Vol 47 No. 7: 548-556 [PDF] [Full Text]
Hyperpigmentation mechanism of methyl 3,5-di-caffeoylquinate through activation of p38 and MITF induction of tyrosinase
Hyo Jung Kim1,†, Jin Sook Kim2,†, Je-Tae Woo1,3, Ik-Soo Lee2 and Byung-Yoon Cha1,*

1Research Institute for Biological Functions, Chubu University, Kasugai, Aichi 487-8501, Japan
2KM Convergence Research Division, Korea Institute of Oriental Medicine, Daejeon 305-811, Republic of Korea
3Department of Research and Development, Erina Co., Inc., Minato-ku, Tokyo 105-0021, Japan
These authors contributed equally to this work.

Abstract  Methyl 3,5-di-caffeoylquinate (3,5-diCQM) has been used for the treatment of various diseases in oriental medicine, but its effect on melanogenesis has not been reported yet. In this study, the molecular mechanism of 3,5-diCQM-induced melanogenesis was investigated. It was found that 3,5-diCQM induced synthesis of melanin pigments in murine B16F10 melanoma cells in a concentration-dependent manner. Treatment of cells with 3,5-diCQM for 48 h increased extracellular and intracellular melanin production and tyrosinase activity. The expressions of tyrosinase, tyrosinase-related protein 1 (TRP1), and TRP2 were up-regulated in a dose-dependent manner 48 h after 3,5-diCQM treatment. Western blot analysis showed that 3,5-diCQM increased the phosphorylation of p38 mitogen-activated protein kinase and cAMP responsive element binding as well as the expression of microphthalmia-associated transcription factor. In addition, 3,5-diCQM-stimulated cAMP production, and 3,5-diCQM-induced tyrosinase activity and melanin synthesis were attenuated by H89, a protein kinase A inhibitor. These results suggested that 3,5-diCQM-mediated activation of the p38 pathway may represent a novel approach for an effective therapy for vitiligo and hair graying.


Keywords   methyl 3,5-di-caffeoylquinate (3,5-diCQM); melanogenesis; tyrosinase; microphthalmia-associated transcription factor (MITF); p38 mitogen-activated protein kinase (p38 MAPK)


Received   2015-1-7  


Funding  This work was supported by an endowment from Erina Co., Inc. (Tokyo, Japan) (No. 20140070).


* Correspondence address  Tel/Fax: +81-568-51-6189; E-mail: bycha@isc.chubu.ac.jp

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