Inhibitory Effect of Arctigenin from Fructus Arctii Extract on Melanin Synthesis via Repression of Tyrosinase Expression

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 Ar...

Full description

Saved in:
Bibliographic Details
Published in:Evidence-based complementary and alternative medicine 2013-01, Vol.2013 (2013), p.1-10
Main Authors: Song, Kwang Hoon, Park, Hwayong, Jung, Pil Mun, Kim, Ji-Eun, Ro, Hyunju, Kim, Mi Yoon, Ma, Jin Yeul
Format: Article
Language:English
Subjects:
Cyclic AMP
Cytotoxicity
Dermatology
Extracellular signal-regulated kinase
Gene expression
Herbs
Kinases
Kojic acid
Medicinal plants
Melanin
Melanoma
Natural resources
Phosphorylation
Signal transduction
Skin
Transcription factors
Tyrosinase
Tyrosinase gene
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary: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.
ISSN:1741-427X
1741-4288
DOI:10.1155/2013/965312