Partially purified Curcuma longa inhibits alpha-melanocyte-stimulating hormone-stimulated melanogenesis through extracellular signal-regulated kinase or Akt activation-mediated signalling in B16F10 cells

Exp Dermatol. 2009 Aug;18(8):689-94. doi: 10.1111/j.1600-0625.2009.00857.x. Epub 2009 Mar 7.

Abstract

Bioassay-guided fractionation of Curcuma longa by solvent partitioning and purification with octadecylsilane open column chromatography yielded a partial purification. The active 80% methanol chromatographic fraction from the ethyl acetate layer [partial purification from C. longa (PPC)] was used to investigate the alpha-melanocyte-stimulating hormone (alpha-MSH)-stimulated melanogenesis signal pathway in B16F10 cells. In cells stimulated alpha-MSH, PPC inhibited cellular melanin contents, tyrosinase activity and expression of melanogenesis-related proteins including microphthalmia-associated transcription factor (MITF), tyrosinase and tyrosinase-related proteins (TRP). Melanogenesis-regulating signalling such as mitogen-activated protein kinase (MEK)/extracellular signal-regulated kinase (ERK) and phosphatidylinositol 3-kinase (PI3K)/Akt was activated by PPC in alpha-MSH-stimulated B16F10 cells. The suppressive activity of PPC on alpha-MSH-induced melanogenesis was abrogated by selective inhibition of MEK/ERK (PD98059) and PI3K (LY294002). MEK/ERK or Akt activation by PPC may contribute to reduced melanin synthesis via MITF and its downstream signal pathway including tyrosinase and TRPs in alpha-MSH-induced melanogenesis.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Curcuma / metabolism*
  • Enzyme Activation
  • Enzyme Inhibitors / pharmacology
  • Extracellular Signal-Regulated MAP Kinases / metabolism*
  • Gene Expression Regulation, Neoplastic*
  • Melanins / biosynthesis
  • Melanocytes / metabolism*
  • Melanoma, Experimental
  • Mice
  • Microphthalmia-Associated Transcription Factor / metabolism
  • Monophenol Monooxygenase / metabolism
  • Plant Extracts / pharmacology
  • Proto-Oncogene Proteins c-akt / metabolism*
  • Signal Transduction
  • alpha-MSH / metabolism*

Substances

  • Enzyme Inhibitors
  • Melanins
  • Microphthalmia-Associated Transcription Factor
  • Mitf protein, mouse
  • Plant Extracts
  • alpha-MSH
  • Monophenol Monooxygenase
  • Proto-Oncogene Proteins c-akt
  • Extracellular Signal-Regulated MAP Kinases