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The extract of Angelica gigas Nakai by supercritical CO2 increased the expression of collagen synthesis-related proteins in human dermal fibroblast, including type 1(α-2) collagen chain precursor (pI 9.08, MW 129.7), procollagen C-endopeptidase (pI 7.40, MW 47.97), and prolyl 4-hydroxylase (pI 5.49, MW 60.90). It also increased the expression level of interaction-related proteins, α-actinin (pI 5.47, MW 105.5), integrin-β1 (pI 5.27, MW 88.46). The expression levels of these proteins by pure decursin were similar to those by supercritical fluid extract. By the dose concentration experiment, decursin in A. gigas was found to play the major role in expression level increases. Proteome analysis proved that decursin in A. gigas promoted synthesis of proteins related to skin anti-aging in human dermal fibroblasts.

The ability of heartwood extract ofMorus bombycis in controlling the melanogenesis in B16 melanoma was investigated. An inhibitory effect was observed when the dose concentration was less than 10 mg/L. When the dose was 10 mg/L, the extracellular melanin accumulated was only 5% of the control. Proteome analysis with 2-D PAGE and MALDI-TOF showed that there were various proteins involved in inhibitory melanogenesis. It seems that down-regulation of TRP2, vacuolar protontranslocating ATPase 100 kDa subunit isoform a1-I and V-ATPase E2 subunit were involved in melanosome development and regulation that could reduce melanin synthesis.

The extract of Gynostemma pentaphyllum was tested to control the melanogenesis in B16 melanoma. Cytotoxic effect by the extract was observed when the dose concentration was higher than 2 mg/L. Most of the inhibitory effect was obtained by the reduced accumulation of extra-cellular melanin. When the extract was dosed as 2 mg/L, the extra-cellular melanin produced was only 24% of the control. Proteome analysis with 2-D PAGE showed that various proteins involved in melanogenesis were down-regulated by Gynostemma pentaphyllum. In addition to other proteins related to the intra-cellular melanogenesis, Rab-27b and Rab-38 could explain the remarkable decrease in extra-cellular melanin accumulation by reduced melanin transfer to keratinocyte.

Rett syndrome (RTT) is an X-linked dominant neurodevelopmental disorder affecting 1 per 10,000-15,000 female births worldwide. The disease-causing gene has been identified as MECP2 (methyl-CpG-binding protein 2). In this study, we performed diagnostic mutational analysis of the MECP2 gene in RTT patients. Four exons and a putative promoter of the MECP2 gene were analyzed from the peripheral blood of 43 Korean patients with Rett syndrome by PCR-RFLP and direct sequencing. Mutations were detected in the MECP2 gene in approximately 60.5% of patients (26 cases/43 cases). The mutations consisted of 14 different types, including 9 missense mutations, 4 nonsense mutations and 1 frameshift mutation. Of these, three mutations (G161E, T311M, p385fsX409) were newly identified and were determined to be disease-causing mutations by PCR- RFLP and direct sequencing analysis. Most of the mutations were located within MBD (42.3%) and TRD (50%). T158M, R270X, and R306C mutations were identified at a high frequency. Additionally, an intronic SNP (IVS3+23C>G) was newly identified in three of the patients. IVS3+23C>G may be a disease-related and Korea-specific SNP for RTT. L100V and A201V are apparently disease-causing mutations in Korean RTT, contrary to previous studies. Disease-causing mutations and polymorphisms are important tools for diagnosing RTT in Koreans. The experimental procedures used in this study should be considered for clinical molecular biologic diagnosis.

One of the potential causes of age-related neuronal damage can be reactive oxygen species (ROS), as the brain is particularly sensitive to oxidative damage. In the present study, we investigated the effects of aging and dietary restriction (DR) on ROS generation, lipid peroxidation, and antioxidant enzymes in cerebrum, hippocampus, and cerebellum of 6-, 12-, 18-, and 24-month-old rats. ROS generation significantly increased with age in cerebrum of ad libitum (AL) rats. However, no significant age-difference was observed in hippocampus and cerebellum. DR significantly decreased ROS generation in cerebrum and cerebellum at 24-months. On the other hand, the increased lipid peroxidation of AL rats during aging was significantly reduced by DR in all regions. Our results further showed that catalase activity decreased with age in cerebellum of AL rats, which was reversed by DR, although SOD activity had little change by aging and DR in all regions. In a similar way, glutathione (GSH) peroxidase activity increased with age in cerebrum of AL rats, while DR suppressed it at 24-months. These data further support the evidence that the vulnerability to oxidative stress in the brain is region-specific.