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广谱防晒霜可抑制 UVA 激活的基质金属蛋白酶 1、3 和 9 的合成。

UVA-activated synthesis of metalloproteinases 1, 3 and 9 is prevented by a broad-spectrum sunscreen.

机构信息

Institut National de la Santé et de la Recherche Médicale, CHU Purpan, Toulouse, France.

出版信息

Photodermatol Photoimmunol Photomed. 2011 Dec;27(6):318-24. doi: 10.1111/j.1600-0781.2011.00627.x.

DOI:10.1111/j.1600-0781.2011.00627.x
PMID:22092736
Abstract

BACKGROUND

Specific sunscreens against ultraviolet (UV) A and B radiations are essential to prevent matrix degradation and the activation of intracellular signaling pathways involved in photoaging and photocarcinogenesis. Matrix degradation results from UVA-induced production of matrix metalloproteinases (MMP) and activation of intracellular pathways in fibroblasts and keratinocytes. In particular, in keratinocytes, UVA radiation induces β-catenin nuclear translocation and stimulates MMP gene transcription. Our study was aimed at assessing the efficacy of a specific broad-spectrum sunscreen in preventing β-catenin translocation and MMPs enhanced expression in cultured keratinocytes after UVA irradiation.

METHODS

Sunscreen or the vehicle was spread on quartz sheet. Irradiation of HaCaT cells with 6 J/cm(2) UVA was performed through the sheet, and cells were collected for β-catenin immunostaining then visualization by confocal microscopy, and quantitative real-time polymerase chain reaction analysis of MMP-1, -3 and -9 gene expression.

RESULTS

As shown by immunostaining and confocal microscopy, the sunscreen abrogated UVA-induced beta-catenin translocation to the nucleus, in comparison with control groups. MMP-1, -3 and -9 mRNA expression was enhanced by 7, 7 and 4 folds (P < 0.0001, P < 0.001 and P < 0.01, respectively) in unprotected UVA-irradiated cells compared to the non-irradiated control. Sunscreen protection of the cells significantly reduced UVA-induced expression of MMP-1, -3 and -9 by 83% (P < 0.01), 80% (P < 0.01) and 65% (P < 0.05), respectively.

CONCLUSION

This study demonstrated the efficacy of this broad-spectrum sunscreen in preventing UVA-induced effects on the markers of photoaging and photocarcinogenesis in vitro. It was able to protect HaCaT keratinocytes from UVA-induced β-catenin translocation to the nucleus and MMPs expression.

摘要

背景

针对紫外线 (UV) A 和 B 辐射的特定防晒霜对于预防基质降解以及细胞内信号通路的激活至关重要,这些信号通路与光老化和光致癌作用有关。基质降解是由 UVA 诱导的基质金属蛋白酶 (MMP) 的产生以及成纤维细胞和角质细胞内途径的激活引起的。特别是在角质细胞中,UVA 辐射会诱导β-连环蛋白核转位,并刺激 MMP 基因转录。我们的研究旨在评估特定广谱防晒霜在预防 UVA 照射后培养角质细胞中β-连环蛋白易位和 MMP 表达增强方面的功效。

方法

将防晒霜或载体涂抹在石英片上。通过该片对 HaCaT 细胞进行 6 J/cm2 的 UVA 照射,然后收集细胞进行β-连环蛋白免疫染色,通过共聚焦显微镜观察,并进行 MMP-1、-3 和 -9 基因表达的实时定量聚合酶链反应分析。

结果

与对照组相比,免疫染色和共聚焦显微镜显示,防晒霜可阻断 UVA 诱导的β-连环蛋白向核内易位。与非照射对照相比,未受保护的 UVA 照射细胞中 MMP-1、-3 和 -9 的 mRNA 表达分别增强了 7、7 和 4 倍(P < 0.0001、P < 0.001 和 P < 0.01)。细胞的防晒霜保护显著降低了 UVA 诱导的 MMP-1、-3 和 -9 表达 83%(P < 0.01)、80%(P < 0.01)和 65%(P < 0.05)。

结论

本研究证明了这种广谱防晒霜在预防体外光老化和光致癌作用的标志物方面的功效。它能够保护 HaCaT 角质细胞免受 UVA 诱导的β-连环蛋白核转位和 MMP 表达。

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