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首页> 外文期刊>Life sciences >The activation of melanogenesis by p-CREB and MITF signaling with extremely low-frequency electromagnetic fields on B16F10 melanoma
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The activation of melanogenesis by p-CREB and MITF signaling with extremely low-frequency electromagnetic fields on B16F10 melanoma

机译:p-CREB和MITF信号通过极低频电磁场激活B16F10黑色素瘤的黑色素生成

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Melanin in the skin determines the skin color, and decreased melanin causes many hypopigmentation disorders and increased damage to skin by ultraviolet B (UVB) light irradiation. Here, we stimulate melanogenesis in B16F10 melanoma cells by using specific frequencies of ELF-EMFs. In this study, we focus on the melanogenesis of EMF-ELFs and find that 60-75 Hz ELF-EMFs upregulate melanin synthesis by stimulated expression of tyrosinase and TRP-1 through inhibition of phosphorylation ERK, activation of CREB, and MITF up-regulation in B16F10 melanoma cells. The results show that 60-75 Hz ELF-EMFs significantly increase secreted melanin, cellular melanin content, and tyrosinase activity, and the cell mitochondria activity, cell viability, and cell membrane condition are unchanged. Furthermore, the protein expression level of MITF and p-CREB signaling pathway are significantly increased. Moreover, 60 Hz ELF-EMFs reduce the phosphorylate of ERK in B16F10 melanoma cells. These findings indicate that stimulation of melanogenesis by using ELF-EMFs has therapeutic potential for treating hypopigmentation disorders such as vitiligo. (C) 2016 The Authors. Published by Elsevier Inc. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
机译:皮肤中的黑色素决定皮肤的颜色,黑色素的减少会导致许多色素沉着障碍,并受到紫外线B(UVB)光照射对皮肤的伤害增加。在这里,我们通过使用特定频率的ELF-EMF刺激B16F10黑色素瘤细胞中的黑色素生成。在这项研究中,我们专注于EMF-ELF的黑色素生成,发现60-75 Hz ELF-EMFs通过抑制磷酸化ERK,激活CREB和MITF上调,通过刺激酪氨酸酶和TRP-1的表达来上调黑色素的合成。在B16F10黑色素瘤细胞中结果表明,60-75 Hz ELF-EMFs显着增加了分泌的黑色素,细胞黑色素含量和酪氨酸酶活性,而细胞线粒体活性,细胞活力和细胞膜条件均未改变。此外,MITF和p-CREB信号通路的蛋白质表达水平显着增加。此外,60 Hz ELF-EMF可以减少B16F10黑色素瘤细胞中ERK的磷酸化。这些发现表明,通过使用ELF-EMF刺激黑素生成具有治疗色素沉着障碍(如白癜风)的治疗潜力。 (C)2016作者。由Elsevier Inc.发行。这是CC BY-NC-ND许可下的开放获取文章(http://creativecommons.org/licenses/by-nc-nd/4.0/)。

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