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圣塔玛丽娜通过抑制丝裂原活化蛋白激酶/活化蛋白-1（MAPK/AP-1）并刺激转化生长因子-β/信号转导和转录激活因子（TGF-β/Smad）信号通路，在紫外线A（UVA）照射的人皮肤成纤维细胞（HDFs）中显示出抗光老化特性。

Santamarine Shows Anti-Photoaging Properties via Inhibition of MAPK/AP-1 and Stimulation of TGF-β/Smad Signaling in UVA-Irradiated HDFs.

作者信息

Oh Jung Hwan, Kim Junse, Karadeniz Fatih, Kim Hye Ran, Park So Young, Seo Youngwan, Kong Chang-Suk

机构信息

Marine Biotechnology Center for Pharmaceuticals and Foods, College of Medical and Life Sciences, Silla University, Busan 46958, Korea.

Division of Marine Bioscience, Korea Maritime and Ocean University, Busan 49112, Korea.

出版信息

Molecules. 2021 Jun 11;26(12):3585. doi: 10.3390/molecules26123585.

DOI:10.3390/molecules26123585
PMID:34208202
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8230857/
Abstract

Chronic UVA exposure results in elevated reactive oxygen species in skin which leads to photoaging characterized as upregulated matrix metalloproteinase (MMP)-1 and loss of collagen. Therefore, natural antioxidants are hailed as promising agents to be utilized against photoaging. In the current study, reynosin and santamarine, two known sesquiterpene lactones isolated from , were analyzed for their anti-photoaging properties in UVA-irradiated human dermal fibroblasts (HDFs). Results showed that UVA irradiation (8 J/cm) upregulated the MMP-1 secretion and expression, and suppressed collagen production, which were significantly reverted by santamarine treatment (10 µM). Although both reynosin and santamarine exhibited ROS scavenging abilities, reynosin failed to significantly diminish UVA-stimulated MMP-1 release. UVA-irradiated HDFs showed increased collagen production when treated with santamarine. As a mechanism to suppress MMP-1, santamarine significantly suppressed the UVA-induced phosphorylation of p38 and JNK and nuclear translocation of p-c-Fos and p-c-Jun. Santamarine promoted collagen I production via relieving the UVA-induced suppression on TGF-β and its downstream activator Smad2/3 complex. Antioxidant properties of santamarine were also shown to arise from stimulating Nrf2-dependent expression of antioxidant enzymes SOD-1 and HO-1 in UVA-irradiated HDFs. In conclusion, santamarine was found to be a promising natural antioxidant with anti-photoaging properties against UVA-induced damages in HDFs.

摘要

长期暴露于紫外线A会导致皮肤中活性氧水平升高，进而引发光老化，其特征表现为基质金属蛋白酶（MMP）-1上调和胶原蛋白流失。因此，天然抗氧化剂被誉为对抗光老化的有前景的药物。在本研究中，对从[未提及的来源]中分离出的两种已知倍半萜内酯类化合物雷诺辛和圣塔马林在紫外线A照射的人皮肤成纤维细胞（HDFs）中的抗光老化特性进行了分析。结果表明，紫外线A照射（8 J/cm²）上调了MMP-1的分泌和表达，并抑制了胶原蛋白的产生，而圣塔马林（10 μM）处理可显著逆转这些变化。尽管雷诺辛和圣塔马林都表现出清除活性氧的能力，但雷诺辛未能显著减少紫外线A刺激的MMP-1释放。用圣塔马林处理紫外线A照射的HDFs时，胶原蛋白的产生增加。作为抑制MMP-1的一种机制，圣塔马林显著抑制了紫外线A诱导的p38和JNK磷酸化以及p-c-Fos和p-c-Jun的核转位。圣塔马林通过缓解紫外线A诱导的对转化生长因子-β及其下游激活剂Smad2/3复合物的抑制作用来促进I型胶原蛋白的产生。圣塔马林的抗氧化特性还表现为在紫外线A照射的HDFs中刺激Nrf2依赖性抗氧化酶SOD-1和HO-1的表达。总之，发现圣塔马林是一种有前景的天然抗氧化剂，对紫外线A诱导的HDFs损伤具有抗光老化特性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5cfc/8230857/8fce00be235b/molecules-26-03585-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5cfc/8230857/6fc9ce6d1540/molecules-26-03585-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5cfc/8230857/af988bc40867/molecules-26-03585-sch001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5cfc/8230857/720716cd2589/molecules-26-03585-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5cfc/8230857/88467705fbc6/molecules-26-03585-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5cfc/8230857/8c234343a748/molecules-26-03585-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5cfc/8230857/90763e516168/molecules-26-03585-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5cfc/8230857/1880c2c76eea/molecules-26-03585-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5cfc/8230857/a9037a200efd/molecules-26-03585-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5cfc/8230857/8fce00be235b/molecules-26-03585-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5cfc/8230857/6fc9ce6d1540/molecules-26-03585-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5cfc/8230857/af988bc40867/molecules-26-03585-sch001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5cfc/8230857/720716cd2589/molecules-26-03585-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5cfc/8230857/88467705fbc6/molecules-26-03585-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5cfc/8230857/8c234343a748/molecules-26-03585-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5cfc/8230857/90763e516168/molecules-26-03585-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5cfc/8230857/1880c2c76eea/molecules-26-03585-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5cfc/8230857/a9037a200efd/molecules-26-03585-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5cfc/8230857/8fce00be235b/molecules-26-03585-g008.jpg

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