Isoliquiritigenin inhibits melanogenesis, melanocyte dendricity and melanosome transport by regulating ERK-mediated MITF degradation.


Journal

Experimental dermatology
ISSN: 1600-0625
Titre abrégé: Exp Dermatol
Pays: Denmark
ID NLM: 9301549

Informations de publication

Date de publication:
02 2020
Historique:
received: 27 06 2019
revised: 05 11 2019
accepted: 25 11 2019
pubmed: 1 12 2019
medline: 16 6 2021
entrez: 1 12 2019
Statut: ppublish

Résumé

Isoliquiritigenin (ISL), a flavonoid component from the hydrolysis products of licorice root. It has been reported that ISL inhibited melanogenesis by suppressing the tyrosinase activity in human melanocytes. Recently, ISL was found to induce melanin degradation in human epidermal keratinocytes. However, the role of ISL in pigmentation is not fully understood. In the current study, we aimed to investigate the effects of ISL on pigmentation, and further explored the underlying mechanism. Our results suggested that ISL suppressed basal and α-MSH-, ACTH- and UV-induced melanin synthesis, in addition to inhibiting melanocyte dendricity and melanosome transport. ISL played these roles mainly by activating the extracellular signal-regulated protein kinase pathway. Once activated, it induced microphthalmia-associated transcription factor degradation and decreased the expression of tyrosinase, TRP-1, DCT, Rab27a and Cdc42, finally inhibited melanogenesis, melanocyte dendricity and melanosome transport. Our findings suggested that ISL exhibited no cytotoxicity in our research, it may prove quite useful as a safer natural skin-whitening agent.

Identifiants

pubmed: 31785162
doi: 10.1111/exd.14066
doi:

Substances chimiques

Chalcones 0
Enzyme Inhibitors 0
Melanins 0
Microphthalmia-Associated Transcription Factor 0
alpha-MSH 581-05-5
Adrenocorticotropic Hormone 9002-60-2
isoliquiritigenin B9CTI9GB8F
Monophenol Monooxygenase EC 1.14.18.1
PRSS1 protein, human EC 3.4.21.4
Trypsin EC 3.4.21.4
Intramolecular Oxidoreductases EC 5.3.-
dopachrome isomerase EC 5.3.3.12

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

149-157

Subventions

Organisme : The Fund of Changzhou Sci&Tech Program
ID : CJ20180007
Pays : International

Informations de copyright

© 2019 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.

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Auteurs

Jinpeng Lv (J)

College of Pharmaceutical Engineering and Life Sciences, Changzhou University, Changzhou, China.
Shanghai Institute of Pharmaceutical Industry, Shanghai, China.
Yabang Medical Research Institute, Changzhou, China.

Ying Fu (Y)

College of Pharmaceutical Engineering and Life Sciences, Changzhou University, Changzhou, China.

Yan Cao (Y)

Department of Dermatology, The Affiliated Changzhou No. 2 People's Hospital of Nanjing Medical University, Changzhou, China.

Songzhou Jiang (S)

College of Pharmaceutical Engineering and Life Sciences, Changzhou University, Changzhou, China.

Ying Yang (Y)

College of Pharmaceutical Engineering and Life Sciences, Changzhou University, Changzhou, China.

Guoqiang Song (G)

College of Pharmaceutical Engineering and Life Sciences, Changzhou University, Changzhou, China.

Changjun Yun (C)

Changzhou Wujin People's Hospital, Changzhou, China.

Rongyin Gao (R)

Department of Pharmacy, The First people's Hospital of Changzhou, The Third Affiliated Hospital of Soochow University, Changzhou, China.

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