Year: 2025
Type: article
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.
Source: Frontiers in Endocrinology
Authors: Xu Yu, Hao Wu, Lei Zhou, Gaoxiang Wang, Xinyi Sun, Junjun Miao, Meijie Ben, Rongwei Shi, Shimei Wan, Shasha Li, Xiaoci Wang, Xiqiao Zhou, Yue Zhao
Institution: Nanjing University of Chinese Medicine
Language: English
Subfield: Ophthalmology
Field: Medicine
Domain: Health Sciences
Open Access status: gold
Estimated APC paid: $3,801
Funder: Government of Jiangsu Province
OpenAlex ID: W4410039513
