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Antimelanogenesis Activity of Hydrolyzed Ginseng Extract (GINST) via Inhibition of JNK Mitogen‐activated Protein Kinase in B16F10 Cells
Author(s) -
Han JoonSeung,
Sung Jong Hwan,
Lee Seung Kwon
Publication year - 2016
Publication title -
journal of food science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.772
H-Index - 150
eISSN - 1750-3841
pISSN - 0022-1147
DOI - 10.1111/1750-3841.13380
Subject(s) - microphthalmia associated transcription factor , tyrosinase , kinase , mapk/erk pathway , p38 mitogen activated protein kinases , protein kinase a , chemistry , ginseng , biochemistry , signal transduction , mitogen activated protein kinase , melanin , microbiology and biotechnology , biology , enzyme , medicine , alternative medicine , pathology
GINST is a hydrolyzed ginseng extract produced by an in vitro process that imitates the metabolic function of bacteria in the human digestive track and has approved by the Ministry of Food and Drug Safety of Korea for the management of postprandial hyperglycemia. Additionally, GINST has been reported to have other physiological functions including anti‐aging and antioxidant effects. The objectives of this study are to compare the antimelanogenic effects of fresh ginseng extract (FGE) and GINST extract and to elucidate the functional mechanism. The concentration of total ginsenosides in FGE and GINST was measured using ultraperformance liquid chromatography with a C18 column. B16F10 cells were treated with FGE and GINST for 72 h to assess melanin content, tyrosinase activity, and protein levels of microphthalmia‐associated transcription factor (MITF) and tyrosinase‐related protein‐1 (TRP‐1). The activity of kinases involved in mitogen‐activated protein kinase (MAPK) signaling, such as extracellular signal‐regulated kinases (ERK), c‐Jun N‐terminal kinases (JNK), and p38 mitogen‐activated protein kinases (p38), were measured using western blots. While neither FGE nor GINST inhibited the activity of mushroom tyrosinase directly, GINST decreased melanogenesis and tyrosinase activity markedly. Furthermore, our results indicate that GINST downregulated the levels of MITF and TRP‐1 possibly by suppressing JNK signaling. We concluded that, when compared to FGE, GINST has a superior antimelanogenic effect mediated by the downregulation of MITF, TRP‐1, and intracellular tyrosinase activity via the JNK signaling pathway. Thus, we suggest that GINST has the potential to be used as a novel skin whitening agent.