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没食子酸表没食子儿茶素酯修饰胶原膜的评价及对许旺细胞的影响。

Evaluation of Epigallocatechin-3-gallate Modified Collagen Membrane and Concerns on Schwann Cells.

机构信息

State Key Laboratory of Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu 610041, China.

China-Japan Friendship Hospital, Department of Stomatology, Beijing 100029, China.

出版信息

Biomed Res Int. 2017;2017:9641801. doi: 10.1155/2017/9641801. Epub 2017 Aug 15.

DOI:10.1155/2017/9641801
PMID:28894753
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5574217/
Abstract

Collagen is an essential component of the extracellular matrix (ECM) and is a suitable material for nerve repair during tissue remodeling for fracture repair. Epigallocatechin-3-gallate (EGCG), an extract of green tea, shows various biological activities that are beneficial to nerve repair. Here, we developed modified collagen containing different concentrations of EGCG (0.0064%, 0.064%, and 0.64%, resp.) to induce Schwann cell proliferation and differentiation. Cell Counting Kit-8 test, live/dead assay, and SEM showed that collagen cross-linked by EGCG induced Schwann cell proliferation. Real-time polymerase chain reaction, enzyme-linked immunosorbent assay, and Western blotting revealed that EGCG-modified collagen induced Schwann cell differentiation and downregulated reactive oxygen species (ROS) levels by downregulating the MAPK P38 signaling pathway. Our results indicate that collagen cross-linked with an appropriate concentration of EGCG induces the proliferation and differentiation of Schwann cells. The EGCG-modified collagen membrane may be applicable for nerve repair and guided tissue regeneration applications.

摘要

胶原蛋白是细胞外基质(ECM)的重要组成部分,是组织重塑过程中修复骨折时神经修复的合适材料。表没食子儿茶素没食子酸酯(EGCG)是绿茶的提取物,具有多种有益于神经修复的生物活性。在这里,我们开发了含有不同浓度 EGCG(分别为 0.0064%、0.064%和 0.64%)的改性胶原蛋白,以诱导雪旺细胞增殖和分化。细胞计数试剂盒-8 测试、活/死检测和 SEM 表明,EGCG 交联的胶原蛋白诱导雪旺细胞增殖。实时聚合酶链反应、酶联免疫吸附测定和 Western blot 显示,EGCG 改性胶原蛋白通过下调 MAPK P38 信号通路诱导雪旺细胞分化并降低活性氧(ROS)水平。我们的结果表明,适当浓度的 EGCG 交联的胶原蛋白诱导雪旺细胞的增殖和分化。EGCG 改性胶原膜可能适用于神经修复和引导组织再生应用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/107b/5574217/24dbb32948e6/BMRI2017-9641801.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/107b/5574217/a3a9f495a302/BMRI2017-9641801.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/107b/5574217/1c15425c3706/BMRI2017-9641801.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/107b/5574217/d7234909f2a8/BMRI2017-9641801.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/107b/5574217/24dbb32948e6/BMRI2017-9641801.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/107b/5574217/a3a9f495a302/BMRI2017-9641801.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/107b/5574217/1c15425c3706/BMRI2017-9641801.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/107b/5574217/d7234909f2a8/BMRI2017-9641801.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/107b/5574217/24dbb32948e6/BMRI2017-9641801.004.jpg

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