Inhibitory Effect of Arctigenin from Fructus Arctii Extract on Melanin Synthesis via Repression of Tyrosinase ExpressionReport as inadecuate

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Evidence-Based Complementary and Alternative MedicineVolume 2013 2013, Article ID 965312, 10 pages

Research Article

KM-Based Herbal Drug Research Group, Korea Institute of Oriental Medicine, Yuseong-Daero 1672, Yuseong-Gu, Daejeon 305-811, Republic of Korea

Department of Biological Sciences, College of Biosciences and Biotechnology, Chungnam National University, Daehak-Ro 99, Yuseong-Gu, Daejeon 305-764, Republic of Korea

Department of Dermatology, School of Medicine, Chungnam National University, Munhwa-Ro 266, Daejeon 301-747, Republic of Korea

Received 5 February 2013; Revised 29 April 2013; Accepted 13 May 2013

Academic Editor: André-Michael Beer

Copyright © 2013 Hwayong Park et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


To identify the active compound arctigenin in Fructus Arctii dried seed of medicinal plant Arctium lappa and to elucidate the inhibitory mechanism in melanogenesis, we analyzed melanin content and tyrosinase activity on B16BL6 murine melanoma and melan-A cell cultures. Water extracts of Fructus Arctii were shown to inhibit tyrosinase activity in vitro and melanin content in α-melanocyte stimulating hormone-stimulated cells to similar levels as the well-known kojic acid and arbutin, respectively. The active compound arctigenin of Fructus Arctii displayed little or no cytotoxicity at all concentrations examined and decreased the relative melanin content and tyrosinase activity in a dose-dependent manner. Melanogenic inhibitory activity was also identified in vivo with zebrafish embryo. To determine the mechanism of inhibition, the effects of arctigenin on tyrosinase gene expression and tyrosinase promoter activity were examined. Also in addition, in the signaling cascade, arctigenin dose dependently decreased the cAMP level and promoted the phosphorylation of extracellular signal-regulated kinase. This result suggests that arctigenin downregulates cAMP and the tyrosinase enzyme through its gene promoter and subsequently upregulates extracellular signal-regulated kinase activity by increasing phosphorylation in the melanogenesis signaling pathway, which leads to a lower melanin content.

Author: Hwayong Park, Kwang Hoon Song, Pil Mun Jung, Ji-Eun Kim, Hyunju Ro, Mi Yoon Kim, and Jin Yeul Ma



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