Abstract

The mode of action of spent coffee grounds supercritical fluid CO2 extract (SFE) in melanogenesis has never been reported. In the study, the spent coffee grounds were extracted by the supercritical fluid CO2 extraction method; the chemical constituents of the SFE were investigated by gas chromatography-mass spectrometry (GC-MS). The effects of the SFE and its major fatty acid components on melanogenesis were evaluated by mushroom tyrosinase activity assay and determination of intracellular tyrosinase activity and melanin content. The expression level of melanogenesis-related proteins was analyzed by western blotting assay. The results revealed that the SFE of spent coffee grounds (1–10 mg/mL) and its major fatty acids such as linoleic acid and oleic acid (6.25–50 μM) effectively suppressed melanogenesis in the B16F10 murine melanoma cells. Furthermore, the SFE decreased the expression of melanocortin 1 receptor (MC1R), microphthalmia-associated transcription factor (MITF), tyrosinase, tyrosinase-related protein-1 (TRP-1), and tyrosinase-related protein-2 (TRP-2). The SFE also decreased the protein expression levels of p-JNK, p-p38, p-ERK, and p-CREB. Our results revealed that the SFE of spent coffee grounds attenuated melanogenesis in B16F10 cells by downregulation of protein kinase A (PKA), phosphatidylinositol-3-kinase (PI3K/Akt), and mitogen-activated protein kinases (MAPK) signaling pathways, which may be due to linoleic acid and oleic acid.

Highlights

  • Melanin is produced and secreted by melanocytes that are distributed in the basal layer of the skin epidermis [1]

  • It is predicted that linoleic acid and oleic acid in the supercritical fluid CO2 extract (SFE) may contribute to their antimelanogenic activities

  • The results indicate that 1–10 mg/mL of spent coffee grounds SFE treatment led to a reduced level of microphthalmiaassociated transcription factor (MITF), tyrosinase, tyrosinase-related protein1 (TRP-1), and tyrosinase-related protein-2 (TRP-2)

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Summary

Introduction

Melanin is produced and secreted by melanocytes that are distributed in the basal layer of the skin epidermis [1]. It is reported that accumulation of an excessive level of epidermal melanin resulted in various dermatological disorders. Those skin hyperpigmented syndromes include melasma, postinflammatory melanoderma, age spots, freckles, and sites of actinic damage [2]. The inhibitors of melanogenesis have been increasingly applied in skin care products for the treatment or prevention of skin hyperpigmented disorders [3]. It is well known that tyrosinase (EC 1.14.18.1) catalyzes the first two steps of melanin synthesis. It first hydroxylates L-tyrosine to L3, 4-dihydroxyphenylalanine (L-DOPA), and L-DOPA is further oxidized into the corresponding o-dopaquinone [4].

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