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ORIGINAL RESEARCH article
Front. Endocrinol.
Sec. Clinical Diabetes
Volume 16 - 2025 | doi: 10.3389/fendo.2025.1556310
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Aims: To evaluate the role of hyperoside in ameliorating retinal injury of DR rats and dysfunction of retinal endothelial cells (RECs) in high-glucose. Methods: RECs were cultured in varied groups including high-glucose and different concentrations of hyperoside. The viability, migration and tube formation of RECs, and the expressions of TGF-β1/miR-200b/VEGF in each group were assayed. Meanwhile, Sprague Dawley rats were used for DR modeling and treated by hyperoside. The tissue pathology of rat retina, and the expressions of TGF-β1/miR-200b/VEGF of retinal tissues in each group were tested. 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 normal rats. The expressions of TGF-β1 and VEGF in high-glucose-induced RECs group and DR rats retina were markedly up-regulated, but miR-200b levels were obviously down-regulated. However, hyperoside could significantly inhibit high-glucose-induced over-proliferation, migration and tube formation of RECs, alleviate retinal injury of DR rats, and reverse the expressions of TGF-β1/miR-200b/VEGF in high-glucose-induced RECs and DR rats retina, dose-dependently. Conclusions: Hyperoside could ameliorate DR rats retinal injury and high-glucose-induced RECs dysfunction by regulating TGF-β1/miR-200b/VEGF pathway.
Keywords: Hyperoside, Diabetic Retinopathy, Retinal endothelial cells, TGF-β1, MiR-200b, VEGF
Received: 18 Feb 2025; Accepted: 03 Apr 2025.
Copyright: © 2025 Yu, Wu, Zhou, Wang, Sun, Miao, Ben, Shi, Wan, Li, Wang, Zhou and Zhao. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence:
Yue Zhao, Department of Endocrinology, Affiliated Hospital of Nanjing University of Chinese Medicine, Jiangsu Province Hospital of Chinese Medicine, Nanjing, China
Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.
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