Lotus Sprout Extract Induces Selective Melanosomal Autophagy and Reduces Pigmentation.

autophagy hyperpigmentation melanin melanogenesis melanosomes

Journal

Journal of cosmetic dermatology
ISSN: 1473-2165
Titre abrégé: J Cosmet Dermatol
Pays: England
ID NLM: 101130964

Informations de publication

Date de publication:
21 Sep 2024
Historique:
revised: 29 08 2024
received: 09 04 2024
accepted: 03 09 2024
medline: 21 9 2024
pubmed: 21 9 2024
entrez: 21 9 2024
Statut: aheadofprint

Résumé

Hyperpigmentation disorders are caused by the excess production and irregular accumulation of melanin. Existing treatments often have limited efficacy and adverse effects, necessitating the development of new skin-brightening agents. Lotus sprout extract (LSE) was identified as a potential pigment-correcting agent. However, the active compounds responsible for driving mechanisms related to this activity remain unknown. This study aimed to investigate the effects of LSE and its active components, neferine and liensinine, on melanin accumulation and to understand how LSE reduces skin pigmentation. Melanin accumulation was analyzed in MNT-1 human melanoma cells and MelanoDerm human skin equivalents following neferine, liensinine, or LSE treatment. The effects of the compounds on different pathways regulating melanin levels were evaluated by gene expression, biochemical assays, and western blotting. Melanosome ultrastructure was monitored using transmission electron microscopy (TEM). Neferine and liensinine reduced melanin accumulation in MNT-1 cells without downregulating melanogenesis-related genes or inhibiting tyrosinase activity. Instead, these compounds increased autophagic flux, suggesting that the reduction in pigmentation was due to increased melanin degradation. LSE also reduced melanin accumulation and activated autophagy in normal human melanocytes and MelanoDerm tissue. Autophagosomes induced by LSE treatment contained only melanosomes, and structural changes in melanosomes suggested that LSE may disrupt melanosome maturation. This study revealed a novel mechanism for LSE, neferine, and liensinine in reducing pigmentation, potentially through the induction of autophagy and subsequent melanosome degradation. These findings suggest that LSE and its enriched bioactive compounds could be promising agents for treating hyperpigmentation.

Sections du résumé

BACKGROUND BACKGROUND
Hyperpigmentation disorders are caused by the excess production and irregular accumulation of melanin. Existing treatments often have limited efficacy and adverse effects, necessitating the development of new skin-brightening agents. Lotus sprout extract (LSE) was identified as a potential pigment-correcting agent. However, the active compounds responsible for driving mechanisms related to this activity remain unknown.
AIMS OBJECTIVE
This study aimed to investigate the effects of LSE and its active components, neferine and liensinine, on melanin accumulation and to understand how LSE reduces skin pigmentation.
METHODS METHODS
Melanin accumulation was analyzed in MNT-1 human melanoma cells and MelanoDerm human skin equivalents following neferine, liensinine, or LSE treatment. The effects of the compounds on different pathways regulating melanin levels were evaluated by gene expression, biochemical assays, and western blotting. Melanosome ultrastructure was monitored using transmission electron microscopy (TEM).
RESULTS RESULTS
Neferine and liensinine reduced melanin accumulation in MNT-1 cells without downregulating melanogenesis-related genes or inhibiting tyrosinase activity. Instead, these compounds increased autophagic flux, suggesting that the reduction in pigmentation was due to increased melanin degradation. LSE also reduced melanin accumulation and activated autophagy in normal human melanocytes and MelanoDerm tissue. Autophagosomes induced by LSE treatment contained only melanosomes, and structural changes in melanosomes suggested that LSE may disrupt melanosome maturation.
CONCLUSION CONCLUSIONS
This study revealed a novel mechanism for LSE, neferine, and liensinine in reducing pigmentation, potentially through the induction of autophagy and subsequent melanosome degradation. These findings suggest that LSE and its enriched bioactive compounds could be promising agents for treating hyperpigmentation.

Identifiants

pubmed: 39305105
doi: 10.1111/jocd.16587
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Informations de copyright

© 2024 The Author(s). Journal of Cosmetic Dermatology published by Wiley Periodicals LLC.

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Auteurs

Mikhail Geyfman (M)

Allergan Aesthetics, An AbbVie Company, Irvine, California, USA.

Robin Chung (R)

Allergan Aesthetics, An AbbVie Company, Irvine, California, USA.

Raymond Boissy (R)

University of Cincinnati, Cincinnati, Ohio, USA.

Neil Poloso (N)

Allergan Aesthetics, An AbbVie Company, Irvine, California, USA.

Kuniko Kadoya (K)

Allergan Aesthetics, An AbbVie Company, Irvine, California, USA.

Prithwiraj Maitra (P)

Allergan Aesthetics, An AbbVie Company, Irvine, California, USA.

Rahul Mehta (R)

Allergan Aesthetics, An AbbVie Company, Irvine, California, USA.

Classifications MeSH