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马来酸依那普利在小鼠皮肤紫外线B诱导皱纹修复过程中对细胞外基质成分的恢复作用。

Recovery of extracellular matrix components by enalapril maleate during the repair process of ultraviolet B-induced wrinkles in mouse skin.

作者信息

Matsuura-Hachiya Yuko, Nakai Yuji, Abe Keiko, Nishiyama Toshio, Arai Koji Y

机构信息

Scleroprotein Research Institute, Faculty of Agriculture, Tokyo University of Agriculture and Technology, Fuchu, Tokyo 183-8509, Japan.

Institute for Food Sciences, Hirosaki University, 2-1-1 Yanagawa, Aomori, 038-0012, Japan.

出版信息

Biochem Biophys Rep. 2015 Sep 21;4:180-186. doi: 10.1016/j.bbrep.2015.09.012. eCollection 2015 Dec.

DOI:10.1016/j.bbrep.2015.09.012
PMID:29124203
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5668924/
Abstract

The renin-angiotensin system is known to be involved in skin remodeling and inflammation. Previously, we reported that ultraviolet B (UVB) irradiation enhanced angiotensin-converting enzyme (ACE) expression and angiotensin II levels in hairless mouse skin, and an ACE inhibitor, enalapril maleate (EM), accelerated repair of UVB-induced wrinkles. In this study, we analyzed gene expression profiles by DNA microarray and protein distribution patterns using an immunofluorescence method to clarify the process of EM-accelerated wrinkle repair in UVB-irradiated hairless mouse skin. In the microarray analysis, we detected EM-induced up-regulation of various extracellular matrix (ECM)-related genes in the UVB-irradiated skin. In the immunofluorescence, we confirmed that type I collagen α1 chain, fibrillin 1, elastin and dystroglycan 1 in the skin decreased after repeated UVB irradiation but staining for these proteins was improved by EM treatment. In addition, ADAMTS2 and MMP-14 also increased in the EM-treated skin. Although the relationship between these molecules and wrinkle formation is not clear yet, our present data suggest that the molecules are involved in the repair of UVB-induced wrinkles.

摘要

已知肾素-血管紧张素系统参与皮肤重塑和炎症反应。此前,我们报道过紫外线B(UVB)照射可增强无毛小鼠皮肤中血管紧张素转换酶(ACE)的表达及血管紧张素II水平,而一种ACE抑制剂马来酸依那普利(EM)可加速UVB诱导皱纹的修复。在本研究中,我们通过DNA微阵列分析基因表达谱,并采用免疫荧光法分析蛋白质分布模式,以阐明EM加速UVB照射的无毛小鼠皮肤皱纹修复的过程。在微阵列分析中,我们检测到EM可诱导UVB照射皮肤中各种细胞外基质(ECM)相关基因上调。在免疫荧光实验中,我们证实反复UVB照射后皮肤中的I型胶原α1链、原纤蛋白1、弹性蛋白和抗肌萎缩蛋白聚糖1减少,但EM处理可改善这些蛋白质的染色情况。此外,ADAMTS2和MMP-14在EM处理的皮肤中也有所增加。尽管这些分子与皱纹形成之间的关系尚不清楚,但我们目前的数据表明这些分子参与了UVB诱导皱纹的修复。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0457/5668924/cf9d259b42da/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0457/5668924/15514b27f689/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0457/5668924/cf9d259b42da/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0457/5668924/15514b27f689/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0457/5668924/cf9d259b42da/gr2.jpg

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