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N-(4-甲氧基苯基)咖啡酰胺诱导的黑色素生成抑制机制。

N-(4-methoxyphenyl) caffeamide-induced melanogenesis inhibition mechanisms.

作者信息

Kuo Yueh-Hsiung, Chen Chien-Chia, Wu Po-Yuan, Wu Chin-Sheng, Sung Ping-Jyun, Lin Chien-Yih, Chiang Hsiu-Mei

机构信息

Department of Chinese Pharmaceutical Sciences and Chinese Medicine Resources, China Medical University, Taichung, 404, Taiwan.

Department of Biotechnology, Asia University, Taichung, 413, Taiwan.

出版信息

BMC Complement Altern Med. 2017 Jan 23;17(1):71. doi: 10.1186/s12906-016-1554-6.

DOI:10.1186/s12906-016-1554-6
PMID:28114924
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5259883/
Abstract

BACKGROUND

The derivative of caffeamide exhibits antioxidant and antityrosinase activity. The activity and mechanism of N-(4-methoxyphenyl) caffeamide (K36E) on melanogenesis was investigated.

METHODS

B16F0 cells were treated with various concentrations of K36E; the melanin contents and related signal transduction were studied. Western blotting assay was applied to determine the protein expression, and spectrophotometry was performed to identify the tyrosinase activity and melanin content.

RESULTS

Our results indicated that K36E reduced α-melanocyte-stimulating hormone (α-MSH)-induced melanin content and tyrosinase activity in B16F0 cells. In addition, K36E inhibited the expression of phospho-cyclic adenosine monophosphate (cAMP)-response element-binding protein, microphthalmia-associated transcription factor (MITF), tyrosinase, and tyrosinase-related protein-1 (TRP-1). K36E activated the phosphorylation of protein kinase B (AKT) and glycogen synthase kinase 3 beta (GSK3β), leading to the inhibition of MITF transcription activity. K36E attenuated α-MSH induced cAMP pathways, contributing to hypopigmentation.

CONCLUSIONS

K36E regulated melanin synthesis through reducing the expression of downstream proteins including p-CREB, p-AKT, p-GSK3β, tyrosinase, and TRP-1, and activated the transcription factor, MITF. K36E may have the potential to be developed as a skin whitening agent.

摘要

背景

咖啡酰胺衍生物具有抗氧化和抗酪氨酸酶活性。研究了N-(4-甲氧基苯基)咖啡酰胺（K36E）对黑色素生成的活性及机制。

方法

用不同浓度的K36E处理B16F0细胞；研究黑色素含量及相关信号转导。采用蛋白质印迹法检测蛋白质表达，用分光光度法测定酪氨酸酶活性和黑色素含量。

结果

我们的结果表明，K36E可降低α-黑素细胞刺激素（α-MSH）诱导的B16F0细胞中黑色素含量和酪氨酸酶活性。此外，K36E抑制磷酸化环磷酸腺苷（cAMP）反应元件结合蛋白、小眼畸形相关转录因子（MITF）、酪氨酸酶和酪氨酸酶相关蛋白-1（TRP-1）的表达。K36E激活蛋白激酶B（AKT）和糖原合酶激酶3β（GSK3β）的磷酸化，导致MITF转录活性受到抑制。K36E减弱α-MSH诱导的cAMP通路，导致色素减退。

结论

K36E通过降低包括p-CREB、p-AKT、p-GSK3β、酪氨酸酶和TRP-1在内的下游蛋白的表达来调节黑色素合成，并激活转录因子MITF。K36E可能有开发成为皮肤美白剂的潜力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e877/5259883/9e58d022a1d6/12906_2016_1554_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e877/5259883/6bdd1be1378f/12906_2016_1554_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e877/5259883/4d5b78d9b727/12906_2016_1554_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e877/5259883/c4672beaf71c/12906_2016_1554_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e877/5259883/04bc3b06a0f6/12906_2016_1554_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e877/5259883/9874c8509bd7/12906_2016_1554_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e877/5259883/655934468a32/12906_2016_1554_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e877/5259883/06a3bc41a8cb/12906_2016_1554_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e877/5259883/9e58d022a1d6/12906_2016_1554_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e877/5259883/6bdd1be1378f/12906_2016_1554_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e877/5259883/4d5b78d9b727/12906_2016_1554_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e877/5259883/c4672beaf71c/12906_2016_1554_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e877/5259883/04bc3b06a0f6/12906_2016_1554_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e877/5259883/9874c8509bd7/12906_2016_1554_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e877/5259883/655934468a32/12906_2016_1554_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e877/5259883/06a3bc41a8cb/12906_2016_1554_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e877/5259883/9e58d022a1d6/12906_2016_1554_Fig8_HTML.jpg

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