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Molecules 2013, 18(12), 15724-15736; doi:10.3390/molecules181215724
Article

Madecassoside Inhibits Melanin Synthesis by Blocking Ultraviolet-Induced Inflammation

1
,
1
,
1
,
1
,
2
 and
1,*
1 Biospectrum Life Science Institute, Eines Platz 11th FL, 442-13 Sangdaewon Dong, Seongnam City, 462-807 Gyunggi Do, Korea 2 Dermiskin Life Science Institute, 44-9 Cheongho Ri, Pyeongtaek City, 451-862 Gyunggi Do, Korea
* Author to whom correspondence should be addressed.
Received: 29 October 2013 / Revised: 10 December 2013 / Accepted: 11 December 2013 / Published: 16 December 2013
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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.
Keywords: post-inflammatory pigmentation; madecassoside; PAR-2; UVR post-inflammatory pigmentation; madecassoside; PAR-2; UVR
This is an open access article distributed under the Creative Commons Attribution License (CC BY 3.0).

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Jung, E.; Lee, J.-A.; Shin, S.; Roh, K.-B.; Kim, J.-H.; Park, D. Madecassoside Inhibits Melanin Synthesis by Blocking Ultraviolet-Induced Inflammation. Molecules 2013, 18, 15724-15736.

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