ArticleFrontiers in endocrinology2025
Ameliorative effect and potential mechanism of hyperoside on diabetic retinopathy.
Article in Frontiers in endocrinology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed.
- Protopanaxatriol ameliorates diabetic retinopathy by regulating mTOR/G6PD mediated pentose phosphate pathway.Journal of natural medicines · 2026Article
- Anti-diabetic retinopathy molecular mechanism of Dihuang Yinzi: insights from network pharmacology, metabolomics, and microbiome analysis.Frontiers in medicine · 2026Article
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Authors and funding
13 authors.
Funding
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Abstract
Aims: This study aimed to evaluate the role of hyperoside in ameliorating the retinal injury of diabetic retinopathy (DR) rats and the dysfunction of retinal endothelial cells (RECs) in high glucose. Methods: RECs were cultured in various groups including high glucose and different concentrations of hyperoside. The viability, migration, and tube formation of RECs and the expression of transforming growth factor-beta 1 (TGF-β1)/micro-RNA 200b (miR-200b)/vascular endothelial growth factor (VEGF) in each group were assayed. Sprague-Dawley rats were used for DR modeling and were treated with hyperoside. The tissue pathology of the rat retina and the expression of TGF-β1/miR-200b/VEGF in the retinal tissues of each group were examined. Results: Excessive proliferation, migration, and tube formation of RECs were induced by high glucose. The retinal pathological changes and vasculopathy in DR rats were more serious compared with those in normal rats. The expression levels of TGF-β1 and VEGF in the high glucose-induced REC group and in DR rat retina were markedly upregulated, but those of miR-200b were noticeably downregulated. However, hyperoside could significantly inhibit the high glucose-induced overproliferation, migration, and tube formation of RECs, alleviate the retinal injury in DR rats, and reverse the expression of TGF-β1/miR-200b/VEGF in the high glucose-induced REC and DR rat retina, dose-dependently. Conclusions: Hyperoside could ameliorate retinal injury in DR rats and the high glucose-induced dysfunction of RECs by regulating the TGF-β1/miR-200b/VEGF pathway.
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