Aglycone of Rh₄ Inhibits Melanin Synthesis in B16 Melanoma Cells : Possible Involvement of the Protein Kinase A Pathway

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  • JEONG Yun-Mi
    Department of Applied Bioscience, CHA University Stem Cell Research Laboratory, CHA Stem Cell Institute
  • OH Won Keun
    BK21 Project Team, College of Pharmacy, Chosun University
  • TRAN Tien Lam
    BK21 Project Team, College of Pharmacy, Chosun University
  • KIM Wang-Kyun
    Stem Cell Research Laboratory, CHA Stem Cell Institute Department of Applied Bioscience, CHA University
  • SUNG Sang Hyun
    Department of Pharmaconogy, College of Pharmacy, Seoul National University
  • BAE Kyeol
    Deaprtment of Biomedical Science, CHA University
  • LEE Suman
    Deaprtment of Biomedical Science, CHA University
  • SUNG Jong-Hyuk
    Stem Cell Research Laboratory, CHA Stem Cell Institute BK21 Project Team, College of Pharmacy, Chosun University Department of Applied Bioscience, CHA University

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  • Aglycone of Rh<sub>4</sub> Inhibits Melanin Synthesis in B16 Melanoma Cells: Possible Involvement of the Protein Kinase A Pathway

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To our knowledge, there is no report that directly shows an inhibitory effect of ginsenoside on melanin synthesis in B16 melanoma cells. Hence, we investigated whether the aglycone of Rh4 (A-Rh4) inhibits melanin synthesis in B16 melanoma cells, and determined the mechanism of melanin inhibition. We isolated 12 ginsenoside compounds from leaves of Panax ginseng and tested them in B16 melanoma cells. It significantly reduced melanin content and tyrosinase activity under alpha-melanocyte stimulating hormone- and forskolin-stimulated conditions. It significantly reduced the cyclic AMP (cAMP) level in B16 melanoma cells, and this might be responsible for the regulation down of MITF and tyrosinase. Phosphorylation of a downstream molecule, a cAMP response-element binding protein, was significantly decreased according to Western blotting and immunofluorescence assay. These data suggest that A-Rh4 has an anti-melanogenic effect via the protein kinase A pathway.

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