These results suggest gene expression profiles that are associated with AD and this implied that fibroblasts may play important roles in the AD pathogenesis. We provided new insights into three candidate genes such as HAS2, TNFAIP6 and IL-8 with respect to their involvement in AD disease.

The inhibition of tyrosinase has attracted considerable attention for potential medicinal and cosmetic applications, as well as in agriculture. This study investigated the inhibition effects of thiol-associated Cu(2+) chelators and deduced a strategy for designing and/or selecting tyrosinase inhibitors. Among the several compounds tested, dithioglycerine (DTGC) was selected for further experiments on the inhibition kinetics on tyrosinase. Different types of tyrosinases derived from mushroom and from the transient overexpression in HEK293 cells were tested individually. The results showed that DTGC significantly inhibited human tyrosinase in a complex manner (slope-parabolic mixed-type inhibition), which was comparable to mushroom tyrosinase. The affinity of DTGC affinity to human tyrosinase was evaluated by setting up a K(i slope) equation. The results suggest that a Cu(2+) chelator modified with thiol groups has potential as a whitening agent. In addition, a strategy for designing and/or selecting tyrosinase inhibitors that target the active enzyme site was also suggested.

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We conducted the proteomic studies to detect the dysregulated proteins in the atopic dermatitis (AD) proteome obtained from the patient-derived primary cultured fibroblasts. Acetaldehyde dehydrogenase 1 (ALDH1) was detected as being significantly down-regulated at the pH ranges of 6-9 and 4-7. The transcriptional levels of ALDH1, as detected by RT-PCR and real-time PCR, further confirmed the down-regulated phenomena for all the AD-fibroblasts (n = 20). The expression levels of ALDH1 in the whole skin tissue samples were further supported by the results of the primary cultured samples. These findings clearly demonstrate that ALDH1 can be a dermal biomarker for AD disease.

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