Inhibitory effects of ursolic acid on oxygen-induced mouse retinal neovascularization via intravitreal injection.

IF 1.4 3区医学 Q4 BIOCHEMISTRY & MOLECULAR BIOLOGY

Molecular Vision Pub Date : 2025-04-10 eCollection Date: 2025-01-01

Lu Yang, Fen Yang, Weiliang Zhang, Yanhua Wang, Peng Chen, Shufang Du, Xiaoyan Liu, Yan Gao, Junhua Shi, Peng Wang, Rui Li, Qiang Su

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引用次数: 0

Abstract

Objective: This study aimed to explore the effects and mechanisms of ursolic acid (UA) on oxygen-induced retinal neovascularization (RNV) in mice and its inhibitory effects on human retinal capillary endothelial cells (HRCECs) under high-glucose conditions.

Methods: Neonatal mice were divided into five groups: one normal group and four with oxygen-induced retinopathy (OIR), including OIR, phosphate-buffered saline, UA and Lucentis groups. On postnatal day 17 (P17), mice were euthanized and one eye was collected for retinal analysis using fluorescence microscopy. Protein and messenger ribonucleic acid (mRNA) levels of vascular endothelial growth factor (VEGF), matrix metalloproteinase (MMP)-2, MMP-9 and cyclo-oxygenase-2 (COX-2) were detected. HRCECs cultured under high-glucose conditions were treated with UA to assess its effects on proliferation and molecular expression.

Results: UA significantly reduced RNV area in OIR mice and protected astrocytes from hypoxia-induced damage (p<0.01). VEGF, MMP-2, MMP-9 and COX-2 levels were lower in the UA group compared with the OIR and phosphate-buffered saline groups (p<0.05), but slightly higher than in normal controls (p<0.01). Lucentis reduced VEGF levels but did not significantly affect MMP-2, MMP-9 or COX-2. In HRCECs, UA inhibited high-glucose-induced proliferation and reduced VEGF, MMP-2, MMP-9 and COX-2 expression in a time- and dose-dependent manner.

Conclusions: UA inhibits RNV by reducing VEGF, MMP-2, MMP-9 and COX-2 expression, protecting astrocytes and suppressing HRCEC proliferation under high-glucose conditions, highlighting its therapeutic potential for retinal neovascular diseases.

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熊果酸通过玻璃体内注射对氧诱导小鼠视网膜新生血管的抑制作用。

目的：探讨熊果酸（UA）对高糖条件下小鼠氧诱导视网膜新生血管（RNV）的影响及其机制，以及对人视网膜毛细血管内皮细胞（HRCECs）的抑制作用。方法：将新生小鼠分为正常组和氧致视网膜病变（OIR）组，分别为OIR组、磷酸盐缓冲盐水组、UA组和Lucentis组。在出生后第17天（P17），对小鼠实施安乐死，取一只眼荧光显微镜进行视网膜分析。检测血管内皮生长因子（VEGF）、基质金属蛋白酶(MMP)-2、MMP-9、环氧化酶-2 （COX-2）蛋白和信使核糖核酸（mRNA）水平。采用UA处理高糖条件下培养的HRCECs，评估其增殖和分子表达的影响。结论：UA通过降低高糖条件下VEGF、MMP-2、MMP-9和COX-2的表达，保护星形胶质细胞，抑制HRCEC的增殖，从而抑制RNV的表达，显示了其对视网膜新生血管疾病的治疗潜力。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Molecular Vision 生物-生化与分子生物学

CiteScore

4.40

自引率

0.00%

发文量

审稿时长

1 months

期刊介绍： Molecular Vision is a peer-reviewed journal dedicated to the dissemination of research results in molecular biology, cell biology, and the genetics of the visual system (ocular and cortical). Molecular Vision publishes articles presenting original research that has not previously been published and comprehensive articles reviewing the current status of a particular field or topic. Submissions to Molecular Vision are subjected to rigorous peer review. Molecular Vision does NOT publish preprints. For authors, Molecular Vision provides a rapid means of communicating important results. Access to Molecular Vision is free and unrestricted, allowing the widest possible audience for your article. Digital publishing allows you to use color images freely (and without fees). Additionally, you may publish animations, sounds, or other supplementary information that clarifies or supports your article. Each of the authors of an article may also list an electronic mail address (which will be updated upon request) to give interested readers easy access to authors.