retard cutaneous skin aging after topical or systemic use. Here, we investigated the effects of the atomic hydrogen surrounded by water molecules, H(H2O)m, on acute UV-induced responses and as well as skin aging. Interestingly, we observed that H(H2O)m application to human skin prevented UV-induced erythema and DNA damage. And H(H2O)m significantly prevented UV-induced MMP-1, COX-2, IL-6 and IL-1β mRNA expressions in human skin in vivo. We found that H(H2O)m prevented UV-induced ROS generation and inhibited UV-induced MMP-1, COX-2 and IL-6 expressions, and UV-induced JNK and c-Jun phosphorylation in HaCaT cells. Next, we investigated the effects of H(H2O)m on intrinsically aged or photoaged skin of elderly subjects. In intrinsically aged skin, H(H2O)m application significantly reduced constitutive expressions of MMP-1, IL-6, and IL-1β mRNA. Additionally, H(H2O)m significantly increased procollagen mRNA and also decreased MMP-1 and IL-6 mRNA expressions in photoaged facial skin. These results demonstrated that local application of H(H2O)m may prevent UV-induced skin inflammation and can modulate intrinsic skin aging and photoaging processes. Therefore, we suggest that modifying the atmospheric gas environment within a room may be a new way to regulate skin functions or skin aging.

Highlights

  • Acute exposure to ultraviolet (UV) radiation leads to inflammatory responses such as skin erythema and sunburn, whereas chronic exposure to UV causes carcinogenesis and photoaging of the skin

  • In the result of immunofluorescence staining, UV-induced phospho-cJun expression was decreased by H(H2O)m (Figure 5C). These results suggest that H(H2O)m inhibits UV-induced matrix metalloproteases (MMPs)-1 expression and that this inhibition may be mediated by a reduction in the level of phosphorylated c-Jun, which is known to be closely associated with UV-induced activator protein (AP)-1 activation

  • This study demonstrated that H(H2O)m prevented UV-induced erythema and DNA damage in human skin and inhibited UVinduced MMP-1, COX-2, IL-6 and IL-1b expressions significantly

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Summary

Introduction

Acute exposure to ultraviolet (UV) radiation leads to inflammatory responses such as skin erythema and sunburn, whereas chronic exposure to UV causes carcinogenesis and photoaging of the skin. Activation of cell surface receptors, such as epidermal growth factor receptor, by UV stimulates mitogen-activated protein kinase (MAPK) signal transduction pathways [10]. Many studies have indicated that UV exposure of human skin causes extracellular matrix degradation via induction of transcription factor AP-1 and subsequently by increased MMP production [10,15]. Another important transcription factor activated in response to UV irradiation is nuclear factor kappa B (NF-kB) [16]. Activation of the NF-kB pathway by UV stimulates inflammatory cytokine expression, and contributes to UV-induced skin damage, such as photoaging

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