Abstract
We investigated the potential melanogenic effect of compounds from Zingiber cassumunar Roxb. Our data revealed that chloroform-soluble extract of Z. cassumunar enhanced melanin synthesis in B16F10 melanoma cells. Among the components of the chloroform extract, (E)-4-(3,4-dimethoxyphenyl)but-3-en-1-ol (DMPB) increased melanogenesis in both B16F10 cells and human primary melanocytes. In B16F10 cells, DMPB enhanced the activation of ERK and p38, and the level of tyrosinase. Although the level of microphthalmia-associated transcription factor was unchanged in DMPB-treated B16F10 cells, DMPB increased levels and nuclear localization of upstream stimulating factor-1 (USF1). Consistently, DMPB-mediated melanin synthesis was diminished in USF1-knockdown cells. Furthermore, DMPB induced hyperpigmentation in brown guinea pigs in vivo. Together, these data suggest that DMPB may promote melanin synthesis via USF1 dependent fashion and could be used as a clinical therapeutic agent against hypopigmentation-associated diseases.
Highlights
Melanin, which is synthesized in the melanosomes of melanocytes, serves a number of valuable functions, such as determining the appearance of the skin and protecting it from the harmful effects of ultra violet (UV) radiation, toxic drugs and chemicals [1]
We provide the first evidence that DMPB isolated from Z. cassumunar stimulates melanin synthesis via the extracellular signal-regulated kinase (ERK) and p38 mitogen-activated protein kinase (MAPK) signaling pathways
The DMPB-induced melanogenic response in B16F10 cells was comparable to that induced by α-MSH treatment
Summary
Melanin, which is synthesized in the melanosomes of melanocytes, serves a number of valuable functions, such as determining the appearance of the skin and protecting it from the harmful effects of ultra violet (UV) radiation (and skin cancer), toxic drugs and chemicals [1]. A number of natural products have been reported to inhibit melanogenesis by regulating melanogenic enzymes, including Hoelen extracts [8], sesamol (3,4-methylenedioxyphenol) [9]. Arthrophytum scoparium extract [10], Caffeoylserotonin [11] and the aqueous fraction from Cuscuta japonica [12] have been shown to inhibit melanogenesis by regulating MITF. These agents have all been used to develop anti-melanogenic agents for the treatment of hyperpigmentation disorders. Rosmarinic acid promotes expression of tyrosinase by activating PKA/ CREB pathway They have been suggested as photo-protecting and pro-melanogenic agents. We investigated the effects of Z. cassumunar on melanogenesis
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