上海交通大学学报（医学版）

上海交通大学学报（医学版） ›› 2019, Vol. 39 ›› Issue (10): 1122-.doi: 10.3969/j.issn.1674-8115.2019.10.004

• 论著·基础研究 • 上一篇    下一篇

增生性瘢痕中血管内皮功能障碍对成纤维细胞功能的影响

奚 箐，郑捷新，王西樵   

  1. 上海交通大学医学院附属瑞金医院灼伤整形科，上海 200025
  • 出版日期:2019-10-28 发布日期:2019-11-22
  • 通讯作者: 王西樵，电子信箱：wxqiao2002@hotmail.com。
  • 作者简介:奚 箐（1969—），女，主治医师，硕士；电子信箱：xj10707@rjh.com.cn。
  • 基金资助:
    国家自然科学基金（30872686，81671914）

Effect of endothelial dysfunction in hypertrophic scars on fibroblasts biology

XI Jing, ZHENG Jie-xin, WANG Xi-qiao   

  1. Burn and Plastic Center, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China
  • Online:2019-10-28 Published:2019-11-22
  • Supported by:
    National Natural Science Foundation of China, 30872686, 81671914

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摘要： 目的·探索增生性瘢痕在演变过程中血管内皮功能障碍对成纤维细胞功能的影响。方法·分离和培养正常皮肤，以及增生期、消退期和成熟期瘢痕的血管内皮细胞，然后收集其培养上清液，加入正常皮肤来源的成纤维细胞中；48 h后收集成纤维细胞，利用Alamar blue测定细胞增殖活性，天狼星红染色测定胶原含量，TUNEL法检测细胞凋亡情况。另外，以血管内皮生长因子（vascular endothelial growth factor，VEGF）抗体、血小板衍生的生长因子（platelet derived growth factor，PDGF）抗体、转化生长因子β1（transforming growth factor-β1，TGF-β1）抗体、内皮素1（endothelin 1，ET-1）抗体和碱性成纤维细胞生长因子（basic fibroblast growth factor，bFGF）抗体中和血管内皮细胞培养液中的相应生长因子，观察对成纤维细胞增殖、凋亡和胶原产生的影响。结果·与对照组相比，消退期瘢痕来源的血管内皮细胞培养液能够显著抑制成纤维细胞的增殖活性和胶原生成，促进细胞凋亡（均Pβ1、PDGF或bFGF后，成纤维细胞增殖和胶原产生被明显抑制（均PP结论·瘢痕中血管内皮功能障碍能够抑制成纤维细胞的增殖和胶原蛋白生成，诱导细胞凋亡，尤其以消退期瘢痕血管内皮细胞作用更为显著；该过程中TGF-β1、PDGF和bFGF可能发挥主要作用。

关键词: 增生性瘢痕, 血管内皮功能障碍, 内皮细胞, 成纤维细胞, 瘢痕消退

Abstract:

Objective · To investigate the effect of endothelial dysfunction in hypertrophic scar regression on the fibroblasts biology. Methods · Scar-derived endothelial cells were isolated and cultured proliferative scars, regressive scars and mature scars, and the endothelial cells normal skin as control. After 6 h of culture, the endothelial cell culture medium (ECCM) was harvested. In addition, the fibroblasts normal skin were cultured and treated with the ECCM. After 48 h, the cell viability, total collagen production, and cell apoptosis were assessedAlamar blue, sirius red staining, and TUNEL assay, respectively. Furthermore, anti-VEGF (vascular endothelial growth factor), anti-PDGF (platelet derived growth factor), anti-TGF-β1 (transforming growth factor-β1), anti-ET-1 (endothelin 1), and anti-bFGF (basic fibroblast growth factor) neutralizing antibodies were individually added to the ECCM to identify their effects on fibroblasts biology. Results · The results revealed that the ECCM regressive scars inhibited fibroblasts viability and collagen production, and induced apoptosis (PPPConclusion · Vascular endothelial dysfunction in hypertrophic scars can inhibit fibroblast proliferation and collagen production, and induce cell apoptosis, especially in regressive scars. TGF-β1, PDGF and bFGF may play a major role in this process.

Key words: hypertrophic scar, endothelial dysfunction, endothelial cell, fibroblast, scar regression

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