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水曲柳醇通过 CREB/MITF 信号通路刺激 B16F10 小鼠黑色素瘤细胞中的黑色素生成。

Fraxinol Stimulates Melanogenesis in B16F10 Mouse Melanoma Cells through CREB/MITF Signaling.

机构信息

Division of Applied Life Science (BK21), PMBBRC and Research Institute of Life Sciences, Gyeongsang National University, Jinju 52828, Korea.

Division of Life Science, College of Natural Sciences, Gyeongsang National University, Jinju 52828, Korea.

出版信息

Molecules. 2022 Feb 25;27(5):1549. doi: 10.3390/molecules27051549.

DOI:10.3390/molecules27051549
PMID:35268650
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8911637/
Abstract

Melanin pigment produced in melanocytes plays a protective role against ultraviolet radiation. Selective destruction of melanocytes causes chronic depigmentation conditions such as vitiligo, for which there are very few specific medical treatments. Here, we found that fraxinol, a natural coumarin from plants, effectively stimulated melanogenesis. Treatment of B16-F10 cells with fraxinol increased the melanin content and tyrosinase activity in a concentration-dependent manner without causing cytotoxicity. Additionally, fraxinol enhanced the mRNA expression of melanogenic enzymes such as tyrosinase, tyrosinase-related protein-1, and tyrosinase-related protein-2. Fraxinol also increased the expression of microphthalmia-associated transcription factor at both mRNA and protein levels. Fraxinol upregulated the phosphorylation of cyclic adenosine monophosphate (cAMP) response element-binding protein (CREB). Furthermore, H89, a cAMP-dependent protein kinase A inhibitor, decreased fraxinol-induced CREB phosphorylation and microphthalmia-associated transcription factor expression and significantly attenuated the fraxinol-induced melanin content and intracellular tyrosinase activity. These results suggest that fraxinol enhances melanogenesis via a protein kinase A-mediated mechanism, which may be useful for developing potent melanogenesis stimulators.

摘要

黑素细胞产生的黑色素对紫外线辐射起到保护作用。黑素细胞的选择性破坏会导致慢性色素减退症，如白癜风，目前针对这种疾病几乎没有特定的医学治疗方法。在这里，我们发现，一种来自植物的天然香豆素——秦皮乙素能有效刺激黑色素生成。秦皮乙素处理 B16-F10 细胞能在不产生细胞毒性的情况下，浓度依赖性地增加黑色素含量和酪氨酸酶活性。此外，秦皮乙素还能增强黑色素生成酶如酪氨酸酶、酪氨酸酶相关蛋白-1 和酪氨酸酶相关蛋白-2 的 mRNA 表达。秦皮乙素还能在 mRNA 和蛋白水平上增加小眼畸形相关转录因子的表达。秦皮乙素能上调环腺苷酸反应元件结合蛋白（CREB）的磷酸化。此外，cAMP 依赖性蛋白激酶 A 抑制剂 H89 能降低秦皮乙素诱导的 CREB 磷酸化和小眼畸形相关转录因子的表达，并显著减弱秦皮乙素诱导的黑色素含量和细胞内酪氨酸酶活性。这些结果表明，秦皮乙素通过蛋白激酶 A 介导的机制增强黑色素生成，这可能有助于开发有效的黑色素生成刺激剂。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8df1/8911637/8ef52102c45b/molecules-27-01549-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8df1/8911637/27a299aff0c3/molecules-27-01549-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8df1/8911637/f4cdd651ae9e/molecules-27-01549-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8df1/8911637/794be32d0cd3/molecules-27-01549-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8df1/8911637/1445d628bb79/molecules-27-01549-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8df1/8911637/d38bce473170/molecules-27-01549-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8df1/8911637/8ef52102c45b/molecules-27-01549-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8df1/8911637/27a299aff0c3/molecules-27-01549-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8df1/8911637/f4cdd651ae9e/molecules-27-01549-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8df1/8911637/794be32d0cd3/molecules-27-01549-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8df1/8911637/1445d628bb79/molecules-27-01549-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8df1/8911637/d38bce473170/molecules-27-01549-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8df1/8911637/8ef52102c45b/molecules-27-01549-g006.jpg

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