Ginsenosides, the major active ingredient of ginseng, show a variety of biomedical efficacies such as anti‐aging, anti‐oxidation and anti‐inflammatory activities. To understand the effects of 20‐O‐β‐D‐glucopyranosyl‐20 (S)‐protopanaxadiol (compound K), one of the major metabolites of ginsenosides on the skin, we assessed the expression level of approximately 100 transcripts in compound K‐treated HaCaT cells using cDNA microarray analysis. Compound K treatment induced differential expression of 40 genes, which have been reported to be involved in the organization of the structure of the extracellular matrix as well as defense responses in human skin cells. One of the most interesting findings is a two‐fold increase in hyaluronan synthase2 (HAS2) gene expression by compound K. We found that change in expression of HAS2 gene represents a specific response of HaCaT cells to compound K because hyaluronan synthase 1,3 was not changed by treatment with compound K. We also demonstrated that the compound K effectively induced hyaluronan synthesis in human skin cells and hairless mouse skin. A human clinical study indicated that topical application of compound K containing oil‐in‐water emulsion showed improvement of xerosis, wrinkle and fine lines in the aged skin. We concluded that compound K has anti‐aging effects by the induction of HAS2 gene expression and following hyaluronan synthase.
Lipoteichoic acid (LTA), a cell wall component of gram-positive bacteria, is recognized by Toll-like receptor 2, expressed on certain mammalian cell surfaces, initiating signaling cascades that include nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) and mitogen-activated protein kinase. There are many structural and functional varieties of LTA, which vary according to the different species of gram-positive bacteria that produce them. In this study, we examined whether LTA isolated from (aLTA) affects the expression of junction proteins in keratinocytes. In HaCaT cells, tight junction-related gene expression was not affected by aLTA, whereas adherens junction-related gene expression was modified. High doses of aLTA induced the phosphorylation of extracellular signal-regulated protein kinases 1 and 2, which in turn induced the epithelial-mesenchymal transition (EMT) of HaCaT cells. When cells were given a low dose of aLTA, however, NF-κB was activated and the total cell population increased. Taken together, our study suggests that LTA from infections in the skin may contribute both to the outbreak of EMT-mediated carcinogenesis and to the genesis of wound healing in a dose-dependent manner.
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