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• W2148711700 abstract "Background N-Acetylglucosamine (GlcNAc) and its derivates have been utilized in dietary supplements and for therapeutic development due to their unique characteristics. GlcNAc is recognized primarily for its function as a precursor to hyaluronic acid, which plays a significant role in the structure and hydration of the extracellular matrix in skin, in both the epidermis and the dermis. Objective We investigated the protective effects of GlcNAc on immortalized human skin fibroblasts (HS68) against UVB damage. We then explored the inhibitory effects of GlcNAc on UVB-induced collagenases and investigated the molecular mechanism underlying those effects. Methods Those effects were assessed by semi-quantitative PCR, Western blotting and enzymatic activity assays. Results GlcNAc increased the viability of, and inhibited ROS production in, HS68 cells exposed to UVB irradiation. Pre-treatment of HS68 cells with GlcNAc inhibited UVB-induced production of the collagenases MMP-1 and MMP-13. Western blot analysis further revealed that GlcNAc markedly suppressed the enhancement of collagen degradation in UVB-exposed HS68 cells. GlcNAc also suppressed UVB-induced activation of c-Jun, c-Fos and NF-κB and the phosphorylation of MAPKs and PI3K/Akt, upstream modulators of AP-1 and NF-κB. Moreover, GlcNAc decreased the UVB-induced influx of Ca2+ into HS68 cells and the phosphorylation of Ca2+/calmodulin-dependent kinases (CaMKs). Conclusion The results indicate that GlcNAc inhibited UVB-induced collagenolytic MMP production by interfering with Ca2+-dependent Akt and MAPKs/AP-1 and NF-κB signaling. They may thus be potentially useful in the prevention and treatment of skin photoaging. N-Acetylglucosamine (GlcNAc) and its derivates have been utilized in dietary supplements and for therapeutic development due to their unique characteristics. GlcNAc is recognized primarily for its function as a precursor to hyaluronic acid, which plays a significant role in the structure and hydration of the extracellular matrix in skin, in both the epidermis and the dermis. We investigated the protective effects of GlcNAc on immortalized human skin fibroblasts (HS68) against UVB damage. We then explored the inhibitory effects of GlcNAc on UVB-induced collagenases and investigated the molecular mechanism underlying those effects. Those effects were assessed by semi-quantitative PCR, Western blotting and enzymatic activity assays. GlcNAc increased the viability of, and inhibited ROS production in, HS68 cells exposed to UVB irradiation. Pre-treatment of HS68 cells with GlcNAc inhibited UVB-induced production of the collagenases MMP-1 and MMP-13. Western blot analysis further revealed that GlcNAc markedly suppressed the enhancement of collagen degradation in UVB-exposed HS68 cells. GlcNAc also suppressed UVB-induced activation of c-Jun, c-Fos and NF-κB and the phosphorylation of MAPKs and PI3K/Akt, upstream modulators of AP-1 and NF-κB. Moreover, GlcNAc decreased the UVB-induced influx of Ca2+ into HS68 cells and the phosphorylation of Ca2+/calmodulin-dependent kinases (CaMKs). The results indicate that GlcNAc inhibited UVB-induced collagenolytic MMP production by interfering with Ca2+-dependent Akt and MAPKs/AP-1 and NF-κB signaling. They may thus be potentially useful in the prevention and treatment of skin photoaging." @default.
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• W2148711700 date "2011-08-01" @default.
• W2148711700 modified "2023-10-16" @default.
• W2148711700 title "N-Acetylglucosamine suppress collagenases activation in ultraviolet B-irradiated human dermal fibroblasts: Involvement of calcium ions and mitogen-activated protein kinases" @default.
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• W2148711700 doi "https://doi.org/10.1016/j.jdermsci.2011.04.008" @default.
• W2148711700 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/21600739" @default.
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