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叉头框蛋白抑制剂-6 抑制大鼠碱烧伤后角膜新生血管形成及随后的纤维化。

Forkhead Domain Inhibitor-6 Suppresses Corneal Neovascularization and Subsequent Fibrosis After Alkali Burn in Rats.

机构信息

The First Affiliated Hospital of Fujian Medical University, Fuzhou, Fujian, China.

Sichuan Provincial Key Laboratory for Human Disease Gene Study, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chengdu, Sichuan, China.

出版信息

Invest Ophthalmol Vis Sci. 2022 Apr 1;63(4):14. doi: 10.1167/iovs.63.4.14.

DOI:10.1167/iovs.63.4.14
PMID:35446346
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9034725/
Abstract

PURPOSE

The purpose of this study was to investigate the effects of Forkhead Domain Inhibitor-6 (FDI-6) on regulating inflammatory corneal angiogenesis and subsequent fibrosis induced by alkali burn.

METHODS

A corneal alkali burn model was established in Sprague Dawley rats using NaOH and the rat eyes were topically treated with FDI-6 (40 µM) or a control vehicle four times daily for 7 days. Corneal neovascularization, inflammation and epithelial defects were observed on days 1, 4, and 7 under a slit lamp microscope after corneal alkali burn. Analysis of angiogenesis-, inflammation-, and fibrosis-related indicators was conducted on day 7. Murine macrophages (RAW264.7 cells) and mouse retinal microvascular endothelial cells (MRMECs) were used to examine the effects of FDI-6 on inflammatory angiogenesis in vitro.

RESULTS

Topical delivery of FDI-6 significantly attenuated alkali burn-induced corneal inflammation, neovascularization, and fibrosis. FDI-6 suppressed the expression of angiogenic factors (vascular epidermal growth factor, CD31, matrix metalloproteinase-9, and endothelial NO synthase), fibrotic factors (α-smooth muscle actin and fibronectin), and pro-inflammatory factor interleukin-6 in alkali-injured corneas. FDI-6 downregulated the expression of monocyte chemotactic protein-1, pro-inflammatory cytokines (interleukin-1β and tumor necrosis factor-alpha), nucleotide-binding oligomerization domain-like receptor family pyrin domain-containing 3, and vascular endothelial growth factor in RAW264.7 cells and inhibited the proliferation, migration, and tube formation of MRMECs in vitro.

CONCLUSIONS

FDI-6 can attenuate corneal neovascularization, inflammation, and fibrosis in alkali-injured corneas.

摘要

目的

本研究旨在探讨叉头框蛋白抑制剂-6（FDI-6）在调节碱烧伤诱导的炎症性角膜血管生成和随后的纤维化中的作用。

方法

采用 NaOH 建立 Sprague Dawley 大鼠角膜碱烧伤模型，用 FDI-6（40μM）或对照载体每日 4 次局部处理大鼠眼睛，共处理 7 天。角膜碱烧伤后第 1、4、7 天，裂隙灯显微镜下观察角膜新生血管、炎症和上皮缺损情况。第 7 天分析血管生成、炎症和纤维化相关指标。体外实验中，采用小鼠巨噬细胞（RAW264.7 细胞）和小鼠视网膜微血管内皮细胞（MRMECs）研究 FDI-6 对炎症性血管生成的影响。

结果

局部给予 FDI-6 可显著减轻碱烧伤诱导的角膜炎症、新生血管形成和纤维化。FDI-6 抑制了血管生成因子（血管表皮生长因子、CD31、基质金属蛋白酶-9 和内皮型一氧化氮合酶）、纤维化因子（α-平滑肌肌动蛋白和纤维连接蛋白）和促炎因子白细胞介素-6 在碱烧伤角膜中的表达。FDI-6 下调了 RAW264.7 细胞中单核细胞趋化蛋白-1、促炎细胞因子（白细胞介素-1β和肿瘤坏死因子-α）、核苷酸结合寡聚化结构域样受体家族富含亮氨酸重复序列 3 和血管内皮生长因子的表达，并抑制了 MRMECs 的增殖、迁移和管腔形成。

结论

FDI-6 可减轻碱烧伤诱导的角膜新生血管形成、炎症和纤维化。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/76c7/9034725/a5949adcb370/iovs-63-4-14-f006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/76c7/9034725/4c86290d8464/iovs-63-4-14-f001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/76c7/9034725/429cf4172866/iovs-63-4-14-f002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/76c7/9034725/eb440461cdfe/iovs-63-4-14-f003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/76c7/9034725/3f0521f4ba60/iovs-63-4-14-f004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/76c7/9034725/9c7ea59ec15c/iovs-63-4-14-f005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/76c7/9034725/a5949adcb370/iovs-63-4-14-f006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/76c7/9034725/4c86290d8464/iovs-63-4-14-f001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/76c7/9034725/429cf4172866/iovs-63-4-14-f002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/76c7/9034725/eb440461cdfe/iovs-63-4-14-f003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/76c7/9034725/3f0521f4ba60/iovs-63-4-14-f004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/76c7/9034725/9c7ea59ec15c/iovs-63-4-14-f005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/76c7/9034725/a5949adcb370/iovs-63-4-14-f006.jpg

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