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新型海洋营养保健品对 UVB 辐射人黑素细胞来源细胞中 IL-1α 介导的 TNF-α 释放的影响。

Effect of novel marine nutraceuticals on IL-1α-mediated TNF-α release from UVB-irradiated human melanocyte-derived cells.

机构信息

School of Medical Sciences, RMIT University, P.O. Box 71, Bundoora, VIC 3083, Australia.

出版信息

Oxid Med Cell Longev. 2011;2011:728645. doi: 10.1155/2011/728645. Epub 2011 Sep 22.

DOI:10.1155/2011/728645
PMID:21961050
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3179886/
Abstract

UV-induced inflammation and reactive oxygen species formation are involved in the development of melanoma. Natural products like 5β-scymnol and CO(2)-supercritical fluid extract (CO(2)-SFE) of mussel oil contain anti-inflammatory and antioxidant properties that may aid in reducing the deleterious effects of UV radiation. Therefore, their effect on the release of the proinflammatory cytokine, tumour necrosis factor-α (TNF-α), from UVB-irradiated human melanocytic cells was examined. Human epidermal melanocytes (HEM) and MM96L melanoma cells were exposed to UVB radiation and IL-1α. Cell viability and TNF-α levels were determined 24 hours after-irradiation while p38 mitogen-activated protein kinase (MAPK) activation was observed at 15 min after-irradiation. When α-tocopherol, CO(2)-SFE mussel oil, and 5β-scymnol were added to the UVB-irradiated HEM cells treated with IL-1α, TNF-α levels fell by 53%, 65%, and 76%, respectively, while no inhibition was evident in MM96L cells. This effect was not due to inhibition of the intracellular p38 MAPK signalling pathway. These compounds may be useful in preventing inflammation-induced damage to normal melanocytes.

摘要

UV 诱导的炎症和活性氧形成参与了黑色素瘤的发展。像 5β-石竹烯和贻贝油的 CO2 超临界流体提取物(CO2-SFE)这样的天然产物具有抗炎和抗氧化特性,可能有助于减少 UV 辐射的有害影响。因此,研究了它们对 UVB 照射的人黑素细胞中促炎细胞因子肿瘤坏死因子-α(TNF-α)释放的影响。将人表皮黑素细胞(HEM)和 MM96L 黑色素瘤细胞暴露于 UVB 辐射和 IL-1α 下。在照射后 24 小时测定细胞活力和 TNF-α 水平,而在照射后 15 分钟观察到 p38 丝裂原活化蛋白激酶(MAPK)的激活。当 α-生育酚、CO2-SFE 贻贝油和 5β-石竹烯被添加到用 IL-1α 处理的 UVB 照射的 HEM 细胞中时,TNF-α 水平分别下降了 53%、65%和 76%,而 MM96L 细胞中没有明显的抑制作用。这种作用不是由于抑制细胞内 p38 MAPK 信号通路。这些化合物可能有助于预防炎症引起的正常黑素细胞损伤。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/10a6/3179886/6aec688f03d3/OXIMED2011-728645.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/10a6/3179886/290093affe61/OXIMED2011-728645.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/10a6/3179886/d314d05266ae/OXIMED2011-728645.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/10a6/3179886/d158270b471b/OXIMED2011-728645.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/10a6/3179886/6aec688f03d3/OXIMED2011-728645.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/10a6/3179886/290093affe61/OXIMED2011-728645.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/10a6/3179886/d314d05266ae/OXIMED2011-728645.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/10a6/3179886/d158270b471b/OXIMED2011-728645.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/10a6/3179886/6aec688f03d3/OXIMED2011-728645.004.jpg

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