Photobiomodulation Using 830 nm Lighting-Emitting Diode Inhibits Melanogenesis via FOXO3a in Human Melanocyte

IF 3.9 3区 医学 Q2 CELL BIOLOGY
Yanjun Dan, Li Chen, Shanglin Jin, Xiaoxue Xing, Yijian Zhu, Min Jiang, Chengfeng Zhang, Leihong Flora Xiang
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Abstract

Photobiomodulation (PBM) using 830 nm light-emitting diode (LED) benefits tissue regeneration, wound healing and neural stimulation. However, there is not much exploration of its effect on melanocytes and ex vivo skin model. This study aims to investigate the mechanism behind the anti-melanogenic activity of 830 nm LED and provides evidence for its activity in human ex vivo skin model. Our results showed that 830 nm LED at fluences ranging from 5 to 20 J/cm2 inhibited melanosome maturation and reduced melanin content, tyrosinase activity and melanogenesis-related proteins. 830 nm LED inhibited the phosphorylation of AKT and its downstream FOXO3a, leading to nuclear translocation of FOXO3a. Furthermore, FOXO3a knockdown and AKT activator like SC79 could reverse the melanogenesis inhibition phenotype induced by 830 nm LED. In human ex vivo skin model, Fontana–Masson staining revealed a decrease in epidermal basal pigmentation after 830 nm LED irradiation. Taken together, 830 nm LED demonstrated the anti-melanogenic activity via FOXO3a.

Abstract Image

使用 830 纳米发光二极管进行光生物调节可通过 FOXO3a 抑制人类黑色素细胞的黑色素生成
使用 830 纳米发光二极管(LED)进行光生物调制(PBM)有利于组织再生、伤口愈合和神经刺激。然而,有关其对黑色素细胞和体外皮肤模型影响的研究还不多。本研究旨在探究 830 纳米 LED 抗黑色素生成活性的机制,并为其在人体体外皮肤模型中的活性提供证据。我们的研究结果表明,830 nm LED 在 5 到 20 J/cm2 的通量范围内可抑制黑色素小体的成熟,降低黑色素含量、酪氨酸酶活性和黑色素生成相关蛋白。830 nm LED抑制了AKT及其下游FOXO3a的磷酸化,导致FOXO3a的核转位。此外,FOXO3a基因敲除和AKT激活剂(如SC79)可以逆转830 nm LED诱导的黑色素生成抑制表型。在人体体外皮肤模型中,Fontana-Masson 染色显示,830 nm LED 照射后表皮基底色素沉着减少。综上所述,830 纳米 LED 通过 FOXO3a 显示了抗黑色素生成的活性。
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来源期刊
Pigment Cell & Melanoma Research
Pigment Cell & Melanoma Research 医学-皮肤病学
CiteScore
8.90
自引率
2.30%
发文量
54
审稿时长
6-12 weeks
期刊介绍: Pigment Cell & Melanoma Researchpublishes manuscripts on all aspects of pigment cells including development, cell and molecular biology, genetics, diseases of pigment cells including melanoma. Papers that provide insights into the causes and progression of melanoma including the process of metastasis and invasion, proliferation, senescence, apoptosis or gene regulation are especially welcome, as are papers that use the melanocyte system to answer questions of general biological relevance. Papers that are purely descriptive or make only minor advances to our knowledge of pigment cells or melanoma in particular are not suitable for this journal. Keywords Pigment Cell & Melanoma Research, cell biology, melatonin, biochemistry, chemistry, comparative biology, dermatology, developmental biology, genetics, hormones, intracellular signalling, melanoma, molecular biology, ocular and extracutaneous melanin, pharmacology, photobiology, physics, pigmentary disorders
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