N-Acetyl-Glucosamine Protects Skin from UV Radiation

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 Ca(2+) into HS68 cells and the phosphorylation of Ca(2+)/calmodulin-dependent kinases (CaMKs).

CONCLUSION:
The results indicate that GlcNAc inhibited UVB-induced collagenolytic MMP production by interfering with Ca(2+)-dependent Akt and MAPKs/AP-1 and NF-κB signaling. They may thus be potentially useful in the prevention and treatment of skin photoaging.