Autor: |
Lee, Ki won, Ryu, Hyung Won, Oh, Sang‐seok, Park, Soojong, Madhi, Hamadi, Yoo, Jiyun, Park, Ki‐Hun, Kim, Kwang Dong |
Předmět: |
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Zdroj: |
Experimental Dermatology; Jul2017, Vol. 26 Issue 7, p585-591, 10p |
Abstrakt: |
Melanogenesis is a key pathway for the regulation of skin pigmentation and the development of skin-lightening/skin-whitening drugs or cosmetics. In this study, we found that β-mangostin from seedcases of Garcinia mangostana inhibited α-melanocyte-stimulating hormone (α- MSH)-mediated melanogenesis in B16F10 melanoma cells and a three-dimensional human skin model. β-Mangostin significantly inhibited the protein level of tyrosinase induced by α- MSH in UPS (ubiquitin proteasome system)-independent and lysosome-dependent manner. The inhibition of autophagy by 3-methyladenine treatment or ATG5 knockdown effectively recovered premelanosome protein as well as tyrosinase degraded by the β-mangostin treatment. However, rapamycin, a representative non-selective autophagy inducer, triggered autophagy in α- MSH-stimulated cells, which was characterized by a considerable decrease in p62, but it was unable to inhibit melanogenesis. Melanosome-engulfing autophagosomes were observed using transmission electron microscopy. Furthermore, previously formed melanin could be degraded effectively in an autophagy-dependent manner in β-mangostin-treated cells. Taken together, our results suggest that β-mangostin inhibits the melanogenesis induced by α- MSH via an autophagy-dependent mechanism, and thus, the depigmentation effect of β-mangostin may depend on autophagy targeted at the melanosome rather than non-selective autophagy. [ABSTRACT FROM AUTHOR] |
Databáze: |
Complementary Index |
Externí odkaz: |
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