Ultraviolet‐ and infrared‐induced 11 beta‐hydroxysteroid dehydrogenase type 1 activating skin photoaging is inhibited by red ginseng extract containing high concentration of ginsenoside Rg3(S)

Summary Background Sun irradiation is one of major extrinsic stressors responsible for premature skin aging through activation and expression of 11 beta‐hydroxysteroid dehydrogenase type 1 (11β‐ HSD 1), which converts inactive cortisone to active cortisol. The aim of this study was to evaluate the inhibitory effects of red ginseng extract containing high concentrations of ginsenoside Rg3 (S) ( GER g3) on 11β‐ HSD 1‐induced skin photoaging. Methods To evaluate the inhibitory effects of GER g3 on ultraviolet‐ ( UV ) or infrared ( IR )‐induced skin photoaging, human dermal fibroblasts or a normal human 3D skin model was exposed to UV or an IR . RT ‐ PCR , ELISA , Western blot, and H&E staining were used for evaluations. GER g3 was isolated from crude red ginseng. Results GER g3 inhibited the increased expressions of 11β‐ HSD 1, interleukin ( IL )‐6, and matrix metalloproteinase‐1 ( MMP ‐1) in UVB ‐ or IR ‐exposed Hs68 cells. Additionally, the increased cortisol, IL ‐6, and MMP ‐1 expressions were effectively reduced by GER g3 in UVA ‐exposed 3D skin models. The photoinduced decrease in type 1 procollagen also recovered as a result of GER g3 treatment in Hs68 cells and the 3D skin model. In addition, the UVA ‐exposed dermal thickness was decreased in comparison with the UVA ‐protected 3D skin model, recovered with GER g3 treatment. Conclusion GER g3 had antiphotoaging effects in UV ‐ or IR ‐exposed human dermal fibroblasts and normal human 3D skin model.