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发酵鱼胶原蛋白通过减少 UV 诱导的氧化应激来减弱黑色素生成。

Fermented Fish Collagen Attenuates Melanogenesis via Decreasing UV-Induced Oxidative Stress.

机构信息

Department of Anatomy & Cell Biology, College of Medicine, Gachon University, Incheon 21936, Republic of Korea.

LIBON Inc., Incheon 22006, Republic of Korea.

出版信息

Mar Drugs. 2024 Sep 15;22(9):421. doi: 10.3390/md22090421.

DOI:10.3390/md22090421
PMID:39330302
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11433465/
Abstract

Excessive melanogenesis leads to hyperpigmentation-related cosmetic problems. UV exposure increases oxidative stress, which promotes melanogenesis-related signal pathways such as the PKA, microphthalmia-associated transcription factor (MITF), tyrosinase (TYR), tyrosinase-related protein-1 (TRP1), and tyrosinase-related protein-2 (TRP2) pathways. Glycine is a source of endogenous antioxidants, including glutathione. Fermented fish collagen (FC) contains glycine; thus, we evaluated the effect of FC on decreasing melanogenesis via decreasing oxidative stress. The glycine receptor (GlyR) and glycine transporter-1 (GlyT1) levels were decreased in UV-irradiated keratinocytes; however, the expression levels of these proteins increased upon treatment with FC. The FC decreased oxidative stress, as indicated by the decreasing expression of NOX1/2/4, increased expression of GSH/GSSG, increased SOD activity, and decreased 8-OHdG expression in UV-irradiated keratinocytes. Administration of conditioned media from FC-treated keratinocytes to melanocytes led to decreased p38, PKC, MITF, TRP1, and TRP2 expression. These changes induced by the FC were also observed in UV-irradiated animal skin. FC treatment increased the expression of GlyR and GlyT, which was accompanied by decreased oxidative stress in the UV-irradiated skin. Moreover, the FC negatively regulated the melanogenesis signaling pathways, leading to decreased melanin content in the UV-irradiated skin. In conclusion, FC decreased UV-induced oxidative stress and melanogenesis in melanocytes and animal skin. FC could be used in the treatment of UV-induced hyperpigmentation problems.

摘要

过量的黑色素生成会导致与色素沉着相关的美容问题。紫外线照射会增加氧化应激，从而促进黑色素生成相关的信号通路，如蛋白激酶 A（PKA）、小眼畸形相关转录因子（MITF）、酪氨酸酶（TYR）、酪氨酸酶相关蛋白-1（TRP1）和酪氨酸酶相关蛋白-2（TRP2）通路。甘氨酸是内源性抗氧化剂的来源，包括谷胱甘肽。发酵鱼胶原蛋白（FC）含有甘氨酸；因此，我们评估了 FC 通过减少氧化应激来减少黑色素生成的效果。UV 照射的角质细胞中甘氨酸受体（GlyR）和甘氨酸转运蛋白-1（GlyT1）的表达水平降低，但用 FC 处理后这些蛋白的表达水平增加。FC 降低了氧化应激，这表现在 NOX1/2/4 的表达减少、GSH/GSSG 的表达增加、SOD 活性增加和 8-OHdG 表达减少。用 FC 处理的角质细胞条件培养基处理黑素细胞会导致 p38、PKC、MITF、TRP1 和 TRP2 的表达减少。在 UV 照射的动物皮肤中也观察到了由 FC 引起的这些变化。FC 处理增加了 GlyR 和 GlyT 的表达，同时伴随着 UV 照射皮肤中氧化应激的减少。此外，FC 负调控黑色素生成信号通路，导致 UV 照射皮肤中黑色素含量减少。总之，FC 减少了黑素细胞和动物皮肤中 UV 诱导的氧化应激和黑色素生成。FC 可用于治疗 UV 诱导的色素沉着问题。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7ba1/11433465/8c9fce5b7c80/marinedrugs-22-00421-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7ba1/11433465/69fe903dc5a0/marinedrugs-22-00421-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7ba1/11433465/912f668e0c93/marinedrugs-22-00421-g002a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7ba1/11433465/fa9864e337f3/marinedrugs-22-00421-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7ba1/11433465/8c9fce5b7c80/marinedrugs-22-00421-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7ba1/11433465/69fe903dc5a0/marinedrugs-22-00421-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7ba1/11433465/912f668e0c93/marinedrugs-22-00421-g002a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7ba1/11433465/fa9864e337f3/marinedrugs-22-00421-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7ba1/11433465/8c9fce5b7c80/marinedrugs-22-00421-g004.jpg

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