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没食子儿茶素-3-没食子酸酯(EGCG)抑制人眼Tenon 囊成纤维细胞的肌成纤维细胞转化。

Epigallocatechin-3-gallate (EGCG) inhibits myofibroblast transformation of human Tenon's fibroblasts.

机构信息

Department of Ophthalmology, Guangdong Eye Institute, Guangdong Provincial People's Hospital and Guangdong Academy of Medical Sciences. Guangzhou, China; Shantou University Medical College, Shantou, China.

Department of Ophthalmology, Guangdong Eye Institute, Guangdong Provincial People's Hospital and Guangdong Academy of Medical Sciences. Guangzhou, China.

出版信息

Exp Eye Res. 2020 Aug;197:108119. doi: 10.1016/j.exer.2020.108119. Epub 2020 Jun 27.

DOI:10.1016/j.exer.2020.108119
PMID:32603658
Abstract

Myofibroblast transformation of human Tenon's fibroblasts severely challenges the outcome of glaucoma filtration surgery. epigallocatechin-3-gallate (EGCG) is considered as a potential reagent to overcome this issue for its anti-fibrosis effect on various human diseases, but it is unclear on the fibrosis of Tenon's fibroblasts. This study was conducted to investigate the effect of EGCG on TGF-β1-induced myofibroblast transformation of human Tenon's fibroblasts. The human Tenon's fibroblasts were incubated in the medium containing 10 ng/mL TGF-β1, and subsequently treated with EGCG or mitomycin C (MMC). The cell proliferation and migration were analyzed. The expression of alpha-smooth muscle actin (α-SMA), type I collagen (Col-I), and p-Smad2/3 were also evaluated. It showed that EGCG and MMC strongly inhibited the elevation in cell number in tissue explants compared to the tissues treated with TGF-β1 alone. Scratch-Wound assay showed that 48 h after TGF-β1 induction, only 10% of the wound width remained. But cells treated with EGCG still showed over 93% wound width. Further, EGCG effectively inhibited TGF-β1-induced expression of α-SMA and Col-I as well as phosphorylation of Smad2/3 in Tenon's fibroblasts. Altogether, we concluded that EGCG suppressed the myofibroblast transformation in Tenon's fibroblasts through inactivating TGF-β1/Smad signaling. These findings demonstrate that EGCG can be considered as one of the possible antifibrotic reagents for preventing postoperative scarring in glaucoma filtration surgery.

摘要

人眼Tenon 氏纤维成肌纤维细胞的转化严重影响青光眼滤过手术的结果。表没食子儿茶素没食子酸酯(EGCG)因其对各种人类疾病的抗纤维化作用而被认为是克服这一问题的潜在试剂,但它对 Tenon 氏成纤维细胞的纤维化作用尚不清楚。本研究旨在探讨 EGCG 对 TGF-β1 诱导的人眼Tenon 氏成纤维细胞成肌纤维细胞转化的影响。将人眼 Tenon 氏成纤维细胞在含有 10ng/ml TGF-β1 的培养基中孵育,随后用 EGCG 或丝裂霉素 C(MMC)处理。分析细胞增殖和迁移。还评估了α-平滑肌肌动蛋白(α-SMA)、I 型胶原(Col-I)和 p-Smad2/3 的表达。结果表明,与 TGF-β1 单独处理的组织相比,EGCG 和 MMC 强烈抑制组织外植体中细胞数量的增加。划痕实验结果显示,在 TGF-β1 诱导 48 小时后,仅 10%的伤口宽度保持不变。但用 EGCG 处理的细胞仍显示超过 93%的伤口宽度。此外,EGCG 有效抑制了 TGF-β1 诱导的 Tenon 氏成纤维细胞中 α-SMA 和 Col-I 的表达以及 Smad2/3 的磷酸化。总之,我们得出结论,EGCG 通过抑制 TGF-β1/Smad 信号通路抑制了 Tenon 氏成纤维细胞的成肌纤维细胞转化。这些发现表明,EGCG 可被视为预防青光眼滤过手术术后瘢痕形成的潜在抗纤维化试剂之一。

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