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Madecassoside inhibits melanin synthesis by blocking ultraviolet-induced inflammation.
Jung, Eunsun; Lee, Jung-A; Shin, Seoungwoo; Roh, Kyung-Baeg; Kim, Jang-Hyun; Park, Deokhoon.
Afiliación
  • Park D; Biospectrum Life Science Institute, Eines Platz 11th FL, 442-13 Sangdaewon Dong, Seongnam City, 462-807 Gyunggi Do, Korea. pdh@biospectrum.com.
Molecules ; 18(12): 15724-36, 2013 Dec 16.
Article en En | MEDLINE | ID: mdl-24352025
ABSTRACT
Madecassoside (MA), a pentacyclic triterpene isolated from Centella asitica (L.), is used as a therapeutic agent in wound healing and also as an anti-inflammatory and anti-aging agent. However, the involvement of MA in skin-pigmentation has not been reported. This study was conducted to investigate the effects of MA on ultraviolet (UV)-induced melanogenesis and mechanisms in a co-culture system of keratinocytes and melanocytes. MA significantly inhibited UVR-induced melanin synthesis and melanosome transfer in the co-culture system. These effects were further demonstrated by the MA-induced inhibition of protease-activated receptor-2 expression and its signaling pathway, cyclooxygenase-2, prostaglandin E2 and prostaglandin F2 alpha in keratinocytes. The clinical efficacy of MA was confirmed on artificially tanned human skin. MA significantly reduced UV-induced melanin index at 8 weeks after topical application. Overall, the study demonstrated significant benefits of MA use in the inhibition of hyperpigmentation caused by UV irradiation.
Asunto(s)

Texto completo: 1 Colección: 01-internacional Banco de datos: MEDLINE Asunto principal: Triterpenos / Rayos Ultravioleta / Vías Biosintéticas / Inflamación / Melaninas Límite: Humans Idioma: En Revista: Molecules Asunto de la revista: BIOLOGIA Año: 2013 Tipo del documento: Article

Texto completo: 1 Colección: 01-internacional Banco de datos: MEDLINE Asunto principal: Triterpenos / Rayos Ultravioleta / Vías Biosintéticas / Inflamación / Melaninas Límite: Humans Idioma: En Revista: Molecules Asunto de la revista: BIOLOGIA Año: 2013 Tipo del documento: Article