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莫林通过激活 B16F10 小鼠黑素瘤细胞中的 MAPK 信号通路诱导黑色素生成。

Morin Induces Melanogenesis via Activation of MAPK Signaling Pathways in B16F10 Mouse Melanoma Cells.

机构信息

Department of Pharmaceutical Engineering, Dongshin University, 185 gunjae-ro Naju, Jeonnam 58245, Korea.

出版信息

Molecules. 2021 Apr 8;26(8):2150. doi: 10.3390/molecules26082150.

DOI:10.3390/molecules26082150
PMID:33917985
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8068350/
Abstract

Morin is a well-known flavonoid, and has been reported to have various properties, such as anti-cell death, antioxidant, and anti-inflammatory properties. Although studies on the biochemical and biological actions of morin have been reported, the melanin biosynthesis effects and molecular mechanisms are unknown. In this study, we first found that morin has the effect of enhancing melanin biosynthesis in B16F10 mouse melanoma cells, and analyzed the molecular mechanism. In this study, we examined the effects of morin on the melanin contents and tyrosinase activity, as well as the protein expression levels of the melanogenic enzymes TRP-1, TRP-2, and microphtalmia-associated transcription factor (MITF) in B16F10 mouse melanoma cells. Morin showed no cytotoxicity in the concentration range of 5-100 μM, and significantly increased the intracellular tyrosinase activity and melanin contents. In mechanism analysis, morin increased the protein expression of TRP-1, TRP-2, and MITF associated with melanogenesis. Furthermore, morin increased phosphorylated ERK and p38 at the early time, and decreased phosphorylated ERK after 12 h. The results suggest that morin enhances melanin synthesis through the MAPK signaling pathways in B16F10 mouse melanoma cells.

摘要

莫林是一种众所周知的类黄酮,据报道具有多种特性,如抗细胞死亡、抗氧化和抗炎特性。尽管已经报道了关于莫林的生化和生物学作用的研究,但黑色素生物合成的作用和分子机制尚不清楚。在本研究中,我们首先发现莫林具有增强 B16F10 小鼠黑色素瘤细胞中黑色素生物合成的作用,并分析了其分子机制。在本研究中,我们检测了莫林对 B16F10 小鼠黑色素瘤细胞中黑色素含量和酪氨酸酶活性以及黑色素生成酶 TRP-1、TRP-2 和小眼畸形相关转录因子(MITF)的蛋白表达水平的影响。莫林在 5-100 μM 的浓度范围内没有细胞毒性,并且显著增加了细胞内酪氨酸酶活性和黑色素含量。在机制分析中,莫林增加了与黑色素生成相关的 TRP-1、TRP-2 和 MITF 的蛋白表达。此外,莫林在早期增加了磷酸化 ERK 和 p38 的表达,而在 12 小时后降低了磷酸化 ERK 的表达。结果表明,莫林通过 MAPK 信号通路增强了 B16F10 小鼠黑色素瘤细胞中的黑色素合成。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2687/8068350/8eee49710926/molecules-26-02150-g007.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2687/8068350/ff3d0a4a4587/molecules-26-02150-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2687/8068350/e61bf36cb9f3/molecules-26-02150-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2687/8068350/8eee49710926/molecules-26-02150-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2687/8068350/74c5c4e30700/molecules-26-02150-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2687/8068350/87664dda2a8f/molecules-26-02150-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2687/8068350/4d8a0805a17e/molecules-26-02150-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2687/8068350/fc17510d1f7e/molecules-26-02150-g004.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2687/8068350/8eee49710926/molecules-26-02150-g007.jpg

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