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ERK Activation by Fucoidan Leads to Inhibition of Melanogenesis in Mel-Ab Cells
The Korean Journal of Physiology and Pharmacology ; : 29-34, 2015.
Artículo en Inglés | WPRIM | ID: wpr-727829
ABSTRACT
Fucoidan, a fucose-rich sulfated polysaccharide derived from brown seaweed in the class Phaeophyceae, has been widely studied for its possible health benefits. However, the potential of fucoidan as a possible treatment for hyperpigmentation is not fully understood. This study investigated the effects of fucoidan on melanogenesis and related signaling pathways using Mel-Ab cells. Fucoidan significantly decreased melanin content. While fucoidan treatment decreased tyrosinase activity, it did not do so directly. Western blot analysis indicated that fucoidan downregulated microphthalmia-associated transcription factor and reduced tyrosinase protein expression. Further investigation showed that fucoidan activated the extracellular signal-regulated kinase (ERK) pathway, suggesting a possible mechanism for the inhibition of melanin synthesis. Treatment with PD98059, a specific ERK inhibitor, resulted in the recovery of melanin production. Taken together, these findings suggest that fucoidan inhibits melanogenesis via ERK phosphorylation.
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Texto completo: Disponible Índice: WPRIM (Pacífico Occidental) Asunto principal: Fosforilación / Fosfotransferasas / Algas Marinas / Western Blotting / Monofenol Monooxigenasa / Hiperpigmentación / Phaeophyceae / Factor de Transcripción Asociado a Microftalmía / Beneficios del Seguro / Melaninas Idioma: Inglés Revista: The Korean Journal of Physiology and Pharmacology Año: 2015 Tipo del documento: Artículo

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Texto completo: Disponible Índice: WPRIM (Pacífico Occidental) Asunto principal: Fosforilación / Fosfotransferasas / Algas Marinas / Western Blotting / Monofenol Monooxigenasa / Hiperpigmentación / Phaeophyceae / Factor de Transcripción Asociado a Microftalmía / Beneficios del Seguro / Melaninas Idioma: Inglés Revista: The Korean Journal of Physiology and Pharmacology Año: 2015 Tipo del documento: Artículo