title: Light-emitting diodes at 830 and 850 nm inhibit melanin synthesis in vitro.
abstract: Treatment of hyperpigmentation remains a challenge. Because of the positive effects of low-energy Nd:YAG lasers on the treatment of melasma, it is suggested that laser-like light-emitting diodes (LEDs) can potentially ameliorate hyperpigmentation. We evaluated the effect of seven different LED wavelengths on melanogenesis. LED irradiation at 830 nm (dose-dependent, from 1 to 20 J/cm2) and 850 nm (1 J/cm2) significantly reduced melanin production and tyrosinase expression, not only in a normal human melanocyte monoculture both with and without forskolin stimulation but also in a three-dimensional multiple cell type culture. It reduced melanin content via inactivation of the apoptosis signal-regulating kinase and extracellular signal-regulated kinase 1/2 pathways. The level of phosphorylated cyclic AMP response element-binding protein was also decreased by LED irradiation. Moreover, LED irradiation reduced melanogenesis through decreased expression of tyrosinase family genes (tyrosinase-related protein-1 and 2, and microphthalmia-associated transcription factor). These results indicate that LEDs could potentially be used to treat melanin-overproducing skin conditions.
authors.affiliation: Dongguk University Research Institute of Biotechnology Medical Science Research Center, Gyeonggi-do, Korea.
authors.forename: Jeong Mo
authors.initials: JM
authors.lastname: Kim
authors.forename: Nan-Hyung
authors.initials: NH
authors.lastname: Kim
authors.forename: Yu Shun
authors.initials: YS
authors.lastname: Tian
authors.forename: Ai Young
authors.initials: AY
authors.lastname: Lee
mesh_terms: D002478:Cells, Cultured; D005576:Colforsin / Q000494:pharmacology; D000242:Cyclic AMP / Q000378:metabolism; D017362:Cyclic AMP Response Element-Binding Protein / Q000378:metabolism; D004307:Dose-Response Relationship, Radiation; D004789:Enzyme Activation; D006801:Humans; D019746:Intramolecular Oxidoreductases / Q000378:metabolism; D054023:Lasers, Semiconductor; D020930:MAP Kinase Kinase Kinases / Q000378:metabolism; D008543:Melanins / Q000096:biosynthesis*; D008544:Melanocytes / Q000187:drug effects / Q000378:metabolism / Q000528:radiation effects*; D008562:Membrane Glycoproteins / Q000378:metabolism; D051739:Microphthalmia-Associated Transcription Factor / Q000378:metabolism; D019950:Mitogen-Activated Protein Kinase 1 / Q000378:metabolism; D048052:Mitogen-Activated Protein Kinase 3 / Q000378:metabolism; D014442:Monophenol Monooxygenase / Q000378:metabolism; D010088:Oxidoreductases / Q000378:metabolism; D010766:Phosphorylation; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism; D015398:Signal Transduction / Q000528:radiation effects; D012880:Skin Pigmentation / Q000187:drug effects / Q000528:radiation effects*
chemical_list: C115163:CREB1 protein, human; D017362:Cyclic AMP Response Element-Binding Protein; C497234:MITF protein, human; D008543:Melanins; D008562:Membrane Glycoproteins; D051739:Microphthalmia-Associated Transcription Factor; D005576:Colforsin; D000242:Cyclic AMP; D010088:Oxidoreductases; C489799:TYRP1 protein, human; D014442:Monophenol Monooxygenase; D051057:Proto-Oncogene Proteins c-akt; C535150:MAPK1 protein, human; D019950:Mitogen-Activated Protein Kinase 1; D048052:Mitogen-Activated Protein Kinase 3; D020930:MAP Kinase Kinase Kinases; D019746:Intramolecular Oxidoreductases; C042501:dopachrome isomerase