Reduced or defective melanin skin pigmentation may cause many hypopigmentation disorders and increase the risk of damage to\r\nthe skin triggered byUVirradiation.Ginsenosides Rb1 and Rg1 havemanymolecular targets including thecAMP-response elementbinding\r\nprotein (CREB), which is involved in melanogenesis. This study aimed to investigate the effects of ginsenosides Rb1 and\r\nRg1 on melanogenesis in human melanocytes and their related mechanisms. The effects of Rb1 and Rg1 on cell viability, tyrosinase\r\nactivity, cellular melanin content and protein levels of tyrosinase, microphthalmia-associated transcription factor (MITF), and\r\nactivation of CREB in melanocytes were assessed. Results showed that Rb1 or Rg1 significantly increased cellular melanin content\r\nand tyrosinase activity in a dose-dependent manner. By contrast, the cell viability of melanocytes remained unchanged. After\r\nexposure to Rb1 or Rg1, the protein levels of tyrosinase, MITF, and phosphorylated CREBwere significantly increased. Furthermore,\r\npretreatmentwith the selective PKAinhibitor H-89 significantly blocked the Rb1- or Rg1-induced increase of melanin content. These\r\nfindings indicated that Rb1 and Rg1 increased melanogenesis and tyrosinase activity in human melanocytes, which was associated\r\nwith activation of PKA/CREB/MITF signaling. The effects and mechanisms of Rb1 or Rg1 on skin pigmentation deserve further\r\nstudy.
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