Abstract
The effects of essential oil from Eucalyptus camaldulensis flowers oil on melanogenesis and the oil’s antioxidant characteristics were investigated. Assays of mushroom and cellular tyrosinase activities and melanin content of mouse melanoma cells were performed spectrophotometrically, and the expression of melanogenesis-related proteins was determined by Western blotting. The possible signaling pathways involved in essential oil-mediated depigmentation were also investigated using specific protein kinase inhibitors. The results revealed that E. camaldulensis flower essential oil effectively suppresses intracellular tyrosinase activity and decreases melanin amount in B16F10 mouse melanoma cells. The essential oil also exhibits antioxidant properties and effectively decreases intracellular reactive oxygen species (ROS) levels. The volatile chemical composition of the essential oil was analyzed with gas chromatography–mass spectrometry (GC/MS). The chemical constituents in the essential oil are predominately oxygenated monoterpenes (34.9%), followed by oxygenated sesquiterpenes (31.8%), monoterpene hydrocarbons (29.0%) and sesquiterpene hydrocarbons (4.3%). Our results indicated that E. camaldulensis flower essential oil inhibits melanogenesis through its antioxidant properties and by down-regulating both mitogen-activated protein kinases (MAPK) and protein kinase A (PKA) signaling pathways. The present study indicates that the essential oil has the potential to be developed into a skin care product.
Highlights
Melanin is responsible for skin coloration and protects the skin from damage induced by ultraviolet (UV) light
The results indicated that the JNK-mediated signaling pathway, which is involved in melanin production, was affected by E. camaldulensis flower essential oil
Differences were considered as statistically significant for p < 0.05. This is the first report regarding the effect of E. camaldulensis flower essential oil on melanin production
Summary
Melanin is responsible for skin coloration and protects the skin from damage induced by ultraviolet (UV) light. UV-induced skin hyperpigmentation causes abnormal melanin production and accumulation [1]. Several skin hyperpigmentation disorders such as freckles, age spots, melasma, post-inflammatory melanoderma and other hyperpigmentation syndromes are the result of abnormal melanin accumulation [3]. Many tyrosinase inhibitors such as kojic acid [4], arbutin [5] and azelaic acid [6] are used in skin whitening products to prevent or treat abnormal skin pigmentation [7]. It has been reported that whitening products with chemical skin depigmenting agents can have significant side effects, including pigmented contact dermatitis caused by kojic acid [8], genotoxicity caused by arbutin [9] and transient erythema or skin irritation caused by azelaic acid [10]. The search for an effective and safe skin depigmenting agent is still ongoing in the field of cosmetic research and development
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