Royal jelly (RJ) is one of the most attractive functional foods that have been a commercial product, especially in dietetics and cosmetics in many countries. However, RJ has been evoked with dermatitis, acute asthma and anaphylaxis because of major RJ proteins. Therefore, to access water soluble royal jelly (WSRJ) that removed allergy-induced proteins as an effective whitening agent for cosmetics and potential external treatment for topical use, we investigated its ability to inhibit melanin biosynthesis. B16F1 cells were treated with 10 nM α-melanocyte-stimulating hormone (α -MSH) for 48hr, and then were treated with various doses of WSRJ for 36hr. WSRJ (1-10ug/ml) inhibited direct tyrosinase activity and cellular tyrosinase activity, which lead to the decrease of melanin synthesis in α-MSH stimulated B16F1 melanoma cells. In addition, we examined RT-PCR and Western blotting for melanogenesis-related genes such as tyrosinase, tyrosinase related protein 1 (TRP-1) and 2. WSRJ suppressed mRNA and protein expression of tyrosinase, tyrosinase related protein (TRP)-1 and TRP-2 in α-MSH stimulated B16F1 cells, and similar to positive control, arbutin. Our findings suggest that WSRJ induced the downregulation of melanogenesis by inhibiting tyrosinase, TRP-1 and 2 activations. It may serve as a new candidate in the new skin-whitening agents.

Royal jelly (RJ) is exclusive food that is secreted from the hypopharyngeal and mandibular glands of worker honeybees, and it is well known to be a necessary for the growth of the queen honeybee Although fresh royal jelly have been demonstrated to enhance wound healing, the wound healing effects of water soluble royal jelly (WSRJ) have not been elucidated. We investigated whether WSRJ promotes the migration, attachment, and proliferation of human dermal fibroblasts (HDFs) during in vitro wound healing. HDFs were treated with 1-5ug/ml WSRJ and RJ for up to 24hr following wound formation. Cell migration was assessed by measuring recovery from wound margin, while cell attachment and proliferation were determined by MTT assay. By observing the numbers of cell attached, we confirmed that not only WSRJ but also RJ did not affect on the initial cell adhesion. WSRJ (5 ug/ml) enhanced cell migration rate approximately 84.3% in HDFs at 24hr, whereas RJ (5 ug/ml) increased cell migration rate 71.3% in HDFs at 24hr, which is similar to cell migration rate of WSRJ 1 ug/ml (73.7%). In cell proliferation assays, WSRJ induced an increase in the number of HDFs, compared with control and RJ. In conclusion, WSRJ promotes cell migration with increased cell proliferation in an in vitro wound healing model.