[6]-Shogaol Inhibits α-MSH-Induced Melanogenesis through the Acceleration of ERK and PI3KAkt-Mediated MITF Degradation

Abstract EN

[6]-Shogaol is the main biologically active component of ginger.

Previous reports showed that [6]-shogaol has several pharmacological characteristics, such as antioxidative, anti-inflammatory, antimicrobial, and anticarcinogenic properties.

However, the effects of [6]-shogaol on melanogenesis remain to be elucidated.

The study aimed to evaluate the potential skin whitening mechanisms of [6]-shogaol.

The effects of [6]-shogaol on cell viability, melanin content, tyrosinase activity, and the expression of the tyrosinase and microphthalmia-associated transcription factor (MITF) were measured.

The results revealed that [6]-shogaol effectively suppresses tyrosinase activity and the amount of melanin and that those effects are more pronounced than those of arbutin.

It was also found that [6]-shogaol decreased the protein expression levels of tyrosinase-related protein 1 (TRP-1) and microphthalmia-associated transcriptional factor (MITF).

In addition, the MITF mRNA levels were also effectively decreased in the presence of 20 μM [6]-shogaol.

The degradation of MITF protein was inhibited by the MEK 1-inhibitor (U0126) or phosphatidylinositol-3-kinase inhibitor (PI3K inhibitor) (LY294002).

Further immunofluorescence staining assay implied the involvement of the proteasome in the downregulation of MITF by [6]-shogaol.

Our confocal assay results also confirmed that [6]-shogaol inhibited α-melanocyte stimulating hormone- (α-MSH-) induced melanogenesis through the acceleration of extracellular responsive kinase (ERK) and phosphatidylinositol-3-kinase- (PI3K/Akt-) mediated MITF degradation.