Abstract
S-Methylmethionine sulfonium (SMMS) was reported to have wound-healing effects; we therefore have investigated the photoprotective effect of SMMS in the present study. SMMS increased the viability of keratinocyte progenitor cells (KPCs) and human dermal fibroblasts (hDFs) following ultraviolet B (UVB) irradiation, and reduced the UVB-induced apoptosis in these cells. SMMS increased the phosphorylation of extracellular signal-regulated kinases (ERK), and the inhibitor of the mitogen-activated protein kinase pathway significantly decreased the SMMS-induced viability of KPCs and hDFs. In addition, SMMS attenuated the UVB-induced reactive oxygen species (ROS) generation in KPCs and hDFs. SMMS induced the collagen synthesis and reduced the matrix metalloproteinase-1 expression in UVB-irradiated hDFs. In animal studies, application of 5% and 10% SMMS before and after UVB-irradiation significantly decreased the UVB-induced erythema index and depletion of Langerhans cells. In summary, SMMS protects KPCs and hDFs from UVB irradiation, and reduces UVB-induced skin erythema and immune suppression. Therefore, SMMS can be used as a cosmetic raw material, and protect skin from UVB.
Highlights
Ultraviolet (UV) light is a carcinogenic component of sunlight and widely known as one of the most relevant risk factors for skin cancers [1,2]
We monitored the proliferation of keratinocyte progenitor cells (KPCs) treated with various concentrations of the S-Methylmethionine sulfonium (SMMS) (1, 10, 100, 500, and 1000 μM), but there is no difference in KPC proliferation
We investigated the protective mechanism of SMMS in KPCs from ultraviolet B (UVB) irradiation, and found that SMMS (1 and 10 μM) reduced the UVB-induced reactive oxygen species (ROS) generation in KPCs (Figure 1C, n = 1)
Summary
Ultraviolet (UV) light is a carcinogenic component of sunlight and widely known as one of the most relevant risk factors for skin cancers [1,2]. UVB irradiation induces skin erythema, and changes the morphology and function of epidermal Langerhans cells (LCs). Taguchi et al reported that UVB irradiation induced the migration of epidermal LCs to the draining lymph nodes, resulting in a depletion of the epidermal LCs [6]. The anti-inflammatory, anti-depressant and cytoprotective effects of SMMS have been reported [10,11,12]. The activation of extracellular receptor kinase 1/2 (ERK1/2) mediated the SMMS-induced proliferation and migration of hDFs [8]. Signaling pathways and underlying molecular mechanisms are investigated in KPCs and hDFs. The in vivo photoprotective effect of SMMS was evaluated in hairless rats by quantitatively measuring the UVB-induced skin erythema and by conducting an immunohistochemical analysis of the depletion of epidermal LCs after
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