Oral administration of royal jelly (RJ) promotes wound healing in diabetic mice. Concerns have arisen regarding the efficacy of RJ on the wound healing process of normal skin cells. In this study, a wound was created by scratching normal human dermal fibroblasts, one of the major cells involved in the wound healing process. The area was promptly treated with RJ at varying concentrations of 0.1, 1.0, or 5 mg/ml for up to 48 hrs and migration was analyzed by evaluating closure of the wound margins. Furthermore, altered levels of lipids, which were recently reported to participate in the wound healing process, were analyzed by HPTLC and HPLC. Migration of fibroblasts peaked at 24 hrs after wounding. RJ treatment significantly accelerated the migration of fibroblasts in a dose-dependent manner at 8 hrs. Although RJ also accelerated the migration of fibroblasts at both 20 hrs and 24 hrs after wounding, the efficacy was less potent than at 8 hrs. Among various lipid classes within fibroblasts, the level of cholesterol was significantly decreased at 8 hrs following administration of both 0.1 ug/ml and 5 mg/ml RJ. Despite a dose-dependent increase in sphinganines, the levels of sphingosines, ceramides, and glucosylceramides were not altered with any concentration of RJ. We demonstrated that RJ enhances the migration of fibroblasts and alters the levels of various lipids involved in the wound healing process.
Administration, Oral ; Animals ; Ceramides ; Cholesterol ; Chromatography, High Pressure Liquid ; Fatty Acids ; Fibroblasts ; Glucosylceramides ; Humans ; Mice ; Skin ; Sphingosine ; Wound Healing

AIMTo study the bioactive components from Helicia nilagirica.

METHODSCompounds were separated with a combination of multi-chromatography. Their chemical structures were determined on the basis of spectral analysis and chemical evidence.

RESULTSTwo compounds were isolated from the leaves of Helicia nilagirica. Compound 1 was elucidated as 1-O-3-D-glucopyranosyl-(2S,3S,4R,8Z)-2-[(2'R)-2'-hyd roxylignocenoyl-amino]-8-octadecene-1, 3, 4-triol. Compound 2 was an analogue of 1.

CONCLUSIONThe two compounds are new cerebrosides.

Cerebrosides ; chemistry ; isolation & purification ; Glucosylceramides ; chemistry ; isolation & purification ; Molecular Conformation ; Molecular Structure ; Plant Leaves ; chemistry ; Plants, Medicinal ; chemistry ; Proteaceae ; chemistry

OBJECTIVETo design and make trial of a new therapy for Gaucher disease.

METHODSA substrate analogue of beta-Glc (glucocerebroside analogue, GCA) was used as a molecular chaperon. Normal and mutant skin fibroblasts were cultured with or without GCA. The activity of beta-Glc was assayed by fluorescent enzymologic techniques. The amount of beta-Glc was determined using Western blot. The beta -Glc was localized by double cell stain experiment. The degradation of glucocerebroside was assessed by thin layer chromatography (TLC) experiment using 14C-Serine.

RESULTSIt was found that GCA could enhance the activity and amount of beta-Glc with F213I mutation. It also promoted the beta-Glc with F213I mutation to the lysosome and accelerated the degradation of glucocerebroside.

CONCLUSIONThe low molecular compound analogous to beta-Glc substrate (GCA ) may be a new therapeutic strategy for Gaucher's disease with F213I mutation.

Amino Acid Substitution ; Blotting, Western ; Cells, Cultured ; Enzyme Induction ; drug effects ; Gaucher Disease ; drug therapy ; enzymology ; genetics ; Glucosylceramidase ; biosynthesis ; genetics ; metabolism ; Glucosylceramides ; metabolism ; pharmacology ; Humans ; Immunohistochemistry ; Mutation ; Substrate Specificity