Abstract
Ultraviolet irradiation-induced hyperpigmentation of the skin is associated with excessive melanin production in melanocytes. Tyrosinase (TYR) is a key enzyme catalyzing the rate-limiting step in melanogenesis. TYR expression is controlled by microphthalmia-associated transcription factor (MITF) expression. Sorghum is a cereal crop widely used in a variety of foods worldwide. Sorghum contains many bioactive compounds and is beneficial to human health. However, the effects of sorghum in anti-melanogenesis have not been well characterized. In this study, the biological activity of sorghum ethanolic extract (SEE) on α-melanocyte-stimulating hormone (α-MSH)-induced TYR expression was evaluated in B16F10 melanoma cells. SEE attenuated α-MSH-induced TYR gene promoter activity through the downregulation of the transcription factor MITF. We found that paired box gene 3 (Pax3) contributes to the maximal induction of MITF gene promoter activity. Further analysis demonstrated that SEE inhibited α-MSH-induced Pax3 expression. The collective results indicate that SEE attenuates α-MSH-induced TYR expression through the suppression of Pax3-mediated MITF gene promoter activity. Targeting the Pax3-MITF axis pathway could be considered a potential strategy to increase the efficacy of anti-melanogenesis.
Highlights
Melanin in the skin is a natural pigment induced by ultraviolet (UV) radiation of solar light
Activated melanocortin-1 receptor (MC1R) triggers the stimulation of adenylate cyclase and subsequently increases the cyclic adenosine monophosphate level, leading to the activation of cAMP-dependent protein kinase (PKA), which in turn phosphorylates the transcription factor cAMP response element-binding protein (CREB) [2,3]
To evaluate the effect of sorghum ethanolic extract (SEE) on TYR expression, B16F10 cells were pre-treated with SEE before stimulation with α-melanocyte-stimulating hormone (α-MSH), and TYR protein levels were examined using immunoblot analysis
Summary
Melanin in the skin is a natural pigment induced by ultraviolet (UV) radiation of solar light. Activated MC1R triggers the stimulation of adenylate cyclase and subsequently increases the cyclic adenosine monophosphate (cAMP) level, leading to the activation of cAMP-dependent protein kinase (PKA), which in turn phosphorylates the transcription factor cAMP response element-binding protein (CREB) [2,3]. The phosphorylated CREB becomes active and binds to the cAMP response element (CRE) site within the promoter region of the microphthalmia-associated transcription factor (MITF) gene, a master regulator of melanogenesis [2]. The accumulated MITF protein activates the transcription of several genes involved in melanin biosynthesis, including tyrosinase (TYR), tyrosinase-related protein 1 (TRP1), and tyrosinase-related protein 2 (TRP2, known as dopachrome tautomerase) [4]. Various TYR inhibitors are widely used in skin depigmentation [11]
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